Kuchera - Osteopathic Considerations in Somatic Dysfunction

Osteopathic Considerations
in Systemic Dysfunction
Revised Second Edition
Michael L. Kuchera, D.O., F. A. A.O
Professor and Chairman
William A. Kuchera, D.O., F.A. A. 0
Professor
Osteopathic Considerations
in Systemic Dysfunction
Michael Kuchera, D.O., F.A.A.O.
William Kuchera, D.O., F .A.A.O.
Greyden Press, LLC
_ Dayton, Ohio
Original Works
Greyden Press, LLC Original Works Books Dayton, Ohio
Osteopathic Considerations in Systemic Dysfunction
Copyright 1994 by Michael & William Kuchera. All rights reserved. Printed in the United States of America.
Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed
in any form or by any means, or stored in a data base retrieval system, without prior written permission of the publisher.
ISBN 1-57074-154-9
Printer/ Binder: Greyden Press, LLC
"Osteopathic physicians must be able to give a reason for the treatment
they give, not so much to the patient, but to themselves.
"1
A.T. Still, M.D.
"The inevitable result of the rapid strides in the study of bacteriology,
and pathologic change in tissues and secretions, nd the comparatively
slow progress which has been made in studying the patient, has been an
undue emphasis of the importance of the disease, and a minimizing of the
importance of the patient who has it. The dawning of a better day in
medicine, however, is now evident ...
"2
F.M. Pottenger, M.D.
"(Neuroscience) studies are establishing the physiological bases for
determination in man of the visceral consequences of spinal syndromes
for which manipulative therapy is advocated.
"3
Horace W. Magoun, Ph.D.
1. Truhlar R Doctor A.T. Still in the Living. Cleveland, privately printed, 1950, P 112.
2. Pottenger FM Symptoms of Visceral Disease. St Louis, CV Mosby Co, 7th ed, 1953, P 34.
3. Magoun H: Neuroscience studies in Goldstein M (ed) The Research Status of Spinal Manipulative Thera, Bethesda
MD, US Department of Health, Education and Welfare (NINCDS Monograph #15), 1975, p 210.
THIS PAGE INTENTIONALLY LEFT BLANK
FORWOR
Osteopathy is relatively a young profession in the history of medicine. Slightly
over 10 years ago, A.T. Still introduced his philosophy of medical care to the
world. The frst schol of osteopathy was established in Krksville, Missouri in
1892. It was in this sme time period that the germ theory was proposed and
eventually the allopathic profession adopted the prsptive that this was "the
answer to all dises proesses." With the discovery of Salversn and
eventually penicillin, the allopathic profession launched into an all-out effort to
fnd medicines which would be the "magic bullets." The germ theory of disese
promoted the concept that health would be restored and secure if the offending
"germ" was found and medically removed.
Because of this majority prspective there are thousands of articles and texts
reporting experiences and trials in the use of medications for the treatment of
systemic diseses. On the other hand there is relatively little published about
augmenting homestasis or treting host factors in systemic diseases. This text
was written to augment the latter category and stresses the structure and function
that are pertinent t this prspctive. Without specifc knowledge of anatomy
and physiology, the osteopathic approach would become to "time consuming"
and would not be fnancially fesible to offer a patient with systemic disese.
Osteopathic physicians are educated to use and understand all current
medications and surgica proedures for the purpose of promoting health,
fghting the disease and supporting the host's physiology. Palpatory and
manipulative skills c be used effectively a well as effciently to aid in
diagnosis and tretment of patients with systemic disese or dysfunction.
This text has ben divided into sverl sections in order to present an
osteopathic approach to dysfunction manifesting in a particular system or
prtinent to a common clinical presentation. These divisions have been
primarily group by their common autonomic and lymphatic elements but the
physician must not b limited to management of the patient within a given
system (or section of this text). Because ech patient is a unit, dysfunction or
disease affecting one part can have far-reching manifestations.
This text does not propse to replace the many reference texts of medicine ad
dos not include a complete differential diagnosis or a complete tretment plan
for the clinical situations that are discussed. Its purpse is to explore selected
structural and functional considerations which may prouce symptoms or
iv
compromise homeostasis. It also demonstrates, by example, clinical application
of the osteopathic philosophy in selected situations. Lstly, it attempts to show
where osteopathic manipulative tretments c be prescribed as primary or
adjunctive modalities available to the D. O. as they assist patients in reching
their maximum health potential.
Even if the patient dos not have specifc joint somatic dysfunction,
manipulative management c be designed to address the following goals:
o .. support the patient's body systems that will be stressed by the
pathophysiology of the disese
o .. support the patient's natural protective and homeostatic rections to disese
o .. neutralize detrimental responses of the patient's body to the disease process
o .. provide a synergistic and physiologic approach to the patient's medical
and/or surgical management
o .. provide a rpid and long-lasting beneft toward improving the patient's level
of health and immediate comfort
Dysfunction of the soma and its related elements plays a signifcant role in the
prouction of a variety of patient complaints, signs, and/or symptoms and
frequently accompanies underlying visceral dysfunction. For these reasons,
palpation for somatic dysfunction is an imprtant part of an osteopathic
approach to making a differential diagnosis ad it provides essntial data for
developing a rational total tretment progrm for the patient. Becaus
osteopathic manipulative tretment is designed to tret the patient's soma and/or
to support systemic protetive and homeostatic mechanisms, a therapeutic trial
of manipulation which addresses the patient's somatic component is an
imprtant par of a rational treatment protool for ech patient's visit.
By studying anatomy and physiology from the philosophical vantage point
need to formulate "rational ostepathic tretment," the osteopathic student
discovers a unique and valuable prspctive of helth and disese.
Interrettion of somatic clues through understanding of the physiology
underlying symptom development allows the physician to surmise the
dysfnction or pathophysiology ocurring in a given individual patient and
offers valuable direction and information for the physical examination and the
differential diagnosis. Rather than simply diagnosing and treting symptoms or
symptom complexes, the osteopathic physician sk to augment the health that
is found within the individual.
v
The following relevant comments are found in Pottenger's Symptoms of
Visceral Disease
!
:
"Variability of symptoms is the rule in clinical medicine, a fact which
can be readily appreciated by understanding the nere and chemical
control of physiologic function and the factors which infuence them,
both physical and psychic. "
"It is not only necessy to understnd that symptoms produced by a
given disse may differ in different individuals and in the sme
individual at different times, but it is equally necessary to bear in mind
that while the stimulus which would be expcted to produce a given
symptom is present, the symptom may not appear or its reverse may
appear if the stimulus to the nere is excessive, or the neuron itself is
hyperexcitable or a certain ionic concentration exists in the body cells.
It is necessary, therefore, always to ber in mind that infammation in
organs gives origin to stimuli which have a tendency to produce such and
such symptoms, although the symptoms themselves may not
materialize. "
"Most of the imprtant symptoms arising from diseses of interal
viscera are refex in nature. In order to understad these symptoms, one
must study the innervation of the various viscera and the
interrelationship which exists between them, also the interrelationship
which exists between the viscera and the skeletal structures. "
This text encourages the reder to reexamine familiar medical facts, anatomic
relationships and physiologic functions from the osteopathic perspective. This
prsptive can then be carried into the diagnostic and therapeutic decisions
which will repatedly b required of the medical student and the osteopathic
physician for the rest of their professional lives.
1. Pottenger FM Symptoms of Visceral Disease. St Louis, CV Mosby Co,
7th ed, 1953, 140.
vi
TABLE OF CONTENTS
1 J1C1I( ........... 1
Introuction . . . . . . . . . . .. .. . . ... ... . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . .. . . . . . . . . . .. . . . . . . . . ... .. .. . 1
Pathophysiology . .. ... .. . . . . .. . . . . . . . . . . .. . . . . . . . . . . . .. . . . . . .. . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . 2
Refex Connections . . . . . . ... . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . .. . . . . . . 2
Sympathetics . . . . . . . . . . . .... . . . . . . . . . .... . . . . . . . . . . . .. . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Parasympathetics . . . . . . . . . . . .. . .. . . . . . . . . . . . . . . .. . . . .. . .. . . . . . . . . . . . . . . . . . . . . .. . . . . . . 4
Venous And Lymphatic Systems . . . . .. . . . . . . . . .. . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Neur System . . . .. .. . . . . . . . . . . . . . . ... . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . 6
Somatic System . . . . . . . . . . . .. . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . .. . .. . . . . . . . . . . . . . . .. . . . . . . 8
Tretment .. .. . . . . . . . . . .. . . . .. . .. . . . . . .. . . . .. . . . . . ... . .. . . . . . . . . . . . . . .... . . .. . . . . . . . . . . ... . .. 12
The Eye . . . . . .. .. . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. .... .. . . . . 13
The Er . ... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . .. . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 14
The Nos . . . . . . . .... . .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . .. . . . . . . . . . . . . . . . .. 16
The Throat. . . . . ... . . . . . . ... .. .. . . . . . . . . . . . . .. . . . . . . . . . .. . .. . . . . . . . ... . . . . . . . . . . . . . . .. 17
The ENT Unit .. ... . . .. .. . . . . . . . . . . . . . .. .. . . . . . . . . . . . . . . . . . . ... . . . . . . . . . . . . . . .. . . . .. 17
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
Additional EENT Bibliography .......................................................... 19
References .................................................................................. 19
1I <(( <( .................................................................... 23
Introuction ................................................................................ 23
Pathophysiology ........................................................................... 24
Tretment ................................................................................... 25
Summary .................................................................................... 29
References .................................................................................. 30
WWE RPI TORY DISORDERS .................................................. 33
Normal Functional Respiration .......................................................... 33
Pathophysiology . . . . . . . . . . .. . . . . . .. . . . .. . . . .... . . . .. . .. . . .. . . . . . . . . . .. . . .. . . . . . . . . . . . . . . .. . 36
Refex Action During Infection . . . . . . . . . . . . .. . . . . . . .. . . . . . . . . . . . . . .. . ... . .. . .. . . . 36
Sympathetics . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . 36
Parasympathetics ................................................................... 38
Somatic System ..................................................................... 38
Lymphatics .......................................................................... 39
vii
Tretment .......................................................... ......................... 40
Pneumonia ..... . ........... .......... ......... . . . ......... . ...... . .......... . . ....... 40
Sample of Tretment Protool For Pneumonia .. . ...................... 45
Prevention of Postoprative Pulmonary Complications ....................... 46
Chronic Obstructive Pulmonary Dises ............ . ........................... 48
Asthma ....................... ............................ ............ . . . . ............ 48
Summary .................................................................................... 51
References .................................................................................. 51
CARDIOVASCUAR DISORDERS ........................................................ 53
Introduction ................................................................................ 53
Pathophysiology ........................................................................... 53
Sympathetics ..................................... ................................... 53
Parasympathetics ......................... .. ........................................ 55
Lymphatics ............................. . .. ........... ............................... 56
Somatic system .................................... . .......... . ............... ...... 57
Referred Patters ......................................... . ................ . .. . . ... . 58
Treatment Summary ................................................................ . ... . . 59
Myoardial Infarction . .................... ........................ . . ............... 59
Essential Hyprtension ........................................ . .................... 61
Congestive Heart Failure ........................ . . ............... .. ............... 66
Arrhythmias ......................................................................... 67
Clinically Relevant Abstracts--Bibliography .................................... . ...... 68
Autonomic Nerous System ........................................... ........... 68
Lymphatics ..... .. .......... . ........................................................ 70
Text References ...................... . ......................................... ............ 73
Additional Cardiac References ..................... . . .. ............................. . . . . 76
UPPER GI DISORDERS ...................................................................... 79
Introduction ........... . ............ ... . . ...................... . ............... . .. . . . . . . . . .. 79
Pathophysiology ........................................................... . ............... 79
Viscerosensory And Visceromotor .......................................... . .... 79
Sympathetics ................................................................ . ... . ... 83
Parasympathetics ................. . ................................................. 84
Lymphatics . . .......................................... .............................. 85
Somatic System .................................. ........................ ........... 86
The Philosophy of Tretment ............................... ........... .. . ............... 87
Osteopathic Tretment ..... ................................... . ............... . ........... 89
Lymphatics And Fascias ................................... ........................ 89
Sympathetics ............................................................... . ........ 90
Parasympathetics ................................................................... 92
Summary ...................................... . ........ ... . . ..... .... . .............. . ....... 93
References .......... ........................................................................ 93
viii
WWER BOWEL DISORDERS ............................................................. 95
Introduction ............................................................................ .... 95
Pathophysiology ..................................... .................. .................... 96
Sympathetics ........................................................................ 96
Parasympathetics ................................................................ ... 97
Lymphatics .......................................................................... 98
Viscerosensory And Visceromotor ............................................. 10
Somatic ............................................................................ 100
Osteopathic Manipulative Tretment ................................................. 101
Sympathetic Dominant Complaints............................................ 104
Parasympathetic Dominant Complaints ............................. .......... 104
Other Complaints ................................................................. 105
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106
References. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 106
ITABLE BOWEL SYNDROM...................................................... 109
Introduction .............................................................................. 109
Physiology..... . ................ .. . . . ...... . . . . . . .. . ......... . . . . . . .... .. . . .. . .. .. . ....... 111
Intrinsic Nere Control.......................................................... 111
Extrinsic Nere Control ......................................................... 112
Sympathetic Innervation......................................................... 112
Parasympathetic Innervation .................................................... 112
Characteristics ........................................................................... 113
Tretment Considerations .............................................................. 116
Pharmacologic Tretment ....................................................... 116
Osteopathic Manipulative Treatment ................................................. 117
Affecting The Somatic Compnent............................................ 118
Affeting Sympathetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 118
Affecting Parasympathetics ..................................................... 119
Affecting The Lymphatic System .............................................. 120
Summary .................................................................................. 121
References.. .. .. . . .. .. ....... . .. . . . . . . . .. . . .. . .. ... .. ........ .. . . . . ...... . . ........ 122
GENITO'ARY TACT DISORDERS ............................................. 123
Introduction .............................................................................. 123
Kidneys, Ureters And Bladder ......................................................... 124
Sympathetics ...................................................................... 125
Parasympathetics ................................................................. 126
Lymphatics ........................................................................ 127
Viscerosensory/Visceromotor Refexes ...... ..... ..... ....................... 127
Somatic System................................................................... 127
ix
Genital/Reprouctive System .......................................................... 129
Sympathetics And Parasympathetics ........................................... 129
Lymphatics ............... ....................................... . .. . . . ... . .... ... . 130
Viscerosnsory And Visceromotor ............................................. 131
Somatic S
y
stem................................................................... 132
Tretment Conslderations ....... ......... . ..... .. . . .. . . ... . . .. . .. .. . . .. . ..... . .... ..... 133
Urnary Tract Infections ......................................................... 134
Renal Dis..................................................................... 135
Prostatitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 136
Ureterolithiasis ................................................................. '" 137
Dysmenorrhe .............. .... . . . ..... . .. ..... .. ..... ...... .... ................. 139
Sexual Dysfunction ............................................................... 142
Eretile Dysfunction ... ... ..................... ........................... 142
Premature Ejaculation .................................................... 143
Dyspareunia ................................................................ 143
Infertility ................................................................... 144
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
TIE OBSTETRCAL PATIT .......................................................... 149
Existing Stresses Aggravated By Pregnancy ......... ..... . ... ..... ... . . .. . . . ... ..... 149
Gravity ............................................................................. 149
A Basic Physiological Relationship .................. ............ ...... . .. ..... 149
The Unique Valveless Venous System ........................................ 150
Stresses Added Speifcally By Pregnancy .......................................... 151
Mechanical ..... . . ................................................... ... . . .... . .... 151
Physiological.. . ... ... . . . . ....... . . ... . . .. . . .... . . . . . . .. . . . . . ... . . . . . . ... . . ... . . . .. 151
Lymphatic ................... ....................... .... .. ........ . . . . . .... ... ..... 151
Venous ............................................................................. 152
Hormonal.... . . . ........ . . . . . . . .. ..... . . . . . .. .. ... . . ... . . . ... . . . .. ... . . . .... . .. . . .. 152
Relative Contraindications to OMT................................................... 152
Distinctive Ostepathic Thinkng ..................................... .... .. ... . .... .. 152
An Aid in Preventative Care ...... ............... . ...................... ........ 153
A Diagnostic Aid....................................... . . . . . ... . . . . . . . .. . .. .. . . .. 153
A Tretment Advantage......................................................... 153
Distinctive Ostepathic Tretment .................................................... 153
The Structural Stage .................................. .... . . ..................... 153
The Congestive Stage............................................................ 155
The Preparatory Stage ........................................................... 156
Lbor and Delivery ....... .................. ................ ..................... 157
The Reovery And Maintenance Stage........................................ 157
References ............ ........................ ..... .. .... .. . ........................ ...... 158
x
RU TOWGIC DISORDERS ....................................................... 159
Introuction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 159
Pathophysiology... . . . . . . . . . .. . . . .. . . . . . . .. . . . . ..... .. . . . . . . . ... . . . . ..... .... . . .... . ..... 159
Sympathetics ...................................................................... 160
Somatic System................................................................... 161
Lymphatics ........................................................................ 162
Parasympathetics ................................................................. 163
Other Factors ..................................................................... 163
Tretment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 163
Osteopathic Manipulative Techniques ......................................... 164
Other Management Concers................................................... 166
Summary. . .. ..... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... .... . . . .. . .... .. . . . . . . . .. . . .. 167
" (I ] ................... 169
Manipulation In The Pediatric Patient................................................ 171
Osteopathic Considerations In Psychiatry (Bibliography) ......................... 181
Osteopathic Considerations In Immunology (Bibliography) ....................... 182
Hypersympathetic Activity On Selected Tissues (Korr) ........................... 183
Autonomic Infuence On Selected Tissues........................................... 187
Osteopathic Manipulative Treatment In Systemic Dysfunction................... 189
Basic Plan And Goals............................................................ 189
Chart: Sympathetic/Parasympathetic Innervation ............................ 192
Ventral Abdominal Techniques:
Indications and Contraindications....................................... 227
Chapman I s Charts ................................................................ 232
PRACTICAL EX FOR OSTEOPATHIC
MULATIVE TECHIQUE I SYSTEMC DISEAS .000000000000000000 234
xi
IEX OF FIGU
Figure 1 All Parasympathethic Ganglia of Hed and Neck. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Figure 2 Sympathetic Innervation to Hed and Nek ... ...... . . . . ...... ..... . . . ... . ....... 2
Figure 3 Anterior Chapman Points to Hed, Neck, Bronchi .. . . . .... . . . . .. . . . . . . . . . . . . . .. 3
Figure 4 Ciliary Ganglion to Eye (parasympathetic) .... . . . . . . . . . . . . .. . . . . . . .. . . . .. . ....... 5
Figure 5 Parasympathetic Inneration to Hed and Neck ....................... ........... 5
Figure 6 Sphenopalatine Ganglion to Nasal Mucos and Lcrimal Gland ... . ..... . . .... 5
Figure 7 Richardson's Eye Exercise Chart . . . . . ............................................. 13
Figure 8 Cerical Sympathetic Ganglia ............................. ....... . ...... . ..... . . . . 26
Figure 9 Imprtant Lndmarks of Normal Thoracic Inlet ... ........................... . . 27
Figure 10 Sphenopalatine Ganglion (parasympathetics to Lcrimal Gland
and Respiratory Mucos of Sinuses ......... ..... . ...... . . . . .. . ........ . . . . .. 29
Figure 11 Diaphragmatic Action (A Maor Lymphatic Pump) ...... ....... . . . ..... . ... . . 33
Figure 12 Innervation of the Lung
and Viscerovisceral and Viscerosomatic Refexes . .. . .. . . . . . . . . . . . . . . . . . . . . 34
Figure 13 Anterior Chapman Points of Cardiopulmonary System . . . .... . . . . ... . ... . . . . . 37
Figure 14 Diaphragmatic Action (A Major Lymphatic Pump) .. . . ... . . . . . . ... . . . ... . . . . . 39
Figure 15 Common Lymphatic Drainage of the boy ................................ . ..... 40
Figure 16 General Movement of Ribs and Sterum During Respiration ............... . 44
Figure 17 Sympathetic Inneration of Het ..... ................ . ............. . . ... . ....... . 54
Figure 18 Diagram of Sympathetic Innervation of Boy ..... . . ...... . . ..... . . ............ 54
Figure 19 Parasympathetic Inneration of the Boy .. ..... ... ........ . ......... . . . . . . . . .... 55
Figure 20 Lymphatic Drainage of the Body ...................................... . . . . . . . .... 56
Figure 21 Travell Pectoralis Major Trigger Point
Assoiated With Tachyarrhythmias . .... .......... . ... ..... . .. . .... . ... . . .... 57
Figure 22 Etiologies for Chest Pain .............. . . . . .... . . ........ . . . . . . .... ... .. . . . . . . . . . . . 58
Figure 23 Cardiac Pain Patter ............................. .......... . ....... . . ...... . . . . . . . . . 58
Figure 24 B' s Palpatory Study Somatic Dysfunction
in Patients With Cardiovascular Dis ......... . . . . ... . ... . . . . . ....... . . . . 59
Figure 25 Chart of Stile's Work Regarding OMT in ICU Patients With MI ...... . ... . 6
Figure 26 A Classifcation for Hyprtension .............. .................... .............. 61
Figure 27 Mechanisms of Hyprtension
(potentiators of Increased Peripheral Resistance) ............... . . ......... 61
Figure 28 OMT Interention in Hyprtension (Effets Stress Lvels) . . . . ............... 62
Figure 29 OMT Interention in Hyprtension (Effets Kidneys and Adrenals) ...... . . 63
Figure 30 OMT Interention in Hypertension (Effects Peripheral Resistance) .. .... ... 63
Figure 31 Hypothesis for Stress and Sympathicotonia
in Pathogenesis of Essential Hyprtension .................................. 6
Figure 32 Location for OMT to Chapman's Posterior Adrenal Points .. . . . . ............ 65
Figure 33 True Viseral Pain .................................................................. 80
Figure 34 Viscerosensory Pain (Viscerosomatic Pain) ..................................... 80
Figure 35 Peritoneutaneus Refex of Morley
(Diret Visceral-Somatic Extension of Pain) ............................... 81
Figure 36 Phrenic Nere Pain Referral ...................................................... 81
Figure 37 Mayo Clinic Pain Patter lllustrations .... . . ..... .......... ......... . . ........... 82
Figure 38 Sympathetic Inneration of GI Trct . ... .. . . .......... .. .................. . ...... 83
xii
Figure 39 Sympathetic Inneration of Body ................................................. 83
Figure 40 Parasympathetic Inneration of the GI Tract. ................................... 84
Figure 41 Lymphatic Drainage of Upper GI Tract ......................................... 86
Figure 42 Tretment Approaches to Uppr GI Disorders ............ . .................... 87
Figure 43 Posterior Attachments of Mesenteries ............................................ 89
Figure 44 Anterior Chapman Refexes From Uppr GI Tract ............................ 90
Figure 45 Collateral Sympathetic Ganglia Loations .......... ............................. 91
Figure 46 Viscerosomatic Refex of Colon to Iliotibial Bands .................... ........ 96
Figure 47 Anterior/Posterior Chapman's Refexes from Colon Dysfunction ........... 96
Figure 48 Sympathetic Inneration of the Boy ........ ..... .. .. ........... . ............... 97
Figure 49 Parasympathetic Inneration of Intestinal Tract ................................ 97
Figure 50 Posterior Attachments of Abdominal Mesenteries ............................. 98
Figure 51 Cross Section Pelvic Flor and Ischiorectal Foss ............................. 99
Figure 52 Anterior Chapman's Refexes
From Genitourinary System Dysfunction ................................. 125
Figure 53 Inneration for Micturition and Neurologic Bladder Disorders ............ 126
Figure 54 Inguinal Heria and Effects of Intra-abdominal/Pelvic Pressure ........... 128
Figure 55 Referred Pain Patters of Iliolumbar Ligament Syndrome.................. 128
Figure 56 Coronal Setion Through Urogenitl Triangle ................................ 130
Figure 57 Pain Patter and Mechanisms of Psoas Syndrome ........................... 132
Figure 58 Prostatoynia and Prostatitis .................................................... 137
Figure 59 Etiology, Symptoms and Signs of Ureteral Irritation ............. . .......... 138
Figure 60 Genital Inneration for Sexual Function ....................................... 143
Figure 61 Diagram of Congestion In Pregnancy .......................................... 149
Figure 62 Autonomic Nerous System In Rheumatology ............................... 160
Figure 63 Circulation and Lymphatic and Venous Drainage of a loint. ............... 162
Figure 6 Location of Collateral Sympathetic Ganglia .................................. 199
Figure 65 Cerical Sympathetic Ganglia ........ . .......................................... 202
Figure 66 Diagnostic Ares Related to Regional Congestion ........................... 206
Figure 67 Compnsted and Uncompnsted Patters of Zink ... ...................... 207
Figure 68 Static Lndmarks For Diagnosis
of Fascial Diaphrgm at the Thoracic Inlet ............................... 209
Figure 69 Fascial Thoracic Inlet Sidebent and Rotated to the Right ................... 211
Figure 70 Fascial Thoracic Inlet Sidebent and Rotated to the Left. .................... 212
xiii
IEX OF TABLE
Table 1 Travell Triggers With EENT Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
Table 2 Differential Points Assoiated with Functional E Compnents . . . . . . . . . . . . . . 11
Table 3 Chart of OMT for Patients With EENT Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
Table 4 Chart of OMT for Patients With Upper Respiratory Disorders . . . . . . . . . . . . . . . . 31
Table 5 1918 Flu Epidemic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
Table 6 Prevention of Postoprative Pulmonary Complications (Henshaw) . . . . . . . . . . . 47
Table 7 Chart of OMT for Patients With Lower Respiratory Disorders . . . . . . . . . . . . . . . . 50
Table 8 Postulated Time Interals for Onset of OMT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66
Table 9 Chart of OMT for Patients With Cardiovascular Disorders . . . . . . . . . . . . . . . . . . . . 67
Table 10 Chart of OMT for Patients With Uppr GI Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . 94
Table 11 Prevention and Tretment of Postoprative Paralytic Ileus (Herrmann) . . . 103
Table 12 Chart of OM for Patients With Lwer GI Disorders........................ 107
Table 13 Slow Wave Ratios For Normal Patients And Patients With IBS . . . . . . . . . . . . 113
Table 14 Chart of OMT For Patients With Genitourinary Disorder . . . . . . . . . . . . . . . . . . . 133
Table 15 Chart of OMT for Patients With Dysmenorrhe . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Table 16 Chart of OMT For Patients With Rheumatologic Disorders................. 167
Table 17 Vision And Interest Of Infant (Chart)
From Birth to 12 Months . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
Table 18 Autonomic Nerous Infuence in Seleted Ares . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 187
Table 19 Chart of OMT For Patients With Systemic Disorders . . . . . . . . . . . . . . . . . . . . . . . . 190
Table 20 Chart of Autonomic Innerations of the By . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192
Table 21 Muscles Used In Tretment of Rib Somatic Dysfunctions . . . . . . . . . . . . . . . . . . . 198
Table 22 Common Symptoms and Signs of Congestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204
Table 23 Other Symptoms and Signs of Fascial Dysfunction........................... 205
Table 24 Ventrl Abdominal Fascial Release and Pump Treatments . . . . . . . . . . . . . . . . . . 227
Table 25 Anterior Chapman's Refexes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232
Table 26 Posterior Chapman's Refexes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
xiv
"My object is to make the Osteopath a philosopher,
and place him on the rock of reason."
--A. T. Still, M.D.
OSTEOPATIIIC CONSIERATIONS I EET DYSFNCTION
"All alergic maniestation have a 3-ol etiolog: heredit, the
allergen, and the strctural problem, which is the most fndamental
becaue it lowers resistance and invites malnction. Wile nothing can
be dn about heredit, resistance ma be built up to the all
E
rgen or it
ma be avoided. Te baic approach is through strcture. "
I. ITRODUCTION
A wide variety of symptoms and signs referable to the eyes, ers, nose, and/or
throat (BEN) will be presented by the patients sen in a busy general practice.
EEN pain and/or dysfunction as either a presenting complaint or as a fmding
of the clinical history and/or physical examination neds careful and thoughtfl
evaluation by the generalist. The osteopathic practitioner combines somatic
palpatory clues and the knowledge of the interrelationships between structure
and function with a thorough history and a directed physical examination of the
EENT.
Osteopathic manipulative treatment to the
somatic component and considerations
toward enhancing body homeostatic
mechanisms c play a signifcant role in
designing effective tretment for these
patients. Ofen a successful therapeutic
trial with OMT direted at localized
dysfunctional states will eliminate the need
. for systemic tretment or for a more
extensive and expensive work-up seeking a
non-existent systemic etiology.
Common presenting symptoms or
conditions in the EENT system are
presented in this setion for inclusion in
differential diagnosis ad tretment design.
The somatic compnent or dysfunctional
state ocurng with each clinical example
is representative of dysfunction in that
region.
Because of the interrelationship between structure and function, the presence of
dysfunction does not eliminate the possibility of coexisting structural etiologies.
1
l. PATHOPHYSIOWGY
REFEX CONNECTIONS:
Because of a variety of refex connetions, impulses arising from EEN tissues
c prouce symptoms or dysfnctional states in other structures.
2
Asthma,
cephalgia and vertigo are all symptoms which may result from nasal and sinus
affections. Stimulation of vagal afferents by the irritation of a plug of wax
lodged against the tympanic membrane is clinically associated with a recurrent
cough refex
3
or with dizziness.
4
Both of these symptoms disappear when the
wax-irritant is removed.
Impulses originating from outside the EEN may also initiate EEN symptoms
because of refex connections: Cough and hoarseness may be produced by
stimulation of pulmonary and pleural tissue;
5
increased nasal and pharyngeal
secretions may be produced by stimuli originating in either the lung or the upper
gastrointestinal tract.
6
The ouloerical refex which c be used benefcially
in muscle energy osteopathic manipulative techniques has been implicated in the
cerical vertigo symptomatology which occurs in cerical spondylosis, cervical
inertial injuries (whiplash), cerical somatic dysfunction and cerical disk
disease.
An understanding of the
anatomy, physiology and
pathophysiology of the head,
neck and uppr thorcic re
gion is vital if the clinician is
intent on providing optimum
care for patients with EEN
dysfunction.
SYMATETICS:
EEN structures derive their
sympathetic inneration from
cell boies loated in spinal
levels Tl-4 with synapss
betwen the pre-and post
ganglionic fbers ocurring
in the uppr thoracic or cer
vical sympathetic ganglia.
The sympathetic neres gen
erally follow the arterial
supply to peripheral tissues.
Plane Ners
2
Dp
Plo
Infer
Spetc
Gglion
OA
A
} Torc
Inle
(Crc
Torc
Jun;'
Visceral afferent neres, stimulated by organ dysfunction, often follow the sme
pathways as sympathetic inneration. Excessive input from a viscera of the
hed or nek prouces facilitation of the uppr thoracic cord segments and
results in refex stimulation of somatic tissues innerated by TI-4. The
facilitated cord sgment also encourages excessive sympathetic outfow from
that sgment to its assoiate viscera (T1-4, to the hed and nek); it is also
believed t be the basis for estblishment of Chapman myofascial tender pints
related to visceral dysfnction.
Palpatory changes in the upper thoracic and cervical paraspinal tissues as well as
traditional Chapman's refex loations therefore indicate incresed functional
activity of the sympathetic nerous system in this region. On the other hand,
physical fndings such as Homer's syndrome
7
(constricted pupil, ptosis, and
facial anhidrosis on the involved side) ofen indicate signifcant structural
involvement or blokage of the sympathetic nervous system; this needs to be
considered in the differential diagnostic process.
Incresed sympathetic activity to the
eye, e, nose, and/or throat as well
as the upper thoracic musculature
augment the normal physiologic
respnses that those tissues are
capable of providing. In general,
the most common physiologic
respnse is vanstriction leding
to diminished nutrient supply to the
tissues and reuced lymphatico
venous drainage. The boy's ability
t mount a immune respnse and
to obtn effective concentrations of
medications are reduced in areas of
vasoonstriction and tissue
congestion.
Chapman's Reflexes:
Upper Respiratory Tract
Er
Pharnx
Tonsils
Lrnx
With chronic iritation, nasal and pharynge seretions from prolonged
sympathetic stimulation of the respiratory epithelium beomes thick and sticky
due t the incresed number of goblet cells and deresed vascular elements.
Sympathetic stimulation of the nasopharyngeal mucous membranes produces
vasoonstrction, inhibits secretion, and results in dryness in several acute
situations, including fever.
8
Ofen, dryness and cracking of the mucos result
in a breakdown of normal mucosal defense mechanisms and prmits seondary
bacteral infetions to ocur.
3
Dilation of the pupil (mydriasis) ocurs with incresed sympathetic activity to
the eye; pupillary constriction results from a reduction or loss of sympathetic
activity. Long term uppr thoracic and cerical dysfunction with
sympathicotonia have ben implicated in the development of cloudiness of the
lens.
9
I exophthalmic goiter, prolonged sympathetic activity producing
contraction of the Mullerian orbital muscle combined with edema and lymphoid
infltration,
1
0
results in protrusion of the eyeball. Other eye phenomena in this
sme condition are due to hyprarasympathetic activity, such a the failure of
the uppr lid to follow the core when the eyes are lowered or a widening of
the lid slits due to incresed tone of the levator palpebrae muscle.
Sympathetic fbers innerate blo vessels which supply the thyroid and also
innerate the cells which produce thyroid secretion. Increased loal sympathetic
activation, generalized adrenal activity or increased thyrotropic hormone from
the anterior pituitary (any of these) increases thyroid glandular secretion.
11
Common EEN signs and/or symptoms assoiated with incresed sympathetic
activity include photophobia, unstediness (slight vertigo), tinnitus, and
thickened nasopharyngeal secretions. Hyperesthesia of the pharyngeal tissues
usually makes patients anxious, causing them to "rasp, cough and exptorate to
rid themselves of non-existing mucosities or some imaginary foreign body in the
throat. " Sweting is augmented and the patient may experience incresed
fatigue, palpitations, tachycardia, and insomnia. With mydriasis (a hypr
sympathetic event), narow angle glaucoma may be made worse and intraoular
pressures elevated.
While there are an abundance of symptoms produced by hypersympathetic
activity, objetive signs are diffcult to mesure with screning physical
diagnostic tests. Palpatory changes a described erlier are accurate indicators
and when present, war t consideration in both the diagnostic and theraputic
arenas.
PARASYA TIETCS:
Parsympathetic nere fbers to the pupil are supplied by the third cranial nere
( oulomotor nere). They synapse in the ciliary ganglia and then pass to the
ciliary muscle where parasympathetic contraction of the pupil oppses
sympathetic dilation. Contraction, from parasympathetic activity affecting the
lens, shortens the eye's foal pint. According to Pottenger, "When the
excitability of the motor cells in the oulomotor nerve is very high, it may result
in accommoation spasm.
,,
1
2
4
Parasympathetic nerve fbers to the
lacrimal gland as well as to the
nasopharyngeal mucos travel via
the sventh crnial nere (facial).
They synapse in the sphenopalatine
ganglia. Parasympathetic hyper
activity is respnsible for the
production of tes from the
lacrimal glands and profuse, clear,
thin secretions from the mucos of
the nasopharynx and sinuses.
Great Petrosl N.
In the absence of histo
logical changes which
may be prouced by
prolonged sympathicoto
nia, irritation of the
nasopharyngeal mucos
results in a "runny nose"
and watery eyes. A
sphenopalatine syndrome
is described as redness
and n engorgement of the
mucous membraes,
photophobia, tearng and
pain behind the eyeball,
nose, neck, e or
temple. ,,
1
3
(Parasympathetic) Superior
Foraen
Pangea Ne.
This syndrome is sid to
worsen cases of asthma due
to lowered resistnce of
nas mucos to foreign
protein and inadeuate
conditioning of the air
entering the lungs.
Parasympathetic neres to
the thyroid aris from the
supror and inferior
laryngeal neres and a
branch from the main vagus
nere (cranial nere X).
VII Salivatory
Nucleus
Sp
Si
N_YI 'r.
()
5
At this pint its physiologic role in thyroid function is unknown; it is believed
to be neither an activator nor an inhibitor of thyroid activity.
VEOUS A LYMHATIC SYSTE:
85 % of the venous drainage from the hed is accomplished via the jugular veins
which pass through the right and lef jugular foramina, formed in the
ocipitomastoid sutures between the ocipital and the temporal bones. Venous
congestion of the hed leds to symptoms of cephalgia and anxiety.
The frst sign of lymphatic congestion affecting EEN structures and
attributable to fascial somatic dysfunction will appear a fllness in the
suprclavicular tissues. The pre-auricular, post-aurcular, tonsilar,
submaxillary, submental, and psterior cervical lymph nodes should also be
palpated for evidence of infection. Manipulative goals are directed toward
opning lymphatic pathways while avoiding direct manipulation over swollen
lymph nodes.
Lymphatic congestion leads to boggy, edematous tissues which are generally
uncomfortable and which change local biochemical conditions and hinder
homeostatic mechanisms. In nasopharyngel dysfunction there will be
diminished transprt of nutrients to the tissues and a reduction in the movement
of metabolic wastes from the mucos. This hampers healing while incresing
the pssibilities of nasopharyngeal adhesions from repeated or serious infection.
Where the sclera, corea, iris and ligamentum pectinatum meet is defned as the
angle of the anterior chamber of the eye. "Upon the integrity of this angle
depnds the proper circulation of lymph to nourish the anterior portion of the
eye";
14
glaucomatous changes have frequently been linked to por lymphatic
drinage of the eye.
In the inner e, absorption of endolymph is believed to be important in the
prevention of both endolymphatic hydrops ("glaucoma of the e" 1
5
) and
fbrosis of the endolymphatic duct which ocurs in Meniere'S disease.
Meniere's disese is accompanied by symptoms of tinnitus, diminished hearing,
and vertigo.
NUAL SYSTE:
A varety of EEN symptoms c be primarily explained by the effect of
somatic dysfunction on motor or sensory nerves in the cranial and/or cerical
regions. (Table 1, page 9)
A trauma history is important as EEN symptoms in a child or an adult ofen
have their onset as a consequence of a difcult delivery or a truma such as the
6
inertal injury (whiplash) incurred in a motor vehicle accident. Dental trauma
should als b a routine part of the historical questioning beus of its
propnsity for creting crnial somatic dysfnction.
While the two most common pathophysiologic causes of extraoular muscle
palsy are diabetes mellitus and aneurysm, extraoular muscle dysfunction is also
a frequent sign of cranial somatic dysfnction and often respnds well to
ostepathic manipulative tretment directed at the attachments of the
ptrosphenoidalligament. Beause this ligament is formed by the anterior
extensions of the fxed margins of the tentorum cerebelli to the body of the
sphenoidal bone, tretment is typically directed to its attachments, particularly
to the tempral and sphenoid bones.
Inneration to the extraoular muscles--crnial neres ill, IV and VI--is
particularly vulnerable to durl stress as these neres pass in close relationship
to the ptrosphenoidal ligament. Post-traumatically, symptoms of cranial nere
VI are the most common beause this is the most vulnerable of the three neres
as it passes under the ptro sphenoidal ligament.
16
Cranial nere VI innervates
the lateral retus muscle so its dysfunction leads to medial strabismus. The
effet of extraoular muscle dysfnction ranges from mild eye fatigue, hedache
and blurred or double vision to amblyopia, mild nystagmus, or strabismus. Any
of thes dysfunctions may respnd favorably to OMT of the cranium.
17
Other crnial neres may be affecte and led to EEN symptoms.
Dysfunction involving the olfactory nere
18
(cranial nere I) may led to an
altered snse of smell or to an impression of an oor that is not present. The
trigemina nere (CN V) carries sensory information from many structures
including the anterior and middle cranial fosse, the tentorum cerebelli, the
mastoid air cells, the nasal mucos, the corea, and the tempromandibular
joints. Dysfunction of the ffh cranial nerve may led to hedache
19
perceived
in the anterior foss, eyebrows, or sinuses; it is also considered in the
differential diagnosis and tretment of trigeminal neuralgia (tic douloureuxr
2
0
The buccal branch of cranial nere V may be entrpped by trgger points2
in
the lateral pterygoid muscle and prouce tingling in the chek.
Dysfunction of crnial nere VI is assoiated with complaint of a metallic taste
or altered slivation. Finding somatic dysfunction in the cranium which could
affet the facial nere (CN VI is also quite helpfl in the differential diagnosis
ad tretment of Bell's palsy. 2 Vertigo, nystgmus and tinnitus are symptoms
which may arise from involvement of the vestibuloohler nere (CN VIII).
2
3
With dysfunction of crnial neres IX and X, infants may have pr suckling2
4
or failure t thrive beaus of pr SWallowing. Dysrthria may result from
dysfnction of crnial nere XII.
7
Palpation of the cranium for obvious strn patters, ocipitl compression, and
tempral malalignment is extremely helpful in ruling out cranial dysfunctional
states which could led t EEN symptoms. Tretment of any somatic
dysfunction found is helpfl in addressing the physiologic prtion of the
tretment protool.
TE SOMTIC SYSTE:
The myofascial system plays a signifcant role i EEN symptomatology. A
number of myofascial trigger points (s) have been well doumented by
Travell and Simons that refer pain to, and/or caus dysfunction of, the eye, er,
nose, Eustachian tube, and throat. Specifc questions relating t the activation
of the prtinent muscles outlined in Table 1 (age 9) should therefore be posed.
All myofascial trigger pints and particularly those i the head and neck region,
are aggrvated by cold and emotional stress. I this are, emotional stress
symptoms
2
5
such as bruxism and clenching of the teeth are particularly pertinent
as they prouce TPs in the masseter and pterygoid muscles. Frowning or
squinting sts up TPs
2
6
in the orbicularis ouli and ocipitalis muscles. These
muscles are also activated by excessive gum chewing, wor teeth or dentures,
oclusl disharmony, TM, and prolonged dental procedures.
Symptoms referred by myofascial dysfnction to the eye are most prominently
sen with TPs in the steral division of the steroleidomastoid muscle.
2
7
Motor vehicle accidents, espially those from the rear
28
when the head is
tured, frequently cause trigger pints in the sterocleidomastoid, splenius
cericis, and trapzius muscles. Postural disorders must be ruled out
2
9
as a
prtuating factor in those cases where the trigger points are difcult to
eradicate.
Baus of ipsilaterl visual disturbances including bluring, diminution of
prceived light and apparent ptosis from spasm of the orbicularis ouli in the
reference zone, the patient may reprt a need to tip the head backwards to look
up. TPs in the obicularis ouli muscle will also cause excess ipsilateral
lacrmation and conjunctival reddening due to vascular engorgement.
30
TPs in
the orbicularis ouli muscle may result in patient complaints of "jumpy print"
while reding.
31
Splenius cericis TPs
3
2
will prouce ipsilateral blurring of
ne vision without conjunctivitis or dizziness as well a pain in the eye and
orbit. Thos in the ocipitis muscle refer pain behind the eye and in the
eyeball and eyelid while thos in the trapzius might refer pain to the back of
the orbit.
The underlying cause of functional er symptoms should be carefully ad
systematically sorted out. The role of cranial nere dysfunction and lymphatic
congestion has alredy been discussed with regard to tinnitus, vertigo, and/or
hearing disorders. Crial somatic dysfunction is a frequent cause of functional
8
symptoms. Exteral rotation of the tempral bone is assoiated with low
pitche roaring tinnitus; fxed interal rotation assoiated with high-pitched
tinnitus; ad both ptentially causing vertigo.
33
TA I: TVL TRIGGERS WITH EEHT SYTOMS;
EYE SYMTOMS AD/OR PAIN:
Sternal Division of Sternocleidomastoid Muscle
Splenius Cervicis Muscle
Occipitalis Muscle
Orbicularis Oculi Muscle
Trapezius Muscle
E PAIN, TINITS, A/OR DIMINISHED BEARING:
Deep Portion of Masseter Muscle
Clavicular Portion of Sternocleidomastoid Muscle
Medial Pterygoid Muscle
Occipitalis Muscle (Possible)
EUSTACHIA TE DYSFCTION:
NOSE PAIN:
Orbicularis Oculi Muscle
MILY SINS PAIN AD/OR SINUS SYTOMS:
Lateral Pterygoid Muscle
Masseter Muscle
Sternal Division of Sternocleidomastoid Muscle
THROAT PAIN AD/OR PAIN OR DIFFICUTY SWAOWING:
Digastric Muscle
CRIA HRV EM:
VA
(Buccal Nerve Branch) : Lateral Pterygoid Muscle
XI
.
Sternocleidomastoid Muscle .
9
Otalgia c be referred
34
from teeth, tongue, tonsils, esophagus, TM and from
cerical/cranial somatic dysfunction through cranial neres V, IX and X or Cl-
2. To thes factors c be added Eustachian tube dysfunction and myofascial
trigger pints.
Bth seretory and acute otitis media often arise from Eustachian tube
dysfunction. The middle e is normally ventilated 3-4 times pr minute as the
Eustachian tube opns during swallowing, snezing or yawning. Even mild
infetion c cause mucosl swelling suffcient to blok the Eustachian tube
35
leding to pressure changes within the middle e, retraction of the tympanic
membrane, srous otitis and hering loss. Under these conditions oxygen is
absorbed through the blo vessels in the mucous membrane of the middle e.
In the pathogenesis of secretory otitis media, a relative negative pressure
develops with Eustachian tube dysfunction leding to mild retraction of the
tympanic membrane. This c be demonstrated on physical examination by
abnormal light refection on the tympanic membrane and by por insuffation.
The negative middle e pressure causes a transudate from the blood vessels of
the mucous membrane of the middle e. This produces an amber to gray
colored appce to the tympanic membrane, a fuid level and bubbles may be
seen on otologic examination. A conductive heing defcit develops in patients
with secretory otitis and it may last for months.
Stein I s textbok, Interal Medicine, states that the most important predisposing
factor in developing acute otitis media is an acute nasopharyngeal infection,
usually virl, causing Eustachian tube dysfunction that allows microbial
proliferation and infection in the middle e, especially when combined with
other inadequate host factors.
36
Cranial somatic dysfunction has also proven to
be a predisposing factor for recurent pediatric otitis media.
3
7
Eustachian tube dysfunction may ocur from tissue swelling, edema, and/or
adhesions forming after tonsillectomy or after repeated or serious infections. It
may also arise from trigger points in the medial pterygoid
3
8
muscle or from
dysfunction of crnial nere X. Additionally, it has been assoiated with cranial
somatic dysfunction
3
9
--espially interal rotation of the tempral bone or
torsion or sidebending-rotation of the sphenobasilar symphysis. Regardless of
the etiology, Eustachian tube dysfunction has ben assoiated with a variety of
patient signs, symptoms, or disorders including diminishe hering, pain with
altitude changes, tinnitus, reurrent infetions, secretory and acute otitis media,
asymmetrical elevation of the uvula upon phonation, and vertigo. Because any
of these symptoms may arise from Eustachian tube dysfunction, physical
examination of the psterior pharynx, palpation of the medial pterygoid muscle
and cranium, and visualiztion with insufation of the tympanic membrane
should be prforme.
10
TABE 2: SELECTED DIFFERIA POINS IN DIAGNOSES
ASSOCIATED WITH FCIONA E COMONENS
DIAGNOSIS E TINITS DECRASED
SESATION HING
Meniere's Disease Fullness 85-90% Unilateral 85-95% Unilateral
10-15% Bilateral
Hypothyroidim (-) (-) Bilateral
Hyperthyroidism (-) Bilateral (-)
Eustachian Fullness (+) Unilateral Conductive
Dysfunction Unilaterally
Labyrinthitis (+/-) (-) (+)
Temporal Bone with OA or (+/-) Unilateral (+/-)
Somatic Dysfunction vagal involv.
TP Deep Masseter Deep Pain Unilateral (-)
TP Clavicular (+/-) (-) Unilateral
Portion of
Sternocleidomastoid
TP Medial Pterygoid Stuffiness (-) (-)
TP Occipitalis Ache (-) Slightly
Post-Concussion (-) (+/-) Sensorineural
Syndrome
Salicylate Toxicity (-) Bilateral (-)
VERTIG/
DIZZINESS
Vertigo
Dizzy
I

llghtheadedness
.
(? )
Dizzy
Dizzy or
Vertigo
(-)
contributes to
Carsickness
Seasickness
(-)
(-)
Vertigo
(-)
Other e symptoms attrbutable to myofascial trigger points (TPs) include those
in the deep prtion of the masseter, the clavicular portion of the
steroleidomastoid (SCM), the medial pterygoid, and according to Kellgren,
the ocipitalis muscle. Variables in the presentation of these points and other
differentials are detaile in Table 2 on page 11.
The low roarng tinnitus exprienced in TPs from the deep prtion of the
masseter
40
muscle will often vary when the jaw is opned wide. The stufness
in the e caused by TPs in the medial pterygoid
4
1
muscle is felt to be due to
Eustachian tube dysfunction which arises from inability of the tensor veli
palatini muscle to move the medial pterygoid and assoiated fascia aside to open
that structure. Not included in Table 2, are the TPs of the trapezius
4
2
which
includes among its many other referral sites, the posturicular area.
Sinus symtoms c also arise from myofascial structures. TPs in the lateral
pterygoid muscle refer svere pain to the maxillary region as well as
autonomically stimulating excessive secretions from the maxillary sinuses. Pain
referred from this TP and from TPs in the superfcial upper pron of the
masseter muscle give rise to complaints of "sinus attack" and often result in
incorrect and therefore ineffective treatment for sinusitis. Dysfunctional TPs in
the steral division of the steroleidomastoid
44
cause coryz and maxillary
sinus congestion. Nose pain, per se, is rarely caused by TPs other than those in
the orbicularis ouli
45
muscle.
Throat pain arises from myofascial triggers in either the medial pterygoid
46
and
digastric
4
7
muscles. Swallowing is painful with the former and diffcult with
the latter.
il. TAT
Afer a thorough diagnostic evaluation, a tentative diagnosis is made.
Formation of a rational osteopathic treatment for this initial diagnosis must:
o .. consider the patient's body as a unit
o .. supprt structure and functional components
o .. supprt and enhance the homeostatic mechanisms involved
The most effective tretment plan is direted at the cause of the complaints and
not at the symptoms.
In general, this setion will consider primarily the manipulative tehniques
which flfll the objectives mentioned in the previous paragrph. Tretment of
the uppr thoracic and cervical regions effectively addresses the sympathetic
compnent. Lymphatic congestion is best accomplished by frst opening the
pathways--espcially the thoracic inlet and anterior and posterior cerical sof
12
tissues--and then enhancing the fuid movement with diaphragmatic techniques,
lymph pumps and effeurage. Tretment of the parsympathetic component,
when it is present, often involves use of manipulative techniques to the cranium
ad/or ocipitoerical junction. In certn circumstances, spifc manipulative
techniques, exerciss or diety considerations may be applied to the general
tretment plan outlined above.
TE EYE:
3

A

2

Effeurage over the eyelid and globe

is often benefcial with eema of the

eyelid and sleral eema. Avoid
8 5
9
stroking over the lid when the

patient is wearing contacts or if any

other ophthalmic foreign boy is

suspted.

B

4
Some patients have an impaired
BEH
ability to fous their eyes and,
whether ne- or far-sighted, may
beneft from a sries of eye
exerciss develope by H. A.
Richardson, D. O.
48 TRBAE
I HEZBFD
Using an enlarged chart like the one
FOSGACNHO
illustrated above, this is one of six
eye exerciss that Dr. Richardson
ROD B A E D F H P Z
had his patients prform.
O MD V L R W C X P Z AO
-To b effetive the patient must b mtivate enough t prform the exercis
regularly. Pin a large -A- tet char on the wall with the fgure 5 on a diret line wit
the end of your nose. Std te inches away ad se that your nos is on a direct line
wit the fgure 5. Now lok at No.
1
, then at No.2, then back t No.1. Do this fve
tim, strtching the musle of the eyes ech time. Then shif fom No.
3
t No.
4
,
fve times ech way. Do not move the head. Then shif fom No.
8
t No.
9
fve times
ech way. Then lok up at A ad dow at B fve times up and dow. Then while you
remin the s distance from the chart, starting at A, shif the eye fom one dot t
the other all te way around the circle back t A. Do this fve times t the right, then
fve time t the lef. Blink ech tim that you lok a a dot; but do not mve your
hed when exercising. Now clos the eyes tightly fve tims. Then lok at No.5 ad
clos the eye for a sond; ten open them and lok at No. 5 again. O ad close
them fve time, loking at No. 5 again. On and clos them fve time, loking at
No. 5 ech time. This exercis bth the interl ad exter rt musle at the
s time. Now clos your eyes and cover them with the palms of the hands, bing
sure t exclude all light ad relax in this position for fve minutes. If one eye is weer
13
t the other, you should cover the stronger eye ad do more exercising with the
weaer eye. Now tae your st at abut ten fet fom te A test chart ad red all
of the letters on the card, shifing the eyes rapidly fom te bttom to the top of ech
letter, blining every time you shif the eyes.
Afer you have read all of the letters on te card at lest once, you should
again cover the eye with the palms of the hd ad relax for a few minutes
bing carefl not to put ay presure on the eyeballs .
4
9
T.J. Ruddy, D. O. ,
50
an ostepathic ophthalmologist, also developed a series of
muscle energy tehniques designed to balance extr-oular muscle tone. These
techniques utilize traditional muscle energy principles with the physician
applying resistance against the oular globe as the patient attempts to lok in a
spcifc direction. This form of OMT, combined with cranial techniques to
improve the structure-fnction relationship of extraoular muscle innervation,
has ben helpful in patients with functional diplopia, strabismus, cephalgia
secondary to eye strn, amblyopia, and other conditions in which somatic
dysfunction of the extroular muscles plays a role.
Another tehnique applied directly to the globe has been utilized for patients
with mild chronic glaucoma.
51
The purse of this technique is to improve
fuid drainage and constitutes part of a total tretment program. With the
patient' s eyes closed, the physician places a fnger across the eyelid from lateral
to medial. With a fnger of the other hand, a light prcussion is performed over
fnger that lies on the closed eyelid. In one study, intraoular tension averaged
3-5 mm Hg reduction 6 minutes afer an OMT regimen.
52
In a double blind,
randomize study of introular pressure of normal and chronic, open angle
glaucoma patients, signifcant pressure changes were also seen 6 to 6 minutes
after ostepathic manipUlative tretment.
53
Acute closed-angle glaucoma, on
the other hand, is an oular emergency which may prouce blindness in 3-5
days unless treted medically.
Where structural problems such as entropion or extropion lead to functional
disorders such as por drainage of tears through the nasolacrimal system or
chronic recurrent pathophysiology such as the infammation seen in chronic
conjunctivitis, the best tretment is probably surgical repair of the structural
disorder. However, where functional problems led to eye pain, blurred vision
or reddening, manipUlative or spry-and-stretch techniques should be applied to
spcifc trigger muscles. (See Table I, page 9. )
T EA:
In patients with signifcant cranial somatic dysfunction who are also
expriencing vertigo or tinnitus, a therapeutic trial of manipulation is warted.
Goals include achieving a balance between the temporal bones, normalizing the
14
cranial rhythmic impulse, and removing ares of dural strain. In addition, ech
of the musles listed in Table 2 page 1 1 that meet the patient' s presentation
should be palpated and treted if a myofascial tgger is found.
Patients with structural adhesions affeting the Eustachian tube may complain of
defness, otlgia with altitude changes, reurent otitis media, vertigo and/or
tinnitis. They may beneft from lysis of thes nasopharyngel adhesions. A
tehniue, referred t as "fnger surgery" , was ppularized by C. H. Muncie,
M. D. i It is often effetive in moifying the structure suffciently to restore
normal Eustachian tube function.
Yawning and swallowing are essential to normal Eustachian tube function,
therefore dysfunction affecting crnial neres IX, or V, or any of the myofascial
structures involved in these actions can compromise maximal Eustachian tube
function. Myofascial dysfunction in the medial pterygoid muscles and those
attached to the hyoid bone are particularly likely to disturb the opening of the
Eustachian tube. These dysfunctions respond well to OMT.
The frequency of pediatric otitis media is incresed in relation to a number of
somatic factors (number of cranial strain patters,
55
presence of plagioephaly,
or Eustachian tube dysfunction
56
) , environmental factors (expsure to tobacco
smokng
57
and woheting,
58
or participation in day care) , and familial factors
(history of sibling or parental otitis media) .
59
The tretment of choice for acute otitis media would address the underlying
Eustachian tube dysfunction, provide antibiotics capable of managing both
Strept pneuonia and Hemophilu inuenza
6
0
and support host elements. Such
a regimen prmits the boy' s homeostatic elements the best opprtunity to
interrupt the natural progress of the dis, spntaneous prforation of the
tympaic membrne with closure and retur of hearing in 1-2 weeks. Bause
sretory otitis media has a sterile effusion, antibiotics are not helpful unless it
is assoiated with a bacterial rhinitis, sinusitis, or nasopharyngitis.
Psudophedrine for vasoonstriction may be of some symptomatic relief, but
the ostepathic physician should go back and tret any underying
nasopharyngeal structural or functional condition which may be causing the
Eustachian tube dysfunction. Antihistamines may only be appropriate when
allergic factors are assoiated with Eustachian tube dysfunction.
ManipUlative tretment in Meniere's dis has ben spifcally descrbed as
"benefcial . ,,
61
One study of OMT in Meniere' s patients reveale excellent
results or signifcant improvement in 79% of cases.
62
OMT addressing dural
restrictions, and espcially those assoiated with tempral bone dysfnction,
63
is
particularly helpful in our exprience as are diagnosis and tretment of the
lymphatic and autonomic compnents.
15
TE NOSE A SISE:
w. Hadley Hon Ill, D. O. in his article, "Current concepts i management of
sinus disese, " states, "OMT should be included in the tretment of sinusitis. "
He notes that OMT should address parasympathetic and sympathetic fbers as
homeostasis of teir autonomic functions may prevent ostial oclusion. Sensory
fbers to the sinuss (originating in the trigeminal nere) should also be
addressed.
Stimulation of the sphenopalatine gaglia
65
results in a brief priod in which
there is proucton of profuse, thin nasal secretions, a parasympathetic
respnse. This may prove helpful in the symptomatic relief of patients with
sinusitis or patients whose thick nasal seretions have been diffcult to cler
from the nasal passgeways. The pressure applied to the site needed to affect
the sphenopalatine ganglion will elicit "exquisite" tenderess if active lateral
pterygoid myofascial trigger points are present.
66
Ofen the referred maxillary
sinus pain and autonomically induced excessive secretions will resolve with the
inhibition that ocurs with this technique.
67
Reserch utilizing rhinomanometry
has shown that following osteopathic manipulative tretment there is a reduction
in the amount of work required by the nose during breathing.
68
Manipulative techniques to free somatic dysfunction in the cranium
69
(especialy
the frontal-ethmoidal and facial bones) or to improve the pumping motion
through the vomer are benefcial for imprOVed nasal sinus function. They are
extremely helpful in patients with dysfunctional, allergic, or infectious
etiologies for rhinitis, acute sinusitis, or the pharyngitis resulting from post
nasl drainage. CV 4 cranial technique is felt to act through fuid mobiliztion
and incresed pump ptency; regardless of mechanism, shortly afer applying
this tehnique, most patients note signifcant clearng of the sinuses.
Tretment to normalize the body' s response to sensory input along branches of
the trigeminal is helpful in reducing refex symptoms rging from sinus
hedache to sneezing. This may be accomplished with gentle rotatory
stimulation over the bony foramina of the supraorbit and infraorbital neres.
(Se the next setion entitled "Osteopathic Considerations in the Common
Cold. ")
In patients with structural abnormalities such as nasal septal deformity or
chronic sinusitis, surgery beomes the osteopathic tretment of choice.
70
When
fnctional and otherise transient changes in acute sinusitis are inadequately
treted, irreversible structural changes may result. Thus, in chronic sinusitis,
when the normal ciliated epithelium is replaced with stratifed squamous cells
incapable of homeostatic clece mechanisms,
71
antibiotic and manipulative
therapy is rendered ineffective. Hoyt notes, "Functional sinus surgery offers
16
new hop to the patient who has failed to respnd to conserative ostepathic
medical tretment"
72
and can relieve associated somatic cephalgic
manifestations.
TE THOAT:
The tehniques described previously for the Eustachian tube and sphenopalatine
ganglia are also indicated to tret dysfunctions of the pharynx. Soft tissue
tehniques t the anterior cerical fascia and gentle manipulation to correct any
hyoid dysfnction are also extremely benefcial in restablishing normal
function in this region and prmits the patient signifcant symptomatic relief.
Addressing the anterior cerical fascias and hyoid bone is frequently helpful in
thyroid dysfunction, but beause this is an endorine gland and under the
control of the pituitary, evaluation and tretment of any cranial dysfunction
73
should also be prformed.
TE EN UT:
Mandibular drainage technique is effective in encouraging drinage from the
nasopharyngeal are and opning the Eustachian tube. It is therefore helpful in
decongestion of a large part of the ENT unit.
The proedure is described by Angus Cathie, D.O. (after Galbreth) in his
discussion of the sinobronchial syndrome
74
and is also mentioned by Harold 1.
Magoun, D.0.
1
5
The patient is treated in the supine psition with a slight
elevation of the head which is rotated 900 to the non-involved side. The
oprator stabilizes the fontoparietal region with one hand and places his/her
fngers of the other hand below the zygomatic arch and over the T with the
heel ner the symphysis menti. The patient is instructe to relax his/her jaw
while the oprtor applies a slow, frm pressure downward, forward, and
medial. This is relesed and repated alterately to apply a "make/break
tension" to the pterygoid muscles. This deongests the rich pterygoid venous
plexus which drains the tissues noted above. Relaxation of the medial pterygoid
muscle also enables the tensor veli palatini muscle to functionally opn the
Eustachian tube.
While usually utilized to facilitate diagnosis, tretment of ENT Chapman' s
pints with generalized soft tissue techniques or spcifc rotatory stimulation can
be pstulated to benefcially moify sympathetic outfow. It is noted that
symptomatic relief is afforded the uppr respiratory tract when these refex
pints are treted a a system. For comfort and practicality, the psterior pints
are treted frst and the anterior pints may be gently treated if they remain.
17
t CRI t Endolymphatic Flow
Oculocervical - Muscle Energy
Cervicals C3-S (Phrenic Nerve)
Tl-12 and Ribs 1-12 (Somatic Nerves and Respiration)
Thoracolumbar Junction (Diaphragm Attachment)
Medial pterygoid muscle
Somatic Dysfunction Hyoid Soft Tissue for Eustachian Tube
facH. seg.
Sympathetics
I
Parasympathetics I
I
Rib Raising
Tl-4
Cervical Fascias
(Cerv. Ganglia)
Chapman's Reflexes
I
Eye:
Tl-2
Ciliospinal Center
SYATHETIC EFCTS
t Tone:
t Vasoconstriction
TREATMNT PL FOR
EENT DYSFUNCTION
Lymphatics
Thoracic Inlets
Abdominal Diaphragm
Effleurage
Lymphatic Pumps
1
Ruddy's Resistive Duction
Ocular - Muscle Energy
Stroking (Ocular)
Sphenopala
Ganglion
Cranial OM
Cranial N
(Cranial
t Thickens Secretions (t Number of Goblet Cells)
. Drainage
Mydriasis Worsening of Glaucoma
LYHATIC EFCTS
Impaired Lymph Flow:
. Drainage
t Congestion
t Endolymphatic Pressure Possible Fibrosis of
Endolymphatic Channel
L
with stasis
Meniee's Disease
PARASYATETIC EFCTS
t Tone:
t Thinning of Secretions
Improved Drainage
18
tine
Technique,
T to Affect
erves
N-VII )
I. SUARY
Refex mehanisms are extremely active in integrated EEN functions. Somatic
dysfunction moifes normal refex activities and may prouce dysfunctional
states whos symptoms must be differentiated a t whether they are fnctional
(smatic dysfunction) or pathological. In dis situations, smatic
dysfunction reduces the effcacy of the boy' s homeostatic mechanism.
Successfl manipulation of somatic dysfnction constitutes either a theraputic
trial or an imprtant supprt to homeostsis. Its incorration into the tretment
program speds healing and decreses morbidity while simultaneously providing
symptomatic relief for the patient.
ADDITIONAL EENT BmLIOGRAPHY:
Norfolk DF: Cranial nere syndromes: relationship to musculoskeletal lesions
of the cerical spine. The Joural of Osteopathy 1962; 69(8) : 17-22.
Gayral L, Neuwirth E: Oto-neuro-ophalmologic manifestations of cervical
origin. New York State J Med 1954; 54: 1920-1922.
RFCE:
1. Magoun il: Oe in the Crial Field. Kirksville, Joural Printing
Co, 3rd e, 1976, P 276.
7th ed, 1953. pp 239-40, 374-391.
3. O cit p 381.
4. Travell JG, Simons DG Myofascial Pain and Dysfunction: The Trigr
Point Manual. Baltimore, Williams and Wilkins, 1983, p 209.
5. Pottenger FM Soms of Visceral Disease. St Louis, CV Mosby Co,
7th ed, 1953, p 239.
6. O cit pp 239-240, 378.
7. Stein JH (e) Intra Meicne. Boston, Little, Brown & Co, 3rd ed,
1990, P 1 897.
7th e, 1953, pp 377-8.
9. Cole W: Exprimental evidence, in Hoag JM (ed) Osteopathic Meicine.
New York, M
C
Graw-Hill, 1969, ch 8, p 1 19.
10. Pottenger FM Soms of Visral Dis. St Louis, CV Mosby Co,
7th ed, 1953, pp 384-6.
1 1. Cole W: Exprimental evidence, in Hoag JM (ed) Osteathic Meicne.
New York, McGraw-Hill, 1969, ch 8, P 1 19.
12. Pottenger FM Ss of Viscerl Dis. St Louis, CV Mosby Co,
7th ed, 1953, P 385.
13. Magoun H: Neuroscience studies in Goldstein M (ed) The ReSeh
S
of Snal Manipulve T, Bethesda MD, US Department of
19
Health, Eucation and Welfare (NINCDS Monograph #15) , 1975, pp
213-6.
14. Wolf AH: Ostepathic manipulation in eye, e, nose, and throat disease.
AAO Y 1962: 133-40
15. Gibson WR: The diagnosis and tretment of Meniere' s disease. The
Practitioner 1978; 221 : 718-722.
16. Magoun HI Ostthy in the Cranial Field. Kirksville, Joural Printing
Company, 3rd ed, 1976, P 293.
17. O cit pp 267,284, 293.
18. O cit P 167.
19. Op cit pp 76, 185, 290.
20. O cit pp 294-30.
21 . Travell JG, Simons DG Myofascial Pain and Dysfunction: A Trig r Point
Manual. Baltimore, Williams & Wilkins, 1983, p 266.
22. Magoun HI Osteathy in the Cranial Field. Kirksville, Joural Printing
Company, 3rd ed, 1976, P 269.
23. Op cit P 150.
24. O cit p 234.
25. Travell JG, Simons DG Myofascial Pain and Dysfunction: A Trigr Point
Manual. Baltimore, Williams & Wilkins, 1983, pp 219, 249.
26. Op cit pp 285, 293.
27. O cit P 203.
28. Op cit P 299.
29. Op cit pp 103- 1 14.
30. Op cit P 203.
31 . O cit pp 296, 298.
32. Op cit pp 285, 288.
33. Magoun HI Ostepathy in the Cranial Field. Kirksville, Joural Printing
Company, 3rd ed, 1976, pp 151 , 215.
34. O cit P 286.
35. More K Clinicly Oriente Anatomy. Baltimore, Williams & Wilkins,
2nd ed, 1985, P 970.
36. Stein JH Interal Medicine. Boston, Little, Brown, & Co, 3rd ed, 1990, P
1262.
37. Degenhardt BD, Kuchera ML: The prevalence of cranial dysfunction in
children with a history of otitis media from kindergarten to third grade.
Med-Johnson Fellowship Papr, 1993.
38. Travell JG, Simons DG Myofascial Pain and Dysfunction: A TrgPoint
Maual. Baltimore, Williams & Wilkins, 1983, p 249.
39. Magoun HI Ostathy in the Cranial Field. Kirksville, Joural Printing
Company, 3rd ed, 1976, pp 151 , 215.
40. O cit p 221 .
41 . Op cit p 249.
42. Op cit p 184.
43. O cit pp 263-4.
44. Op cit p 203.
45. Op cit p 282.
46. O cit p 252.
47. Op cit p 276.
2 0
48. Richardson R Increasing The Strength Of The Eyes a the Eye Mus
W the Aid of G. Kanss City, The Eyesight and Helth
Assoiation, 1925.
49. Op cit pp 52-53.
50. Ruddy TJ: Ostepathic manipulation in eye, e, nose, and throat disese.
AAO Y 1962: pp 133-40.
51 . Ibid
52. Misischia PJ: The evaluation of intraoular tension following ostepathic
manipulation. JAOA July 1981 , 80:750.
53. Feely R, Castillo TA, Greiner JV. Osteopathic manipulative tretment
and intraoular pressure. JAOA Sept 82, 82: 60.
54. Muncie CH Prevention and Cure of Defness Through Muncie
Rstive Metho. 1960.
children with a history of otitis media from kndergarten to third grade.
56. Stein H Interal Meicne. Boston, Little, Brown & Co, 3rd ed, 1990, P
1262.
57. Hinton AE: Surgery for otitis media with effusion in children and its
relationship to parental smoking. J Lngol Otol 103: 550, 1989.
58. Degenhardt BD, Kuchera ML: The prevalence of cranial dysfnction in
59. Degenhardt BD, Kucher ML: The prevalence of crnial dysfunction in
6. Stein H Intra Meicne. Boston, Little, Brown & Co, 3rd ed, 1990, P
1262.
61. Cole W: Disorders of the nerous system, in Hoag 1 (ed) Otic
Meicine. New York, McGraw-Hill, 1969, ch 20, p 315.
62. Korr 1M (ed) The Neurobiologic Mehanisms in Manipulative T.
New York, Plenum Press, 1977, p 61 .
63. Magoun m Oepathy in the Cranial Field. Kirksville, Joural Printing
Co, 3rd ed, 1976, p 281 .
6. Hoyt (III) W: Current concepts in management of sinus disese. JAOA
October 1990; 90(10); pp 913-919.
65. O cit p 183.
66. Travell JG, Simons DG Myof Pain ad Dysfunction: A Trigr Point
M
. Baltimore, Williams & Wilkins, 1983, p 265 .
67. Op cit p 263.
68. Kaluz, Sherbin M: "The physiologic respnse of the nose to osteopathic
manipUlative tretment: Preliminary report. " JAOA May 83, 82: 654-60
69. Magoun m Oepathy in the Cranial Field. Kirksville, Joural Printing
Co, 3rd ed, 1976, pp 289-291 .
70. Rebik JM, McIntire LD, Hoyt W (III), McIntire K: Ethmoid sinus
dis and nasal septal deformities as etiologies of chronic cephalgia:
Results of surgical management. JAOA (October 1990) : 897-907.
71. Stein H Intra Mediine. Boston, Little, Brown & Co, 3rd ed, 1990, P
1262.
72. Hoyt (III) W: Current concepts in management of sinus disease. JAOA
Otober 1990; 90(10); p 918.
2 1
73. Magoun HI Othy in the Cria Field. Kirkville, Joural Prnting
Co, 3rd ed, 1976, p 214.
74. Catie A: Sino-bronchia syndrome. AAO Yearbok, 1974: 180-l .
75. Magoun HI Ohin the C Field. Kirkville, Joural Printing
Co, 3rd ed, 1976, P 215.
2 2
OSTEOPATHIC CONSIERATIONS I TE COMON COL
A OTHER UPPER REPIATORY ICTIONS
I. ITODUCTION
Probably no dises causes so much aggravation t so many people as the
common cold. Its vir etiology makes tretment with antibiotics ineffetive; in
fact, studies indicate that the use of antibiotics in a viral infetion only prolongs
the symptomatic stage of the infection. Moder medical tretment consists of
symptomatic care with a plypharmacy that ofen includes antihistamines,
analgesics and deongestants administered by spray, tablets or capsules. This is
a less than optimum protool.
The common cold affects the function of the uppr respiratory tract--nasl
passages, sinuses, ers, pharynx and bronchial tubes. The nas passges are a
very small part of the total human anatomy but they have a very imprtant role
in the maintenance of health. Though they are only 4 inches in length from the
nares to the psterior pharynx, air from a single inhalation travels that distance
in 114 second, is warmed to 96.8 degrees, 75% humidifed, and practically
fltered cle regardless of the condition of the air outside the body.
A special type of respiratory epithelium, composed of a combination of ciliated
columnar and goblet cells, provides the mens of effetively fltering and
moisturzing the air. In a state of helth, the epithelial ratio of goblet to ciliated
cells is maintained by a predominant infuence from its parasympathetic
inneration. The resulting seretion is present in two layers and normally the
layer of mucus next to the cells is cler with a saliva-like consistency.
Inhaled air is warmed and humidifed by the structural nature of three nas
turbinates which line ech nas passage. These turbinates increse the surface
area to which inhaled air is expsed and dilation of their abundant thin-walled
blo vessls effectively warms the air, even in a very cold exteral
environment.
Baus of their shap and loation, the turbulence of the inhaled air is
incresed s that foreign particles are thrown against the fuent but sticky
suprfcial layer of the mucous blanket. Freign particles stick to this
suprfcial layer where lysozyme, an enzyme present in this mucus, kills virus
and bacteria on contact. Both layers of the entire mucous blanket are move
slowly toward the back of the pharynx by the action of the ciliated cells as their
cilia move the deepr siva-like layer of mucus.
Mucus that arrives at the psterior pharynx is usually swallowed. The mucous
blanket is completely replaced 3-4 times in every 24 hour prio, amounting to
23
a normal total prouction of 1.5 pints of mucus pr day. Any bacteria or virus
remaining alive after being swallowed will be killed by the gastric acid in the
stomach.
The constant movement of air through the nasl passges would dry out the
mucous membranes without homeosttic mechaisms. In order to protet the
mucosl blanket and the nasl epithelium from drying out, 80% of the normal
ppulation have "nasl cycles." These are alterating patency cycles of te
nasl passges during which one naris assumes the dominant role of air passge
while the other one "rests". When working proprly, this fuctuation is not
noticed because the total air resistance is unchanged. If one or both nares are
unable to dilate because of allergic congestion, infetion, or some structural
problem such as nasal deviation or a fractured nose, the total resistance to the
air passing through the nas passges is gretly incresed. Patients with any of
these conditions interret the usua resting stage of the nasal cycle as "nasl
congestion" .
It is important to remember that the sme stratifed ciliated columnar epithelium
which lines the nasl passges also lines the sinuses and the bronchial tubes.
(Stratifed squamous epithelium in the respiratory tract is found only in the
psterior pharynx.)
l. PATOPHYSIOWGY
Infection begins with deresed resistance of the host. A prson c often reall
many etiological stressful situations which c reduce resistance of the boy.
Initially there apps to be increased parasympathetic activity and the mucus
becomes more profuse and watery. The common cold viruses, such as the
rhinovirus, do not attack the epithelial cell walls but produce infammation with
increased transudation of fuids rich in kinins (bradykinins, lysylbradyknin).
These st up the symptoms of infammation and predispse to bacterial
infetion. Perhaps the boy is trying to functionally fush out or dilute the
pathogen or irritant. As the viral invasion becomes more advanced, visceral
afferent impulses to the spinal cord increse. Most visceral afferent neres
share the fascial pathways traveled by the sympathetic neres which innerate
that organ, so these impulses arive at the sme cord levels as that organ's
sympathetic inneration. Afferent impulses from the sinuses and other hed
structures synaps in the dorsl hors of spinal cord segments Tl-4 and those
from the bronchial tree feed into the spinal cord at the Tl-6 levels.
Reduction in the natural resistance of the boy to protet and defend the air
passages allows secondary bacterial infection to ocur and in the c of the
infuenz virus, a diret attack upn the cell wall of the respirtory epithelium.
Infuenz virus invades the epithelial cells to use the cells' own metabolic
proesses in the prouction of more viruses. The fate of the infected cells
24
depnds upn how sverely the virus disturbs the cells' metabolism. There may
be loal congestion, mucosl ulceration, sloughing, and exudate formation.
Exudate makes an excellent media for bacterial growth and bacteria in the
region tae advantage of the denuded surfaces and "protein rich cellular broth. "
Seondary infetion by Haemophilu inuena and Staphlococcu pyogen
bacteria is common.
A steady strem of visceral afferent impulses from a dysfunctional uppr
respiratory trct "facilitates" the upper four to six thoracic spinal cord sgments
and prmits viscerovisceral refexes that result in excessive sympathetic outut
t the respirtory epithelium of the hed, neck and bronchial tubes. In the
common cold, palpatory evidence of tenderess and spasticity may be evident
from the cerical through the thoracolumbar junction, but espially from Cl to
T3.
1
Presynaptic sympathetic fbers destined for the head and neck synapse in the
cervical sympathetic ganglia while those destined for the lungs and the bronchial
epithelium synapse in the TI-6 paraspinal chain ganglia. Postsynaptic
sympathetic fbers travel through the respiratory plexus to the bronchial
epithelium of the lungs or through the carotid plexus, the deep ptrosl nere,
the nere of the pterygoid canal and then through the sphenopalatine ganglion
(without synapsing) to the respiratory epithelium of the hed.
Hyprsympathetic activity to the respiratory epithelium produces epithelial
hyprlasia. Epithelial hyprplasia is characterized by increased numbers of
goblet cells in relation to ciliated cells and encourages the prouction of
profus, thick, sticky, tenacious, slow-moving mucosl discharge.
il. TRATMT
Meical tretment at an erly stage usually includes a deongestant to
symptomatically reduce the air resistance through the nasal passges and make
brething esier. This tretment is subjectively effective by constricting blo
vessels in the nasl mucos; but in the long run, it actually encourages the
detrimental sympathetic effets listed in the previous paragraph. Sidney Harris
sid, "A bad physician trets the symptoms, a good physician trets the disse,
and a rare physician trets the patient." The osteopathic curriculum strives to
prouce the "go ad rare physician." It is often neessary to tret the
symptoms, for various resons, but kow what will be gained and what may be
lost by doing so.
The principles of ostepathic manipulative tretment ( OMT) in helping the boy
heal itself are outlined in Othic Meicne:
2
1. OMT stimulates blood supply
25
2. OMT incress venous and lymphatic drainage of the organ systems
pssibly affected
3. OMT relieves muscle spasm, reducing restriction on breathing
4. OMT reduces refex disturbances that may be impairing
a. Vasomotor regulation
b. The function of sondarily involved organs
c. Other defense respnses
5. OMT improves circulation to and from the reticulondothelial
system, to aid its respnses to an invading agent"
Simple rib raising manipulation to
the uppr six ribs reduces the
snsitivity of facilitted sgments in
the thorcic are and results in
diminished sympathetic outfow to
the mucos of the nose, sinuses and
bronchial tubes. Tretment of
relate joint somatic dysfunction
reduces facilitation at the cord level
by removing its somatic infuence.
Tretment of cerical myofascial
dysfunction opns fascial pathways
for lymphatic drainage and
simultaneously infuences psterior
Chapman's pints (subocipital
are) through somatovisceral refex
action. Bcause of the fascial ties
and the proximity of the cervical
sympathetic ganglia to the vertebral
joints, treatment of somatic
'NTERIOR POINTS: DIAGNOSTIC AIDS:
A. E
UPPER RESPIRATORY TRACT (T1-)
B. N Snus
{
D. Bonus
CERVICAL SYMPATHETIC CHAIN
t>iSupo CeMI
Gnglion
Midle Cericl
Gnglion
Infer C
Gli
As Sublava
A. ETERNAL RESPIRATION
Lypt
He a Ne
Sytm ."
. . .

t

H a Lungs
t
Aomen --
Pel -
-
-
A
-- -Toracc
-

___ Aominal
-
---
Pel
7
5
% 25%
Venous A Aerial
L7Ph
L
atic
5
%
J
:
Cilla
: ... : .
B. INTERNAL RESPIRATION
FUNCTION OF "A" DETERMINES FUNCTION OF "S"
26
P
u
m
P
s
dysfnction and fasial tension in the cerical are opens pathways for
lymphatic drainage and reduces viseral afferent infuences that are active in
maintaining related facilitated cord sgments. By reducing sympathetic
infuence and allowing the more desirable parsympathetic effets to
predominate, the respiratory epithelium prouces a thinner, more watery
sretion. Tretment of this are frst will also reduce the outfow of
sympathetic impulss via facilitated uppr cord segments.
Following tretment by rib raising, it is benefcial to tur the patient t his/her
side and provide a keding typ sof tissue tretment to the thorcolumbar
junction. This relaxes the patient and the lumbar attachments of the muscular
abdominal diaphragm, preparing the patient for a diaphragm redoming
tretment.
Increased interstitial fuid and mucosal swelling a a result of mucosl irritation,
infammation, and infection prouces an exigency for effective lymphatic
drainage to relieve congestion. Go lymphatic drainage requires unimpded
lymphatic pathways from the site of infection back to the heart and effetive
lymphatic pumping action from a well-domed abdominal diaphragm.
If not alredy accomplishe, the following static landmarks should be examined
at the thoracic inlet. Fascial torsion of the inlet should be diagnosed and
effetively treated to remove any hindrance to this terminal drainage site for the
lef and rght lymphatic ducts.
Infradavicla Spac
/
\

Lf
Right
Lf Cacl
Right Cacaviclar
Agle Agle
L R
Normal Static Landmarks of the Thoracic Inlet
Diagnos ad tret any smatic dysfunction in the midcerical and OA ares.
This insures go phrenic nere inneration to the diaphragm, relaxes the
fasial pathways for lymph fow through the cerical are and c infuence the
parasympathetic respnse in respiration. The diaphragm is then redomed by any
27
one of a number of indirect or diret fascial manipulative techniques. (Se pages
212-217 in the tretment stion of this bok.)
With lymphatic pathways fred and the diaphragm reomed, lymph fow is
initiated by using one of the many manipulative lymphatic pump proures.
The ptoralis lif tretment applied for 2 minutes furishes the pumping effet
of about 5 minutes of the usual intermittent chest pump tretment. This
tehnique is als applicable to patients with osteprosis, metastatic di s,
various typs of pstsurgical conditions and also OB patients with tender,
hyprtrophied brests. The ptoralis lift c ofen b sfely taught to the
patient's family for their us on the patient at home. In addition to moving
fuids, the thoracic lymphatic pump has been shown to modify immune
function. 3,4
Attention is then directed to the face and sinus ares. The physician's fngers
are placed over the infraorbital, and later the supraorbital, foramina. The skn
and subcutaneous tissues are contacted and circular treatment is provided over
the nerve branches of the trigeminal nere as they emerge from the maxillary
and frontal sinuses, resptively. Thes neres provide the impulss which are
interreted as pain from the respiratory epithelium of the sinuses. When the
sinuses ae infected, the patient will be very sensitive to pressure over these
neres as they exit from their formina, a helpful clue to the diagnosis of
sinusitis. If thes ares are not tender to the patient, "sinus tretment" is
probably not indicated. Though the tretment is initially uncomfortable in
patients with sinusitis, resonable manipulative effort over thes nerves helps to
relieve the subject's "sinus pain." Efeurage to the face ofen completes
lymphatic tretment.
Addition of a typ of cranial tretment employs a frontonas suture spred
S
and
encourages the ethmoid bone of the skull t move freely and normally in the
ethmoid notch of the frontl bone. Go functional motion of the ethmoid and
frontal bones encourages a natural pumping action through the cranioscral
mehanism and improves sinus drainage. This cranial technique may be
incorporated by osteopathic students and physicians, even without having
complet training in the craniosacral concept.
In order to infuence parasympathetic outfow to the sinus and nasl respiratory
epithelium it is effcacious to take a minute and tret the right and the left
sphenopalatine ganglia. This tretment has two main effects:
o .. Parasympathetic activity is a primary infuence in the prouction of a
thinner, sliva-like seretion. Stimulation of this parasympathetic
ganglion provides a "interal irgation" by thinning the thickene nasal
scretions and thus providing both symptomatic relief and improved
regional homeostasis.
28
o .. It encourages the autonomic system to establish a more normal cellular ratio
in the mucosl epithelium betwen the goblet and the ciliated columnar
epithelial cells. Parasympathetic impulses reduce the goblet cells and
incres the proprtion of ciliated columnar cells.
The sphenopalatine ganglion is loated in the sphenopalatine foss of the skull
and hangs from the maxillary division of the trigeminal nere. This is a
parasympathetic ganglion and it cannot be reched diretly by the palpating
fnger. It may be reche indiretly, through the opn mouth of te patient, by
passing a cotte fnger over the molars of the uppr jaw, then lateral and
psterior t the maxillary ridge and then cephalad over the pterygoid plates (ust
psterior to the maxillary ridge) to the extent prmitted by the buccal mucos in
the mouth.
6
The patient is then asked to no toward the palpating fnger. Two
or thre reptitions on ech side of the mouth provides adeuate tretment by
indiretly applying tension on the ganglion through the fascias of the pterygoid
muscles. Satisfactory tretment is signaled by tearing of the eye only on the
side of treatment, because the lacrimal gland shares the same parasympathetic
nere supply.
Sp
Siat
Nu VII
(Paap) .
I. SU Y
The osteopathic approach has been reprted
7
to decrese the symptoms and
durton of colds, to supprt the body's homestatic mechanisms against
29
infection, and to prevent complications and reurence. Ostepathic
manipulation provides incresed comfort for the patient, balances and supprts
physiologic protetive and homestatic mechanisms of the boy, and provides
rewarding tretment for a patient with the common cold.
This sction encourages the student of an osteopathic approach to understand,
incorrate, and record the following:
o .. The sympathetic and parasympathetic inneration t structures of the hed
and the effets of ech upn the respiratory epithelium and discharge of
the uppr respiratory tract
o .. The lymphatic drainage patter from the upper respiratory trct
o .. Manipulative tchniques for tretment of the thoracic inlet, redoming the
diaphragm and initiating lymphatic fow
o .. Manipulative tehnique for applying effeurage of the face
o .. Sphenopalatine ganglion intraoral fnger manipUlative technique
o .. The diagnosis and osteopathic treatment of cervical, rib, thoracic, and
thoracolumbar somatic dysfunction is indicated to remove the somatic
compnent of the facilitated spinal cord segments including ocipital
(condylar) decompression, frontal/nasal spread, and CV4 techniques
RFRCE:
1. Zirul EE: Infections caused by viruses, in Hoag JM Osteopathic Meicne.
New York, McGraw-Hill, 1969, ch 45, P 722.
2. Op cit P 720.
3. Measel J, Jr: The effect of the lymphatic pump on the immune respnse:
I. Preliminary studies on the antibody response to pneumoocal
plysaccharide assyed by bacterial agglutination and passive
hemagglutination, JAOA Sept 1982; 82( 1):59-62.
4. Mel J, Kty AA: The effect of the lymphatic pump on the band T
cells in pripheral blo (abst). J AOA; 608.
5. Magoun HI: Othy in the Cranial Field. Kirksville, Joural Printing
Co, 3rd ed, 1976, pp 172, 290.
6. O cit p 216.
7. Schmidt I C: Osteopathic manipUlative therapy as a primary factor in the
management of uppr, middle, and pararespiratory infetions. JAOA
Feb 1982; 81: 382-8.
30
Medial pterygoid muscle
Somatic Dysfunction Hyoid Soft Tissue for Eustachian Tube
facil. seg.
Sympathetics

Parasympathetics I
I
Treatment Plan for:
Rib Raising Sphenopalat' lne
Technique,
to Affect
erves
N-VII)
Tl-4
Cervical Fascias
(Cerv. Ganglia)
Chapman's Reflexes
I
SYATHETIC EFECTS
t Tone:
The Comon Cold,
Rhinopharyngitis and
Upper Respiratory Tract Inf.
Lymphatics
Thoracic Inlets
Abdominal Diaphragm
Effleurage
Lymphatic Pumps
t Vasoconstriction
Ganglion
Cranial OMT
Cranial N
I
(Cranial
t Thickens Secretions (t Number of Goblet Cells)
J Drainage
LYHA TIC EFECTS
J Drainage
t Congestion
PARASYATHETIC EFCTS
t Tone:
t Thinning of Secretions
Improved Drainage
31
NOT:
32
OSTEOPATIC CONSIERATIONS U
T WW REPIATORY DISORDES
I. NORAL FNCTIONAL REPIATION:
Diaphragm
Well Domed Diaphragm
Flatened
/
-+
Respiration is a dynamic
orchestration involving
cordinated refex neural
activity, abdominal
diaphragmatic and various other
muscular contractions, motion of
fascial planes, and the
movement of over 146 joints of
the boy. Effciency of this
orchestration is necessry for
effective inhalation and
exhalation, respiration and for
the prouction of pressure
gradients between the thoracic
and abdominal cavities. The
cyclic pressure gradients act as a
pump for the lymphatic system
and encourage go fow of
lymphatic fuids. It is also
involved in aiding venous fow
and a host of biochemical and
physical rections ocurring in
the blo strem durng
respiration.
Brething and respiration are not the sme. The purse of "brething" is to
move air from outside the boy into the lungs, exchange oxygen in the air for
caron dioxide in the blo strem, and then exhale the air. The purs of
"respiration" is to provide for a similar exchange of thes gases at the cellular
level. If this is to baccomplished with optimal clinical effet, brething must
bcoupled with go circulation in an interstitial tissue environment as fre
from congestion as pssible. The lung maintains its interal environment and
fnction via viserovisceral and viscerosomatic refexes.
Metabolic or respiratory acidosis or alkosis results in a change of the blo's
pH and affets its hemoglobin-oxygen dissoiation cures. This mens that the
ability of hemoglobin to give up its oxygen to the cells will vary according to
the blo's pea
2
and srum pH. Even small increses in oxygen to the tissues
33
is accompanied by a very gret increse in protection of those tissues from
infection.
Niinikoski stated: "Any tretment that augments the loal oxygen supply or
helps to avoid hypprfusion tends t incre the rte of heling and dere
susceptibility to infetion. " Ostepathic manipulative tretment affets the
pulmonary environment through smatosomatic ad somatovisceral refexes. It
als affets the musuloskeletal mechanics involved in brething, respiration and
lymph fow. Thes mehanisms have been researched by such sientists a
Bums, Hix, Olwen Gutensohn, Denslow, Korr, Krogh, Patterson, and Sato just
to name a few.
Decongestion of interstitial tissues and improvement of respiration through
mechanical and neurorefex mehanisms are also encouraged by osteopathic
manipulation.
34
Through improve
ment of the boy's
fascial pathways and
its own slf-regula
tory mehanisms for
protection and
homestasis, ele
trolyte balance, pH
adjustment, and the
delivery of oxygen to
the tissues ocurs
more esily and op
timal tissue resistance
and repair capabilities
are encourged.
In normal respiratory
activity, the slity
nucleus of the respi
ratory center in the
medulla is informe
of the collaps of the
air scs by way of
viscerl afferent
nerve fbers.
These visceral afferents travel in the pathways of the vagus nere. The refex
respns by the nucleus solitius and the respiratory center in the medulla may
be moifed by impulss received fom the carotid boy. The carotid boy is
snsitive t CO2 concentrtions in the blo.
A subsuent refex arch from the nucleus solitarius t the mid-cerical are,
(C3,4,5) prouces a contraction of the diaphragm via the phrenic nere.
Somatic intercostal neres, Tl-12, are also called into action by this refex
proucing stabiliztion of the intercostal spaces but doing little to move the ribs
unless there is a call for very dep inhalation.
When the air scs are flle, visceral afferent refexes inhibit the nucleus
slitarius and the somatic refex pathways cause the diaphrgm and intercostal
muscles to relax.
o .. If the air scs remain partially distended, the person's brething may
become more shallow.
o .. If the srum carbon dioxide content is increased, as in respiratory acidosis,
viscerosomatic refexes are initiated by the carotid boy which result in
an increse in the rate of respiration.
o .. The result of these two actions is a patient with shallow, rapid respirations.
The tubular bronchial system is lined with speial pseudostratifed columnar,
ciliated epithelium which is suppsed to protet and maintain the interal
environment of thos passgeways. It is imprtant to remember that it is the
resultant balance betwen the sympathetic and parasympathetic nere impulss
to the lung that determines the cellular mae-up of the respiratory epithelium.
This mens, espially, "the ratio of ciliated to goblet cells" in the lining of the
bronchial tubes. It is this rtio which determines the basic typ of bronchial
scretions prouced by the respiratory epithelium ad thus determines the
fnctional and protetive environment at the mucosal bronchial membrane
interface of respiration.
Pasympathetic infuence via the vagus neres is dominant in a normal
fnctioning lung. The cellular ratio of the bronchial epithelium is depndent
upn this parasympathetic dominance to prouce a cler, sliva-like (but sticky)
mucous blanket. This typ of mucous blanket is esily move cephalad towad
the epiglottis by the action of the ciliated cells in the respirtory epithelium and
it keps the bronchial passges moist and clen. Becaus of the dominant
parasympathetic:sympathetic infuence in healthy lungs, there is normally a
slight increse in smoth muscle tone of the bronchial tubes.
35
l. PATHOPHYSIOWGY - "REFEX ACTION DUG ICTION:"
Pulmonary dis, whether infectious or not, may be loked upn as the result
of the disruption or undesirable respns of one or more of the protetive
mehanisms. Any disruption of the mucos blanket or irritation of the
epithelial lining of the bronchial tubes will obviously change the bronchial
environment. Constant dysfnction of the lung's normal refex mehanisms is
assiated with predictable pathophysiologic events. 1 Infection--viral or
bacterial--is one of the most common irtants of the respiratory mechanism,
although bronchial irritation prouced by smokng is prbably very common
and, unfortunately, is often unnoticed until cell changes have ocurred.
Viral or bacterial infetions prouces lo irritation of the bronchial epithelium.
An infammatory respnse is st up which may spred into the parenchymal
tissue of the lung. Alveolar surfactant is reduced, exudate forms, and
eventually congestion and even edema of lung tissue ensues. Hours or days
later there is sloughing of some of the injured mucos.
At this pint, the patient has "tissue congestion" and pssibly even sme edema
which begins a compromise of the lung's cellular function in the proess of
respiration. The stage is set for the "signs and symptoms" of an acute viral or
bacterial bronchial infection.
The respiratory mucos of the trache and bronchi is relatively insensitive to
pain, but the movement of mucus and cellular debris over raw ares in the
bronchial tubes activate a cough refex. A cough can prouce pressure changes
of up t 30 mmHg in the lung and can prouce air veloity up to 50 mph.
While coughing is usually prouced by a protetive refex, it may als be
damaging and dangerous to some patients and is a signifcant etiologic caus of
exhalation rib somatic dysfunction.
SYMA THETIC REPNSE:
Bginning with lung dysfunction and mucosal iritation, visceral afferent nerve
endings in the are of tissue injury are stimulate. This results in a viseral
afferent bombardment of the spinal cord from the TI-6 cord levels. When the
lungs are irritate, the six uppr thoracic cord sgments have ben found,
exprimentally, t have low refex thresholds which disharge esily. This ese
of discharge is assoiated with the fnding of sympathetic hypractivity in the
relate lung tissue. Viserosomatic ad somatovisceral refexes ocur in thes
lowered threshold sgments resulting in activation by emotional, smatic, or
viseral stimuli that are unrelated to the lung. This low threshold phenomenon
is termed facilitation.
36
Viserosomatic refexes are the viscera's contribution responsible for initiating
the facilitated cord sgments in this example. Viscerosomatic refexes will also
sgmentally interact with nuclei of somatic nerves in the spinal cord to initiate
refexes which provide the physician with palpable joint and musuloskeletal
indications of lung dysfunction. These increased secondary somatic impulss
prouce palpable musuloskeletal indications of visceral dis in the TI-6 area
(espially T3-4 and somewhat preferentially on the left). Afferent impulss
from thes smatic dysfnctions beome the somatic contrbution t the supprt
and prolongation of the facilitated cord sgments. When the lung parenchyma
is involve, the infammatory condition c produce direct irritation of the chest
wall and intercostl nere with accompanying musculoskeletal dysfunction
adjacent to the lobe(s) involved. This produces pleuritic pain and is ofen
accompanied by a pleural friction rub which c be auscultated.
Primary visceral afferent activity is also felt to be responsible for the formation
of scondary myofascial tender pints called Chapman's refexes.
Cardiopulmonary System (1-6)
Hear

_
__Upper Lung
N Lower Lung
Thes pints have distinct loations and c be used to help diagnose and then to
adjunctively tret the visceral dysfunction of the lungs and other viscer organs.
The anterior Chapman pints for the uppr lung and the lower lung are found in
the third and fourth intercostl space, respctively, next to the sterum.
The sympathetic nerous system is involved in all dis proesss. Prolonged
sympathicotonia results in vanstriction with loal hypprfusion in the lung
and epithelial hyprlasia. It even diretly infuences pulmonary immune
function. Soeman and Soeman sy: "The adaptive, protetive rection might
bfar more damaging to the individual than the noxious agent or the beginning
dysfunction. "
37
Hyprsympathetic effects in the lung are initially respnsible for some dilation
of the bronchial tubes. This is not an undesirable effet at frst; but prsistence
of the protective sympathetic respnses is also respnsible for a relative
vanstriction of the arterioles in the are of tissue injury. Vanstriction
along with interstitial tissue congestion encourages hyprfusion of the lung
tissues, the very tissues that ned oxygen the most.
Another effet of hyprsympathetic activity to the lung from the facilitated
sgment is a proess called epithelial hyprlasia. In this situation, goblet cells
in the bronchial eithelium incres. The ratio of goblet to ciliated cells
incres. Not only is more mucus prouced by the respiratory mucous blanket
but the mucus beomes thick, profuse, tenacious and diffcult to expctorte.
In this condition the patient not only has congested and edematous interstitial
tissues, but also has thick, sticky, profuse tenacious mucus in the bronchial
tubes. Edema of the distal air scs may also be present in pneumonia, further
decreasing the capacity of the respiratory system by partially flling the air scs
of the lung.
PARASYATHETIC REPNSE:
It is known that the Herng-Breuer refex mechanism cannot refexly distinguish
between air scs flled with air and air scs flled with fuid; so the respiratory
center receives information from the vagus nere to limit the excursion of the
diaphragm beause the air scs are flled. At the sme time the respiratory
center receives information from the carotid body that more oxygen is neded
and the abdominal diaphragmatic rate should be incresed. The result is often
shallow brething at a rapid rate.
MSCUSKELETAL REPNSE:
The mehanical and physical compnents of respiration are also stressed by the
pathophysiologic changes just described. The diaphrgm is mehanicly
stressed by relative immobility of ribs and spine (viscerosomatic refexes) and
also by the tissue resistance caused by congestion in the lung. Incresed work
load on the diaphragmatic muscle results in a strain of its attachments to the
lower six ribs and the thoracolumbar junction producing an increse in the
lumbar lordosis and a fattening of the dome of the diaphragm. The clinical
result is often a patient with a spastic, fattene diaphrgm that displaces very
little volume during its contraction and relaxation.
Other palpatory clues to pulmonary dysfunction have been described.
2
TI-6
parspinal tissues, and espially T3-4 on the lef, have increse tone and are
often tender from facilitation through viscerosomatic refexes. Tl-12 may have
incresed paraspinal tissue tone and tenderess when the lung parenchyma is
38
involve. Thes musculoskeletal effets often restrict chest cage excursion and
further diminish homestasis. Another peak incidence of somatic dysfunction
note in numerous studies of patients with pulmonary dis c be palpated at
C2.
3
Coughing incorrates rapid contraction of the intercostal muscles. Persistent
or unexpted coughing often results in exhalation somatic dysfunction of the
ribs which then complicates the homestatic response to the underlying
pulmonary proess involved. In svere chronic obstructive pulmonary diss,
fatigue of the salenes may result in depression of the rust rib or exhalation
somatic dysfnction of rib 2, otherwis infreuent fndings.
LYHTIC SYST RPNSE:
E
!
Diaphragm
Well Domed

Diaphragm
Flattened -
3+
"Breathing, the lymphatic pump."
Normally contractions of the
abdominal diaphragm
prouce changes in volume
betwen the thoracic and
abdominal cavities. When
the diaphragm is well
domed, the volume changes
prouce effetive pressure
grdients between the
thoracic and abdominal
cavities. In this way a pump
action for lymphatic fow is
prouced. Flattening of the
diaphragm seriously
decreses volume
displacement and the
pressure gradient that the
diaphragm is able to prouce
between the thor and
abdominal cavities. In such
a situation there is a dere
in the pressure betwen thes
two ares at any given
moment. Dereased lymph
fow incres congestion of
tissues and c dere
cardiac outut.
Under normal conditions, lymphatic retur to the heart in a 24-hour prio is
eual to the entire srum volume of the body. There is no argument about the
imprtance of maintaining lymphatic fow from the lungs in disese or in heth.
39
Extrapleural lymphatics drain t intercostal vessels, to axillary noes, and then
into the left or rght lymphatic duct; however, the drainage of the pleural sc
and lung tissues travels to pretracheal noes and then into the right lymphatic
duct.
Basic medical and osteopathic
resrch have proven that chronic
lymphatic congestion with resultant
po r oxygenation of the cells is
assiate with incred infection,
incresed mortality, incresed
healing time, and increased fbrosis
and srng if heling dos ocur.
Studies have also shown that tissue
congestion decreses the
effectiveness of medical therapy.
Respiratory therapy, pulmonary
toilet and osteopathic manipulative
tretment all have substantial effects
on the prognosis of a patient when
they are included in a program to
enhance homeostasis.
m. TAT:
PNUONA:
Right
Lymphatic
Duc
Lymphatic Drainage
4
Lower respiratory infetions such as pneumonia typically prouce symptoms of
high fever, hypxia, tachypnea and toxic symptoms such as severe fatigue and
hedache; often the patient will initially have a repetitive, non-prouctive, non
effective cough. Thes patients may have chest pain, espcially with deep
inhalation.
It is also common to fnd patients with lower respiratory infetions in which
thes typical symptoms are not present. This is espcially common in the
elderly patient. Their only complaints may be unexplained "toxic" fatigue,
heviness in the chest and/or a severe hedache. Acceptable supprtive care
consists of bed rest to consere energy, a light but nutritious diet with good
fuid intake, and het to the chest or the back. Fluid and eletrolytes must be
balanced and assured either by mouth or with intrvenous drip.
Medical tretment consists of antibiotics, protection from non-prouctive cough,
losening of seretions, oxygen as required and ocasionally bronchoilators.
Erly recognition of a lower respiratory tract infection is advantageus because
40
this allows erly institution of an antibiotic that is believe to be spcifc or of a
broad enough sptrum before the cultures from deep exptorations and/or
from the blo have ben reprted. When the cultures are retured, the result
of the initial tretment is evaluated and the antibiotic changed if indicated.
Palpatory and ausultatory physical fndings precede radiographic changes by
24-48 hours.
Sometimes the cough may be suppressed by the use of dextromethorhan,
coeine or other antitussive medications, espially if it is non-prouctive and
damaging t the Q|0|, m0bm05d|05|m00580gY00I08 0mMg
the patient more comfortable instead. Realize that thes medications might
make the sretions less fuid and more diffcult to exptorte from the
bronchial system. Tretment may be given to loosen te bronchial secretions
and aid the patient's naturl defenses. Mucolytic expctorants and propr
hydration aid in the elimination of secretions and use of various mechanical
mens such as pstural clopping and intermittent positive-pressure breathing
proedures could be employed to rech this goal. Use of sympathomimetics to
dilate bronchial passges allows the patient to breathe esier but the benefts of
this typ of medication must be weighed against the pssibility of reducing
blo fow to the parenchymal tissues of the lung.
The development of medications and antibiotic tretment for pneumonias has
gretly reduced the patient's suffering from fever, hypxia and systemic
toxemia; and it has reduced the mortality from pneumonias. The effectiveness
of thes medications and the patient's comfor c be maimized by incuding
an intelligent plan for osteopathic manipulative tretments in the patient's
management program. These tretments need not be extensive to be effetive;
in fact, to much manipulation erly in the toxic stages of the infection will tire
the patient, reduce energy resere and not enhance the tretment. 5 Suggeste
protool and plans for providing osteopathic manipulative tretment to patients
with pneumonia are presnted on pages 45 and 50.
100,000 PEOPL WITH VIR INFUENZA IN T 1918 EPIDEMIC
MDICA C OSTEOPATHIC MIPUTION
OVER
MORTAITY 5% 0.25%
MORTAITY IF
PNEUONIA 30-60% 10%
COMLICATION
41
The effectiveness of ostepathic manipulative support for patients who were not
reeiving effective medications was clinically tested during the fu epidemic of
1918. Antibiotics had not yet been discovere to help patients fght bacterial
complications. Even toay, antibiotics are ineffetive against viral infections.
In this study
6
of 10,0pple with infuenz, Smith reported that patients
who reeived ostepathic manipulation had a 0. 25% overall mortality and a
10% mortality rate if they developd pneumonia. The mortality rates for
patients who only reeived meical care and no osteopathic manipulation were
5 % overall and 30-6 % if they developd pneumonia.
Such a study would never be exeuted in toay's scientifc and effective medical
siety; but this erly surey indicates the pwer and effectiveness of
manipulative supprt of the boy's own defenses. Combining medication with
manipulative tretment to support body homeostasis has ben shown effective in
reducing the hospit stay length of stay by 10%.
1
Initial manipulative tretment in pneumonia has three main goals: Reduce
congestion, reduce sympathetic hypractivity to the parenchyma of the lung, and
reduce mehanical impediments to thoracic cage respiratory motions. Effetive
manipUlative tretment accomplishing these three goals would also encourage
removal of waste proucts for detoxifcation by the liver and removal by the
kdneys; reduce vascular constriction in the tissue ares of the pathology;
enhance more predictable antibiotic dose-to-tissue levels; improve respirtion
and make the patient more comfortble. These goals are addressed esily and
effciently applying basic manipUlative tretment tehniques.
Clinically, some variation of rib raising manipulation is commonly prforme
(s page 195) with spial emphasis on the TI-6 are. The patient is usually
supine and the hed of, the bed is elevated to provide ese in respiration for the
comfort of the patient. Rib raising c be administered to one side at a time or
both sides at once. The physician may also pass both hands under the patient's
spine and grasp the eretor spinae mass (EM) with the fngers on one side of
the EM ad the thenar and hypthenar eminences on the other side of the
EM. The physicia's hands are then closed to prouce tolerable inhibitory
pressure on the eretor spinae mass muscle. As this muscle group is grsp,
the typical rib raising psture of the patient ocurs with elevation of the sterum
and ribs. While still grsping the muscle group; one hand or the other is
adjusted by right or left displacement of the patient's spine until pressure
between the two hands and the ESM of the patient seems to be as equal as
pssible. Hold this until the ESM muscles relax; then slowly relese the
pressures.
Rib rising not only relaxes the patient but is considered to effectively increse
the blo supply to the lung tissues by inhibitory sympathetic interference with
42
both vasomotor and bronchomotor control. 8 Prolonged hypersympathetic
infuence t the bronchial epithelium increases the ratio of goblet cells and
encourges thick, sticky mucus. Effective rib raising should therefore reduce
the results of excessively prolonged sympathetic infuence on the respiratory
mucos, deres the goblet cells in the mucos and encourge a thin, sliva
like bronchial scretion. In addition to improving the arterial supply, rib raising
enhances venous and lymphatic drainage from the bronchial and pribronchial
tissues.
9
Rib raising techniques applied for about 30-90 sconds usually relax
the paraspinal musculature and effectively trets sympathetic imbalance.
Manipulation is then directed toward improvement of lymphatic fow. The
thoracic inlet is diagnosed for its fascial preference and is treted with indirect
fasial manipulation or muscle energy direct techniques to prouce fredom of
fasial pathways in this terminal are of lymphatic drainage. Thoracic inlet
somatic dyfnction c also be treted by thrust manipulation but the tissues of
a toxic patent do not tolerate thrust activation a well. The thoracolumbar area
is then relaxed with inhibition of the muscles in the eretor spinae mass or by
keding the sof tissues, to prepare the musculature for redoming of the
diaphragm. The abdominal diaphragm is then tested to determine whether both
sides of this muscle are working effectively. The diaphragm is redomed if
indicated using indirect or direct fascial methods with patient respiratory
coperation, breathing in or out and holding that phase of respiration as the
physician directs the tissue relese. A well-domed diaphrgm prouces greater
pressure gradients between the chest and abdomen durng contraction and
relaxation; this indiretly results in greter efciency in the movement of
interstitial fuids by producing a more effective pumping action upn the fuids
in the closed lymphatic system.
Mehanically the thorcic cage must be able to expad in all three planes for
optimal brething. Somatic dysfunction of any of the 146 joints involved in this
proess may be considered to limit maximal chest cage function and multiple
sites of somatic dysfunction may provoke signs and symptoms.
The usual form of rhythmic compression and relese of the rib cage to
encourge movement of lymphatic fuids and even the pal pump of Dalrymple
may not be tolerated by an overly fatigued and toxic patient.
Lymphatic fow c be sfely accomplished by grasping the ptoralis musle
ner its tendinous attchment, pulling cephalad and slightly medially to tissue
tolerance and then holding for a prio of seonds or a minute or so. In effet,
this proedure pulls superiorly on the attachments of the pctoralis major muscle
to the upper seven rbs. With ech inhalation by the patient this technique
increses the volume of inhaled air. An additional 40 cc of air c be inhaled
with ech breth for ech additional centimeter of chest cage diameter.
43
A=Ordinary Exhalation
B=Quiet Inhalation
C=Deep Inhalation
Ltra v of stum wt frt a sent ribs ated.
T diara iUustat motion of t stucure during respiration.
Exhalation rib
somatic dysfunction
particularly limits
chest expansion,
while causing pain
and splinted
brething.
Exhalation rib
dysfunction is most
frequently caused by
coughing and
therefore plays a
major complicating
role in many primary
respiratory problems.
Rib raising tehniques may mobilize this dysfunction, but often spcifc OM t
the involved rib(s) is necessy to restore the homeostatic benefts obtained from
effetive brething. Examination and treatment should not be limited to rib
dysfunction however; OM to restore normal motion to the thoracic vertebrae,
sterum, and even the shoulder girdle have all been shown to improve the depth
of brething and to reduce the work assoiate with that breth. Thes may be
the only tretments prformed at the initial visit unless the patient also has
smatic dysfunction at the bas of the ociput and/or in the uppr cerical
reglOn.
Hedache is not uncommon in patients with respiratory dysfunction and is often
an obvious clue t the freuently found smatic dysfunction in this region. The
vagus has connections with the frst and second cerical neres and this may be
the functional connetion between the lung problem and the symptom of
hedache. Manipulation of any cerical somatic dysfunction, espially of the
OA or AA should make the patient more comfortable and also normalize
parasympathetic infuence to the lungs through the vagus nere.
Tretment for the hyprsympathetic activity that is found in every dis
proess is ofen trete frst. Hyprsympathetic activity t an organ is enhaced
by a facilittion of the cord sgments relate to the sympathetic inneration for
the affeted organ. The cord sgments beome facilitated by diret visceral
afferent bombardment from excessive afferent impulses originating in the
iritted lung tissues. Manipulation at any other area of the spine would snd
impulses past thes cord segments of low threshold and very likely prouce a
outburst of sympathetic impulses to the lung from those segments. Therefore in
many instances, it is physiologically desirble to calm down the sensitivity of
the facilitated segments before manipulating other ares.
44
On subseuent manipulative tretments the continued function of thes ares is
esily determined and treted a necessary. Other ares and typs of tretment
c then be given as indicated by the patient's symptoms and by examination of
the patient. Administering soft tissue tretment t the paraspinal ares while
communicating with the patient not only provides information neded by the
physician and the patient but als provides a tonic effet, improves comfort and
provides palpatory information t visceral ares needing supprt and
R
alpatory
evidence of the vitality of the patient. Liver pump ad splenic pump 0
manipulation, carefully applied, are believed to encourage detoxifcation and
have ben shown to incre circulation of WBCs, resptively. Manipulation
als tends to prevent the complication of constipation commonly prouced by
inactivity and systemic toxicity.
Osteopathic manipulation in the tretment progrm of a patient with lower
respiratory infection improves the patient's comfort and supprts that patient's
own slf-healing and protetive mehanisms. Osteopathic manipulation is
provided for the patient's needs and by understanding the stresses that a patient
should encounter with a certn disese; there is not a spifc list of tehniques
usd for a patient with a systemic disese. Osteopathic manipulation to supprt
the patient works synergistically with the medical progrm directed toward the
infectious agent and/or the disese.
Staging a patient according to the severity of symptoms has been shown to be
usful when planning an ostepathic manipulative tretment program which will
be benefcial for a patient with pneumonia. The following is a suggested
ostepathic manipulative treatment protool for hospitalized patients with
pneumonia:
11
SAMPLE OF TREATMENT PROTOCOL FOR PNEUMONIA:
Manipulative tretment in the hospitalized patient with pneumonia is suggeste
at lest daily and idelly, thre times a day. Charts and suggestions are only
guides and it is the physician's examination of ech patient that makes the fnal
determination of the systems that should be supprted and the ares that require
manipulative tretment.
STAGE I: Moerate distress, febrile, non-productive cough, usually mildly to
moerately dehydratd, exhibiting some degre of eletrolyte imbalance.
A. Rib raising to pint of tissue relese in the paravertebral are on
ech side. Bgin with the are of gretest involvement. In lobar
pneumonia this would correspnd with the ribs in diret
contiguity with the lobar region of involvement. With bronchial
pneumonia the entire rib cage region frm Tl through 12 is ofen
involve.
45
B. Bilateral soft tissue myofascial relese of the thoracic inlet fascias
and similar tretment to the uppr thorcic subscapular muscular
and fascial tensions.
C. Bilateral inhibition of paravertebral muscles in the ocipitoatlantal
are and down at lest to C5.
D. Bilateral ocipital pressures towards cranial extension (CV4) if
able to provide this tretment proprly, is useful espcially if
tempratures are 101-103
0
STAGE IT: Diminished distress, lysis of fever, ely prouctive cough,
restoration of fuids and eletrolyte balance.
A. Bilateral sof tissue myofascial relese of subscapular muscles and
fascia, rib raising by inhibition of parvertebral muscles to pint
of tissue effect. Address tretment especially to tissues which are
most signifcantly effected as determined by palpation.
B. Bilaterl sof tissue myofascial relese tretment to anterior
cerical fascias.
C. Bilateral soft tissue myofascial relese treatment of the intercostal
muscles and fascias.
D. Spcifc mobiliztion of C7 to T4.
E. Gentle inhibition of the suprior cerical segment. Extend this
tretment down to C5.
STAGE m: Convalescent, afebrile, productive cough, restoration of fuid and
eletrolytes balance has been accomplished.
A. Rib raising ech thoracic paravertebral are until tissue effect is
palpable.
B. Lymphatic pump either by bilateral pedal pressure or thoracic
pump.
C. Spcifc mobiliztion of segmental vertebral somatic dysfunction
as indicated.
PRVTION OF PSTOPEATIV PUONAY
COMLICATIONS:
The two most common pstoprative complications are ileus and pulmonary
dysfnction. Uppr gastrointestinal (GI) surgery is more likely to result in
pstoprative pulmonary complications than lower GI surgery, probably due to
the proximity of the surgery to the diaphragm. Somatic dysfunction (C3-5:
phrenic nere) can compromise respiratory homeostasis. Henshaw
1
2
demonstrates the imprtance of treting this are pre-opratively to prevent
respiratory complications following GI surgery.
46
2. 7 %
LOWER ABDOMINAL
SURGERY
Ga Populat
3X
:
INCIDENCE OF POST-OPERATIVE
PULMONARY COMPLICATIONS
38%
8 %
LOWER ABDOMINAL
SOMATIC DYSFUNCTION
C3- C5
UPPER ABDOMINAL
SURGERY
General PopUlation
SURGICL POPULTION WITH PRE-OP
C 3 SOMATIC DYSFUNCTION
I
OMU Prior t
Surger
109 CASES
85. 3%
\
/
5. 3%
Pot - Op
Pulm
Cmplictons
(
3C )
75
16 X
Hn. T D.O . Sp. 6. p 132- 3
31
Post - Op
Pulmonar
Cmplictions
47
2X
69%
UPPER ABDOMINAL
SOMATIC DYSFUNCTION
C3- C5
No OMU Prior
To Surger
CHONIC OBSTUCTE PUONARY DISEASE (COP):
Bth fnctional and structural changes take place in chronic obstructive
pulmonary dise that eventually affet the entire boy unit. Hyprinfation
with alvelar wall destructon leds to a reduction in the total alveolar are of
the lungs and a concomitant loss of pulmonary capillaries. Hypxia results and
pulmonary vascular resistance is incresed as is cardiac output. Pulmonary
hyprtension and right-side heart failure may develop. Structurally, the patient
usually develops a barrel chest and often the accessory muscles of respirtion
beome over used. Hyprtrophied scalenes may cause neurovascular
compromise affecting the uppr extremity.
The general guidelines discusse in the previous stion on pneumonia are also
applicable for supprting homeostasis in patients with chronic obstructive lung
disese. Manipulative tretment to aid in chest cage motion, thoracic drainage,
and diaphragmatic function are "extremely important" 13. Somatic dysfunction
in the upper thoracic and cerical areas is also treted to reduce segmentl
facilitation and to normalize autonomic activity imprtant in both vasomotor and
bronchomotor tone. With better blod fow to the involved tissues, COPD
patients with proprly managed somatic factors are clinically expcted to require
smaller and less frequent doses of medication. 14 Us of osteopathic
manipulative tretment in COPD patients has been doumented 15 to
signifcantly beneft pC02, 02 sturation, total lun
l
capacity, and residual
volume. In a study of chronic bronchitis patients, 1 92 % of the patients in the
OMT group:
- were able to walk greter distances
- had fewer colds and uppr respiratory tract infections
- had less dyspne
. . . than prior to their manipulative management.
ASTA:
Bronchial asthma is characteried by bronchospasm with trapping of both a
and secretions leading to signs and symptoms of dyspne, hypxia, bronchial
expiratory rales, and paroxysmal cough. The secretions are often excessively
visous and sputum is white, frothy, tenacious, mucoid, and shows microsopic
eosinophils and Charcot-Leyden crystals. Both bronchospasm and incresd
bronchial secretions may be caused by overactivity of the bronchial branches of
the vagus nerve.17 Individuals that have hay fever or asthma therefore are
generally vagotonic and also "are particularly prone to parasympathetic refexes
in the gastrointestinal tract. .,18 Often patients with asthma also have high
narrow palates correspnding to the extension cranial mechanics frequently
48
assoiated with this respirtory problem.
1
9 Sudden stress factors -- emotional,
physical, or environmental -- will often trigger an asthmatic attack.
In addition to identifcation of inciting factors with management aimed at
avoidance or hypsensitiztion, various medictions for prevention or
symptomatic relief are ut. In this sction, however, only OMT will be
disussed in detail. The "effcacy (of OMT) in asthma is particularly
remarkable. ,,20 Stiles reprts a 14% reduction in hospital length of stay (pre
DRG) when OMT was added to the medical management of asthmatic
patients.2
1
The text, Ohic Meicine, propses the following:22
"Rather than being merely adjunctive, ostepathic management of
asthma is direted primarily toward the basic disturbance. Asthma is an
outstanding example of a functional derangement. It dramatically
illustrates how unbalanced homestatic control can alter normal
bronchial muscle tone, seretion, and vasomotor fnction to caus a
seriously disbling state and ultimately, ireversible organic damage.
The functional basis strongly suggests that somatoviscerl refexes may
well be contributory or loalizing causes. Such refexes can convert
subjective discomfort into a full-blown attack. "
The goals for the us of osteopathic manipulative tretment durng an attck
may be dramatically different than the goals propsed for the use of OMT
betwen attcks. During an attack, some clinicians may attempt to initially
stimulate the sympathetics for the bronchoilator respnse that results and,
carefully considering the signifcant spasm of the thorcic musculature induced
by viscerosomatic refexes, may assist breathing and respiration with a sted
thorcic pump tehnique. The soft tissues should not be overtreted however.
Pottenger notes23 that either inhibition of the vagus or stimulation of the
sympathetics are physiologically corret in addressing the patient with asthma.
Other clinicians start with CV 4 tehnique, corret the sphenobasilar extension
mehanics, and manipulatate to normalize the vagus.24
Empirically, somatic dysfunction of the third or fourth rib is often demonstrated
and, as with most viscerosomatic induce dysfunctions, respnds porly to high
veloity, low amplitude techniques; other activating forces such as muscle
energy or indiret methos can be quite effective. Tretment of the
sphenopalatine ganglion may also be helpfl. 2 OMT is believed to raise the
threshold to irritating stimuli and to superimpsed psychogenic disturbances. 2
6
Btween attacks, maximal thoracic, steral, and costal motion is sought.
Resch by Perrin T. Wilson and by R.S. Koh demonstrated that OMT
betwen acute asthmatc episoes is able t derese the frequency and sverity
of attacks as well as the ne for medications. 27
49
BASIC PLAN FOR OSTEOPATHIC MULATION OF PATINTS WITH WWE
PULONARY DYSFUCTION:
cervicals C3-S (Phrenic Nerve)
sternum
somatic Dysfunction
facil. seg.
Sympathetics
I
I
Rib Raising
Tl-6 Treatment Plan For
Chapman's Reflexes Pulmonary Dysfunction
I
SYMATHETIC EFCTS
t Tone:
Lymphatics
Thoracic Inlets
Abdominal Diaphragm
Rib Raising
Lymphatic Pumps
1. t Thickening of secretions
2. t Vasoconstriction to Lung Tissue
3. t Bronchiole Dilation
LYMHATIC EFCTS
1. t Tissue Congestion
PARASYMATHETIC EFCTS
t Tone:
1. Thinning of secretions
2. Profuse secretions
3. Relative Bronchiole constriction
50
Parasympathetics
I
OA, A ]
Cranial
I
Vagus
Nerve
I. SUM Y:
The ability to advantageusly integrate and administer the combination of
propr meical care and distinctive ostepathic manipulation to supprt the
patient's respiratory system and compnstory mehanisms, depnds upn a
combination of thes factors:
o .. the ostepathic physician's understanding of normal and altered refex
patters
o .. the pathophysiologic proprties of the dis
o .. the ability of the physician to evaluate the patient's individual rection to
the dis proess
o .. the physician's knowledge ad sklls to provide effective and effcient
manipulative techniques which will reduce hyprsympathetic tone,
remove biomehanical impdiments to optimum chest cage motion,
improve diaphrgmatic function, move lymphatic fuids, and ensure
more approprate parasympathetic respnses so that they c be provided
for the patient when indicated.
A physician must tret the patient according to the present and future neds of
that patient indicated by a physical examination, the estimation of impnding
stresses, the pathophysiological nature of the dis and according to that
physician's trining, belief, and knowledge regarding boy homeostasis and the
diret interelationship of structure and function.
RFCE:
1. Killough, JH: Protective Mehanisms of the Lungs; Pulmonary Diss;
Pleural Disease, in Soeman and Sodeman's (ed) Pathologic Pho.
Philadelphia, W.B. Saunders Company, 1979, ch 16, p 455
2. Beal MC, Morlok J: Somatic dysfunction assoiated with pulmonary
disse. JAOA Oct 1984; 84(2): 179-183.
3. Ibid
4. Killough, JH: Protective Mehanisms of the Lungs; Pulmonary Dis;
Pleural Dis, in Soeman and Soeman's (ed) Pogic Phy.
Philadelphia, W.B. Saunders Company, 1979, ch 16, p 452
5. D' Alonzo A, Evans DJ: Disorders of the respiratory system, in Hoag JM
(ed) Ostic Medicne. New York, McGrw-Hill, 1969, ch 29, p
465.
6. Deth statistics reveal comparative values of ostepath and drug tretments.
Ohic Physician December 1918; 34: 1-2.
and Ostepathy's epidemic record. Ostthic Physician July 1919; 33: 1.
7. Fitzgerald M, (Stiles E): Ostepathic hospitals' slution to DRGs may b
OMT. The DO Nov 1984: 97-101.
51
8. D'Alonzo AF, Evans DJ: Disorders of the respiratory system, in Hoag JM
(ed) Ohic Medicine. New York, McGraw-Hill, 1969, ch 29, p
476.
9. Ibid
10. Purs FM: Infetious disss in children, in Hoag 1M (ed) Ohic
Medicine. New York, McGrw-Hill, 1969, ch 49, pp 747, 751.
11. Chila, T: (Adapte from a clinical reserch project in pneumonia), OU
COM Department of General Prctice.
12. Henshaw The D.. Sept 1963; 132-133.
13. D'Alonzo AF, Evans DJ: Disorders of the respiratory system, in Hoag 1M
(ed) Osteathic Medicine. New York, McGraw-Hill, 1969, ch 29, pp
46-465.
14. Stiles E: Manipulative management of chronic lung disese. Ostathic
Annals Aug 1981; 9(8): 30-304.
15. Howell R, Allen T, Kappler R: The infuence of ostepathic
manipulative therapy in the management of patients with chronic
obstructive lung disese. JAOA Apr 1975; 74: 757-760.
16. Magoun H: Neuroscience studies, in Goldstein M (ed) The R
Status of Spinal Manipulative Thera, Bethesda MD, US Department of
Health, Eucation and Welfare (NINCDS Monograph #15), 1975, pp
295, 301.
7th ed, 1953, P 124.
18. Op cit P 270.
19. Magoun HI Ostehy in the Cranial Field. Kirksville, Joural Printing
Co, 3rd ed, 1976, P 268.
,
20. Umanzio CB: The allergic response, in Hoag JM Ohic Meicne.
New York, McGrw-Hill, 1969, ch 43, p 693.
21. Fitzgerald M, (Stiles E): Osteopathic hospitals' solution to DRGs may be
OMT. The DO Nov 1984: 97-101.
22. Umanzio CB: The allergic response, in Hoag JM (ed) Ostepathi
Medicine. New York, McGraw-Hill, 1969, ch 43, p 696.
7th ed, 1953, p 125.
24. Magoun HI Osteopathy in the Cranial Field. Kirksville, Joural Printing
Co, 3rd ed, 1976, P 268.
25. Op cit p 268.
26. Umanzio CB: The allergic response, in Hoag JM (ed) Oepathic
Meicne. New York, McGraw-Hill, 1969, ch 43, p 696.
27. Northup GW (ed) Ostathic Resech: Growth ad Develoment. AOA,
1987, pp 82-83.
52
OSTEOPATIIC CONSIERATIONS
CARDIOVASCULAR DISORDERS
I. ITRODUCTION
"Te rule of the arer is supreme. "
-- . 1. Still
The autonomic and lymphatic systems and their effects upon the function of the
cardiovascular system have probably been studied more extensively than any
other system. This is refective of the signifcant impact that these elements
have in cardiovascular function and the support of cardiovascular homeostasis in
patients with severe compromise. Osteopathic manipulative treatment (OMT)
has been shown by Stiles to signifcantly decrease both the mortality and the
morbidity of patients with cardiovascular diseses and dysfunctions.
1
Rogers
reprts that OMT has been demonstrated to be of signifcant value in some
patients with coronary insuffciency.
2
This section briefy outlines considerations relevant in hypertension and
atherosclerosis, cardiac arrhythmias, congestive heart failure, and myoardial
infarction. Modalities such as diet, medication, exercise, stress reduction and
cesstion of smoking have gret relevance to the complete osteopathic treatment
program and these should be integrated into a total tretment program for the
patient; however, in this chapter only the manipulative elements will be
considered in depth.
M. PATHOPHYSIOLOGY
SYMATHETICS:
The sympathetic inneration of the heart has its origins in cord segments Tl-6
with synapses ocurring between pre-and post-ganglionic fbers in the upper
thoracic and/or cerical chain ganglia. While not totally ipsilateral, there are
defnite right- and left-sided distrbutions of sympathetic fbers to the heart.
The fbers originating on the right tend to pass to the right deep cardiac plexus
to innerate the right heart and the sinoatrial (SA) node. Hypersympathetic
activity to these right-sided fbers predisposes to supraventricular
tachyarrhythmias.
3
R Left
Cerical
Ganglia
,-
Superior
Sympathetic Innervation of the Heart
Incresed sympathetic tone increases
morbidity following myoardial
infarction, it inhibits the
development of collateral
circulation, and it c adversely
affect the degree of recovery from
myoardial injury. Incresed
sympathetic tone to the coronary
vessels has been linked with
coronary vasospasm.
Sympathetic nere fbers are distribute
to 8 blo vessels and generally cause
constriction of the circular smoth
muscles found in the vascular system.
Sympathetic tone normally maintains
the majority of blo vessels constricted
to one-half their maximum diameter and
therefore reduction of sympathetic tone
produces a relative vasodilation. An
overiew of the sympathetic supply to
vessls of various regions is sen in the
adjacent diagram.
4
The fbers originating on the left
tend to innerate the lef deep
cardiac plexus and the
atrioventricular (A V) nodes.
Hyrsympathetic activity of these
fbers predisposes to ectopic foi
and ventricular fbrillation. 3
Sympathetic stimulation of slected
fbers may increse the force of the
heart bet, shorten the time of
systole, increse ventricular outut
and incres the rate of contraction
of the heart muscle without
incresing blod pressure or raise
the blod pressure without a general
change in vasomotor tone of the
body. Asymmetries in sympathetic
tone may play a role in the genesis
of serous arrhythmias. 4
PMM
L
YMP1Ml
NMV
MP
UM1MNPL
N1LM
PNLt
LUl
a. UM l1M1
|
b
. MPL1N11N

M1 MPLtLN
UMlU
LMPLtLN
Sympathetic Inneration to Blood Vessels
Physiologically, these vasomotor nerves are generally unopposed and their
activation typically prouces vasoonstriction with reduced blo fow to the
boy tissues. Vasoonstriction c produce a shunt of blod from one are to
another; and it usually increses total pripheral resistance and increses cardiac
work-load. Veins are also constricted in respnse to sympathetic stimuli but the
venous respns is weaker than that in the arteries and arterioles. Sympathetic
hypractivity to the vascular supply of the kidney has been implicated as a
pssible cause of essential hypertension.
PARASYA THETICS:
Parasympathetic innervation to ares of the heart is also predominantly
ipsilateral. The right vagus primarily innervates the heart through the sinoatrial
(SA) noe and its hyperactivity predisposes the heart t sinus bradyarrhythmias.
The lef vagus primarily innervates the heart through the atrioventricular (A V)
noe where hypractivity predispses to A V bloks. The heart may be refexly
slowed by stimulating the visceral afferents of selected organs. This seems to
ocur because of their common vagal inneration. Irritation of the pulmonary
branches of the vagus produce the strongest inhibitory refex infuence on the
hert. Irritation of the larynx, pressure on the carotid boy or the pressure on
the globe of the eye (oculodiac refex) will also refexly slow the heart from
stimulation of visceral afferents that activate vagal efferents. Normally, the
ouloardiac refex will provoke a slowing of 5-13 bets pr minute; however,
it will not slow the heart at 8 in sympathecotonic gatients while slowing the
heart 10-12 beats pr minute in vagotonic patients.
Somatic dysfnction of the
ocipitomastoid suture, OA,
AA and/or C2 areas (where
there are signifcant vagal
connections) presumably
prouces effets through this
afferent activation of vagal
refexes.
Parasympathetics are also
involved in regulation of
pripheral arteriolar
vasculature, but only in a
few slet situations. In
thes ares the
parsympathetic respnse in
the loal arterial vessels is
vasoilation:
Lf
Vagus
Parasympathetic (agal) Innervation of Heart
o .. submaxillary gland vessels via fbers in the small petrosal nere (from
crial nere VII)
o .. parotid gland vessels via fbers in the small petrosal nere (from cranial
nere IX)
o .. vessels in the blush region of the face
o .. vessls in the tongue via the lingual nere
o .. vessels of the pnis via the nerus erigens
LYHATICS:
Lymphatic drainage from the heart and lungs is carried back to the heart
primarily by the right lymphatic duct. 7 Impaired lymphatic drainage from the
heart is known t severely compromise homeostasis and has been implicated in
reduced collateral circulation and increased morbidity and mortality from
ischemia and infection. 8
Congestion of cardiac tissues may result in
arrhythmias or changes in the EKG patter
(sick sinus syndrome).9 Peripherally
compromised lymphatic drainage has been
linked to the pathogenesis of atherosclerosis
and to the development of hypertension.
10
It plays a signifcant role in pulmonary
edema, asites, hepatomegaly, and the
pripheral edema sen in congestive heart
failure. Electrolyte imbalance which can
result from the development of pripherl
edema plays a signifcant role in the
@
morbidity sen in patients with congestive
hear failure.
The diameter of the thoracic duct and other large lymphatic channels is also
under sympathetic control. This fact should be considered in any tretment
protool designed to improve lymphatic drainage. Hypersympathetic activity
can reduce lymphatic fow capacity.
b
SOMTIC SYSTE:
Severe soliosis with a thoracic cure greter than 750, sriously compromises
cardiac function. Other pstur changes are more common and have their
effects through somatoviscerl refex changes or segmenta facilitation.
Pectoralis "Arhythmia" Trigger Point
In our experience, patients with
fattened thorcic kyphoses or with
pstural cross-overs in the uppr
thorcic spine tend t have prios
of tachyarrhythmias when stressed.
This is also the case in patients with
a well-doumented Travell
triggerint loated in the right
pectoralis muscle. 11 This
triggerpoint, in which posture may
play an etiologic or prpetuating
role, causes supraventricular
tachyarrhythmias. When this is the
etiology, the cardiac arrhythmia
disppears when the triggerint is
effetively treted.
Compnstory musculoskeletal problems may refexly affect cardiac function.
Tretment of the underlying pstural stressor will usually be necessary before
manipUlative tretment of the compensatory somatic dysfunctions will result in
lasting change.
Gait should also b analyzed and espcially treted in patients with
compromisd functional activity from diminished cardiac output. Abnormal
gait may increse cardiac work by up to 30%1
2
and this may surass the
patient's energy resres. Correction of an abnormal gait may allow a sverely
compromised patient to achieve a degree of indepndence in their activities of
daily living.
Somatic factors also play a signifcant role in the differential diagnosis of
prceived cardiac complaints. Anterior chest wall syndrome is often a generic
term for any one of a variety of somatic elements which caus substeral and/or
chest pains. Anterior chest wall syndrome is frequently misconstrued as
J
represnting cardiac dysfunction. A partial list of spifc entities falling into
this category might include cervical, thoracic, steral, or rib somatic
dysfunction, costohondritis (Tietze's syndrome), intercostal neuritis,
myofascial triggerints in pectorlis major, pctoralis minor, or steralis
musles, or unrecognized rb fracture. It must be emphatically stated that
smatic factors c co-exist with cardiac dis and that spinal segmental
facilitation may augment the severity of one and/or the other. Correction of a
diagnosed somatic problem, while it may relieve some of the cardiac
symptomatology, cannot rule out the need for further cardiovascular diagnostics
and/or therapeutics in a given patient.
R PATS: c be referred from numerous sites
CEST PAIN: Emergence
Pain patters in somatic tissues from
cardiac and coronary dysfunctions
have als been well doumented.
Referre pain via the cardiac
viscerosnsory refex from the
coronary arteries (angina) is
classically described as radiating to
the uppr half of the lef chest, with
referral out and down the inner
surface of the arm and hand to the
ends of the little and ring fngers. It
may als refer up the neck and into
the jaw.
CHEST PAIN: l Emergent
Satc Dsfunction of Ribs and Thoracic Vertebrae
(Is Is often overloked etiolog o chest pain)
8
t
Referred Pain
Myocardial Infarction
This classic pain distribution into dermatomes C8-T3 is particularly true when
the ventricle is involved; when the atria are involved, the pain is found lower
in the chest wall, in ares of the T4-6 dermatomes.
lO TON AD INCDENC O TORCC SOAA TC
DYFNCTON IN N CDIC
100
9 0
8 0
i
7
0
l
60
6
o
5
C
4
0
D
O

3
0
20
10
0
PATENT
92
8
3
5
29
22
18
8 6
0
1
il

1
0
T
8
T7T
6
TsT4T3T
2
T
1
T
1
T
2
T
3
T4TS
Ta Spine Toracc Spine

Ltion
At fo dat b Mon Ba. DO. FAO
"Palpto Tetng for Smatc Dfuncon in
Patent wt Cdiovala Disea"
. 82 (11) pp. 82-8
31
Referrl via the cardiac
viseromotor refex leds to
muscular contraction and spasm in
the upr intercostal muscles.
Lrson 13 B14 and Nicholas 15 ,
f
,
as well as numerous other
osteopathic physicians, have
separately reported the consistency
of palpatory changes primarily on
the left side at the levels of T2, 3, 4
as being assoiated with cardiac
disorders. Palpatory fndings of
somatic dysfunction at Tl -5 on the
left demonstrate 73 % 16 to 79 % 17
accuracy compared to angiography
in determining the presence or
absence of coronary artery disease.
Chapman s refexes from the heart
are also consistent with these
levels. ` The psterior and inferior
walls of the heart are heavily
innerated by cholinergic fbers.
While anterior wall myoardial infarctions predictably demonstrate
viscerosomatic changes in the Tl-4 paraspinal musculoskeletal on the left, 19
psterior or inferior wall myoardial infarctions are accompanied by incresed
acetylcholine and brdyarrhythmias. Thoracic palpatory fndings at T2 are less
predictable in psterior and inferior wall infarctions. In myoardial infarction
(espially with involvement of the psterior or inferior wall), thes palpatory
changes at C2
20
may need some explanation. According to some clinicians, an
autonomic rationale can be pstulate as an explanation beause of the vagal
connections to the C2 are.
The reurrent fnding of somatic dysfunction or pain in the nek,
cericothoracic junction, uppr thoracic are, chest, shoulder or arm should
alert the physician to the pssibility of a signifcant cardiac etiology. Likewise,
while a myofascial triggerint in the pctoralis major may led to functional
cardiac changes, cardiac pathology may refexly prouce triggerints in the
pctoralis myofascial tissues.
2
1
9
m. TREATT SU RY - SELECTED EXALE
MYOCARDIAL IARCTION:
The majority of patients seen within 30 minutes of acute myoardial infarction
demonstrate signs of autonomic disturbance.
22
This is evidenced a
sympathicotonia in the upper six thoracics (particularly T-3 on the lef) in
patients with anterior infarction and as vagal hypractivity (C2 and cranial base)
in patients with inferior wall infarction. All MI patients would theoretically
beneft from reducing the sympathetically assoiated cardioardiac refexes (C8-
T5) s a to prevent ventricular arrhythmias; concer also exists for those with
excessive parasympathetic activity which c led to hyptension and
subsquent diminished coronary blod fow to ischemic areas of the
myoardium.
23
For patients in the intensive care
unit following myocardial infarc
tion, patients with angina, or
patients with other serious cardiac
insults, treatment is therefore
direted at calming the sympathetic
hypractivity especially in the upper
thoracic spine to reduce inappropri
ate crdioardiac refexes, lower the
incidence of ectopic foi and
ventricular fbrillation, and to
remove at lest one factor which
disourages development of collat
eral circulation. This is usually the
frst manipulative goal in the
tretment sequence because ascend
ing input from other manipulative
tehniques might otherwise be
foused through facilitated segments
into the injured myoardial region.
90
80
70
6
0
50
40
30
2
0
1
0
5 Patt wt wInfacn
A NwIb Ed M.
... e
0 No OMT
WtOMT
_... _ ........ _..._._. g, . . ... -............ -.
26
%
_........ .. ..
1
6
%
When integrated with effective medical management for this and other acute
goals, specifc osteopathic manipulative tretment should probably be limited to
indiret techniques to avoid undue transient elevation of sympathetic activity to
the heart from the tretment itself. OMT may also be applied in the form of
generalized paraspinal inhibition to decrease total peripheral resistce
24
and
cardiac workload.
bU
Any thoracic inlet dysfunction is treted with indiret technique and if chest
compressions have ben applied during an emergency cardiac resuscitation, both
the ribs and the sterum may beneft from indirect corection of the
dysfunctions that are most certainly present. An excellent cse can be made to
als include tretment of hyoid dysfunction beause of the fascial continuity to
the meiastinum. Petoral traction would probably b the tretment of choice to
enhance lymphaticovenous retur. The diaphragm may also be redomed using
indiret tehniques. Diagnosis and tretment of C2 supriorly including the
bas of the skull are prformed in an attempt to address parasympathetic activity
to the heart. CV 4 is a technique that is helpful in fuid homeostasis as well as
in lowering the patient's stress levels. Osteopathic manipulative tretment along
the lines outlined in this section have been demonstrated to signifcantly lower
the incidence of arrhythmias and mortality in post-MI patients
25
and to lower
total pripheral resistance.
26
Regardless of the techniques selected, a number of physiologic goals are
considered to be addressed effectively by OMT. Thus OMT has been advoate
for coronary heart disese by osteopathic manipulative spcialists
27
,
28
,
29
and
osteopathic cardioiogists
30
alike.
ESEIL HYPERTENSION:
Hyprtension is a common problem
affeting more than 15 % of the US
adult ppulation. Of thes cases,
approximately 85 % are considered
to have primary or essential
hyprtension.
Most authors postulate essential
hyprtension to have a multifactorial
etiology with a pssible genetic
preispsition aggravated by
environmental and habitual factors
a well as neurogenic, humoral, and
vasular factors.
bJ
HYPERTENSION IN ADULTS IN U.S.A.
Snda 15%
20% Hprnsi
2:1 - Bla:Wite
Functional elements are frequently implicated in the process:
o . . most patients with essential hypertension demonstrate vascular and cardiac
hypr-rectivity to sympathetic stimuli;
31
o .. prolonged sympathetic stimuli to the kdneys cretes a functional retention
of water and slt and elevated arterial pressure;
o . . venoonstriction is se n in the erly labile phas of essntial hyprtension
with an incresed cardiac outut accompanied by inappropriately normal
pripheral resistance.
32
rEMOTIONAL STATE
CEREBRAL
_CORTEX
HYPOTHALMUS
RESET BAROCEPTORS
E
.:..
PERIPHERAL
.. __ -
ANS
RESISTANCE
L
VA5C I
SWEWNG
I INCREASED
SODIUM CONTRACTILIT
RENAL
ISCHEMIA
\
RETENTION _ TUBULR
,
....... NA LOAD
ALTER
J
ELECTROLYTES
ALDOSTERONE
|
...
`(ADRENAL I
NIU
2
Eventually pripheral
resistance increses
and cardiac outut
returs to normal.
With prolonged
hyprtension, the
homeostatic mecha
nism incorrated in
the carotid sinus
baroreceptors resets
and tends to maintain
the increased arterial
pressure.
33
The ad
jacent fgure summa
rizes the physiologic
factors involved in
blo pressure
regulation.
.
t
m
I
ENA
q
"
0-11 TIO-I1
I .
_
Mm Piper sisIc
t

t
L.W. W P.., Glomerular Rltaton
M
1

AHt
''=
1 t BLOOD PRESSURE 14
MWhW Auids J.. .
Boepto r
CN IX
CN X
' Hrensio n
on physiologic mechanisms in these ares, OMT to supprt homeostasis
should b effective in patients with hyprtension. Regular ostepathic
manipulative tretment is therefore felt to break the cycle of incresingly
freuent episoes of sympathicotonia and delay the stage of fxed hyprtension.
According to Ohic Medicine, "Effective management of primary
hyprtension will pstne for years the time when compnstory mechanisms
beome exhausted and the effets of nephrosclerosis are manifested. ,,34 Due to
the widespred distribution of the sympathetic nerous system, treatment is
usually directed to the entire spinal column.
b3
Stress reduction is extremely helpful in reducing cardiovascular manifestations
espially in patients with evidence of the presence of facilitated spinal cord
sgments.
Transiently
Inaeased
Sytemic
Blo Pressure
Incea
Renin
Relea
Cnsticion
of Renal
Efferent Aerioles
Thicening of
Resistant
Vessels
Inaeas Peripheral
Reistanc
Adapte from Kplan NM
m
1979; 1 :56.
Inceasd
Fltration
Facor
Nephroscerosis
Inaeased
Sium
Rorton
Relativ
Auid Volume
Es
Dea
Renin
Relea
This diagram illustrates a hypthesis for the role of stress and the sympathetic
nerous system in the pathogenesis of essential hypertension. It is adapted from
Kaplan N Hyertension 1979; 1: 546.
35
4
Patients with any cardiovascular dysfunction should also be given the beneft of
tretment to address kidney and adrenal function because of these organs'
intimate cordination in the maintenance of boy homeostasis.
One study of hypertensive patients
in which Chapman's psterior
pints to the adrenals were treted
resulte in a blood pressure drop of
15 mm Hg systolic and 8 mm Hg
diastolic pressure
36
and serum
aldosterone levels in hypertensive
patients have been demonstrated to
decres 36 hours pst-OMT.
37
In
another study of 10 hypertensive
patients treted with OMT only,
there was an average drop of 33 mm
Hg systolic (from 199 to 166 mm
Hg) and 9 mm Hg diastolic (from
123 t 114 mm Hg).
38
Rotator stimulation of the posterior Chapman's
points (11-12) depicted above have been
shown to effectively lower blood pressure and
decrease serum aldosterone levels.
38
Rotatory stimulation of the posterior adrenal Chapman's points depicted in the
diagram above has been shown to effectively lower blood pressure and decrease
serum aldosterone levels.
39
Reduction of both systolic and diastolic bloo pressure is the "rule" following
OMT.
4
"Whatever technique is used, it should be slow-moving and gentle to
augment rest and relaxation, promote autonomic balance and relese fascial
contractures. 41 The following chart pstulates mehanisms for the tretment
used in hypertensive patients based on the clinical results seen and the anatomic
are being treated:
b
TRTMNT
OA
PSTUATED MCHANISMS FOR
OSTEOPATIC MUATION
MCHISMS ONSET
OCCIPITOMASTOID NEURAL 30 SEC
TECHNIQUE
RIBS STRESS-
GENERL OMT RELAXATION;
BIOFEEDBACK ANS
THORACOLUMBAR
JUNCTION RENIN-
CHAPMAN'S ANGIOTENSIN;
REFLEXES ANS
FASCIAS BODY FLUID
CV4 SHIFTS
CONGETIVE HEART FAIURE:
30 SEC
2 MIN
10 MIN
FL EFFECT
30 SEC
16 HRS.
?
1-2 DAYS
Physicians should place special emphasis on lymphatic goals when treating
patients with congestive heart failure (CHF) in addition to the general approach
to the autonomics discussed throughout this chapter. In CHF 3 to 40 times the
resting amount of lymphatic retur challenges the system.
42
,
4
3
Dilation of the
thoracic duct to several times its normal size may ocur causing leakage out of
the duct and subseuent ascites. Inability to accept further lymphatic fuid
results in pripheral edema.
Increased venous and lymphatic retur c be translate into incresed cardiac
outut and homeostatic resistance to extension of injury following myoardial
infarction. Optimal respiratory function is vital for the maintenance of
tretment effects directed at lymphatic and venous retur. For this reson
additional time is felt to be well spent on treting diaphragmatic and thoracic
cage somatic dysfunction. Lymphatic pumps and effeurge aid in fuid
homestasis and help to restore protein and electrolyte levels in these patients.
OM should not overload the circulatory system but may derese the
ineffciency of a dilated thoracic duct and restore lymphatic rates to resting
physiologic levels purorted to be maximal at approximately 1 ml pr minute.
ARRHYTHS:
comprehenive approach of osteopathic medicine seem
peculiarly suited to cardiac arrhythmia. Cemotherapy can be
liesaving, but perhaps some of those lie-threatening emergencies
could be avoided i the physician would seek out and treat early
sites of dysfnction however remote fom the hean proper, or
would view the onet of arrhythmia in the light of homeostatic
and strctural mechanisms. M
Rational osteopathic management including OMT is described in the text,
Oic Medicine, for sinus tachycardia, sinus bradycardia, sinoatrial blok,
atroventricular blok, extrasystole, paroxysmal atrial tachycardia, paroxysmal
ventricular tachycardia, atrial futter, atrial fbrillation, and conduction
defcits.
45
Homeostatic support includes OMT directed towards reduction of
segmental facilitation in the upper thoracics and use of techniques to modify
vagal tonicity (such as pressure over the eyes, massang the carotid sinus,
strong forward bending of the head [Erben's refex], Val salva maneuver, or
tretment of ocipital-OA-AA-C2 dysfunction). Structural support also includes
appropriate attention to postural factors and correction of trigger pints,
espially those in the pctoralis (described on page 57) or steralis muscles.
OSTEOPATHIC MPULATION OF A PATIENT WITH CARDIAC
DYSFUNCTION
Somatic Dysfunction
facil. seg.
Sympathetics
Cervical Ganglion
Rib Raising
Tl-6
Chapman's Reflexes
T lO-L2
I
Adrenal
Kidne y
: paraSympatheticsl
Treatment Plan
For
Cardiac Dysfunction
Lymphatics
Thoracic Inlets
Abdominal Diaphragm
Rib Raising
Lymphatic Pumps
J
I
OA, A
J
va
Cranial Ne
gus
rve
SYMATHETIC EFECTS
t Tone
:
Increased
1. t Heart Rate and t Vasoconstriction Cardiac
2
. t Cardiac Irritability Arrhythmias Work
3. Coronary Artery Vasospasm
, Tone:
1. , Venous Capacity
2
. , Ability to Develop Collateral Circulation
LYMHATIC EFCTS
Impaired Flow:
1. t Central Venous Pressure
2
. t Tissue Congestion Decreased 0
2
and Nutrients
to the Myocardium
3. t In Size of Infarction from MI
4. t Risk of Subacute Bacterial Endocarditis
PARASYMATHETIC EFECTS
t Tone:
1. Bradyarrhythmias via SA Node (Right Vagus)
2
. Heart Block via the AV Node (Left Vagus)
3. Hypotension and Diminished Coronary Blood Flow
in Inferior MI
. CLIICALLY RELEVANT ABSTRACTS - BfLIOGRAPHY
The following sction briefy abstracts a few pints supportive of the pstulated
role that structure-function interrelationships and/or homeostatic factors play in
an ostepathic approach to tretment of the cardiovascular system. The reder
is encouraged to review the complete article for specifcs or qualifcations and to
integrate their fndings into the brief descriptions of osteopathic care offered in
this chapter.
AUTONOMC NERVOUS SYSTEM:
1. "The obseration that in the majority of patients seen within 30 minutes afer
the onst of acute myoardial infarction there were signs of 'autonomic
disturbance,' namely signs of sympathetic hyeractivity mostly in patients with
anteror infarction and signs of vagal hyperactivity mostly in patients with
inferior infarction, not only represented a major contribution but also provide a
neessry link between experimental studies and clinical reality. "47
8
2. Active visceral afferent impulses from the heart prouce refex effets which
are mediated at spinal levels through a cardio-cardiac refex (viscerovisceral)
and are involved in extending the degree of myoardial injury in myoardial
infarction. Occlusion of the left circumfex coronary artery in dogs led to
tachycardia. It was also observed that if denervation of the sympathetics was
prformed frst and then a coronary artery was occluded, those dos had smaller
ares of myoardial infarction than dogs that were not denervated. 8
3. "There is a link between the magnitude of sympathetic activity in humans
with myoardial infarction and the hert muscle metabolism, and accompanying
hemoynamics and clinical disorders. The nature of the adrenergic respns
remains mysterious. In particular, it is not known why this respns
(sympathicotonia) is large in one individual and only moderte in another. ,,49
4. Stimulation of sympathetic nerves lowers the cardiac muscle's threshold for
ventricular fbrillation in animals and has been seen to increse coronary
vascular resistance in patients with ischemic het disease. `
5. Sudden deth is the result of ventricular fbrillation. This condition c be
reversed if realized and if equipment is available for tretment. Transient risk
factors induce eletrical instability and in the electrically unstable heart there is
incresed susceptibility to ventricular fbrillation. These transient risk factors
are generally derived from activities higher up in the nerous system:
o . . sympathetic pathways from the hypothalamus are implicated in the genesis
of ventricular arrhythmias
o . . the left stellate ganglion is dominant in the enhancement of sympathetic
efferent activity which predisposes to ventricular fbrillation
o . . stimulation of the left stellate ganglion is assoiated with increses in the
inotropic effect to the heart while right-sided stellate stimulation
increses both chronotropic and inotropic effets
o . . infuence of circulating adrenal cateholamines on cardiac excitability is
considerbly less than the infuence of the neural input to the heart from
the stellate ganglion
In summary, increased sympathetic activity predisposes the heart to ventricular
fbrllation. Protection can be achieved with surgical deneration,
pharmacologic denervation, or procedures which refexly reduce sympathetic
tone. '
6. The most striking and convincing evidence that sympathetic neura inputs are
active in provokng malignant ventricular arhythmias is demonstrated by the
sries of disorders of ventricular repolariztion known colletively a the long
Q-T syndrome. A vaety of sensory inputs, ranging from emotionally stressful
9
events to noise and exertion, may trigger ventricular tachycardia or ventricular
fbrillation. An imbalance between the right and lef stellate ganglionic
sympathetic impulses to the hert has been pstulated a being the mechanism
respnsible for this. 5
2
7. A cardio-cardiac refex takes place within a few sconds of ischemia and
plays an imprtant role in the genesis of erly ventricular arrhythmias.
Interruytion of visceral afferents from C8-T5 reduces the arrhythmias to a maor
extent. 3
8. On initial examination, patients with sinus tachycardia were found to have
sympathetic overactivity.
Trnsient hyprtension in the absence of sinus tachycardia was also regarded as
evidence of sympathetic activity. Patients with sinus bradycardia or A V block
were considered to have parasympathetic overactivity. Sympathetic and
parasympathetic overactivity may coxist in cardiac patient.
The anatomical distribution of vagal receptors may explain the greater frequency
of parasympathetic overactivity in patients with posterior infarction . . . refex
vagal overactivity may produce A V blok. 54
9. Experiments revealed that when sympathetic nerves to the kidneys are
stimulated continuously for several weeks, fuid retention from reduced renal
function ocurs and results in chronically elevated arterial pressure as long as
the sympathetic stimulation continues. It is therefore logically theorized that
sympathetic stimulation of the kidney produces chronic elevation of arterial
pressure.
Essential hypertension is probably produced by functional retention of water and
salt by the kidneys. 55
LYHATICS:
1. Respiratory activity is the principal mechanism underlying the fow of lymph
from the thoracic duct into the venous system. It appars that the capacity for
trnsfer of lymph is delicately adjusted to the normal rte of lymph prouction.
Patients with systemic or prtal venous circulatory congestion convert the
plasma into lymph at an abnormally high rte. Available evidence indicates that
this excessive volume of lymph, amounting at times to 3-4 times the blo
volume in a 24 hour priod, eventually exceeds the fow capacity of the thoracic
duct/venous junction. The fow capacity of this junction appears to underlay
distension of the duct and the formation of ascites. ,,56
JU
2. "Kellner in 1955 reprted an interesting study of the relationship of lymph
and its pssible role in the pathogenesis of atherosclerosis. "
"It s ms likely that under normal circumstances there is a constant fow of
fuid contaning various srum lipids and protein across the endothelium into the
walls of the blo vessels; this material normally passes through the wall and is
completely removed by way of vasovasorum and lymphatics. In certain
conditions, however, where there are incresed amounts of lipid in the blood or
where there are excessive quantities of certain typs of lipids, the removal of
these particles from the wall of the vessel is incomplete and some remain to
initiate the proess of atherosclerosis."
"In hyprtension, incresed hydrostatic pressure apps to caus an increse in
the quantity of srolipprotein that diffuses across the vessel wall, thereby
incresing the pssibility for incomplete removal and hence for the depsition of
lipids. "
"In this theoretical formulation of the pathogenesis of atherosclerosis, the artery
wall is regarded as an organ which is constantly bathed by a serum transudate
containing, among other things, various serolipoproteins, most of which pass on
through, some of which doubtless are metabolized loally and a few of which
remain behind to cause mischief.
5
7
3. If by anatomic fault or abnormal physiologic mechanisms, lymphaticovenous
communications fail to function, the rate of edema of the limbs or organs in
congestive he failure may be increased or resolution (including respons to
therapy) may be impeded.
"Data so far suggests that lymphaticovenous communications or, more broadly,
adequate lymph fow plays a part in minimizing pathologic manifestations of
disordered lymph fow from a particular organ or limb. "
58
4. There exists at present a "state of insuffcient training of most physicians in
lymphology. ,,
59
5. In a study
60
of 28 dogs and 10 humans: "Insuffciency of the cardiac lymph
circulation has not only a theoretical but also clinical imprtance in the
pathogenesis of arrhythmias. "
In cardiac lymphostasis the following was observed:
o .. dilated lymph vessels, interstitial edema, edematous swelling of the
myofbrils and changes in atrial action potentials
o .. shortened effective refractory perio of atrium and ventricle (irritability)
o .. diminished SA noe automatism
JJ
o .. slowed A V conduction (prolonged P-Q -- A V bloks)
o .. EKG changes similar to sick sinus syndrome
6. The protective role of the pulmonary lymphatic system is dramatically
evident when there is an abrupt development of pulmonary edema in a
previously asymptomatic patient with advanced mitral stenosis. These pople
develop congestive heart failure and ofen demonstrate a functional expansion of
the pulmonary lymphatics over a prio of time. The expansion with incresed
lymph fow may be a compnstory mechanism to remove the overt pulmonary
edema.
61
7. Exprimental evidence by a team of cardiologists at Michael Reese Hospital
(Chicago) notes: Fibrous and elastic tissue increses signifcantly in the
ventricular endoardium when a dog's cardiac lymph fow is chronically
impaired. Impairment of cardiac lymph fow may similarly cause
en do myoardial fbrosis and endocardial fbroelastosis in humans.
Ventricular subendocardial hemorrhages frequently occurre son after lymph
fow obstruction in the heart of dogs. Areas of hemorrhage might led to
fbrosis when cardiac lymph drainage was chronically inadequate. Autologous
blood injected into the lef ventricle of lymph-impeded animals led to marked
fbrosis and changes resembling the pathology sen afer acute myoardial
infarction. This was compared to few abnormalities found in controls with
normal cardiac lymph fow.
Dogs with impaired cardiac lymph drainage were injected with bacteria and
most developed endoarditis of the mitral valve. This was compared to no
ocurrences in controls with normal lymph fow. Reserchers were led to
conclude that chronic interference with lymph fow predispses to infetion and
infammation. If impaired drainage from the heart is one of the factors that
predispose a human to bacterial endocarditis, then "it is conceivable that this is
one of the means by which rheumatic fever predisposes to subsequent bacterial
infection. "
It is unquestionable, the lymphatic system was important in the reparative
proesss sen in dogs after the injection of autologous blo into the
myoardium and lymph fow may prove to be equally signifcant in healing after
acute myoardial infarction. Animals with intact lymphatic drainage of the
heart undergoing the sme injection showed much smaller or absent ares of
infarction and had a lower mortality and morbidity than animals with impaired
lymphatic drainage.
Dr. Dumont of NY University studied the effect of cannulizing and venting nine
patients who were in the fnal stages of heart disese and had huge distended
thoracic ducts from lymph under pressure. Within 24 hours, centrl venous
J2
pressures fell toward normal and distended neck veins, pripheral edema, ascites
and liver tenderess all diminished or disppeared. Liver edges no longer
projeted out under the costal margin.
62
RFCE:
1. Fitzgerald M, (Stiles, E): Osteopathic hospitls' solution to DRGs may be
OMT. The DO Nov 1984: 97-101.
2. Rogers JT, Rogers Je: The role of osteopathic manipulative therapy in the
tretment of coronary heart disease. JAOA Sept 1976; 76: 71-81.
3. Corr PB, Gillis V. Autonomic neurl infuences on the dysrhythmias
resulting from myoardial infarction. Circ R July 1978; 43(1):
1-9.
and Lown B, Verrier V, Rabinowit SH: Neural and psychologic
mechanisms and the problem of sudden cardiac death. Am J Cardio
May 26, 1977; 39: 890-902.
4. Ibid (Lown et al. )
5. J Autonomic Nerous System, 1981.
7th ed, 1953, p 111.
7. Soeman W A, Sodema TM Pathologic Physiolo: Mehanisms of
Disease. Philadelphia, WB Saunders, Sixth Edition, 1979.
8. Miller P! The lymphatic system and cardiac disese, in Mayerson HS
(ed) Lymph and the Lymphatic System, CC Thomas 1968, pp 213-229.
and Lymphatics' role stressed in cardiovascular disease. Me World News
Jan 21, 1966; pp 10-101.
9. Foldi Press in Lympholo, pp 84-85.
10. Mayerson HS: One aspect of the role of the lymphatic system in
cardiovascular function, in National Conference on Cardiovascular
Diseses The Heart and Circulation. Washington, 1965, Vol 1, pp 90-
91.
11. Travell JG, Simons DG Myofascial Pain and Dysfunction: A Trig Point
Manual. Baltimore, Williams Wilkins, 1983, ch 42.
12. Saunders JB: The major determinants in normal and pathological gait.
The Jal of Bne and Joint S Jul 1953; 35-A(3): 543-558.
13. Lrson NJ: Summary of site and ocurence of paraspinal soft tissue
changes of patients in the intensive care unit. JAOA May 1976; 75:
840-842.
14. B MC: Viscerosomatic refexes: A review. JAOA De 1985: 786-801.
15. Nicholas AS, DeBias DA, Ehrenfeuchter W, England , England RW,
Grene CH, Heilig D, Kirschbaum: A somatic compnent to
myoardial infarction. Brit Med J July 6, 1985; 291: 13-17.
16. Cox JM, Gorbis S, Dick LM: Palpable musculoskeletal fndings in
coronary artery disease: Results of a double-blind study. JAOA Jul
1983; 82(11): 832-36.
17. Beal MC, Kleiber GE: Somatic dysfunction as a predictor of coronary
artery dis. l May 85; 85(5): 302-307.
J3
18. Byres TR, Kuchera ML, Guffey JM, Steele , Betty DR, Haman JL,
Lko MD: Correlation of palpatory fndings with visceral
diagnoss. JAOA 92(9):1177, Sept 1992.
19. Rosero H et al: Correlation of palpatory obserations with anatomic lous
of acute myodial infarction. JAOA Feb 1987; 87: 119.
20. B Me: Palpatory testing for somatic dysfunction in patients with
cardiovascular disese. JAOA Jul 1983; 82(11): 822-831.
21. Travell JG, Simons DG Myofascial Pain and Dysfnction: The Trg
Point Manual, Williams Wilkns, 1983, pp 585-586.
22. Schwartz PJ, Stone HL: The role of the autonomic nerous system in
sudden coronary deth. Annals NY Academy of Sces 1982;
382:162-180.
23. Ibid
24. Burchett G, Dickey J, Kuchera M: Somatovisceral effects of osteopathic
manipulative tretment on cardiovascular function in patients (abst).
JAOA 1984; 84(1): 74.
25. Fitzgerald M, (Stiles E): Osteopathic hospitals' solution to DRGs may be
OMT. The DO Nov 1984: 97-101.
26. Burchett G, Dickey J, and Kuchera M: Somatoviscerl effects of
osteopathic manipulative treatment on cardiovascular function in patients
(abst). JAOA 1984; 84(1): 74.
27. Patriquin DA: Manipulation for the patient with myoardial infarction.
Osteathic Sympsium February, 1975; pp 16-17.
28. Stokey JR: OMT for angina. Osteopathic Sympsium March 1975; pp
16-18.
29. Frymann V: Osteopathic manipulation held to aid heart function. Clinical
Trends in Osteopathic Medicine March-April 1976; pp 1, 5.
30. Rogers JT, Rogers JC: The role of osteopathic manipulative therapy in the
tretment of coronary heart disese. JAOA Sept 1976, 76:71-81.
31. Merck Manual, Rahway NJ, MSD Resech Lb, 15th ed, 1987,
Q 390.
32. Op cit p 393.
33. O cit Q 390.
34. Daiber . Disorders of the kidneys in Hoag JM (ed) Osteopathic
Medicine. New York, McGraw-Hill, 1969, ch 39, pp 64-5.
35. Kaplan N: Arerial hyperension, in Stein JH (ed) Intral Meicne.
Boston, Little, Brown and Co, 3rd ed, 1990, Q 240.
36. Mannino JR: The application of neurologic refexes to the treatment of
hyprtension. JAOA; 79(10): 607-608.
37. Mannino JR: The application of neurologic refexes to the tretment of
hypertension. JAOA De 1979; 79: 225-231.
38. Northup TL: Manipulative management of hypertension. JAOA Aug
1961; 60: 973-978.
39. Mannino JR: The application of neurologic refexes to the tretment of
hyprtension. JAOA De 1979; 79: 225-231.
40. Daiber . Disorders of the kidneys in Hoag JM (e) Osteopathic
41. Magoun HI Oeopathy in the Cranial Field. Kirksville, Joural Printing
Co, 3rd ed, 1976, Q 280.
J4
42. Dumont AE, Clauss V, Reed GI: Lymph drainage in patients with
congestive heart failure, comparison with fndings in hepatic cirrhosis.
NEM 1963; 269: 949-952.
43. Lymphatics' role stressed in cardiovascular dis. Me World News
Ianuary 21, 1966: 10-101.
44. Baldwin W, Ir: Cardiac arhythmias, in Hoag 1M (ed) Osteic
45. Op cit pp 480-486.
46. Pottenger FM Soms of Visceral Disea. St Louis, CV Mosby Co,
7t e, 1953, Q 111.
47. Schwartz PI, Stone HL: The role of the autonomic nerous system in
sudden coronary deth. Annals NY Acad S 1982; 82: 162-180.
48. I Autonomic Nervs S, 1981.
49. Circ ReSeh 1981; 48: 6.
50. NM August 21, 1980.
51. Lown B, Verrier V, Rabinowitz SH: Neural and psychologic mechanisms
and the problem of sudden cardiac death. Am I Cardio 1977; 39: 890-
902.
52. DeSilva V. Central nerous system risk factors for sudden cardiac deth.
Annals NY Acad Sci 1982; 382: 143-161.
53. Schwart PI, Stone HL: The role of the autonomic nerous system in
sudden coronary deth. Annals NY Acad Sci 1982; 382: 162-180.
54. Autonomic disturbance at the onset of acute myocardial infarction. N
Mehanisms in Cardiac Arrhythmias, 1978.
55. Guyton Textbok of Physiolo.
56. Am I of the Med S 1975; 269: 3.
57. Mayerson HS: One aspect of the role of the lymphatic system in
cardiovascular function, in National Conference on Cardiovascular
Diseses The Heart and Circulation. Washington, 1965, vol 1, pp 90-
91.
58. Threefot S: Lymphaticovenous communications, in Lymph ad the
LSm. CC Thomas, 1968, ch 2.
59. Foldi Progress 10 Lympholo.
6. Op cit pp 84-85.
61. Mayerson HS Proedings of the Conference on Lymph ad the Lymphatic
Sm. CC Thomas, 1968.
62. Miller P. The lymphatic system and cardiac disese, in Lymph and the
Lymphatic System, CC Thomas, 1968, pp 217-229.
and Lymphatics' role stressed in cardiovascular disese. Med World News
Ian 21, 1966: 10-101.
J
ADDITIONAL CARDIAC BmLIOGRAPHY:
IUNCE PREETLY UNCLASSID
Bal MC: Viscerosomatic refexes: A review. JAOA De 1985; 85: 786-801.
Blo HA: Manipulative management of hyprtension. AAO Yearbook 1964;
189-195.
Burchett GB: Somatic manifestations of ischemic heart dis. Ostehic
Annals Sep 1976; 45-50.
Clymer DO: Effects of osteopathic manipulation on severl different
physiologic functions: Part III. JAOA Oct 1972; 72: 201-207.
Cox JM: Palpable musculoskeletal fndings in coronary artery disease: Results
of a double blind study. JAOA July 1983; 82: 832-836.
Fichera AP, Celander DR: Effect of osteopathic manipulative therapy on
autonomic tone as evidenced by blood pressure changes and activity of
the fbrinolytic system. JAOA Jun 1969; 68: 72-74.
Frymann V: In cardiac patients: Osteopathic manipulation held to aid heart
function. Clinical Trends Osteopathic Medicine Mar-Apr 1976; 2: 1, 5.
Johnson FE: Some obserations on the use of osteopathic therapy in the care of
patients with cardiac disease. JAOA May 1972; 71: 799-804.
Kellner A: Lipid and protein content of tissue fuid in normal and hypr-lipimic
rabbits, in Sympsium on Atherosclerosis. Washington DC, National
Academy of Sciences National Reserch Council Publication, 1955, pp
42-49
Lymphatics role stressed in cardiovascular disese. Medical World News Jan
21, 1966: 100-101.
Malliani A: Evidence for a spinal sympathetic regulation of cardiovascular
functions. Exprentia 1970; 26): 965-966.
Mayerson HS: One aspet of role of lymphatic system in cardiovascular
function in The Heart and Circulation: Vol . (RC 681-AIN 3), pp 90-
91.
Miller A: Effects of sof tissue manipulative therapy and factors regulating
blood pressure. JAOA May 1967; 66: 990-991.
Miller P. The lymphatic system and cardiac disease (Chap. X), in Mayerson
HS (ed) Procein of the Conference on Lymph and the Lymphatic
Stem. CC Thomas, 1968.
Nicholas AS, et al: A Somatic component to myocardial infarction. British
Medical Joural Ju1 6, 1985; 291: 13-17.
Patriquin DA: Manipulation for the patient with myocardial infarction.
Osteopathic Sympsium Feb 1975; 16.
Reder V. The role of the sympathetic nervous system in sudden cardiac deth.
Dru Thera (ospital) Ju1 1978; 43-55.
J
Richmond WO: Infuence of somatic manipulation in coronary artry disese
evaluated by a controlled metho. JAOA Jan 1942; 41: 217-225.
Rogers JL: The role of ostepathic manipulatve therpy in the tretment of
coronary heart disese. JAOA Sep 1976; 76: 21-31.
Stiles E: Congestive hert failure. Osteopathic Medicne Aug 1976; 76-78.
Stiles EO: Osteopathic approach to the hyprtensive patient. Othic
Meicine Apr 1977; 44-45.
Stokey JR: OMT for angina. Ohic Sum Mar 1975; 16-18.
Thomas PE: The role of the autonomic nerous system in arteriosclerosis.
Osteic Annals Jan 1974; 12: 17-20.
Tilley M: The smatic compnent in heart dis. Ohic Annals May
1974; 30-43.
TIlE TORACOLUMAR REGION CHAPMAN' S REFLEX
IUENCE
Mannino JR: The application of neurologic refexes to the tretment of
hypertension. JAOA Dec 1979; 79(4): 225-231.
Comments on hypertension study. JAOA; 79(10): 607-608.
Value of manipulation unresolved by hypertensive study. JAOA; 79(11): 667-
668.
TE CERVICAL REGION IFLUENCE
Johnson W: Palpatory fndings in the cervicothoracic region: Variations in
normotensive and hyprtensive subjects, A preliminary reprt. JAOA
Jan 1980; 79(5): 30-308.
CRNIAL CONCEP IUENCE
Magoui HI Osteathy in the Cranial Field. Kirksville MO, Joural Printing
Co, 3rd ed, 1966, pp 114-115, 176, 179, 280.
Northup Osteopathic cranial technique and its infuence on hyprtension.
AAO Yok 1948: 70-77.
BEHAVIOR MODICATION IUENCE
Combined pharmacological and psychosoial therapies for hyprtension
discussed. Behavi Meicine Sept 1980; 7(9): 3.
Relaxing hyprtension in the long run. Emergency Meicine Jan 15, 1981;
177.
Wadden T, De L Torre C: Relaxation therapy a an adjunct tretment for
essential hyprtension. Jra of Family P 1980; 11(6): 901-
903.
JJ
DITAY CONSIETIONS
Hunt JC: The infuence of diet on hypertension management. Dialogues in
Hyrtension 1980; IV: 37-47.
Silverberg DS: Treting hyprtension with diet. Consultant Jul 1980; 115-120.
RISW CONSIETIONS
Finnerty FA: Hyprtnsion: Curent management, Part I, Selecting and
evaluating the patient. Csul Jan 1978; 163-168.
Thind G: Factors infuencing hyprtension prognosis and tretment. Practical
Cardiolo Apr 1980; 6(4): 31-39.
Klatsky AL: Alcohol and hyprtension: Does drinking increse the risk?
Prima Cardiolo May 1978; 31-35, 6-65.
NOTES:
J8
OSTEOPATIC CONSIERATIONS I UPPER GI DISORDERS
"Manipulative therapy can pla a major role in the management
of the ulcer problem, both specically and supporively, and it
shoul be a routine and continuing feature of the emergenc,
maintenance, and follow-up care of the patient. `
I. ITRODUCTION
Along with backache and the common cold, gastrointestinal (OI) dysfunction is
a very common caus for absence from work. Regardless of the etiology for
the gastrointestinal upst, there will always be general and loal as well as
metabolic and cellular dysfunctions. Oo theraputic results from
manipulation have been clinically reported by osteopathic physicians and
supprted for almost 10 years by patients who have received this distinctive
manipulative treatment as a part of their totl medical management.
Osteopathic manipulative tretment of patients with musculoskeletal dysfunction
is understod by most individuals. The present understanding of
pathophysiologic mechanisms and recent research in refex neurophysiology has
identifed where and how osteopathic manipUlation is also clinically effetive in
systemic dysfunction and disese. The "cause/effect approach" which these
studies suggest should encourage the incororation of directed manipulative care
in tretment programs for patients with systemic disese and should stimulate
more clinical reserch for documentation of the specifc effects of manipulation
in patients with gastrointestinal disease. Osteopathic manipulation is not given
instead of medication nor are its effects upon the body's homeostatic
mehanisms duplicated by the medications. Osteopathic manipulation directed
toward improving the physiologic function of the patient and the use of
pharmaceuticals directed mainly toward the disease work synergistically to
encourage the patient's optimal ability to reover and to stay well.
l. PATOPHYSIOWGY
VISCEROSESORY AND VISCEROMOTOR PATTENS:
Pain patters from viscerosomatic dysfunction are extremely important when
prforming a differential diagnosis on a patient with gastrointestinal (01)
complaints or when making clinical judgment of the severity of the underlying
problem. Propr clinical analysis of these patters requires a thorough
understanding of both 01 anatomy and neuroanatomy. Knowledge of the
sgmental innervation of 01 organs and the loation of the appropriately
79
assoiated collateral sympathetic ganglion (M page 107) is vital for loizing
the source of pain.
Pacinian corpuscles and fre nere
endings are located in the wall of
any given viscera. These receptors
are activated by spasm or stretch;
pain senstion is carried by visceral
afferent fbers which travel a course
similar to the correspnding
splanchnic nerves.
True visceral pain carried by
visceral afferent fbers often spills
over into related right or lef
somatic segments in the back
(depending upon which side the
affected organ is on) and to the
midline of the trunk (in organs
derived from midline embryological
structures) .
2. Viscerosensory pain often called visceroso
matic pain: Tis involves facilitated cord
segments which permit visceral hypersympa
thicotonia as well B paraspinal somatic
changes, joint somatic dysfunction, and der
matome hyperalgesia in somatic areas relat
ed to the viscera's sympathethic innervation.
8mesthe0c
Crtex
t Ta|amus
Vscera
1. True visceral pain: This is early pain from
irritation, stretching, contraction or exag
gerated physiologic motor activity and dys
function. It is midline pain, poorly localized
and described as a vague, deep, diffuse
burning ache.
80
All pain receptors which transmit
impulses through visceral afferent
fbers and the cerebrospinal tract are
found within 2 cm of the gut and
are stimulated by edema, pressure,
torsion, traction, infltration,
bacterial toxins, enzymes, or
friction. More spcifcally, they are
found in the anterior and lateral
parietal peritoneum, the lesser
omentum, the mesentery, and the
mesoolon.
@
3. Percutaneous Reflex of Morley: This
is direct transfer of infammatory irritation
from the viscera to the parietal peritoneum
and abdominal wall without refex through
the visceral afferent nere on a somatic
afferent near the mesentary. It produces
abdominal wall rigidity, pain, and rebound
tenderness.
There are no reeptors for pain in
the visceral pritneum; therefore
the greter omentum and the spleen
and its capsule are pain-insnsitive
structures. Thes structures prouce
awareness of pain only if they affect
some adjacent, pain-snsitive
structure. Visceral pain may
become svere enough to spill over
to ares of corespnding somatic
segmental cerebrospinal distribu
tion. Erly in most diM
proesss, smoth muscle spasm or
stretch will elicit visceral pain
which is prly loalized and ofen
described as gnawing, buring, or
cramping. Sweting, nause,
vomiting, pallor, and a relentless
attempt to squirm away from the
pain is particularly characteristic of
patients who are experiencing
visceral pain. None of these
common symptoms of visceral pain
accompany somatic pain.
Somatic pain ariss when the underlying viscer proess progresses past the
viseral sers and stimulates adjacent somatic sensory neres. Somatic pain is
well-loalized, asymmetric, and aggravated by jarring motions. Somatic pain
may be added to the visceral pain patter or it may overwhelm and mask it.
Phrenic pain (C3-5 referral are)
ocurs when either the hemi
diaphrgm or Glissn's capsule of
the liver is stimulated. Its somatic
zone of referred pain is the
ipsilateral shoulder cap. In 5 % of
patients, the fbers of the right
phrenic nere also rech the lesser
omentum. In thos pople,
stimulation of the lesser omentum
would also prouce phrenic typ
referred pain referral to te soma.
81
As a consequence of the spinal cord region becoming facilitated from increased
and prolonged viscera afferent input, palpatory tissue changes and tenderess to
palpation becomes evident in the segmental T5-9 parspinal tissues, collateral
ganglia and Chapman's refex sites (page 232). Posteriorly, the smal rotatores
paraspinal muscles s m to be more frequently affete and their motion
characteristics ad the loation of their dysfunction is a key t the source of the
viseral dysfnction, They tend to exhibit the non-neutral typ motion with a
preference for backward bending and rotation and sidebending to the sme side
as the organ involved. While not contraindicated, high veloity, low amplitude
(VLA) OMT, is ofen found to be ineffective and is met with a rubbery
resistance when applied to viscerosomatic dysfunction of this sort. This
respns should alert the clinician to lok for an underlying visceral cause. If
sondary somatic dysfunction is successfully treted with OMT, it often reurs;
therefore, recurrent thoracic or rib somatic dysfunction without an apparent
primary biomechanical cause should provoke a thorough examination for
assoiated visceral organ dysfunction.
Common pain patters for perforated and non-perforated uppr abdominal
problems were compiled by a group of physicians from the Mayo Clinic.
2
The
following fgures are illustrations adapted from that atlas.
TYPICAL PAIN PATERN
PEPTIC ULCER
82
TYPICAL PAIN PATTERN
CHOLELITHIASIS WITH COLIC
SYATHETICS:
The autonomic nerous system (ANS) innerates the viscera and most
physiologists consider it sley an efferent system. Viseral afferent fbers reprt
viseral dysfunction and they usually travel afferently along adjacent pathways
d the correspnding efferent thoracic and lumbar sympathetic splanchnic
neres.
lme
mm
L
1 - Lel
8-C Lel
L4L-- ..
Somatic clues seondary to visceral dysfunction are mediated by viscerl
afferents to the cord and related somatic efferent fbers to the soma. These
refexes are called viscerosomatic refexes.
Thes refexes are respnsible for much of the typical objective somatic pain
patters seen from visceral problems. They are also respnsible for palpable
Chapman I s refexes, and the characteristic paraspinal tissue texture changes
related to facilitate cord segments T5-9 and Tl O- l l . Visceral afferent activity
is respnsible for the erly tissue chages palpable over the midline collateral
sympathetic ganglia.
The sympathetic prtion of the ANS has the unique ability to prouce rapid and
widespred organ and smatic changes required to meet stressful situations.
Activation of one sympathetic fber prouces anywhere from four to forty pst
ganglionic fber activations. This is not always benefcial in dysfunction,
illness, or disese where the patient has no need for the "fght or fight"
function of the sympathetic system. Sodeman and Sodeman in Pahologic
Pho Mehanisms of Disease stte, "The adaptive protetive rection
might be far more damaging to the individual than the noxious agent of the
83
beginning dysfunction. ,,3 This is the situation ocurring with prolonged
sympathetic hypractivity in GI dysfunction or diM.
Incresed sympathetic tone decreses mucosl defenss against digestive acids
and enzymes by proucing vdnstriction and altertion of the bicarbonate and
mucous buffers. More patients develop infammation or ulceration in the upper
GI system from reuced mucosl defenss (from sympathicotonia) than from
hypracidity. Sympathetic activity also plays an imprtant role in sphincter tone
within the GI system. The normaliztion of facilitted sgments ad the
assoiated sympathetic outfow from the T5-Tll region reduces gastrointestinal
vasoonstriction and allows an increase i mucous sretion from Brunner's
glands permitting homeostatic mechanisms to operate to protect mucous
membranes. 4
In diseased patients, prolonged hypersympathetic activity can initiate proesses
that are detrimentl to surival. Gilsdorf and his group in 1965 reported in
lAMA that cats with nonlethal pancretitis would develop hemorrhagic
necrotizing pancreatitis leding to the death of the animal when subjete to
increased sympathetic stimulation; Blok and others, writing in Sr
Gecolo and Obstetrics in 1954, indicated that ischemia changed nonlethal
pancreatitis to lethal pancreatitis. From studying the world literature, Dr. Korr
emphatically states, "In every disease process there is hypersympathetic activity;
sustained sympathetic activity is a common factor in disease. "
PARASYATHETICS:
g
LR
vagu Vgu8
,
Paayptetic
lnnmabn V|a
m Vau Ner
w
m Splacnic Nere
84
The parasympathetic prtion of the
ANS tends t dominate inneration
of the viscer during "normal, " long
term, restful activity. In the upper
GI tract, parasympathetic
innervation is supplied by the vagus
nere (eN X) which exits the skull
through the jugular foramen, which
is forme by the joining of the
jugular notch of the tempral and
the jugular notch of the ocipital
bones. The lef vagus supplies the
greter curature of the stomach and
extends to the duoenum; the right
vagus supplies the lesser curature
of the stomach, the small intestines,
the right colon and the organs and
glands up to the mid transverse
colon.
Parasympathetic stimulation will increse the secretion rate of almost all
gastrointestinal glands. 5
The most inferior ganglion of the vagus nere, the gaglion nodosum, extends
into the cerical are and lies in fascias which are just anterior to the OA and
AA joints. The vagus also has connections with the frst two cerical somatic
neres which provide neurologic pathways for fbers carying pain fbers from
the psterior prtion of the hed (Le. the ocipital neres). This connetion
may explain the ocipital hedaches which are often a part of the "subjective"
symptomatology of a patient with uppr GI or pulmonay dises, espcially in
uppr GI viral dysfunctions or viral pneumonia.
This connection may also explain the nause and vomiting that accompanies
certain hedaches and the palpatory clues found at the OA and C2 ares are
related to dysfunction in viscer innerated by the vagus nere. The
parasympathetic system will also often produce symptoms of disese.
Parasympathetic refexes give the physician an explanation for many of the
symptoms which are designate as nerous typ or "functional disorders. "
These include hyprchlorhydria, nause, hypermotility of the intestines, spastic
colon, irritable bowel, bradycardia, asthma, hay fever, epiphoria, cough,
hoarseness and excessive nasal discharge. The parsympathetic nerous system
may also produce changes in tissues of its inneration, makng that organ more
susceptible to infection or chronic trophic change. It appars that all organs
innerated by the vagus nere are intimately bound together and capable of
redily transmitting refexes to and receiving refexes from ech other. This
may be why the larynx is s often involved when there is a problem with some
other part of the GI tract also innerated by crnial nere X.6
LYHATICS:
The lymphatic system is absolutely necessary for god helth and is even more
important and frequently overworked during body dysfunction and dises.
Extensive experimental studies in cats and dogs indicate that the lymphatic
system must be able to increse its normal fow cpacity by 4-5 times with some
body stresses and in some chronic pathological syndromes such as congestive
heart failure, up to 40 times its resting capacity. Bcause of these demands on
its peak function, even a slight mehanical impdance of its lymphatic pathways
or hindrance to the function of the diaphragm (which acts as its extrinsic pump)
might greatly reduce the boy's ability to recover from a dises proess.
Lymph from the GI tract as well as all other organs and systems below the
diaphragm drain from small lymphatic channels into the cistera chyli. This is
an irregular fbromuscular sc about the size of a cigarette, wedged between the
aorta and the right crus of the diaphragm and just in front of the boies of the
85
frst two lumbar vertebrae. It also marks the start of the lef lymphatic duct,
called the thoracic duct.
The thoracic duct is about 18 inches
long and extends from the cistera
chyli up through the fascias of the
left thoracic inlet, into the neck for
a distance of about 1 112 inches
above the clavicle, arches over the
pleur ad apx of the lef lung, and
then passes back through the
thoracic inlet to fnally empty into
the junction of the left interal
jugular and lef subclavian veins.
The vital fow of lymph may be
hindered by a poorly effcient,
fattened diaphragm or by torsion of
the fascias around the lymphatic
channels loated in the mesenteries
or at the thoracic inlet. The frst
sign of terminal lymphatic drainage
dysfunction in the abdomen may be
a palpable fullness in the sub
xiphoid sof tissues.
Upper Gastrointestinal Tract
Studies show that the incidence of pancretitis is incresed in gallbladder disese
if their common lymphatic drainage route is compromised. Lymphatic drainage
from the liver is incresed gretly by minor pressure changes and so lymphatic
drainage is greatly infuenced by the depth of respirtions and manipulative
treatments (such as the liver pump) which crete intermittent pressure charges.
SOMTIC SYSTE:
Locating and correlating palpable changes in the musculoskeletal system are
very helpful when considering a diagnosis of visceral diM. Refex muscle
spasm is ofen present in addition to segmental parspinal smatic dysfunction,
Chapman's refexes and collateral ganglion tenderess. Guarding, rigidity and
myofascial trigger pints are all expressions of this phenomenon and all should
be considered when prforming a physical examination. Unless thes ares are
treated, pain patters may be prtuated. Travell reprts, "Pain, which
previously had respnde to medical therapy for a duoenal ulcer, beame
unresponsive and persisted until trigger pints in the abdominal musculature
were found and inactivated."
7
Peptic ulcer disese has been found to be
assoiated with abdominal myofascial trigger pints which in tur continued to
produce a somatic pain referral patter similar to that originally produced by the
86
visceral disturbance; in thes patients, even after the ulcer healed, both the
patient and physician are often misled to believe that a visceral problem
remained. This is believed to be the case in pstcholeystectomy syndrome
where OM commonly alleviates symptoms of gallbladder dysfnction and the
typical gallbladder-typ referred pain which remain even after surgical removal
of the gallbladder.
il. THE PHIOSOPHY OF TEATMT
The exact diagnosis is imprtant when formulating spifc medical ad
manipulative tretment and when predicting the prognosis for a patient with
some type of disese proess; however, from a functional standpoint, specifc
evaluation of the body's attempted homeostatic rections to its dysfnction is
often more useful than the spifc visceral diagnosis when deciding where, how
and what manipulative tretment to give. If the physician understands the
general pathophysiology and respnses of the uppr GI tract to a disese proess
and can determine the respnses of the patient to the dysfunction, manipulation
can be benefcially administered even during the diagnostic work-up stages, to
relax the patient and to supprt body homeostasis.
Protlndins
UPPER GASTROINTESTINAL DISEASE
Cpob
Pori
87
H|sloq
8ymploms
Therefore, the goal is not to diagnos and tret "joint dysfunction. " The goal of
treting patients in this manner involves administering rib raising and paraspinal
inhibition for autonomic imbalance and refex dysfunctions, improving
circulatory and trophic factors, modifying fascial patters which hinder
,
lymphatic pathways and the pumps, and treting the base of the skull and upper
cerical are to affect parsympathetic function. If spifc joint somatic
dysfunction is palpable it should be diagnosed and treted appropriately, because
it represnts a somatic contribution to the maintenance of the facilitated
segments of the cord and thus hinders the viscera by its promotion of
sympathetic hypractivity, termed sympathicotonia.
It is not unusual to M patients suffering from pain and cramping discomfort
due to GI dysfunction of many typs, waiting uncomfortably for 1-3 days while
the "specifc diagnosis" is being obtained through multiple test proedures.
Manipulative tretment for those patients could be started erly. This would not
interfere with the diagnosis in any way, once the search for an organic etiology
was planned and in progress; in fact, the responses of the musculoskeletal
system may help guide a more economical or complete approach to the
diagnosis. It would make the patient more comfortable by beginning
normalization of altered physiologic proesses at a connective tissue or cellular
level. Manipulative tretment would most likely reduce the amount of pain
medication required for patient comfort and would help prepare the patient's
body for better acceptance, distribution and utiliztion of any spifc
medications prescribed once the pathologic diagnosis is seured. If the proess
was functional, then often the "negative" work-up for organic structural causes
will be accompanied by a patient who no longer has complaints.
Ostepathic manipulation for a patient with systemic diM is primarily
directed toward balancing autonomic activity and improving lymphatic fow.
This type of tretment should relieve, improve and enhance the patient's own
abilities:
o to improve visceral respnse to stress
o to relieve congestion
o to improve circulation
o to enhance the removal of waste products from the tissues
o to improve cardiac outut
o to improve oxygenation and nutrition at a cellular level
o to enhance resistance to infection
o to enhance more predictable tissue levels and patient respns to spifc
medications
o to enhance relaxation and comfort of the patient during diagnostic
proedures and any spcifc treatment program
88
I. OSTEOPATIC TREATT FOR PATINT WITH UPPER GI
DYSFUNCTION
LYMHATICS AND FASCIAS:
The visceral organs are suspnde from the dorsl surface of the abdominal
cavity by mesenteries. Through these connective tissue pathways pass the
arterial blo supply, the venous and lymphatic drainage vessels, and the
sympathetic, parasympathetic and visceral afferent neres of the viscera.
Location of Mesenteric Attachments
The most imprtant mesentery to
the osteopathic physician who is
treting uppr GI dysfunction is the
mesentery for attachment of the
small intestines. This mesentery
can be loated in the patient by
constructing an imaginary line from
1 inch to the left and 1 inch above
the umbilicus to a pint in the lower
rght quadrant of the abdomen just
anterior t the right scroiliac joint.
Thirty feet of intestines are attached
to this six-inch mesenteric base.
A manipulative tehnique to reduce congestion and improve circulation to the
small intestines is called a "mesenteric lif" and is helpful in freeing lymphatic
pathways from the small intestines. The small intestines usually lie in the
suprapubic and lower lef abdominal quadrants. This ventral abdominal
technique for the small intestines is prformed by carefully lifting them upward
and to the right side of the abdomen while using the patient's respiratory force
for activation (spage 227). The patient's respiratory force is activated by
having the patient brethe in and hold the breth until air hunger ocurs. The
physician should be snsitive t the tissue respns under the palpating fngers
and keep the patient comfortable while providing a gentle encouragement to the
tissues being treted. About the time the patient neds to take a breth, the
physician will feel a mesnteric relese (although ionally 2-3 breth cycles
will b require before a relese is palpated). Visceral manipulation using
rele tehniques for ech uppr GI organ has been described in detil by Jen
Pierre Bar, D.D.,
s
and may be employed to help maximize visceral function.
Thefascial patter of the thoracic inlet and the inferior thorcic outlet must also
be evaluated. These fasial ares are treted as indicated and the diaphragm
must be well domed. "Domed" means that both leaves of the relaxed
89
diaphrgm are optimally concave inferiorly (convex supriorly) and that they
work symmetrically during respiration. Tretment of a dysfunction of the
thoracoabdominal diaphragm might include soft tissue to the paraspinal muscles
and quadratus lumborum as well d diret or indirect fascial tretment directed
at the diaphragmatic attachments--the thoracolumbar junction, the lower six
ribs, and/or the sterum.
SYATTCS:
Any stress or dys
function of the uppr
GJ tract causes a bar
rage of visceral affer
ent impulses to bom
bard the cord. Vis
ceral afferents from
the upper GJ tract
and small intestines
travel frst through
the celiac or suprior
mesenteric collateral
ganglia. They then
travel through the
chain ganglia to cord
levels T5 to TIL
fZ
R
CHAPMAN'S
REFLEXES
L
Since these impulses tend to travel the sme pathways as correspnding
sympathetic efferents, any resultant facilitated segments are more likely to be at
the levels of sympathetic inneration to the organ in trouble. Studies confrm
that somatic palpatory clues to uppr GJ and small intestinal dysfunction occur
in the paraspinal somatic tissues from T5 to TIL
Chapman I s system of anterior and psterior myofascial tender pints related to
specifc visceral dysfunction are particularly helpful in diagnosis of GJ dysfunc
tion.
10
They are considered to be produced by viscerosomatic refexes which
generally ft a sympathetic refex patter.
Charts for the entire Chapman system of anterior and psterior myofascial
points can be obtained
ll
and are reproduced in diagrams on pages 232 and 233.
The anterior points are most useful as indicators of dysfunction because they are
esily located and are more snsitive to light palpation. They correlate well
with fnal hospital diagnoss.
12
The psterior pints are less tender; therefore,
they are less often usd as diagnostic clues. Some physicians us the psterior
90
pints for loized sof tissue tretment in an attempt to infuence a specifc
organ I s autonomic balance.
The above knowlege helps a physician diagnose and plan manipulative
treatment for uppr GI diss and dysfunction. Tretment to normalize
sympathetic hypractivity is clinically effetive and may be administered in
sveral different ares including the sementally assoiated vertebrae (facilitated
sgments), the ribs (sympathetic chain ganglia), the spifc collateral ganglion,
and the Chapman I s refex tender points.
Any tretment to the sympathetic ganglia will initially stimulate sympathetic
activity to the organs of sympathetic inneration, but this effet is loalized ner
the sgments treted and is short-lived. The lasting effet is believed t be
produced through stimulation of the long very slow sympathetic fbers, which
cause inhibition of sympathetic outfow in the ares treted. This rection is
centrally mediated and is longer acting. It serves to improve blod fow and
maximize homeostasis including mucosal barriers to ares of the GI system
sharing the same segmental distribution.
o .. RIB RAISING: The most common manipulative method to modify
sympathetic activity utilizes rib raising tehniques (page 195) to the
appropriate rib ares, i.e. T5-Tll for the upper GI tract and small
intestines. Since the chain ganglia of the sympathetics lie in the fascias
over the heds of the ribs, rib raising prouces the refexes which
clinically normalize sympathetic activity. This technique L be
administered with the patient in the supine, lateral recumbent or sitting
position. Tretment only needs to be long enough for the physician to
sense palpable tissue change. This may take a few seconds to a few
minutes.
It is known that spinal impulses passing through a facilitated are of the
spinal cord will prouce bursts of sympathetic activity to the viscera
innervated by thos sgments. For this reson, tretment of segmental
spinal somatic dysfunctions related to ares of suspted facilitated cord
segments often preedes manipulative techniques to other tissues in other
ares.
o .. VENTRAL ABDOMINAL INIBITION: Tretment by ventral abdominal
inhibition to the appropriate collateral sympathetic ganglia (page 2()
until tissue change is palpable is also considered t reduce sympathetic
hyprctivity of their respctive spinal levels. It is kown that the
collateral ganglia are able t provide some regional control of the viscera
without relay t the central nerous system and are not "just switching
stations" for autonomic activity.
91
These ganglia are loated in the midline of
the abdomen--anterior to the abdominal
aorta and betwen the xiphoid proess and
the umbilicus. The celiac ganglion is
MOsOotOt|c assoiated with T5-9; the superior
Location of Collateral
Sympathetic Ganglia
mesenteric ganglion with TlO-U; and the
inferior mesenteric ganglion with TI2-L2.
The frst two named ganglia are often
involved in uppr GI disorders while the
inferior mesenteric ganglioh is involved in
lower GI and plvic problems.
0 . . CHAPMAN'S MYOFASCIAL POINS: (See pages 232 and 233)
Sympathetic hypractivity can also be treated by manipulation of
psterior Chapman's refex points. The anterior Chapman's pints are
esily accessible and more tender to manipulation so are use for
diagnosis. Memorize the common anterior Chapman's pints related to
the gastrointestinal system. When performing a physical examination,
these clues to visceral dysfnction can be checked in just a few seconds.
These ganglioform refex pints are believed to be prouced in the deep
myofascial tissues by viscersomatic refexes resulting in increased
hyprsympathetic. If one or more are tender to palpation, ask specifc
questions related organ's dysfunction and correlate this with fndings
from palpation of the collateral sympathetic ganglia and related
paraspinal tissues. To tret the posterior points relate to the uppr GI
tract and small intestines, circular soft tissue pressure of moerate
intensity is administered between the proper intertransvers proesses
until the pints disppar. Posterior Chapman's pints related to the
upper GI system in the intertransverse spaces will usually correlate with
tender anterior Chapman's points located in the respctive ipsilateral
intercostal spaces.
PA S YA THETIC SYSTEM:
Bnefcial tretment to improve parsympathetic inneration to the uppr GI
tract is directed primarily toward removing joint somatic dysfunction of the
cerical spine (espially in the area of the OA and AA joints), treting the sof
tissues of the subocipital are and utilizing condylar deompression techniques
to relieve fascial tensions around the ganglion nodosum and the vagal trunks. If
the physician is trined in cranial treatment techniques, treating somatic
dysfunctions of the ocipitomastoid suture area will relese tensions felt to affect
the vagal nere as it exits the skull through the jugular foramen. This treatment
is also effective in helping to relieve tensions assoiated with subocipitl and
ocipital hedaches which often accompany GI disturbances.
92
VI. SU Y
It has ben shown that removal of musculoskeletal dysfunction may alter
assoiated, sondary viseral dysfunction; however, if the musculoskeletal
etiology remains to long, the refex pathway sems t be "leed by the
cord, " s that the dysfunction of the viscer may be reestablished even after the
smatic dysfunction is removed. Patterson hypthesizes that this may be a basis
for a patient's predispsition to chronic diM and may indicate evidence
supporting erly ostepathic manipulation as a mens of preventing diseases as
well as a mes of supprting a body that has diM.
Osteopathic manipulation provides an additional and synergistic approach to the
usual medical tretment of GI diM and dysfnction. No matter how effective
medicines become, drug spcifcity and sophistication dos not excuse an
osteopathic physician from the responsibility of supprting the patient's own
defenses. Intelligent, physician-directed manipulation provides this supprt for
the patient by enhancing the self-regulatory mechanisms of the body unit using
OMT to improve the boy's structure and fnction.
REFERENCE:
1. Strong W: Disorders of the digestive system, in Hoag 1M (ed)
Osteopathic Medicine. New York, McGraw-Hill, 1969, ch 38, p 573.
2. Smith LA et al An Atl of Pain Patters: Sites and Behavior of Pain in
Certain Common Diseses of the UpAbdomen. Springfeld IL, CC
Thomas, 1961.
3. Sodeman WA, Soeman TM Pathologic Pholo Mehaisms of
Disease. Philadelphia, W Saunders, 6th ed, 1979.
4. Strong W: Disorders of the digestive system, in Hoag 1M (ed)
1953, 7th ed, 262.
6. Op cit pp 211-215.
7. Travell IG, Simons DG Mscal Pain and Dysfunction: A Trigr Point
Manual. Baltimore, Williams & Wilkns, 1983, p 674.
8. Barral IP, Mercier P Vis Maipulation. Settle WA, Estlad Press,
1988.
9. B MC: Viscerosomatic refexes: A review. lAOA De 198; 85: 786-
801.
10. Owens C An Enne Interretation of Chapma's Refex. Carmel
CA, 1963.
11. Contact the Department of Osteopathic Theory and Methos at the
Kirksville College of Osteopathic Medicine, 80 West Jefferson Street,
Kirksville, Mo. 63501
12. Byres TR, Kuchera ML, Guffey 1M, Steele K, Betty DR, Haman JL,
Lko MD: Correlation of palpatory fndings with visceral
diagnoses. JAOA 92(9): 1177, Sept 1992.
93
OSTEOPATIC MULATION OF A PATIT WITH
UPPER GASTROITETIAL DYSFUNCTION
Somatic Dysfunction
facil. seg.
Sympathetics
I
Parasympathetics I
I
Rib Raising
TS-9
TIO-ll
Chapman's Reflexes
I
Collateral
Gan lia g
2&1&D1 E1&D 1O
U@@ G&B1O1D1B11D&1
D_B1UDC11OD
Lymphatics
Thoracic Inlets
Abdominal Diaphragm
Effleurage
Lymphatic Pumps
OA, P C2
Cranial
I
I
- Vagus
Nerve
Mesenteric OMT (Ventral Abdominal Techniques)
SYMATHETIC (PATHO)PHYSIOWGY
t Tone:
1. t Vascular Tone

l 0
2
and Nutrients to tissues

t Mucosal Sensitivity to H+ concentration and Alters
the Mucosal Barrier
2. Relaxation of Gallbladder and Ducts
3. l Peristalsis Constipation
LYMHATIC (PATHO)PHYSIOWGY
1. t Tissue Congestion and Impaired Nutrient Absorption from
the Bowel
2. t Risk of Pancreatic Complications in Gallbladder
Disease/Dysfunction
PARASYMATHETIC (PATHO)PHYSIOWGY
t Tone:
1. t Acid Secretion
2. Contraction of Gallbladder and Ducts
3. Peristalsis Diarrhea
94
OSTEOPATHIC CONSIERATIONS I WWE BOWEL DISORDERS
I. ITRODUCTION
Bginning cellular and organ dysfunctions assoiated with disturbed metabolism,
congested tissues, cloudy swelling, lactic acid accumulation and tissue acidosis
are reversible with erly tretment. Visceral irritaton and dis increse
visceral afferent nere activity and are often assoiated with hyprsympathetic
bombardment of the assoiated organs. Sympathetic nere impulses may
protect the boy from exteral dangers but when they remain hypractive, due
to cord facilitation, they become a roadblok to rapid healing and restoration of
health and c even prouce ptentially lethal conditions. Hyprsympathetic
activity is present in pst-surgical patients and all patients with systemic
diseases.
The rate of healing of boy tissues is dependent upon the ability of the body to
remove waste proucts from the tissues and to deliver oxygen and other
nutrients to the are of tissue dysfunction, injury, or the site of a surgical
intervention. This "is built in" to the boy as self-regulating mechanisms which
in tur require good arterial, venous and lymphatic circulation, as well as a
god nerve supply. These prerequisites of the self-regulating mechanisms
depend upon god circulation and accurate reports from visceral afferent nerves.
Hypoperfusion results in low tissue resistnce to infection and when infected,
these tissues remain infeted longer than tissues with go prfusion and
nutrition. Studies by Niinikosk (1980) reveal that white blo cells sletively
kill bacteria by using suproxide and that "any treatment that augments the local
oxygen supply to the tissues and helps to avoid hypoprfusion incress the rate
of healing and decreses the susceptibility to infection. " Han and McKay
concluded from exprimentation involving animal inoulations of staphylococcal
bacteria that "even small increses in oxygen to a tissue resulted in a relative
large increse in its resistance to infection and greatly increased its ability to
reover from the infection. "
Osteopathic manipulative tretment in bowel disese and bowel dysfunction is
often directed toward and related to improving blod and lymphatic fow and
balancing the autonomic impulses to and from the bowel. Effetive osteopathic
treatment improves the circulation and oxygenation of the tissues. When
prforming or ordering manipUlative tretment for lower GI diseses, certain
functional anatomical and neurologic pculiarities of the colon must be kept in
mind.
95
l. PATOPHYSIOWGY
SYATTICS:
Sympathetic hypractivity refecting
a dises proess is usually
assoiated with facilitated segments
TIO-TIl when the right half of the
colon is involved and facilitation of
T12-L2 when the lef half of the
colon is involved. Disorders of the
colon usually prouce
viscerosomatic refexes which
increase thoracolumbar paraspinal
muscle tension and produce pain in
TlO-11 or T12-L2 areas of the
spine.
CHAPMAN REFLEXES
Sympathetic hyractivity is also
believed to be indicated by
viscerosomatic myofascial tender
points calle Chapman's pints. 1
This myofascial system of diagnosis
and tretment is attrbuted to Frk
Chapman, D.O. The anterior
Chapman's pints are helpfl clues
to colon dysfunction and are found
Posterior Points
as tender, palpable fascial
Cecum
Ascending Colon
Hepatic Flexure
ISigmoid
ganglioform nodulations on the
lateral side of the thighs in the
anterior half of the iliotibial bands
Descending Colon
from the greter trohanters to the
lateral epicondyles of the femur.
,Splenic Flexure
These ares become tender to light
pressure with most colon
dysfunction; however, it has ben
clinically obsered that some colon
cancers may not produce
Aterior Points
Chapman's refexes though it is not known exactly why this is true. It is
therized that tissue infammation and/or irritation is required to initiate these
refexes through the visceral afferent and sympathetic systems.
96
With diseses of the colon, the
inferior collaterl sympathetic
ganglion, loated in the midline of
the abdomen and just above the
umbilicus, is often palpable and
tender. This palpatory change is
als believed to indicate sympathetic
hypractivity to the colon a a result
of viscerl afferent bombardment
with its infuence upn facilitation
of related cord sgments.
The collateral ganglia in the midline
of the abdomen have self-contained
mechanisms which c attempt
control and rection to regional
visceral dysfunction; therefore, they
are capable of controlling function
loally without reporting to the
spinal cord.
Riht Lf
vagusy

Paaptetic
Inlatin of
T Vagus Ners
A
Pelvc Splancnic Nere
Sympathetic Inneration of
The lower Bowel
- C1-2
97

- T2
-
T4
\- T
Clia
Sup. Menteric
Inf. Menteric
.- L
itl Ha of
1_ Tanere Colon,
- Sigid Colon and
Reu
Sympathetic hypractivity of the
lower GI system is assoiated with
fndings and symptoms of ileus,
constipation, abdominal distention
and fatulence.
PA S YA THTICS:
Manipulative techniques to
normalize parsympathetic activity
to the colon may b espcially
usful in the care of patients with
colitis, Crohn' s dis, irritable
bowel syndrome, or idiopathic
diarrhea. The vagus nere provides
parasympathetic innervation to the
right side of the colon.
The left vagal inneration extends only to the greter curature of the stomach
and the pyloric are of the GI tract. The right vagus nerve also innerates the
upper GI tract, including the lesser curvature of the stomach, the liver and gall
bladder and then continues on to innerate al of the small intestines and the
right half of the colon. The plvic splanchnic neres with their origin from
cord segments S2,3,4, supply the parasympathetic inneration of the lef half of
the colon and the plvis.
This split in parsympathetic innervation must be kept in mind when loking for
smatic dysfunction which could have an affet on the right or the lef half of
the colon.
Parasympathetic hypractivity in the lower GI system increses bowel motility
and glandular seretions and is assoiated with diarrhe. Hypactivity of the
parasympathetic system results in the opposite manifesttions of bowel function,
namely decreased bowel motility and glandular secretion as well as constipation.
When there is hypractivity of both the parasympathetic and. the sympathetic
systems to the bowel the functional disorder tends to manifest as an irritable
bowel syndrome. (See Irritable Bwel Syndrome, page 10.)
LYHATICS:
With dysfunction of the tissues of the colon there are cellular and tissue
metabolic changes which lead to incresed interstitial fuids and tissue
congestion. The result is accumulation of waste products, reduced oxygenation
and decresed nutrition to the cells. These changes increse the colon's
susceptibility to infammation and infection and increases its healing time when
stressed. Congestion also increses the likelihood of fbrosis with increased
srng in the healing proess. Fibrosis can worsen the prognosis in patients
with colitis or Crohn' s disease.
Locaton of Mesenteric Attachments
98
One Inch over
Si
Inches
log
Vessels and neres to and from the intestines must travel in mesntries.
Though these mesenteries are broad, the very thin walls of the lymphatic and
venous channels are vulnerable to pressure from surrounding edematous tissues.
Canine studies indicate that tissue congestion interferes with the effetive
medical tretment of disese proesses. 2
In thes studies there was uneven distribution and accumulation of the active
drug in the dogs' tissues and the drug's by-proucts accumulated in the
congested tissues; often the tissues which needed the active component the most
were the tissues that got the lest concentration.
According to Sam Threefot, M.D., director of the New Orlens Research
Institute, "When lymphatic fo channels fail to fnction beause of anatomical
fault or abnormal physiologic mehanisms, therapy is impeded. ,,3
Because the interstitial fuids from a congested colon drain through the thoracic
duct, any restriction of the lymphatic pathways to the duct, the fascias through
which the duct passes, or the fascias at the thoracic inlet would be assoiated
with incresed tissue congestion. Thoracic diaphragm function should be
ascertained becaus of its imprtance in moving both venous and lymphatic
fuids. The ability of the plvic diaphragm to passively and synchronously
move with the abdominal diaphragm should also be considered when treting
conditions assoiated with abdominopelvic congestion.
It is possible that patients with disease processes or prior surgery involving the
lower sigmoid, retum, and anal areas will have asymmetry or spasm of the
plvic diaphragm. The plvic diaphragm is a fnnel-shaped muscle attaching to
the lateral walls of the true pelvis and angling inferiorly and medially to attach
t the urogenital diaphragm and the midline structures of the urogenital and anal
triangles. There are right and lef leves of the pelvic diaphragm.
99
1. Pelvic Diaphragm
2. Ischiorectal Fossa
3. Obturator Internus Muscle
4. Ischial Tuberosity
5. Iliacus (Bone)
6. Acetabulum
7. Acock's Canal (Pudendal Canal)
8. Eternal Anal Sphincter
9. Rectum
10. Tendinous Arch of Obturator
Internus Fascia
11. Anal Canal
The spaces below the plvic diaphragm and between the diaphragm and the
structures on the lateral walls of the true plvis are flled with fat and are called
the ischiorectal fosse. The plvic diaphragm is innerated by the pudendal
nere originating from scral rots S2,3,4. As mentioned erlier, thes sme
cord sgments provide the origin for the pelvic splanchnic neres which supply
the parasympathetic innervation to the lef half of the colon, plvis, and
prineum. The plvic diaphragm works most effectively when it is relaxed and
c work passively and synchronously with the abdominal diaphragm.
Tension of the plvic diaphragm is diagnosed by gently but fmly insrting the
extended fngers of one hand into the later margin of one ischiorectal foss,
along the later side of the rectal triangle of the perineum. The sme
examination is carried out on the other side and the tensions of the muscle on
the two sides are compared. An indication of the pelvic diaphragm tnsion
could also be obtned during the performance of the usual rect or vaginal
examination. OMT to this region is described on page 216.
VISCEROSENSORY AND VISCEROMOTOR PATTERNS
The general principles listed in the previous chapter (Osteopathic Considerations
in Upper GI Disorders) are also pertinent for the lower bowel.
SOMATIC
It is well doumented that severe insult, such as a vertebral fracture, to
thorcolumbar segmental levels will cause a somatovisceral refex resulting in
paralytic ileus. Travell and Simons report
4
several other visceral symptoms
resulting from abdominal myofascial trigger points including diarrhe,
vomiting, belching, fo intolerance, and colic in the infant or excessive
burping in an adult.
The somatic compnent of the viscerosomatic refex that takes place because of
the handling of the bowel during some surgeries is capable of initiating a
secondary somatoviscerl refex which results in and maintns a paralytic post
oprative ileus. (Se study of effects of osteopathic manipulation in prevention
and tretment of pst-op ileus pages 103.) Treatment of the somatic compnent
alleviates the symptoms of the resulting visceral dysfunction.
100
m. OSTEOPATHIC MULATIVE TREATMT OF COWN
DYSFUNCTION
SUGGETED PROTOCOL FOR PROVIIG OSTEOPATHIC
MULATIVE TREATMT TO PST-OPERATIVE
PATITS:
ADMINISTRATION IN GENERAL:
This protool is espcially useful in tretment of patients who have had
abdominoplvic surgery. Optimum tretment frequency is thre times a day
until bowel sounds are herd regularly. Osteopathic manipulative technique and
dosge must be moifed depnding upn the surgical site, placement of
drainage tubes and lotion of incision and dressings.
STAGE I:
In the immediate pst-operative period there are unequilibrated
hemodynamics and electrolyte imbalance. Bowel sounds are very
p r or absent on auscultation. There is shalow brething from
neuromuscular splinting. Palpation reveals signifcant refex
hyprtonicity of paraspinal muscles from surgical interruption of
assoiated dermatome and myotome segments while
viscerosomatic refexes from the surgical and manual irritation of
the viscera also contribute to the paraspinal hyprtonicity.
TREATMENT:
A. Gentle inhibition of hypertonic paravertebral muscles to
pint of tissue relaxation (2-5 minutes total time)
B. Gentle inhibition of hypertonic paravertebral muscles in
thoracic region. This is most effectively directed toward
spinal segments which are assoiated with the surgical site
via supplying sympathetic inneration to the involved
visera.
C. Indiret metho fascial relese manipulation of the
diaphragm, thoracic inlet and mid-cerical spine
STAGE II:
In this stage, there is less refex neuromuscular splinting.
Hemoynamics and electrolytes are ner normal. Bowel sounds
are present. The patient may be ting oral fuids. The
brething patter has improved.
101
TREATMEN:
A. Apply inhibition to paravertebral muscles, espially at the
parvertebrl segments related t the sympathetic
inneration of viscer involved in the are of surgery.
Tret the segments until there is tissue change under the
treting fngers
B. Rib raising ech side (1-3 minutes)
C. Indiret metho fascial relese t thoracic and steral region
myofascial tissues
D. Indiret metho fascial relese to tissues ner surgical site
E. Inhibition of cervical paravertebral ares as indicated by
palpatory evaluation of the patient
STAGE III.
In this stage the patient is ambulating fairly well. Or intake is
improving. There is minimal refex neuromuscular splinting.
TREATMENT:
A. Inhibition of paravertebral muscles at parvertebral segments
assoiated with surgery (1-3 minutes)
B. Spcifc mobiliztion of segmental vertebrl units or regions
as indicated
C. Pectoral traction with modifed classic lymphatic pump or
pdal pump as pssible and determined by evaluation of
the patient (2 minutes as tolerated)
FOR OPTIMAL TREATMENT:
Add bilater condylar decompression and CV 4 tretment. This
is a signifcant beneft to patients at al post-oprative stages.
Providing the CV 4 treatment in these patients is limited only by
the physician's ability to use it properly.
Abdominal mesenteric lif techniques help to decongest the colon and may be
use when no abscess, abdominal aneurysm or acute infection is present in the
are of tretment. Lymph fow is encouraged by appropriate lymphatic pumps
(intermittent chest pressure, pectoralis lift or by utilizing a roking motion of
the abdominal contents through production of intermittent cephalad pressure
through the lower extremities). See page 227 for ventral abdominal techniques
and page 218 for lymphatic pumps. Visceral manipulations for ech lower GI
structure and plvic organ have also been describe in detail by Bar5 and may
be employeed to maximize viscerl function.
102
IEUS PRVETION TRATMT:
317 CSES
SURGERY
9 CSES
SURGERY
1-- OU --I
1--NO OU-_
ILEUS RTE 0.3 %
1/317
ILUS RTE 7.S %
OMT X 2 MINUTES
BOWL SOUNDS
AVRGE OF 5.7 HOURS
Hen. T 0 0 ,O. 6, pp 163
GAS PASSED
AVERGE OF 8 HOURS
TREATMENT
AVERGE OF 3 DAYS
Te above ileus prevention study
6
demonstrates the general importce and
effcacy of osteopathic manipulative tretment in interrupting inappropriate
viserosmatic-smatovisceral cycles.
103
SUPPRTIVE MULATION FOR PATITS WITH SPECIC
FUNCTIONAL PROBLES AND COMLAITS:
PATINTS WITH SYATETIC DOMANT COMLAITS:
constipation, abdominal pain, fatulence, and distention.
In thes patients the physician should palpate the iliotibial bands loking for
diagnostic anterior Chapman pints which might be related to colon irritation.
The lumbothoracic and the lumboscral areas are then relaxed with keding
and stretching sof tissue tretment. This addresses the imprtant sympathetic
levels while simultneusly relaxing the posterior attachments of the abdominal
diaphragm. It als accomplishes tretment of the psterior Chapman pints.
The psterior Chapman pints for the colon are loated in a triangular are on
ech side of the lumbar spine. This are c be outlined (see page 96) by
drawing an imaginary line from the crest of each ilium to the spine, then
passing up the spine to the superior level of L2, ad then connecting that point
with the crest of the ilium again. Chapman found that light circular pressure or
kneading to the triangular psterior Chapman area in the lumbar paraspinal
tissues or light circular pressure and soft tissue to the iliotiqial bands greatly
reduces detrimental sympathetic outfow to the colon.
Hypersympathetic activity to the right colon is effectively reduced by rib raising
in the TlO-12 are and by parspinal sof tissue techniques administered to the
T12-L2 area of the spine. With the patient in the supine position, the midline of
the abdomen betwen the xiphoid proess and the umbilicus is palpated for
tenderess, especially just above the umbilicus over the inferior mesenteric
ganglion. If it is palpable and tender, carefully controlled inhibitory pressure is
applied until a palpable relaxation of the tissues occurs in that are. It is
clinically observed that manipulative treatments directed toward reducing
sympathetic outfow reduce the pain experienced by patients with colon
dysfunction. Manipulative tretment in the form of paraspinal inhibition to the
thoracolumbar are also initiates bowel activity in patients with ileus and rapidly
diminishes abdominal bloating.
PATITS WITH PARASYPATHETIC DOMANT
COMLAITS: headache, nausea, vomiting, diarrhea, cramps or pain
from the GI tract.
When associated with right-sided colon dysfunction, examination and
manipulation are usually directed to the OA, AA, and ocipitomastoid suture
ares. More tissue dysfunction would be expected in the right subocipital are
104
beus the right vagus nere innervates the right colon. The right and left
ganglia noosum of the vagus lie in the fascial tissues just anterior to the OA
and AA joints. Thes ganglia lie in and just below the jugular foramina of the
skull. Thes ares should be examined for fascial tension or spifc joint
somatic dysfunction; the motion patter and mobility of the cranium should also
be determine. Condylar deompression and cranial tehniques to ensure
symmetry of motion in the ocipitotemporal region (if the physician is trained in
cranial manipulation) is effetive tretment in a patient expressing symptoms
related to the parasympathetic system. While in the are, the physician may as
well palpate for somatic dysfunction of C3-5, becaus this are infuences the
phrenic nere and function of the abdominal diaphragm.
When assoiated with lef-side colon dysfunction or pain, diagnose and
manipulate somatic dysfnction of the scrum, innominates, and lumboscral
regions. It is particularly imprtant to check for unilateral scral sher somatic
dysfunction and the ability of the scrum to passively rok about its involuntary
suprior transvers axis (the respiratory axis) between the innominates.
PATITS WIT OTHE RLATE COMLAITS: I all dee
of the colon, fatigue, constipation, diarrhea, pain and cramps may be
related to lymphatic congestion of the colon.
The frst step toward incresing lymphatic drainage from the colon is to check
for fascial torsions and joint somatic dysfunction at the thoracic inlet. This
includes examination of ribs 1 and 2, the frst four thoracic vertebrae and the
manubrium of the sterum. Any joint or fascial somatic dysfunction related to
thes tissues should be treted.
The patient may then be tured to the lateral recumbent position and given sof
tissue treatment to relax the tissues of the lumbosacral junction. Ll,2,3, is the
are of the spinal attachment of the diaphragm and must be relaxed before the
diaphragm c be redomed. The abdominal diaphragm also attaches t the
lower 6 rbs and the xiphoid proess. The diaphragm may be redomed with
diret or indiret fascial tehniques. It must be functioning properly in order to
provide the effective pressure gradients needed to "pump" lymph from the
abdomen to the thor.
The pelvic diaphragm should be palpated and if treatment is indicated it c be
accomplished by using an ischioretal foss technique (s page 216),
Relaxation of the plvic diaphragm through ischiorectal fossa techniques (or
through transvaginal and anal digital inhibition treatment) helps to relieve
congestion and pain originating in the pelvis and also relieves prineural edema
105
of the pelvic parasympathetic neres or the somatic pudendal nere (both having
their origin from nere rots S2,3,4).
I. SUY
Ostepathic manipulation is physiologic tretment of a patient that may be
direted toward systemic dysfunction and/or the boy's respons to a disese
proess. It is the condition of the boy itself which determines whether, how
effciently and how completely a prson will recover from a surgery, a systemic
disse or an infetive proess. The development and the us of more pwerful
and specifc drugs a a mens of improving a patient's recovery will have
varying effects depnding upn the physician's ability (or inability) to improve
or restore that patient's own physiologic mechanisms and resistance.
Remember, for antibiotics to be effective, host resistance must be active no
matter how goo or how spifc the medical treatments become. Osteopathic
manipulative tretment enhances the homeostasis mechanisms of the patient who
has the illness or dysfunction.
RFNCE:
1. Owens C An Endorine Interretation of Chapman's Refexes. Carmel CA,
1963.
2. Miller A: The lymphatic system and cardiac disese, in Lymph ad the
Lymphatic Sem, CC Thomas, 1968, pp 213-229.
3. Threefot S: Lymphaticovenous communications, in Mayerson HS (ed)
Lymph and the Lymphatic System. Springfeld IL, CC Thomas, 1968,
ch 2, pp 17-52.
Manua, Baltimore, Williams & Wilkins, 1983, p 672.
5. Barral JP, Mercier P Viscer Manipulation. Seattle WA, Estland Press,
1988.
6. Herrmann E, The D., Ot. 1965, pp 163-4.
106
SYMPATHETIC INNERVATION OF THE GI TRACT AND PLN FOR USE OF
OSTEOPATHIC MANIPULTIVE TREATMENT
Aatomical Nam.. Aatomical No. Group Functlonal lnneraUon Collateral Sympathetic Ganglon
Greater
Splanchnic Nere
Lesser
Splanchnic Nere
TS-9
1 TS-9 -Stomach, Uver -Celiac Ganglion
(1 0) Pancreas, Duodenum
Least Splanchnic
Nere
T10-11 1
T10-11 -Small Intestines -Superior Mesenteric Ganglion
(12)
and Right Colon
T12
Lumbar Splanchnic
Nere Ll-2
Somatc Dysfunction
facilitated cord
segment
Sympathetics
Rib Raising
T5-10
Tl0-12
L 1-2 (inhibition)
Chapmn's Refexes
Collateral Ganglia
I
T12-L2 - Left Colon and -Inferior Mesenteric Ganglion
Pelvic Organs
Treatment Plan
GI Disease or Dysfunction
Lymphatics
Thoracic Inlets
Abdominal Diaphragm
Mesenteries
Pelvic Diaphragm
Initiate Flow
107
I
I
Parasympathetics
OA,M
Cranial
Sacroiliac
Sacral
I
Pelvic Bone
(innominate)
I
Vagus Neres
Pelvic Splanchnic
Nerves
NOT:
108
OSTEOPATIIC CONSIERATIONS
I IRITABLE BOWEL SYROM
"T high incidnce of co-eisting muculoskletal dfects a
contributing factors maks this (irritable bowel) sndrome
paricularly interesting to the osteopathic physician. ,1
I. ITRODUCTION
The gastrointestinal tract is in a constant state of physiologic and biohemical
activity, yet man is usually unaware of its function until it "rebels" causing gas,
pain, or a change in frequency or type of bowel movements. It has been
reprted physicians will fail to discover an objective diagnosis or organic cause
for 50% of pople presenting with intestinal complaints.
For almost 10 yers, osteopathic physicians have clinically used viscerosomatic
refexes to help them in their diagnosis and treatment of visceral and systemic
disorders and disese. Thrugh the work of Denslow, Hix, Kor, Patterson and
Sato, these refexes have been scientifcally established. In spite of this
evidence, these functional refexes are seldom considered in present day medical
texts and jourals. They are also seldom referred to as an explanation for the
pathogenesis of gastrointestinal disease processes, its symptoms or functional
disorders.
In medical circles, "functional" ofen mens that the symptoms can't be
explained by present structural or biohemical knowledge; some physicians
equate "functional" with psychological. One defnition was found which
conceded that there is a physiologic basis for the symptoms exprienced by
patients with functional disease.
Iritable bowel syndrome (BS) is one of these functional diseases and has quite
a common ocurrence. It is a complex that is chronic, recurrent, intermittent,
non-contagious and apparently non-pathological. Its importnce to physicians is
related to the fact that these patients present with symptoms which could be a
part of any number of serious diseses. Major symptoms include complaints of
abdominal pain usually related to meals and abnormal or irregular bowel habits,
diarrhe and/or constipation. Secon(ary complaints may be distention of the
abdomen, bloating, fatulence, and a sense of incomplete emptying of the
bowel.
Once these symptoms are established in a prson with IBS they rrely disppar;
neither do they progress. If the symptoms of a person with IBS change
rdically, the physician must consider that a pathologic organic dis may be
developing. These patients often have a high degree of stress in their lives.
109
They typically are rigid thinkers, orderly, and conscientious. They are usually
preocupied with planning and details. It has been reported that 70-80% of the
patients with IBS have neurotic personalities but these traits are usually mild.
Some studies have reported that psychiatric illness of the patient ofen precedes
the diagnosis of iritable bowel syndrome. Actually many general practice
physicians feel this psychiatric factor has been over-emphasized. Depression is
common but it is ofen hidden by somatic complaints.
IBS should not be a wastebasket diagnosis given to a patient when symptoms do
not ft other GI diseases. The typical patient with IBS is less than forty yers of
age but not over ffty, with recurrent abdominal pains and a history of an altered
bowel habit. Since this history also fts so many organic pathologic diseases,
the diagnosis of IBS is dependent upon the exclusion of pathologic problems.
These organic disese pssibilities include: Crohn' s disease, ulcerative colitis,
cancer of the colon, gastric/duodenal ulcer, cholelithiasis and amebiasis.
Unlike the diseases mentioned above, patients with the functional irritable bowel
syndrome:
o .. Do not lose weight.
o .. Do not have fever.
o .. Do not have rectal ulcerations.
o .. Do not have rectal bleeding.
o .. Do not have anemia.
o .. Are not more likely to develop cancer of the colon than people who do not
have IBS.
Erly work-up of the patient relieves the anxiety of both the physician and the
patient. It certainly prevents the physician from later performing piece-meal
and repted investigations because of an ambiguous understanding of the
patient's symptoms and the chronic and frustrating nature of this "disease".
Minimal basic work-up might include any or all of the following:
o .. CBC and Sed Rate--evidence of anemia or infection,
o .. Thre stol specimens for ocult blo, ova and parasites (including
Giardia),
o .. Sigmoidoscopy and a warm slide prep for amoba; biopsy if needed.
o .. A double contrast barium study loking for ulcerations, plyps, tumors or
spasm.
If the patient also complains of dyspepsia, a gallbladder study should be
ordered. If there is a complaint of diarrhea as well, a small bowel study should
be ordered.
110
l. PHYSIOWGY OF TE ITETIAL TACT
The intestines have both an extrinsic and an intrinsic control system.
Intrinsically, the smoth musle membranes of the bowel pssss spntaneous
eletrophysiologic mehanisms capable of actively generating electrohemical
gradients. Thes gradients c b stored and then disharged as eletrical
curents. The resultant cyclic activity of the smoth muscle of the gut is called
"slow wave activity." Since spike potentials are prouced in the sme are of
ech slow wave and ech results in a contraction, it is the slow wave frequency
that determines the typ of motor activity found in the intestines. There are two
major slow wave frequencies: 6 and 3 cycle pr minute. The normal smoth
muscle membrane of the bowel in a prson without bowel dysfunction or
dis, has a balance of 90% of the 6 cpm and 10% of the 3 cpm slow waves.
(See table page 113)
Functionally, these are the contractions normally found in the bowel:
o . . "propulsive contractions"--moves material through the gut.
o . . "retropulive contractions"--moves contents back toward the stomach.
The retropulsive contractions are more common in the ascending and
transverse colon in order to slow the forward fow of the feces and to
allow time for storage and additional time for absortion of fuids.
o .. "non-propulive contractions"--just mix the contents of the bowel and
move the material from one haustra to the next.
0 .. "mas movement"--normally ocur once or twice a day. This contraction
suezes off the main fecal mass stored in the ceum and ascending
colon and moves it rpidly (in just a few minutes) over to the sigmoid
colon.
o .. "gatrocolic refex"--is a mass movement that ocurs shortly afer a meal.
Unless it is frequent and excessive, it is considered a normal event. It is
usually initiated by the hormone called gastrin.
The nerous control of the intestinal tract may be generally divide into two
divisions, the intrinsic and the extrinsic prtions. The function of the plexi,
their nere pathways and the overall beneft to the fnction of the entire boy
determines whether a given stress for a patient becomes consious or remains
subconscious; whether the rection will be long-lasting or feting; or whether
the respnse will set the stage for visceral pathology or not.
T ISIC NVE CONTROL SYSTE OF TE ITETI:
The intrinsic control system consists of the autonomic plexi within the wall of
the intestines at which synapses betwen visceral afferents, the parasympathetic,
and sympathetic nere endings tke place. At any one place along the intestine,
the are's plexus moifes autonomic activity according to the loal neds of
111
that region of intestine. Smoth muscle in a sction of the intestine c
therefore respnd to its loal environment and c digest and move fo along
even if the extrinsic nere supply has been surgically svered. Baus this ty
of control is entirely unrelated to the exteral environment, it is termed
vegetative and primitive. It is unrelated to the needs of the rest of the boy as a
whole.
TIE EXTRISIC NERVE CONTROL SYSTEM OF TIE ITETI:
The
Gl
tract cordinates its activity with other body systems and the exteral
environment by way of the extrinsic autonomic nerous system. This extrinsic
control of the intestine with its parasympathetic and sympathetic connetions
between the gut, the spinal cord, and the brain provides continuity and
cordination between the interal control system and the rest of the boy
systems and the environment.
Baus of its extrinsic connections, the
G
l tract c respond and its functions
c b altered whenever the body is stressed psychologically, physically,
chemically or traumatically.
TE SYATIETIC INERVATION OF TIlE ITETI:
Sympathetic inneration to the
Gl
tract has its orgin in cord segments T5-L2
and innerates the intestines by way of the collateral sympathetic ganglia in the
abdomen. The collateral ganglia are labeled celiac, superior mesenteric, and
inferior mesenteric.
TIlE PARASYMATHETIC INERVATION OF TIlE ITETI:
Parasympathetic innervation is supplied by the vagus (cranial nere X) to the
uppr
Gl
, small intestines and right half of the colon; the plvic splanchnic
neres (S2,3,4) supply parasympathetic inneration to the left half of the colon
and the plvis.
Reserch moels indicate that dysfunction of the musculoskeletl system c
prouce visceral dysfnction in related viscera. This ocurs via a
somatoviseral refex. If the musculoskeletal somatic dysfunction was remove
"sn enough," the sondary visceral dysfunction disppared.
If, however, the somatic dysfunction was left "to long," the visceral
dysfunctions initially improved slightly but then become fully established again,
even though the joint somatic dysfunction did not retur. Apparently the refex
patter was "bured into the nerous system" (leed). It has therefore been
therized that a direted program to keep pople free from musculoskeletal
112
somatic dysfunction could become a progrm for prevention of later interal
dis. Further reserch is warranted in this are.
f. CHARACTSTCS OF A PAT WI I ABLE BOWEL
SYROM:
The slow wave ratio in the intestine change: In irritable bowel disese the
patient's intestines have a different ratio of the 2 slow wave typs: The 6 cpm
waves are reduced from 90 to 60 % and the 3 cpm waves are incresed from 10
to 40%.
NORAL BOWEL IBS
SLOW WAVES PATIENT PATIENT
6 cpm 90% 60%
3 cpm 10% 40%
This new ratio hinders the forard fow of fecal contents and therefore prouces
a "functional obstruction." The change in the ratio of slow waves is present
whether or not the patient is having symptoms. It is interesting to note that the
incre in 3 cpm slow waves found in IBS patients is not found in patients with
"pathologic disss" such as ulcerative colitis or pancretitis.
Patients with irritable bowel have the following functional characteristics:
Delayed and prolonged reactions to stimuli: In the fasting state, the spike
ptentials of a normal patient and the patient with irritable bowel syndrome are
about the sme. Afer a mel the normal patient has a rapid increse in spike
ptentials reching a pak at about 40 minutes and shortly after returing to a
normal resting level. This is considered a normal gastroolic refex. In the
patient with irritable bowel syndrome, there is a delay and then a stedy ris of
the spike ptentials. They only rech about 6% of their p levels at 40
minutes ad do not rech their peak until 90 minutes. The IDS patient's
respns is delayed and prolonged to normal changes in the interal
environment. This is not in the best interest of the patient's totl helth.
Decreased nerve threshold levels encouraging excessive reaction to stimuli
that would otherwise be considered to be nonal: In a study demonstrating
this phenomenon, a ballon was placed in the retosigmoid region of normal
patients and als in patients with IDS. Just placement of the ballon into that
region of the intestine cause immediate and delayed contractions in the patient
113
with irritable bowel syndrome. Then, with 6 cc of air in the ballon, 55 % of
the patients with ms complained of pain while only 6% of the "normal
patients" had pain. Even with only 20 c of air in the ballon, 50% of the
patients with IBS still had pain.
Apparently, excessive contractility of the bowel over a long prio of time
reduces the bowel's threshold to distension. As a result, even the usual amounts
of intestinal gas caus the patient to have pain. The gut will remain overactive
long after the stimulus is removed.
Intense emotional reactions: One of the most important factors determining
"intensity of rection" in patients with IBS, is the emotional level at which they
live their lives. Anxiety should trigger sympathetic over activity ad therefore
reuced bowel function and activity should be expected.
2
Gillhor at the
University of Minnesota suggested that "the hypthalamus can tune against
itself."
3
By this he ment that once the initial panic has subsided, the
sympathetic effect is overruled by excessive induction of parasympathetic
stimuli. A hypothalamic tuning can be either parasympathetic or sympathetic in
respnse and may extend to related viscera such as the small intestine or the
urinary tract.
Abnoral contraction patter of the intestines: IBS patients may have
"narrowing" of the intestines which produces diarrhea. This patter is ofen
found in the terminal small bowel and abnormal contractions in the ceum and
ascending colon. They may have "segmentation" which is another abnormal
patter of contractions assoiated with the pain and fatulence of spastic
constipation. This latter typ of contraction causes "functional obstruction." If
narrowing and segmentation ocur together, the result is abdominal pain with
constipation and stol with excessive mucus--but no blood.
Ecessive ga: Man normally prouces 6-8 liters of gas in the intestine every
day, so gas is not abnormal in the intestinal tract.
The gas may be obtained from our exteral environment through swallowing
air. This accounts mainly for the presence of nitrogen and oxygen. The gas
prouced in the normal bowel itself is the source of its carbon dioxide and
hydrogen gas, but 30% of patients also prouce methane gas. This gas is
apparently prouced through the action of some intestinal bacteria that still
remain unidentifed. If it were pssible to develop a practical way to identify
the pople who produce methane gas, they could be watched closely; becaus
85 % of these patients will develop cancer of the colon. People who develop
cancer of the colon also produce methane gas in their colons.
All of the gases mentioned up to this point are odorless. Offensive oors from
intestinal gas indicates the presence of trace gases which contain sulfa or various
114
amine compunds and are more likely to be present when there is some bowel
dysfunction.
Gas in the bowel c be absorbed if the partial pressures between the intestine
and the gas in the capillary is appropriate, if the blo fow around the lumen is
suffcient, and if the pristaltic activity is normal. Intestinal gas c be
absrbed, passe retally, belched, or, in certain cases, excreted by the lungs.
A medical resercher has obsered and reprted that patients with excessive
fatulence often have incresed low back lordosis. He might be describing the
smatic effets of viscerosomatic refexes activated through visceral afferent
neres from the colon and small intestine to the somatic neres in the
thoracolumbar are. The lordosis of the low back are might also be affeting
the function of the intestine via a somatovisceral refex.
Pain in the abdomen: Abdominal pain is a common complaint and results
from a complex interlay of emotions, snsory factors and motor activity as
well as neurologic and hormonal infuences. 65 % of the patients complain of
pain below the umbilicus, 10% above the umbilicus: 25 % complain of pain
above and below the umbilicus at the sme time.
The pain lasts for minutes in 30%, hours in 50% and days in 20%. Though
pain loated in the upper rght quadrant does not ocur very often, it must be
carefully distinguished fom pain caused by gallbladder disease or cholelithiasis.
If a gallbladder is removed unnecessarily in a patient with ms, the so-called
"gallbladder pain" will increse because there is an increase, and constant
rele, of choleystoknin (CCK) into the intestine afer choleystetomy. This
enzyme incress bowel spasms.
Abdominal pain is due to various mechanisms:
I Distention pain
Distention pain is not prouced by stretching in the bowel wall, but by an
attempt to stretch the mesnteries and srosl covering of the bowel beyond its
normal length. Mesnteric and sros tissues do not stretch. Distention is
therefore limite by the sros and mesenteric circumference allowed by the
intestine. Lymphatic edema or venous congestion of the mesenteric tissue of the
gut wall would reduce the amount of gas tolerated before pain from mesnteric
pull would ocur.
115
Contraction pain
Contraction pain is prouced by contraction of the intestine on a fxed and
incompressible mass of stol.
Compres ion pain
Compression pain is due to bowel contraction on an empty lumen and is
apparently produced by pressure on sensitive mucosl and submucosal
structures.
Bth contraction pain and compression pain can be helped with the us of bulk
and by reducing parasympathetic infuence through some physical or medical
mes such as an anticholinergic agent.
I. TREATNT CONSIERATIONS
Tretment of irritable bowel syndrome is important and often consists of some
combination of OM, dietary counselling, and medical prescription. The basic
aim of all treatment is to remove the cause when a cause is present. When a
caus is not evident, the tretment is symptomatic.
PHARMACOWGIC TEATNT:
o .. Antispasmodics taken before meals reduce the degre of gastroolic refex
rection in some people and also reduce the intrlumenal pressure of the
intestine.
o .. Tranquilizers or a tricyclic, like Elavil, may be helpful to control
depression. Tranquilizers probably work best in right-sided abdominal
pains becaus nervous, anxious patients usually have increased ileal
intestinal fow. Many pople think it is the atropine effect of thes drugs
that provide the benefcial effets on the GI tract.
o .. Antacids and/or H
2
inhibitors may be used to reduce the hydrogen radicals
available for rection with the bicarbonates found in the secretions of the .
gallbladder, pancres and bowel. This reduces their rection with
bicarbonates to form water and carbon dioxide gas, further incresing
intestinal gas and intestinal distention. Recall that antacids c
themselves infuence te bowel toward constipation or diarrhe
depending on their formulation.
116
DITARY TREATT:
o . . Non-absorbable bulk: Bulk in the diet in adeuate amounts will provide
50% reduction in the bowel symptoms. Patients will complain of less
abdominal pain beaus of reduced intralumenal pressure and they will
have reduce mucorrhe.
o . . Whet bran, 2 TIs pr day, divided and taken with mels, may be
successfl; or a plycarbophil tablet with mels may provide a gelatinous
stol.
o . . Bulk should be started slowly and incred slowly becaus sudden
incresed bulk in the diet will itself upset the intestinal tract.
o . . Reduce the lactos intake. Lctose is the sugar found in milk. Lctase is a
natural enzyme which prmits normal breakdown of lactose. Lctase
levels c be low in pople anywhere in the world and is not an
uncommon fnding. The patient can be tested by removing milk from
the diet for a 2-wek prio to s if the symptoms of bowel dysfunction
are reduced. Lctase c also be adde to milk and milk proucts to aid
digestion.
o . . Restrct fat from the diet because fat stimulates bowel spasm and it also
rects with the bicarbonate radical in the small bowel to prouce carbon
dioxide gas.
OSTEOPATIJC MUATIE TREATMT:
Irritable bowel syndrome is considered a "functional condition" without a
known caus, but charcterized by certain identifable "functional ad
physiologic rections. " IBS patients rect excessively to interal stimuli and are
infuenced hevily by exteral stimuli through the extrinsic autonomic control
connetions.
For thes resons, osteopathic manipulation is effective by improving function
structure relationships. Medicine, dietary modifcations and osteopathic
manipulative tretment in the management of this fnctional dis provide
increased patient comfort ad clinical improvement far beyond that expted by
ech typ of tretment usd alone. The physician' s goals should be to normalize
autonomic activity to the intestine, promote go lymphatic fow, and normalize
joint smatic dysfunction--espially in the areas of sympathetic inneration to
the GJ tract. (Se page 107 Tretment directed toward the support of the
boy's own self-regulatory mehanisms in a patient with a functional dis, is
a practical conclusion based on a understanding of anatomy and physiology.
Successful tretment of the patient with ms often depnds upn how much
effort the physician exerts toward understnding the mehaisms of the disese
117
proess or the dysfunction. Osteopathic considerations in systemic dysfunction
therefore should begin with a thorough understanding of the pathophysiology of
IDS.
Supprt provided by spifc osteopathic manipulative techniques is designed to:
o .. balance the extrinsic autonomic nerous system, both sympathetic and
parasympathetic.
o .. relieve lymphatic and venous congestion in the intestinal tract.
o .. remove chronic joint smatic dysfunctions which play a role in prptuating
detrimental facilitate cord sgments.
MANIUATION AFECTIG THE SOMATIC COMNENT:
It has been reprted that somatic dysfunction can be assoiated with, or
ptentiated by, visceral dysfunction; and a vicious cycle of viscerosomatic and
somatovisceral refexes c be pstulated. Palpable somatic paraspinal fndings
prouce by viscerosomatic refex pathways c be used as clues to the loation
of interal visceral dysfunction. General stress, structural problems, abnormal
psture, and trauma c ech prouce spinal joint somatic dysfunction. Somatic
dysfunction of joints is also assoiated with the facilitated segment and
sympathicotonia.
MANIUATION AFCTIG SYATHETICS:
Though sympathetic activity may help in "fght or fight" situations, its
prptuation is detrimental to the healing proess. With the understanding that
hypersympathetic activity is present in all dysfunctions and diseses,
hyprsympathetic activity c be treted by osteopathic manipulation at a
number of sites ad in the following ways:
Rib raising and segmental osteopathic manipulative tretment:
In IBS, supine parspinal "rib raising" inhibition (see page 195) and sof tissue
to the thoracolumbar are (T1O-L2) is especially benefcial.
Tretment of the collateral sympathetic ganglia:
Us inhibitory ventral abdominal techniques. In a patient with IDS, the midline
are betwen the xiphoid proess and the umbilicus is tense to palpation and it is
tender to the patient even when palpated lightly. Just a few seconds of stedy
118
"humane" pressure over the ganglia reduces the palpable tension and relieves
the patient's subjective discomfort.
I Tretment of Chapman's refexes:
Chapman's refexes are believed to be produced by viscerosomatic, visceral
afferent induce refexes referred from visceral dysfunction to the sma. They
c b very spifcally mappd out on the boy and charts are available. (efer
t pages 232 and 233.)
Most physicians us the anterior pints to identify the organ which may have
dysfunction. Anterior pints for the small intestine refer to the anterior
intercostal spaces 8, 9, and 10 on ech side. Chapman's refexes from the colon
are found in the iliotibial bands, a 2-inch strip on the lateral side of ech thigh.
These c be treted with sof tissue keding, a mechanical prcussion
hammer, or other typs of vibration to produce an effective somatovisceral
infuence on the sympathetic inneration to the colon.
MUATION AFECTIG PARASYATHETICS:
The effets of manipulation direted toward normaliztion of parasympathetic
activity have relatively little exprimental verifcation. Clinical effects,
however, are obsre. The plvic splanchnic nere provides parasympathetic
inneration to the left half of the colon and plvic organs while the vagus
provides inneration to the rest of the GI tract.
Tretment of somatic dysfunction of the scroiliac joints:
The plvic splanchnics have an S2,3,4 origin while the scroiliac joint
incorrtes scrl segments 1, 2, and 3. Because of this anatomic proximity,
IDS symptomatology is considered to be affected by somatic dysfunctions of the
scrm--torsion, rotations, shes--or by scroiliac somatic dysfunction-
anterior, psterior and suprior innominate shear. Therefore, somatic
dysfnctions of thes ares are spcifcally manipulated to normalize the
parasympathetic activity to the lef colon.
Anterior pressure and roking over the scrum of a patient, prone on the table,
has ben found t clinically moify parasympathetic tone, even in the absence
of spifc scral somatic dysfunction.
119
Tretment of the OA, AA, C2 and use of condylar decompression:
The right vagus nere supplies parasympathetic inneration to the right half of
the colon and small intestines and may be affected by somatic dysfnction at the
OA, AA, C2 and the lambdoidal suture of the cranium, espcially in the are of
the jugular foramen and the ocipitomastoid suture. Osteopathic manipulation
of smatic dysfunction palpable in these areas is effetive in normalizing
parasympathetic activity to the proximal GI tract and the right half of the colon.
MULATON AFCTG TE LYHATC SYSTE:
With organ and tissue dysfunction there will be lymphatic and venous
congestion. This interferes with blo, nere, nutrition and oxygenation of
tissues and results in the increase of toxic waste products in and around the
cells. Congestion also hinders the plexi for intrinsic autonomic control and
reduces the intestine's ability to inform the CNS of the exact nature of loal
conditions. This information is necessary so that the loal responses will be
appropriate to the needs of the entire body and to its exteral environment.
Techniques ofen used to affect the lymphaticovenous system include:
Soft tissue tretment to the thoracolumbar junction:
This prepares the fascias and other sof tissues for abdominal diaphragmatic
redoming.
Tretment to the thoracic inlet and redoming of the abdominal diaphragm:
Basic for opning the pathway for lymphatic drainage and for support of the
extrinsic lymphatic pump.
I Ventral abdominal techniques:
Thes are directed toward the mesenteries to help relieve the congestive effets
of visceroptosis, to fre the fascial planes of the mesnteries, to reduce
abdominal pain, to provide better circulation to the intestines, to improve
lymphatic fow, and t insure more appropriate autonomic respnses.
120
VI. SUARY
Osteopathic physicians have the ability to us proven pharmacologic and dietary
tretment wisly and t provide manipulative supprt t the patient's own boy
mehanisms. The boy also has inherent mechanisms t combat dysfunction or
dis. They reognize that thes mehanisms may not always be working at
their optimal level of effciency as evidenced by the wide variety and rge of
respnss obsred in a group of patients expsed to a similar stress. It is esy
t comprehend that inherent compnstory mehanisms often require assistance
to prmit them t function at their optimal levels and capacities.
The result of osteopathic manipulative tretment is palpable in the tissues.
Functional changes ae clinically obsrable and subjetive improvements are
voiced by the patients. Go results are not limited to the offce visit or the
immediate pst-tretment prio, but continue on; apparently it is pssible to
tune the intrinsic mechanisms to a new level of performance.
Manipulation, as a part of the management of a patient with irritable bowel
syndrome, allows the physician to better control that patient's responses to life
stress and helps to give the patient physiologic relief from his symptoms.
Osteopathic manipulation benefts the patient by providing relaxation,
normalizing extrinsic and intrinsic autonomic control mechanisms and relieving
congestion.
Osteopathic manipulation is directed toward the patient, for the patient who has
dysfunction or dis. It allows a prsonal manipulative prescription for the
spcifc needs of that particular patient.
RECOME READIG FOR OSTEOPATHIC CONSIERATIONS
I PATITS WITH IRITABLE BOWEL SYNDROM:
Sleisenger MH, Fordtran JS Gtrointestinal Diseases. Saunders Co, 3rd ed,
1983.
Seroka T, Jacobson E Gtrointstina Physiolo. Williams and Wilkins,
1983.
Battle W, Kohen S, Snap W: Inhibition of pstrandial colonic immobility
after ingestion of an amino acid mixture. Digve Diseases
a
Sciences Sep 1980; 25(9): 67-652.
Ritchie JA, Truelove SE: Comparisons of various tretment for irritable
syndrome. Brtish Medical Jal Nov 15, 1980; 281: 1317-1319.
Sullivan M, Kohen S, Snap W: Colonic myoelectric activity in irritable bowel
syndrome. Ef of Eting ad Anticholinergics: 878-883.
Kailbinger H, Weilkauch T: Drugs incresing gastrointestinal pharmacology.
Karger, Basel 1982; 25: 61-72.
121
Patriquin D: Epnym syndrome blindness: Is there a cure? JAOA Mar 1984;
83(7): 516/95-521-10.
Ls B: Overiew of irritable bowel syndrome. JAOA 6/11-20/11.
Masterson E: Irtable bowel syndrome: An osteopathic approach. Oic
Annals Jan 1984; 12(1):-12121-18/31.
Denslow JS: Functional colitis: Etiology. AAO Yearbook Vol 1, 1965, pp
192-197.
McBain: Tretment of functional colon. AAO Yearbok Vol 1, 1965, pp 190-
191.
Round Table: Uppr gastrointestinal diseses. Clinical Challenges 1984; 1(3):
2-83.
Burstok G, O'Brien R, Vrbova G: Somatic and Autonomic Nerve-Mus
Interactions. Amsterdam, Elsvier, 1983, pp 383-351.
RFCE:
1. Strong WB: Disorders of the digestive system, in Hoag JM (ed)
2. Almy TP et al: Alteratives In Colon Function. Gastroentrolo 1949;
12: 425-436.
3. Gilhor in Autonomic Imbalance In The Hythalamus. U of Minnesota
Press, 1957.
122
OSTEOPATHIC CONSIERATIONS
I GEITOUARY TRACT DISORDERS
more the osteopathic urologist maks ue of manipulative
therapy, the sooner (s)he becomes aware that special
manipulative meaures can improve and someti
'
es efect
recover fom varou genitourinar disordrs. "
I. IODUCTION
Por psture and compromised boy mechaics have long been implicated in a
wide range of functional disorders including those affeting the genitourinary
system. Goldthwait in the text, Esntias of Body Mehanics in Heth ad
Disease, disusses the role of bad boy mechanics, chronic passive congestion,
the failure of the diaphragmatic pump and pressure on sympathetic ganglia as
factors promoting irregularities in organ function. "These disturbances, if
continued long enough, may lead to diseases in later life. Faulty body
mehanics in erly life, then, becomes a vital factor in the production of the
vicious cycle of chronic disese and presents the chief point of attack in its
prevention.
,,
2
Spifcally, Goldthwait suggests that one of the frst goals of treatment might
b to restore go boy mechanics:
" A los kidney is found almost always with a faulty psture. The
droped thorax obliterates the forward thrust of the ribs and relaxes the
diaphragm, thus pushing the liver downward on the kidney to the right.
Because of this pressure, the protecting fat is rapidly lost and ptosis of
the kidney follows. Chronic passive congestion, kinked ureters,
hydronephrosis, orthostatic albuminuria, urinary stasis, stones and
infetion are pssible outcomes, since function of the kidneys is
depndent on full blo and nerve supply and on fre drainage--all of
which ptosis may distur. The normal psition of the kidneys C be
restore, and the proteting fat re8laced, by relieving the downward
pressure of bad boy mechanics.
tf
Osteopathic considerations therefore include not only a complete history and
examination of genitourinary (GU) structures and/or functions, but als extend
to the psture of the patient and to related somatic dysfunction (neural,
lymphatic, and circulatory elements) involved in homeostasis of these organs.
The imprtance of the thoracic and pelvic diaphragms and the fascias
surrounding the GU organs is crucial to a treatment protool stressing
homeostatic supprt of the patient with GU dysfunction.
123
This stion delinetes general somatic, autonomic, circulatory, and fascial
considerations as they prtain to the pathophysiology ocurring in patients with
genitourinary disorders.
M. KNYS, UTE AND BLADDE (KU)
The kdneys control both volume and composition of boy fuids by regulating
the excretion of water and solutes. Urine, formed H the kidneys, contains
metabolic waste proucts, foreign substances (including pharmacologic by
proucts) ad other water-soluble constituents of the boy in quantities
depnding upn homestatic nes and the functional ability of the kidney at
any given time. The kidneys are also involved in blod pressure control and re
blo cell prouction.
The kidneys are retroprtoneal structures encased in fatty tissue. A tough
areolar fascia surrounds the kidney, splits into two layers which are not
continuous inferiorly, allowing the kidneys to move downward with the
diaphragm during inhalation. This factor is utiliz in the routine physical
examination by having the patient take a deep inhalation so the kidney will
move downward and allow itself to be more easily palpated. A "foating
kidney" may be detected in this manner and kidney enlargement may refect
hydronephrosis, cancer, or plycystic kidney disese. Because of the continuity
of fascias, diaphragmatic descent is the chief factor in venous as well as
lymphatic retur from the GU viscera. Diaphragmatic motion can be reduced
by somatic dysfunction of the thoracolumbar junction or lower ribs,
hyprlordosis, smatic dysfunction affecting the phrenic nere (C3-5) and/or
spasm of the quadratus lumborum or psoas muscles.
The psas muscle courss obliquely causing lateral displacement of the lower
ples of ech kidney. Any limitation of motion in the uppr lumbar vertebrae
(as can ocur with psoas spasm) will result in fascial restriction of the motion of
the kidneys. The ureters adhere directly to the peritoneum and descend on the
psoas fascia, cross the genitofemoral nere, and continue into the plvis to the
bladder. Psoas contracture or spasm may also cause the fascias to adversly
affet ureteral function.
The bladder and urethra carry with them the sme inneration as the systems
from which they were embryologically derived. The sphincter, trigone and
ureter orifces are activated by the sympathetics (whose cell boies originate
from cord segments T12-L2) and are inhibited by the parasympathetics
(originating from S2-4). The bladder wall is activated by the parasympathetics
and inhibited by the sympathetics.
124
SYATETICS:
Sympathetic inneration t the kidneys and ureters begins in sympathetic cell
boies in the spinal cord at the level of TIO-Ll. The preganglionic fbers for
kdney and uppr ureter synaps primarily in the suprior mesnteric collateral
ganglion; while thos for the lower ureter synaps primarily in the inferior
mesntric ganglion. The sympathetic preganglionic fbers t the bladder arise
fom cll boies in the T12-L2 level of the cord and synaps in the inferior
mesnteric collateral ganglion. Sympathetic stimulation causs vanstriction
of afferent arterioles, dereses the glomerular fltration rate (GFR), and results
in dereasd urine volume.
4
This response is exaggerated with emotional
stress.
5
Increase sympathetic tone decreses ureteral pristatic waves and may
caus ureterospasm. Ureteral stimulation, as might ocur with a ureter stone,
slets the kidney as a target organ for sympathetic discharge triggered by
rostral refex centers.
6
Functional urinary obstruction C ocur with
visceromotor refex alterations arising from somatic dysfunction. 7 89 It also
relaxes the bladder wall, which may result in refux and incomplete emptying of
the bladder. Guyton suggests a role for chronic sympathicotonia to the kidneys
in the etiology of essential hyprtension. His physiology text suggests that
essntial hyprtension is probably invoked by a ''nctional retention" of water
and st by the kdneys:
". . . expriments show when sympathetic neres to kidneys are stimulated
continuously for sveral weks, renal retention of fuid ocurs and causs
chronically elevated arterial pressure as long as the sympathetic stimulation
continues. Therefore, it is pssible for nerous stimulation of the kidneys to
caus chronic elevation of aerial pressure.
,,10
Anterior Chapman's
viserosomatic
refexes 11 for the
bladder are loated
priumbilically with
thos referble t the
kdney loated on the
ipsilateral side, one
inch lateral and one
inch suprior to the
umbilicus.
12b
CHAPMAN'S POINTS RELTED TO THE
GENITO-URINARY SYSTEM (T10-l;
Suprior Mesnteric Ganglion,
Inferio Menteric Gaglion)
Key t palpating pernent points:
A. Arenals
B. Kdney
C. Blader
D. Prstate or Broad
Ugaent
E. Gonads
F. Uterus
Posterior Chapman's pints are loated in the intertransvers space (midway
between spines and transvers proess tips of Ll-2 and T12-Ll respctively.
PARASYATETICS:
The parasympathetics which supply the kidney aris from the vagus nere. The
proximal prtion of the ureters are supplied by the vagus and the distal prtion
by the plvic splanchnic neres (S2-4). The bladder's parsympathetic neres
come only from the plvic splanchnic neres. It is not kown how the
parasympathetic neres affect the kdney but in the ureters they maintain normal
pristaltic waves.
As the bladder flls, visceral afferents in the bladder wall transmit impulses to
Ll-2 to snse "fullness"; at the sme time, visceral afferents to S2-4 initiate a
parasympathetic refex to increase the bladder wall tone and, eventually, a
simultaneus relaxation of the interal urethrl sphincter. Then, with the
voluntary relaxation of the exteral urethral sphincter via impulses from S2-4
(the pudendal nerve) and the simultaneous mpathetic relaxation to the exteral
urinary sphincter, micturation takes place. 1 While the exteral urethral
sphincter is primarily under voluntary control, sympathetic relaxation must also
simultaneously ocur during voiding .
UHlNAHY
lNNbHVATlON
Cricl or Crticspinal Lesion
_+a.-..
"Cn't feel fullness but
inaeased pressure cuss
need to urinate."
Trasection Abv Scum
[A9
N
i
9
1
t_
"C feel fullnes b
empting is a refle."
Cuda Equina or
Pelvic Splancnic Lesion
g;f
q
hi#
Eliddenj
.=Inhibit Urination
Crebrum and
Thalamus
aea near leg region of crex
=Initiates Urination
by cnstant cntracting
abominal musces
.Infant Urination' Reflex
Inferior Mesenteric
Ganglion
Pudendal Nere
12
LYMHATICS:
Renal lymphatics drining the capsule and parenchyma fow into the preortic
noes before travelling up the thoracic duct to the subclavian vein. The
synchronous motion of thoracic and plvic diaphragms is vital to lymphatic
drinage from the urinary system. The purs of the lymphatics is to drin the
capsule and parenchyma, acting as a "sfety valve system that aids in the
clece of waste proucts of the kdney as well as fuid, eletrolytes, and
infetious or antibiotic proucts. " It has been shown that during acute ureteral
obstruction, renal hilar lymph fow increses up t 30%.13 With renal vein or
uretera obstruction, capsular lymphatics are known to dilate to prevent renal
damage while Babics and Renyl-Vamos ascribe the surival and continued
prformance of the hydronephrotic kdney to the fact that "urine passes from the
renal plvis into the interstitial space of the kidney where it is continuously
absrbed into the lymphatics. "
The countercurrent exchange concept of urine formation visualizes the vas
reta as imprtant in carrying off slt and water. An osmotic gradient must be
maintaine between the interstitium and the plasma for these vessels to function
proprly. This gradient is maintained only through adequate lymphatic
drainage. Interference with lymphatic drainage has been shown to cause a rise
in the oncotic pressure of the interstitium and an inability of the kidney to
concentrate urine.
VISCEROSENSORY IVISCEOMOTOR REFLEXE:
The renal visceromotor refex will cause incresed tonus to the thoracolumbar
junction and a psitive Lloyd s punch test. The renal viscerosensory refex is
usually described as an ache rather than as a pain. It may refer only to the
thoracolumbar are, the fank, or both. The ureter viscerosensory refex
(ureteroolic) usually extends from the lumbar region and the iliac foss over
the front of the abdomen and into the scrotum or labia. The ureteromotor refex
als causs the abdominal, eretor spinae and the cremasteric muscles to become
tens. As a stone passs through the ureters, palpatory changes from
viseromotor refexes will progress from TlO into the lumbar region.
SOMA TIC SYSTEM:
Exteral sphincter tone relies on resonable innervation from the pudendal nere
(S2-). When there is a sudden increse in intra-abdominal pressure, the plvic
diaphragm with the exteral sphincters will contract in response to a protetive
refex arc. If the contrction of the sphincter is inadequate, urinary
incontinence may ocur when that prson coughs, sneezes or lifs a heavy
object. This problem is more frequent in female patients.
127
When the plvic diaphragm has
incresed tone or is spastic and C
not work synchronously with the
thoracic diaphragm, there will ofen
b a resultnt elevation of intra
abdominal/intraplvic pressure.
This C aggravate the symptoms in
patients with inguinal or esophageal
herias. Pelvic for tension
myalgia C also led to a variety of
urinary symptoms rnging from
testicular ache to frequency and
urgency. 14
Inguina Heria
Tt D
1. RmHeria
2. R Ste& on Pelvic Ro
3. Dim|niInta-omina Presure
4. E Surgi Rp|r
Postural disorders, particularly short leg syndrome, and psoas spasm frequently
caus backache and when accompanied by functionally induced urinary changes
are ofen misconstrued as urinary tract infection. 15
T Ililumbar ligament I one o
t earlies auctur . aalned In
ptural deompnston and
should b palpate In all patent
In which thla l auapeced. Pain
may b loalize to t ae of
atachment o my refe Into te
lateral tigh ao groin. X rays
may show ligament clcifcation o
by exoa In mo chronic
psural atraln. Treatent of acute
aymptomatoloy may Include
counteratraln, NSAID and O
c lly lal inje. However,
t unng pural cause
shoul b ientifie and teated.
Apropiate madjuneel
11f In patent wit ahor leg ayn
drom o & uln patent
whdoaia o spondylolls
tIa ofen neesr t
prevent recurances.
Pain patter modified from
Gerge S. Hacket MD, FACS
Referred Pain From
Iliolumb Ugaent
128
Postural disorders have
further been implicated as a
caus of plvic diaphragm
tension myalgia, whos
symptoms are frequently
misdiagnosed as
prostatitis. 1
6
Iliolumbar ligament strn is
also a frequent consequence
of postural disorders and is
acutely activated by lifing.
Because of the mechanism of
onset and of the refered
pain patter into the groin
region, iliolumbar ligament
strain is ofen perceived by
the patient to be caused by
an inguinal heria.
Somatic dysfunction of the pubic symphysis with tension in the urogenital
diaphragm or the puboprostatic or pubovesicular ligaments may cause dysuria,
urgency or frequency of urination. This may be exprienced by postartum
women or patients who have had either cystoscopy or prinel surgery wherein
te smatic dysfunction C be obtained while they are being incorretly helpd
out of the stirrups following the proedure. In children, this somatic
dysfunction has been assoiated with notural enuresis.
Trigger pints in the lower abdomen
17
may cuse urinary frequency and
urgency, sphincter spasm, and residual urne, or pain in the urinary bladder. In
one reprted c, tretment of a tgger pint in an old appendectomy s
relieved the symptoms of frequency and urgency and increased the patient's
bladder capacity by 4
5 %
.
18
M. GENITAL/REPRODUCTIVE SYSTEM
The Mullerian and Wolfan ducts are of epiblastic origin so the muscles that
surround these ducts in the plvis are innerated by the dermal systems
distribution of sympathetic nerves. The Mullerian ducts become the fallopian
tubes and form the uterus and vagina. The Wolfan duct gives origin to the vas
deferens and ejaculatory duct.
SYMATHETICS AND PARASYMATETICS:
The fallopian tubes, uterus, vagina, vas deferens and seminal vesicles (with the
exception of the cerix) are activated by sympathetics having cell boy origins
from TIl t Tl2 in the spinal cord. Bcause of their embryologic origin, the
sympathetic neres are the only inneration t most of these stctures;
however, the cervix, vagina, clitoris and walls of the urethra are supplied with a
few parasympathetic fbers from S2-4. The maority of the synapses betwen
pre- and pst-ganglionic sympathetic fbers occur in the inferior mesenteric
ganglion. A separate nere supply for the cervix is created by the pelvic
splanchnic nerves (parasympathetic) and activates the cervix while proucing
sme inhibitory infuence on the boy of the uterus.
The prostate, as well as the Cowr and Bartholin glands, have secretory
sympathetic fbers originating from TI2-L2. Stimulation of the hypogastric
plexus of neres, which carries the sympathetic fbers from TI2-L2, prouces
true glandular seretion from the prostate gland structure while stimulation of
the pudendal nerve forces the seretions out the urethra by contracting
musculature.
Anterior Chapman's pints to the prostate or broad ligament are located in the
myofascial tissues along the psterior margin of the iliotibial band. Tenderess
129
t moderate pressure over this are or tenderess and a palpatory sens of
resistance to palpation over the inferior mesenteric collateral ganglion or the
T12-L2 paraspinal tissues should increse the level of suspicion of dysfunction
arising from one of thes structures.
Stimulation of parasympathetic fbers from S2-4 will relax the smoth
musulature of the corra caveros in the pnis and results in an erection as
the musle flls with blo. The pnis also has sympathetic fbers from Ll-2
which innervate the smoth musculature involved in orgasm and ejaCUlation.
Imptence may be assoiated with reduction of parasympathetic tone resulting in
the impairment of erectile capabilities; or it may be assoiated with reduction of
sympathetic activity (as ocurs in diabetics), resulting in dysfnctional
ejaculation disorders. Hyprsympathetic tone producing premature ejaculation
could esily come from facilitation of segments at the thoracolumbar level,
espcially Ll-2.
The testes and ovaries (gonadal tissues) prouce hormonal secretions which have
a marked infuence on the growth and energies of the individual. These
sretions are under the control of the sympathetic fbers, originating in the
TIO-ll spinal cord are. They synapse in the superior mesenteric collateral
ganglion. These neres prouce their effect prmarily through their action on
the gonadal vascular supply. Anterior Chapman s points assoiated with the
gonadal tissues are located on the superior surface of the pubic bones.
Parasympathetic supply is from S2-4 but its effects are unknown except for the
fact that it dos not affect secretory activity of the gonads.
LYHATICS:
Pelvic organs are depndent
upn the synchronous
motion of the active thoracic
diaphragm with the passive
plvic diaphragm during
respiration. The prostate
actually flls an anatomical
urogenital defet in the
plvic diaphragm and is
continuously massged by
the passive motion imparted
by respiratory activity when
the plvic for is fre to
move.
Pem ",
Sup
Pub Ru
Otrat /
Ve&& N.
W _
MW
lie Fos
APHHAGM
This anatomical and functional symbiosis is considered necessary for the
establishment of effetive lymphatic fow.
13U
Pelvic congestion als plays a major role in the symptomatology note in
patients with dysmenorrhe, ovarian cysts, or with premenstrual syndrome.
Incresed vaginal leukorrhe has been assoiated with the venous and lymphatic
stasis of plvic congestion.
1
9 In premenstrual syndrome (PMS) congestion and
fuid retention are respnsible for generalized edema, backache, hedache,
mastalgia, plvic pain, nerousness, irritability, emotional instability,
depression and weight gain. The syndrome has a pstulated hormonal basis, but
hormonal manipulation has been less helpful in the tretment than would be
expcted from this theretical etiology. The adjunctive use of diuretics at the
frst indication of PMS and the us of NSAIDs has als been benefcial in some
cass through their effets in moifying congestion, infammation and
prostaglandin activity.
VISCEROSENSORY A VISCEROMOTOR:
Viscerosensory refexes from the gonads are of considerable clinical
imprtance. They prouce pain in the groin which at times seems to radiate
down the thigh. The etiology of pain referred from the iliolumbar ligaments
should be carefully considered in the differential diagnosis of genitourinary tract
disrders. Visceromotor refexes from the genitourinary tract cause rigidity in
the lowest prtion of the abdominal musculature and in the TIO-li paraspinal
musulature.
Motor refexes from the uterus are not very pronounced, however the snsory
refex is defnite and well recognized; pain is a common sign in both uterine and
tubal disorders. Pain arising from the fallopian tubes may be felt in the fank,
iliac foss, and down the anterior thigh to the knee. Uterine pain is felt in the
thoracolumbar junction, the abdomen, and ocasionally in the scral region.
Segmental referred pain
20
and spinal palpatory changes from the female
reprouctive tract has ben most frequently described as being loated at TIO
for the ovaries, Tl l-12 for fallopian tubes, TIO-LI for the uterus, and S2-4 for
the cerix.
The prostate displays viscerosnsry refexes, traveling via its sympathetic and
parsympathetic routes, as pain in both the thoracolumbar and scral regions.
Pain may also be felt in the glans penis with accompanying urinary frequency
and rectal discomfort beause of the common connection of these tissues with
the plvic nerve.
"The pnis is more ofn the subject of refex sensation than the cause of it.
,,
2
1
Bause it is bound to urogenital and rectal structures by flaments of the plvic
nerve, it is subjet to refex sensory disturbances originating from dysfunction
of renal, ureteral, bladder, urethrl, testicular or prostatic tissues. Infection or
13 1
infammation of thes structures will facilitate the Ll-2 segments causing almost
continuous sxual desire.
The mechanisms of many
"aphroisiacs" can be traced to their
ability t irritate or infame the
bladder to set up this typ of
facilitation. The loation of the
inner thigh "erogenous zones" also
L
corelates with ares which when
stimulated would enhance neural
input into the cord at thes levels.
SOMTIC:
Dysfunction of the psoas muscle has
ben implicated in gyneologic dys
fnction because of its anatomic
proximity to affect varous physio
logic mehanisms imprtant to this
system - vascular, neurlogic, and
lymphatic. Chronic psoas spasm
has been reprted to caus anovula
tion
22
and is also refective of the so
called genitoiliopsoatic syndrome
wherein chronic ovarian
infammation causes refex psoas
spasm.
23
Postural disorders, myofascial trigger pints and pelvic smatic dysfunction also
contribute to pain patters and symptoms commonly assoiated with
genitoreprouctive tract disorders. Short leg syndrme is not only implicated in
low back and lower abdominal pain but also in plvic pain.
24
Symptoms of
dysmenorhe are fruently intensifed by trigger pints in the lower rectus
abdominus muscles. Somatic dysfunction of the scroiliac joint or muscle
spasm in that are may refer pain suggestive of uterine cerical disorders.
26
OT:
Psychomotional factors play a very signifcant role in genitoreproductive
functions. Reduction of stress has ben a valuable therputic element in caring
for patients with functional infertility, frigidity and impotence.
132
. TREATMT CONSIEATIONS
The spifc tehniques provided are much less imprtant than accomplishing
goals which supprt patient homeostasis and maximize structure/function
relationships.
PLAN FOR OSTEOPATHIC MULATION OF PATINT WITH
UROWGICAL DYSFUNCTION:
C3-S (Phrenic Nerve)
Sacroiliacs (Pudendal Nerve, S2,3,4)
Somatic Dysfunction
facil. seg.
Sympathetics
|
Parasympathetics I
|
Rib Raising OA, A
.
V
TlO-L2 Treatment Plan Cranial N
Chapan's Reflexes Urologic Dysfunction S2-4 ]
Inferior Mesenteric Sacrum
Ganglion SI Jnts
Adrenal
l
Lymphatics
Kidne y
Thoracic Inlets
Abdominal Diaphragm
Rib Raising
Lymphatic Pumps
SYMATHETIC (ATO)PHYSIOWGY:
t Tone:
. Afferent Arteriole Constriction to Kidney
2. Ureterospasm ad , Peristalsis of Ureters
3. Relaation of Bladder Wall Lding to Refux
4. t Tone to Exteral Urinary Sphincter
Effets:
, GFR . 'Urnary Output
Elevates Blo Pressure
Ureterospasm . 'Urine Flow through the Ureters
Encourages Incomplete Emptying of Bladder
Encourages Ureteral/Prostatic Refux from Bladder
Complaints of Premature or Retrograde Ejaculation
133
agus
erves
Pelvic
Splanch.
Nerves
LYMHATIC (PATO)PHYSIOWGY:
Impaired Lymphatic Flow Effets:
1 . t Oncotic Interstitial Pressure -
Disrupted Countercurrent Exchange -
, Ability to Concentrate Urine Properly
2. t Risk of Kidney Damage Because of Ureteral
Obstruction
PARASYMATHETIC (PA TO)PHYSIOWGY:
t Tone:
1 . t Peristalsis of Ureters
2. t Bladder Wall Tone
3. Relaxes Interal Urinary Sphincter
, Tone:
1 . Incomplete Emptying of Bladder
2. Impotence
3. Tightens Interal Urinary Sphincter
URIARY TRACT IECTIONS (UTn:
Urinary tract infections (UTI) are among the most frequent bacteral infections
encountered and the most common disese proess ocurring in the GU system.
UIs are ten times more frequent in women than men. If there is a kidney
infection and/or psterior pritoneal irritation, the Lloyd's punch test will
usually be psitive. Chapman's refexes, collateral ganglion involvement, and
the patter of segmental somatic dysfunction help establish a corret differential
diagnosis and correlate with the extent of the infammation. Except for some
simple UTIs, investigation is neessry to detect obstructive uropathies, urinary
calculi, or other predispsing or prtuating factors; further investigation is
also statistically war ted in male patients with UTI. It should b noted that
chronic bacterial prostatitis is the most common cause of relapsing bladder
infetion (cystitis) in males.
Osteopathic considerations include ruling out pubic symphyseal and plvic for
somatic dysfunctions which may produce symptoms of dysuria and freuency.
Tretment of plvic for somatic dysfunction is helpful in reducing spifc
mehanical contributions to symptoms as well as aiding in the relief of the
prostatic congestion that these smatic dysfunctions C prouce.
134
Incomplete emptying, refux and loss of normal ureteral peristalsis are risk
ftors for ascending infetion and should be addresse by tretment to both the
thorcolumbar junction (T1O-L2) and the scroiliac joint (SI-3). Treating a
patient t reduce sympathetic hypractivity is felt to help the boy deal with
loal and systemic infections by removing a factor hindering tissue defense and
promoting mehanisms which led to reduced tissue congestion and adequate
tissue antibiotic levels.
Moifcation of urinary pH is often an effective treatment of urinary tract
infetions and can be accomplished with medication or to a lesser degree, with
cranberry juice. Intake of fuids in general is imprtant.
RAL DISEASE:
All appropriate measures to prevent or limit renal structural changes in
infetious or obstructive uropathies should be taken and this goal is maximized
with erly reognition of GU dysfunctional states. With regard to acute
glomerulonephritis, Osteathic Medicine notes
2
7
that somatic dysfunction "at
TIl, T12, and LI should be considered as an etiologic compnent in view of
the proven pathologic changes apparently associated with such (somatic
dysfunction). In this regard manipulative tretment might well be a preventive
aid." A similar statement is made with regard to acute pyelonephritis, "Patients
having (TIl, T12, and LI somatic dysfunction) are much more vulnerable to
acute pyelonephritis and they are much less likely to respnd to treatment, if
spinal manipulation is not part of the program of management. "28 Even when
signifcnt structural change has ocurred, as in chronic glomerulonephritis,
OMT to these ares to limit dysfunctional refex activity while "not curative ...
will improve renal circulation and is considered decongestive. "
29
Renal failure with resultant aotemia and uremia is "one example in which
applied osteopathic manipulative therapy has in the past produced dramatic
results. "30 OMT to the TIO-L2 region in an attempt to maximize renal
circulation in patients with renal failure "prmit a much faster convalescence. "31
Sterritt reprts a c study in which OMT to the thoracolumbar are is credited
with improving urinary outut and substantially decreasing a critically elevated
BUN3Z
The general concept of the ostepathic manipUlative approach is that by
eliminating the somatic dysfunction component with its related effect on neural,
lymphatic and vasular elements the diseased kidney will function maximally
within its existing structurl limitations. Beyond this, any failed or incomplete
homesttic mehanisms are replaced by artifcial mehanisms - medication,
corretion of electrolyte imbalance and acidosis, and potentially dialysis. To
this end, manipulative tretment to assist the homeostatic responses of patients
with renal disorders is not disese-specifc but rather host-specifc.
13b
PROSTATITIS:
Prostatitis is not one dises. Common prostatitis syndromes include acute
bacterial prostatitis, chronic bacterial prostatitis, nonbacterial prostatitis, and
prostatoynia.
33
Tretment varies depnding on the typ of syndrome present.
Acute bacterial prostatitis is characterized by fever, chills, myalgia and/or
arthralgias, dribbling and/or slowed urinary strem, prinel and low back pain.
It may b accompanied by gross hematuria. The gland will be tender, warm
and swollen to palpation. Digital massge in an acutely infeted gland should
b avoided beaus of the risk of bacteremia. Baus cystitis usually
accompanies bacterial prostatitis, culture of voided bladder urine usually allows
identifcation of the pathogen. The chemical structure of trimethoprim prmits
it to pnetrate the prostatic wall achieving high levels in the prostatic secretions.
This makes trimethoprim or the combination of trimethoprim with
sulfamethoxazole the drugs of choice at the present time. OM addressing the
ishioretal foss, T12-L2 and S2-4 regions is the manipulative tretment of
choice in maximizing prostatic levels of antibiotics and in assisting the boy's
natural defenses. Inadequate prostatic tretment in these patients C led to
chronic relapsing urinary tract infections from ascending infection.
Many patients with chronic bacterial prostatitis have no prior history of an acute
prostatitis. Chills and fevers are unusual; dysuria, urgency, frequency and
noturia are common. There are no characteristic palpable prostatic fndings in
this disorder. Because adequate drug concentrtions rarely are achieved in the
prosttic scretions of thes patients, the pathogen obtns sctuary there; thus,
the hallmark in diagnosis of chronic prosttitis is recurring urinary tract
infetions, always prouced by the sme pathogen. Infected prostatic calculi
may or may not b assoiated with chronic bacterial prostatitis. Medical and
manipulative management is the sme as in acute bacterial prostatitis but the
prognosis for complete "cure" is much porer; surgical interention is probably
indicated for those with prostatic calculi.
Chronic non-bacterial prostatitis is more common than bacterial prostatitis;
however, these patients rarely have histories of UTI and cultures fail to grow a
pathogenic organism. Cells found in the prostatic secretions suggest an
infammatory compnent. Beause the cause of non-bacterial prostatitis is
"unkown," tretment is empirical, traditionally involving hot sitz baths and
prioic prostatic massge. While these may prove helpful, the ostepathic
approach adds manipUlative tretment to corret any somatic dysfnction found
in both the T12-L2 and S2-4 regions and to improve the function of the plvic
for; the latter proucing a physiologic "massge" of the prostate, ocurring
ech time the patient takes a breth.
13
U8BTB BVB8TON1A N IB TO O8 BB CAUBBD B
CBON1C NONBVBC1Y1C V8OBTAT1T1B (Adaptd frm Bralia83
1. "PROSTATODYNIA"
W
3. NON-SPECIFIC
LC FACTORS .---- PROSTATITIS
(painful Male
Urethral Syndrome)
t t
(Intraprostatic Reflex)
I
I
INCRASED SYMATHETIC " URETHR
STIMTION
t
DISTAT FACTORS
(Stress, Psychogenic
Causes Etc.)
HYPERTONIA
(Clinical Form)
(Suclinical For)
'
.
2. CHRONIC
PROSTATITIS
(No symptoms)
Since prostatoynia literally mes painfl prostate, a btter term t us might b painfl
mle uretral syndrom. I this syndrome, the incresed urethral tone cu a painfl urethra
ad not pain in te prostate (which in the over-whelming majority of thes L is nontender on
palpation. )
Prostatoynia presnts with variable plvic pain, intermittent urgency,
frequency, noturia and dysuria as well as hesitancy and weakening of the
urinary strem. Bacterial pathogens and infammatory cells are not sen in the
urine or prostatic eresste. Heightened sympathetic tone34 and plvic
diaphragm tension3 are reprted to play a role in this symptom profle. The
sympathetic dyssynergia causs spasm during voiding and sems to play a
particularly snifcant role in patients with certain types of neurogenic
obstruction. 3
Reommended tretment would address the plvic fo7 and sympathetic
mehanisms38 involve a well as any postural, psychic, emotional or cultural
stressrs39 which aggravate thes mehanisms.
URTOLITIASIS (CALCULI):
Approximately 1 11 0adults annually will acutely suffer through the passge of
at lest one calculus through the ureter, bladder, and urethra. While many
137
calculi are "silent ", they typically produce excruciating pain in the
thoracolumbar region radiating into common pain patters in the back, lower
abdomen, fank, and/or thigh.
Bck pain or renal colic may
ocur with calculi in the
calyces, renal plvis, or
uppr ureter; while stones in
the bladder may caus
suprapubic pain.
Naus, vomiting,
abdominal distension, or the
development of ileus are
sondary gastrointestinal
symptoms which may com
plicte or mask the corret
diagnosis. Fever, chills,
urinary frequency and
hematuria are common signs
and symptoms. Occasionally
the ipsilateral kdney will
refexly and transiently
become nonfunctional.
UHbTbHAL|HHlTATlON
W
CUSES:
1. Uretero
2. Clus
3. P Spam
SYMPTOMS I SIGNS
Rk Pain
Paaspinal Spasm
Smatic Dsfunction
Capman's Points (Ureter)
TREATMENT PROTOCOL
Inhibit Paapinals T1 O-L
Treat Capma Point
Treat Psoa Spasm
(Ceck Lt. L for NN)
Treat Smatic Dsfunction
of Thoraclumbar Juncion
other
In cases with unilateral ureteral stones, the ipsilateral kdney becomes
hyprsnsitive to emotional stress. Patients with unilatral renal disas
demonstrate ipsilateral diminished renal blo fow and reduced GFR for 30-50
minutes. 40
Predictable and predictive palpatory fndings can be noted as the stone passes
through the GU system. Bcause the pain is made wors and the passge of a
calculus is slowed by ureterospasm, tretment considerations should include
reduction of hyprsympathicotonia through the us of thoracolumbar paraspinal
inhibition and/or gentle rib raising techniques.
In the choice of pain medication, morhine should b avoided since this narcotic
is more likely than demerol to prouce an incres in smoth muscle spasm.
Demerol dos not caus signifcant ureteral smoth muscle contraction and is
therefore a better pharmacologic choice for analgesia in this situation. The
patient may appreciate paraspinal inhibition manipulation at the spinal level of
refex spasm until the demerol injection takes effet.
13B
In cs of excruciating pain, most other OMT would b delayed until at lest
partal pain management has been achieved. When less pain is being
exprience, the patient may beneft from counterstrain tretment of palpable
anterior myofascial tender pints including common sen genitourinary
Chapman's refex pints and Jones' iliopsoas pints. ' Physiologic ureteral
pristalsis should b assisted in all patients by diagnosing and treting the
scroiliacs as indicated. Also, the imprtance of adequate lymphatic drainage as
a "sfety valve" preventing complications and tissue damage has already been
pinte out in the stion on pathophysiology.
If the stone cannot be successfully passed, sonic disruption, cystoscopic basket
extraction, or surgical removal may be necessry to reestablish normal function
and prevent renal damage.
It is imprtant to try to determine the pathogenesis of the stone so that propr
prophylaxis can b planned to prevent recurrence. Fluids, dietary counselling,
and moifcation of urinary pH along with a manipUlative program designed to
maintn or augment homeostatic GU mechanisms, can then be intelligently
prescribed.
DYSMOREA:
Primary dysmenorhe should be differentiated from the many causes of
sondary dysmenorrhe. The etiology of primary dysmenorrhe is unknown,
but it ocurs only with ovulatory cycles. This complaint of painful menstruation
is quite common among young women. Both primary and secondary
dysmenorrhe are aggravated by stress. An autonomic postural role has been
implicated and the incidence of dysmenorrhea in college women is signifcant
greter in thos with increased lumbar curatures than in control populations.
An acutely antevertd cerix, in which the fundus is tipped anteriorly relative to
the uterus, is one structural factor which is ocasionally assoiated with
dysmenorrhe. The cramp-like pain of dysmenorrhe is usually loated in the
lower abdomen but may include the back and thighs.
Tretment of any assoiated myofascial trigger points in the lower rectus
abdominus will reduce symptoms of dysmenorrhe.
43
Dysmenorrhe may be
assiated with urinary frequency, pelvic soreness, abdominal distension,
naus, diarrhe, hedache, depression, or irritability. Again, stress aggravates
both primary and sondary dysmenorrhe as well as segmental facilittion and
myofasial trigger pints.
"Dysmenorrhe is one of the disorders in which osteopathic manipulative
tretment (se chart on page 141) offers a great potential beneft."
44
The
symptoms of primary dysmenorrhea are felt to arise from an imbalance in both
139
the sympathetic and the parasympathetic systems as well as from somatic
dysfunction causing a signifcant amount of venous and lymphatic congestion.
Tretment t normaliz both the sympathetics arising fom T12-L2 (controlling
uterine contraction and vanstriction) and the parasympathetics arising from
S2-4 (controlling uterine inhibition and vasoilation) is a major goa; yet, this
dos not neessrily men inhibiting one system and stimulating the other.
Tehniques to incre venous ad lymphatic drnage of the plvic organs often
provides signifcat relief and is the other major goal of tretment.
One very effetive manipulative tehnique used in accomplishing the goals
outlined above involves a frm, continuous pressure over the scral bas with
the patient in the prone psition. This tehnique has a effet on the
parsympathetics but is even more effective in fuid mobiliztion. The
tehnique takes the scra base anteriorly or into the "extension phase" of the
cranioscral mechanism and is therefore equivalent to performing a CV 4 cranial
tehnique which is primarily use to help relieve tissue congestion in the body.
Another technique that is effective in the acute phase is accomplished by gently
roking the prone patient' s scrum with its natur rhythm of 10- 14 times a
minute. This is pstulated to improve the patient's parasympathetic outfow to
the involved organs. Aspirn or NSAIDs may also be benefcial because they
antagonize the spasmogenic action of prostglandins and provide mild analgesia.
The monthly appce of some cases of dysmenorrhe would beneft from
monthly OMT t reuce the severity of symptoms. This is particularly true
when they signifcantly impact the patient's abilities to participate in work,
schol, or home activities-of-daily-living. Functional dysmenorrhea may
respnd to an ostepathic manipulative approach which trets the functional
cus. Osteopathic diagnosis and manipulative treatment may be clinically
successful in relieving dysmenorrhe, particularly in the following situations:
o . . Using OMT and progressive heel lift tretment for correction of a short leg
syndrome having a thoracolumbar cross-over and scroiliac strain.
o . . Manipulation of cranioscral somatic dysfunction in a patient whose history
reveals that the dysmenorrhe began afer starting orthodontic tretment.
o . . Manipulation t remove a scral sher in a tenage patient who reprts that
the dysmenorrhe began afer a "pratfall" . (Questioning the patient
about spcifc activities such as roller skating, ice skating, and
gymnastics can be very helpful in triggering the memory of signifcant
trauma of this sort. )
The knee-chest psition is usd as an "exercis" which is frequently helpful in
patients with dysmenorrhe. Requiring only 5-10 minutes to prform, this
proedure is not a muscle strengthening exercise, but rther a body position to
encourage optimal venous and lymphatic drainage from the pelvis and prmit
the uterus to lif out of the plvis.
14U
A PLAN FOR OSTEOPATHIC MULATION OF A PATINT WITH DYSMORRHEA
Somatic Dysfunction
facil. seg.
Sympathetics
|
Parasympathetics I
|
Rib Raising
TlO-ll (Ovary)
T12-L2 (Uterus)
Superior and Inferior
Mesenteric
I
Ganglia
Treatment Plan For
Patient with Dysmenorrhea
Lymphatics
Thoracic Inlets
Abdominal Diaphragm
Rib Raising
Lymphatic Pumps
Knee Chest Position
S2-4
Sacrum
SI Jnts
I
SYMATETIC (PATHO)PHYSIOLOGY (TIO-ll) H0 (T12-L2)
1 Tone:
} Pelvic
Splanchnic
Nerves
1. 1 Vasoconstriction Poor Nutrition and O
2
Exchange
2. 1 uterine contractions
3+ Threshold for Pain (from uterine body)
LYMHATIC (PA THO) PHYSIOLO GY
Impaired Lymphatic Flow:
1. Lymph Flow
2. 1 Tissue Congestion Bloating and Discomfort
PARASYMATHETIC (PATHO)PHYSIOLOGY (S2,3,4)
1 Tone:
1. 1 Relaxation of uterine Muscle
2. 1 Vasodilation
3+ Threshold for Pain (from the cervix)
141
KNbb-CHb1
|O|1|ON
D WA T A IlM Dr
Twt-sond edion, WB Sunder, 1 951
With the ,patient resting her hed and neck and chest down on her arms and with
her plvis raised to a psition just above her knees (the kne-chest psition) , the
abdominal contents will move with the pull of gravity out of the pelvis and
allow decongestion of the uterus. The patient may need to opn the labia
momentarily to prmit air into the vagina before the uterus moves. The patient
should do this exercise before retiring at night to obtain a maximal decongestive
effet.
SEXUAL DYSFNCTION:
Propr sxual functioning involves a complex interaction of smatic,
parasympathetic, and sympathetic refexes and the body unit tenet of the
osteopathic profession incorrating ment, emotional, and spiritual factors
which must be considere in this bodily function. Physiologic mechanisms
approximately parallel one another in men and women. Sexual dysfunction can
esily ocur with imbalance in the autonomic nervous system, with negative
cortical infuence, as well as with damage to neural, vascular or hormonal
mechanisms. OM has ben pstulated to play a signifcant role in correcting
functional compnents of sxual dysfunction in sveral states including the
following:
o . . ERECTIE DYSFNCTION (ITECE): At lest half of the adult
male ppulation has exprienced the inability to complete sexual
intercours in 25 % or more of opportunities because of erectile
dysfunction. Psychic factors are usually the caus; however , other
functional disorders may play a signifcant role in this problem.
Eretion is depndent upn somatic input through the pudendal nerve
(S2-4) and parasympathetic refexes (S2-4) and therefore manipulative
tretment to remove any scroiliac somatic dysfunction may be helpful
when organic resons have been ruled out.
142
In the female, the physiologic equivalent would be dysfunction of
arousl and lubrication. Thes conditions may also play a role in
development of frigidity and/or dyspareunia.
Oenital | nnenatiOn
Sexual |unctiOn
Et
Vs
Fe
1bt
V_a
Sat
Pun Ner
(Smatic)
Pudendal N.
. .
52.3.4 (Somatic)
Pelvic Splancnic N.
52.3.4 (Paaympathetic)
~ Lumbar Splachnic N.
. . . . . . . .
L1 .2 (Sympathetic)
Lumbar Splancnic N.
: :
via Hypgatric N.
(symp.)
t Va. ad Sminal
Vesides
~~
4
~ Va Deferens
mm Seminal Vesides
mmm Prostate
~~~~ Eternal Sphincter
Crpus Cavernosum
Crpora spongiosum
^^ulbocverosum
Dorsal Nere of Penis

Key
P Prostatic Plexu.
1M Infeior Me.enterlc
Ganglion
0 PRT FACUATION: Ejaculation is primarily a
sympathetically-mediate event activate through Ll -2 and aide by
smatic infuence fom S2-4. Ostepathic manipulation t somatic
dysfunctions in the Ll-2 are of the spine and efforts to reduce viscerl
afferent information t Ll-2 (Le. tretment for left colon or plvic
disrders) may help a patient who is having this typ of ejaculation
dysfnction. OM to thes ares reduces facilitation to the Ll-2
sympathetic centers in the spinal cord. Eucating the patient to interrupt
snsry input from the pnis and/or Ll-2 dermatomes prior to orgasm
and ejaculation is also helpful.
0 DYSPAU: This condition may aris from spasm of the vagina,
inadequate lubrication, plvic for spasm, or lesions and abnormalities
of the female genitl tract. The success of osteopathic tretment in
patients with this problem is related to the correction of somatic
143
dysfunction which affets the attachments of the plvic diaphragm and
normaliz parasympathetic refex activity prmitting formation of
adeuate vaginal lubrication. In the atrophic vagina, estrogen crems
may be helpful.
0 ITIITY: Approximately 10% of married couples in the Unite
States have infertility. Bcaus fertility reuires function and
cordination of the physiologic mehanisms of two individuals, there is a
gret ptential for a dysfnctional cause of infertility. Female structural
tubal disrders are only accountable for 30% of the cases. Male gonadal
defciency accounts for 40%, female hormona defciency 20%, and
"hostile" cerical environment 10%.
Bause of cost, mentl duress, and time involved in the investigation of
infertility, the osteopathic general practice approach incorrates a
theraputic trial of OMT, education, reassurance and correction of any
structural, infectious, or emotional stresses which might interfere with
correct fnctioning. Structurally, emphasis is placed on normalizing
thoracolumbar and plvic somatic dysfunction and reucing pstural
disorders which might b involved in perptuating segmentl facilitation.
Crnioscral evaluation and tretment to assure that there is no
functional pituitary-ovarian axis problem are also considered benefcial.
Couples in which irregular menstrual cycles were a complicating factor
ofen reprt they had increased opprtunity for better and less stressful
timing of the critical prio of ovulation and conception after OMT
promoted regularized prios. Preliminary studies have suggested an
elevation in previously low spermatic counts following systemic OMT.
45
Certnly there is a general reduction in stress which, when coupled with
the removal of somatic and visceral components of "the neurologic lens"
(sgmental facilitation) , offers improved physiologic function. This
approach has often rewarded the couple with clinical success, a long
awaited pregnancy.
An infertility workup beomes necessry only when there is failure of a
clinical therputic trial of osteopathic management over a resonable
length of time. This program must be individually designed to tret
infetions and rule out other organic disese, maximize the patients' own
reprouctive function and crete a favorable environment for
implantation and fetal growth.
ADDmONAL GEITOUARY BmLIOGRAPHY:
Goldthwait, Brown, Swain, Kulans Essentials of B Mechanics in Health ad
Disease. 5th e, 1952.
144
Winter CC Practcal Uo. Mosby Co, 1969.
Pottenger FM Ss of Vi Disease. St Louis, CV Mosby Co, 7th ed,
1953.
Szwed et al: The effet of IV mannitol on renal hemoynamics and renal
lymph reovery during acute ureteral obstruction , in Foldi (ed) Ps
in Lympholo. 1967, pp 123-26.
REFCE:
1 . Sterrett Mg Ir: Disorders of the urinary system, in Hoag 1M (ed)
Osthic Meicine. New York, McGraw-Hill, 1969, ch 40, Q 657.
2. Goldthwait, Brown, Swain, Kuhns Estials of B Mehanic in Health
and Disease. 5th ed, 1952.
3. Ibid
4. Hix EL: Viscerovisceral and somatovisceral refex communications, in Korr
1M (ed) , The Physiological Basis of Osteopathic Meicne, New York,
Insight Publ Company Inc, 1975, pp 87-8.
5. Ibid
6. O cit Q 89.
7. Daiber Disorders of the kidneys, in Hoag JM (ed) Ostthic
M
icne. New York, McGraw-Hill, 1969, ch 39, Q 60.
8. Awad SA, Downie . Sympathetic dyssynergia i n the region of the
exteral sphincter: A pssible source of lower urinary tract obstruction.
Joural of U 1977; 1 1 8: 636-60.
9. Barbalias GA, Meres EM, Sant GR: Prostatodynia: Clinical and
uroynamic characteristics. Iral of Urolo 1983; 130: 514-517.
10. Guyton Textok of Pho.
1 1 . Owens C An Endorine Interretation of Chapman' s Refexes. Carmel CA,
1963.
12. Awad SA, Downie . Sympathetic dyssynergia in the region of the
Joura of U 1977; 1 1 8: 636-60.
13. Saunders JB: The major determinants in normal and pathological gait.
Jal of Bone ad Joint Surger luI 1953; 35-A(3): 543-558.
14. Segura , Opitz IL, and Greene LF: Prostatosis, prostatitis or plvic
for tension myalgia? Jural of Urolo 1979: 122: 168-1 69.
15. Sterrett Mg Ir: Disorders of the urinary system, in Hoag JM (ed)
Osthic Meicne. New York, McGraw-Hill, 1969, ch 40, Q 6.
16. Sinak M, Merrtt IL, Sillwell GK: Tension myalgia of the plvic for.
Ma Clin Pro 1977; 52: 717-722.
17. Travell JG, Simons DG Mal Pain ad Disfunction: A TrgPoint
Manual, Baltimore, Williams Wilkins, 19 3, Q 671 .
1 8. Ibid
19. Burows EA: Disorders of the female reproductive system, in Hoag 1M
Othic Medicne. New York, McGraw-Hill, 1969, ch 42, Q 681 .
20. Op cit Q 677.
14b
21 . Pottenger FM Soms of Viscer Disease. St Louis, CV Mosby Co,
1953, 7th e, Q 401 .
22. Dobrik I : Disorders of the iliopsoas muscle and its role i n gyneologic
disss. J Manua Me 1989; 4(4): 130-133.
23. Ibid
24. Ibid
25. Travell JG, Simons DG Myofascial Pain and Dysfunction: A Trig r Point
Maual. Baltimore, Williams Wilkns, 1983, p 665.
26. Burrows EA: Disorders of the female reproductive system, in Hoag 1M
27. Daiber . Disorders of the kidneys, in Hoag JM (ed) Osteathic
28. Op cit Q 639.
29. Ibid
30. Sterrett M, Jr: Disorders of the urinary system, in Hoag JM (ed)
31 . O cit Q 661 .
32. Op cit pp 663-66.
33. Drach GW, Fair , Meres EM and Stamey TA: Classifcation of
benign diseases assoiated with prostatic pain: Prostatitis or
prostatodynia? Jral of Urolo 1978; 120: 266.
34. Barbalias GA, Meares EM, and Sant GR: Prostatodynia: Clinical and
urodynamic characteristics. Joural of Urolo 1983; 130:514-517.
35. Sinaki M, Merritt JL, Sillwell GK: Tension myalgia of the plvic for.
Mayo Clin Pro 1977; 52: 717-722.
36. Awad SA, Downie . Sympathetic dyssynergia in the region of the
Joural of Urolo, 1977; 1 18: 636-60.
37. Segura , Opitz JL, Grene LF: Prostatosis, prostatitis of plvic for
tension myalgia? Joura of Urolo 1979; 122: 168-169.
38. Awad SA, Downie . Sympathetic dyssenergia in the region of the
exteral sphincter: A possible source of lower urinary tract obstruction.
Joural of Urolo 1977; 1 18: 636-640.
39. Nilsson IK, Colleen S, Mardh PA: Relationship between psychological and
laboratory fndings in patients with symptoms of non-acute prostatitis, in
Danielsson D, Juhlin L, and Mardh PA (eds) Genital Infections and
Their Complications. Stokholm, Almquist and Wiksell Inti, 1975, pp
133- 144.
40. Hix EL: Viscerovisceral and somatovisceral refex communication, in
Korr 1M (ed), The Physiologic Basis of Oeopathic Manipul. New
York, Insight Publishing Co, Inc, 1975, p. 91 .
41 . Jones L Strain ad Cnter. AAO, Colorado Springs, 1981 .
42. Jenness M: The role of thermography and postural mesurement in
structural diagnosis, in Goldstein M, The Research Sts of Spinal
Manipulative Thera. Bethesda MD, US Department of Health
Eucation and Welfare (NINCDS Monograph #15) 1975, Q 258.
Manual. Baltimore, Williams Wilkins, 1983, p 665.
14
44. Burrows EA: Disorders of the female reprouctive system, in Hoag JM
(ed) Ostic Meicine. New York, McGraw-Hill, 1969, ch 42, p
682.
45. Sterrett HW, Jr: Disorders of the male genitourinary system, in Hoag JM
(ed) Osteathic Meicine. New York, McGraw-Hill, 1969, ch 41 , p
673.
and G Slattery, DO, PhD -- unpublished case history, KCOM.
46. Ibid (Sterrett)
and Burrows EA: Disorders of the female reprouctive system, in Hoag
1M (ed) Othic Medicine. New York, McGrw-Hill , 1969, ch 42,
p 678.
147
NOT:
148
OSTEOPA TIIIC CONSIERATIONS I T OBSTETRICAL PATIT
"It is physiologically imprative that we provide for optimal growth and
development of the fetus while presring the materal homeostasis." Although
expressed by Dr. Roy Pitkn, an obstetrician from The Iowa University Schol
of Medicine who is note for his knowledge of nutrition in the OB patient, this
als sums up the ostepathic prsptive applied in obstetrics. Total care for the
obstetrical patient is a physician's desire regardless of his medical degree;
however, a physician's ability to provide total care to the patient is, in fact, a
variable.
I. EXISTIG STRESE AGGRA VA T BY PREGNANCY
GRAVITY:
o .. Grvity mainly affects the A-P postural cures aggravating lumbar and
cerical lordoses and thoracic kyphosis ..
o .. Gravity, activity, habits and stresses of motion produce fascial torsions.
o .. The normal aging proess amplifes the effects of gravity and/or fascial
torsions.
A BASIC PHYSIOWGICAL RELATIONSHI: More blood gets to the
tiue than can be retured by the venous system.
Blo gets t the cells via the
arteries and into the interstitial
spaces through the capillaries. The
interstitia tissue fuids get back to
the he via the venous system with
neessry and vital assistance frm
the lymphatic system (which has no
intrinsic pump).
o .. More blod gets to the tissues
than c be removed by the
venous system; therefore the
lymphatic system is essential
if tssue congeston is t be
prevente--in fact, it is
essential for life itslf.
( CONGESTION )

Bka
,
A mic
Pelvis:
Hemor oids
Vulva
Vaie
Mater
Nu
Intaurin
Grow Rardaton
Sll fo
Gesaton Age
Legs:
Vaities
Malais
Cnfusion
Headace
Iritability
Dizin
Nausaomiting
An:
Cnstipation
U Congesion
Paeatic
Cngestion
Vaotor
Instbilit
Legs:
Cap. Edema
Anything which increses circulation to the cells will result in incresed
interstitial tissue fuids and result in increased demands upn the
149
lymphatic system to move these fuids in order to prevent tissue
congestion or edema.
o .. The abdominal diaphragm functions a an "extrinsic" pump for the
lymphatic system. When working well, it prouces effective pressure
gradients betwen the chest and the abdominal cavities. The pressure
gradients, along with the valves in the larger lymphatic vessls, prouce
a most effetive force for the one-way fow of lymph back to the venous
system ad the het. Sympathetic impulss are capable of constrcting
larger lymphatic vessels; therefore, hyprsympathetic tone is a factor
which decreses lymph fow and promotes tissue congestion.
THE UNIQUE VALVELES VEOUS SYSTE: The eNS, spinal cord
and the bony vertebral colu contain a "valveles venous system. "
Physiological factors working upon the valveless venous system of the spine
have the ability to prouce patters of fow which result in venous congestion in
the tissues they are suppse to drain, derease orga function and generally
incres a prson I s level of stress.
o .. Bcause there are no valves in these venous plexuses, blod is free to move
in either direction depnding upon the path of least resistance.
o .. About 80 % of the blod from the brain and its meninges exits the jugular
foramina of the skull by way of the jugular veins. Blo from the spinal
cord, its membranes, and the bony vertebral column (the spine) usually
passes through communicating veins, to enter the veins of the azygos and
hemiazygos system. The communicating veins are also valveless and not
consistently present at ech lumbar and thoracic level. The venous blo
from thes ares usually drains into the heart via the suprior vena cava.
A scondary pathway for drainage of the profuse venous plexuses of the
spinal cord and vertebral system is provided through anastomoses of
thes plexuss with the vertebral and the interal jugular veins at the
bas of the skull.
o .. Venous blod in this closed system is "pushed" by the arterial blod volume
proplled by the contractions of the heart and pulled by pressure
gradients largely arising from respiratory efforts. The amount and
proprtion of venous blo which travels through the valveless
communicating veins or through the anastomoses with the vertebral and
interal jugular veins is affected by any change in the resting pressure in
the thorax or abdomen; fow through this secondary route is also
incresed by any decrese in the gradient of pressure between the
abdominal and thoracic cavities. These physical factors c prouce
150
fow dynamics which led to relative congestion in the eNS, the spinal
membrnes and/or the bony vertebral spine.
l. STSE ADDE SPECIICALLY BY PREGNANCY
Stresss of a normal pregnancy prouce a relatively rapid aging proess which is
usually reversible. Thes stresss are produced through mechanical,
physiological, venous/lymphatic and hormonal changes.
MCHANICAL: The musculoskeletal system and the body's center of
gravity i changed.
Organ hyprtrophy and mechanical stress prouce structural change and a shif
in the boy's center of gravity. The changes brought about by mehanical stress
are accelerated by the effet of circulating hormones of pregnancy which tend to
weaken muscle and supporting ligaments.
It has ben shown that dysfunction in the musculoskeletal system c increse
the energy reuirements of an individual up to 30%.
PHYSIOWGICAL: Intertitial fuids are increased.
Additional prouction of interstitial fuids is brought about by the incresed
circulation neessary to meet the additional metabolic demands of the growing
fetus and placenta and to supprt the hypertrophy of the uterus and other
organs. Incresed levels of estrogen and adrenal hormones also promote fuid
retention in the boy's tissues.
LYMHATIC: There i decreased effciency in the removal of excesive
intertitial fuids.
Fascial torsions hinder the fow of lymph through lymphatic vessels travelling
through the connetive tissues; organ hyprtrophy and downward drag of the
abdominal wall produce volume changes in the abdomen and thorax; structural
stresss (incresed lumbar lordotic cures, thoracic kyphotic cures, tension on
the diaphragm, and anterior scral base) and the downward drag of the
abdominal ad thoracic wall may act singly or in concert to promote pr
diaphrgmatic excursion. All of these factors decrease the diaphragm's ability
t prouce the most effetive pressure gradients neessry t promote go
lymphatic fow and to reduce tissue congestion. It is clinically obsered that
generalized symptoms of lymphatic and venous congestion present as clinical
problems, espially in the last trimester of a patient's prenatal care.
151
VENOUS: There i a tendency for venous congestion of the central nervous
system (CNS).
There is a drastic change in the volume of organs which ocupy the abdomen as
well as changes in the relative volume ad pressure gradients between the
abdominal and thorcic cavities. Thes changes tend t incre the cavity
pressures and encourage a relative reversl of venous blo fow in the valveless
communicting, vertebral and spinal membrae vessls and led to relative
congestion of the central nerous system (eNS). Symptoms of venous
congestion are more evident in the ely part of the frst trimester, the last
trimester, and in the pstpartum priod.
HORMONAL: Increase i horone production encourage tissue
congestion.
Incresed levels of certn hormones during pregnancy promote biological
weakening of muscles and ligaments and encourage fuid retention. These
changes then prmit a fousing of mechanical stress onto certain
biomechanically snsitive ares of the body, reducing effectiveness of the
diaphragm's lymphatic pump action, and directly incresing interstitial fuids
while at the sme time promoting changes which result in obstruction of
lymphatic pathways back to the hert.
RELATIVE CONTRAIDICATIONS TO OMT:
While OMT c be helpful in pre-eclampsia, the seizure threshold is low in
toxemia of pregnancy and OMT is seldom a part of a treatment protool. OMT
is also usually avoided during premature rupture of membranes, premature
labor, abruptio placentae, and etopic pregnancies.
m. DISTICTIVE OSTEOPATIC TIG:
Distinctive osteopathic thinking to improve the compnstion and comfort of the
OB patient is based upn three premises:
o . . There are mehanical, physiological and biological stresses inherent even in
the patient who is destined to have a normal pregnancy.
o .. The boy has self-regulatory mechanisms which will provide optimal
compnstion for the stresses of pregnancy if they are free to work
effciently.
o . . Distinctive osteopathic care is based upn the belief and the clinical
obsratons that within the boy unit, structure and function are
reiproly interrelated and interwoven with optimum homeostasis.
152
AN AID IN PREVENTIVE CARE: Postural analysis and palpatory
examination erly in pregnancy can identify ares of somatic dysfunction which,
if uncorrected, act to fous the stresss of pregnancy on vulnerable sites within
the boy unit.
A DIAGNOSTIC AID: Bth visceral and structural dysfunction are indicated
by palpable changes in the somatic structures.
A TREATMENT ADVANTAGE: Propr osteopathic manipulative tretment to
the ares of structural dysfunction is assoiated with improvement of viscerl
and smatic fnction.
IV. DISTICTIVE OSTEOPATIC TREATMT:
Any licensed physician who accepts the care of obstetrical patients should have
ben trained to take care of her medical and delivery needs. In addition to this,
an ostepathic physician is trained to appreciate and tret the musculoskeletal
and physiological stresses which ocur in pregnancy. Manipulative treatment
normalizes somatic dysfunction which produces andlor fouses mechanical
stress. It also improves the effciency of mechanical and physiologic
compnents of the patient's compnstory and homeostatic proesses. The
energy that is subsequently sved through improved boy effciency and
removal of somatic dysfunction will be available for fetal growth and for the
betterment of materal physical and mental health.
"THE STRUCTURAL STAGE:" Fr viit to 28th week of getation -
Monthly viits:
012 WEEKS:
The patient usually makes her frst visit during the 9th-12th week of pregnancy
ad although she has exprienced some of the early signs and symptoms of
pregnancy, her structure is little affected at this stage. During these frst thre
months, the patient normally gains about 2.5 t 4.5 punds.
At the patient's frst visit the physician obtains a complete history including the
history of past pregnancies, deliveries, family history of signifcant diseses,
and ak about habits--smoking, coffee, alcohol or the use of drugs. If drugs
have ben used it is imprtnt to kow if the patient has stopped them--and if
so, how long ago. The physician should fnd out about the patient's eting
habits.
At the frst visit the physician establishes rapprt with the patient and the patient
establishes a lasting impression of her physician. This is imprtant, but is not
153
unique to osteopathic care. The remainder of this chapter will t to highlight
the ostepathic differences in management.
The ostepathic physician is very interested in any history of past accidents to
the hed or the rest of the musculoskeletl systm. This includes car accidents,
blows to the hed, falls down the stairs, or falls on the buttoks. This may be
just routine information in most medical histories but, to the ostepathic
physician, a psitive respnse to any of these questions must be investigated.
Thes stresses may have resulted in prsistent somatic dysfunction which could
affet the patient's ability to effetively compenste for the stress of pregnancy.
The patient is aske if she has any present musculoskeletal complaints. During
the routine physical, palpatory evidence of thes and other somatic dysfunctions
and structural abnormalities such as a short leg, a scral she, or scoliosis is
sought.
o .. In the standing position quickly observe and record the levelness of the
various regional horizontal planes--occipital, shoulder, iliac crests, PSIS,
and trohanteric. The spine is obsered and palpated for rotoscoliosis as
the patient bends forward at the waist.
o .. In the sitting psition the preference for fascial motion at the thoracic inlet
c be quickly assssed to se whether it is symmetrical or whether it
conforms (or not) to the common compnstory patter as desribed by
the late Dr. Gordon Zink. A problem with the fascial inlet patters must
b differentiated from the somewhat similar fndings of an elevated 1st
rib somatic dysfunction. The ribs and the thoracic and lumbar spine c
also be evaluated for segmental somatic dysfunction in the sitting
psition.
At this time the physician may manipulate any somatic dysfunction that
has been identife. (The sitting or standing pillow technique--utilizing a
pillow to loalize the thrust--is very helpful in treting the pregnant
patient, even during the third trimester.
o .. With the patient in the supine psition, the rest of the regional fascial
pattering (OA, thoracolumbar and lumboscral) c be evaluated and
the plvis c be palpated for somatic dysfunction (SD) of the
innominates or pubic bones. The physician usually proeds to tret the
SD found in thes ares, using any osteopathic manipulative tehnique
tolerated by the patient. Most techniques which would be prformed in
a patient who is not pregnant c be used in the pregnant patient at this
stage of her pregnancy.
o .. In the prone psition (an esy psition to assume during this erly part of
pregnancy) the scrum c be evaluated and treted as indicated. A
scral sher (a non-physiological somatic dysfunction) must be removed
or the patient will be assured of having backaches during pregnancy and
154
manipulative tretments for other somatic dysfunction will not have a
lasting effet.
o .. Finally, have the patient assume the supine psition again and chek the
cerical spine and the crioscral mehanism by palpation and motion
testing. Any smatic dysfunction in these regions should be treted at
this time.
From the history, physical examination, and her subjetive and tissue respns
to tretment, the physician c determine the osteopathic manipulative care
necessy, the probable dosge indicated, and what the manipulative tretments
should be able to accomplish before delivery.
12-28 WEEKS:
During the second half of the structural stage, the physician still sees the patient
at monthly interals, although if indicated, more frequent appointments are
provided. A little extra time now will sve a lot of time and worry later on in
the pregnancy. At ech visit, part of the care is directed toward manipulation of
SD (which may be a part of her complaints) and/or part toward manipulative
supprt of boy structures and proesses which the osteopathic physician knows
will be under stress. This tretment is esily caried out as the patient talks to
the physician and the physician tlks to her. "The time to talk to ech other" is
extremely imprtant to the patient/dotor relationship and to mutual trust.
It is known that during the structur stage (the second trimester), there will be
obvious changes in her boy structure--increased fat storage, growth of the
uters, hyprtrophy of the brest and other tissues, bloo volume expansion,
and a shift in the patient's center of grvity. The plvis will rok forard,
lumbar lordosis will incre, and a compenstory thoracic kyphosis will
develop along with a cerical/subocipital strain. Ne the end of this frst
stage (sond trimester), clinical evidence of tissue congestion may begin t
app.
Musles and ligaments become more vulnerable t the mechanical stresses as
biological effets of incresed levels of hormones ween their strength. Thes
structur effets of stress are often subjetive and are usually very obvious to
the ostepathic physician.
"T CONGETIE STAGE:" Visits Ever 3 Week:
28-36T WEEK:
This p of the pregnancy is called the "congestive phase." Congestion ocurs
when more fuid accumulates in the tissues than c be effetively removed by
the venous and lymphatic systems. This congestion is partly mehanical, partly
155
hormonal, and partly biological. Circulating hormones, in incresed amounts,
have the tendency to encourge the boy to hold watr in the tissues. The
patient's symptoms vary depnding upn which tissues become congested.
Tissue congestion is als assoiated with deresed oxygenation and nutrition of
the cells and is related t incresed accumulation of metabolites in the soft
tissues.
During this stage of pregnancy, the expanding uterus is well above the
umbilicus and is pushing toward the xiphoid proess. It causs a mehanical,
" ball-valve," effect betwen the veins of the legs and their abdominal
connection with the inferior vena cava, and is mehanically respnsible for
sme of the leg edema of late pregnancy. I also makes it diffcult for sme,
women t lie supine without beoming hypotensive. The uterus also pushes up
under the diaphragm and the lower ribs. This limits the chest volume that c
b obtained during respiration and directly affets the thoracic:abdominal
pressure gradients which c be obtained.
The diaphrgm must also work harder against the incresed mass of abdominal
and plvic contents and this results in its incresed tone. The diaphragm at this
stage of the pregnancy is unable to prouce optimal volume displacements
between the thorax and the abdomen during contraction and relaxation and is
assiated with ineffciency in pumping the lymph back to the heart. A greter
volume displacement is achieved through correction of thoracoabdominal and
plvic for dysfunction.
Although the physician must continue to be alert for mehanical decompnstion
and tret to maintain go structure during this seond stage as indicated, it is
most imprtant to check the common compenstory patter (CCP) in order to
maintain freedom of the fascial pathways and thus improve lymphatic drainage.
(Se page 207) Osteopathic manipulative tretment is directed toward
maintaining symmetry of the thoracic inlet, relaxing the thoracolumbar junction
(attachment of the abdominal diaphragm), and keeping the diaphragm well
domed. After OMT, the abdomen feels sofer and more mobile and
diaphragmatic excursion is fuller. This typ of tretment improves the
effciency of the thoracoabdominal pump and therefore improves lymphatic
fow. Lymphatic fow c be "encouraged" by the use of the pctoralis lift
tehnique (s page 230). The usual manipulative "chest pumps" may be
uncomfortable because of hyprtrophy and incresed sensitivity of the brests.
"TIE PREPARATORY STAGE:" 36 WEEKS TO DELIERY - Weeky
viit:
This is the fnal stage of pre-delivery care. If the patient ever expresses a
feling of " really being pregnant," this is the time. During this third stage of
prenatal care, it is neessy to continue to maintain god structural balance and
156
t supprt lymphatic fow, but it is imparative to emphasize two additional areas
of cre for the obstetrical patient:
o .. Bgin to build the psychological supprt that the patient will nee for
delivery. Emphasize the psitive pints in her prenatal exprience and
help her t plan for the delivery.
o .. Carefully chek the crnioscrl mechanism to be sure it has a normal
confguration, rate, and amplitude so that it will aid normal hormonal
and neural function during labor and delivery.
If the osteopathic physician has been able to accomplish the goals
presented to this pint, the labor and delivery will usually go smothly.
If complications should ocur, the patient is in better condition to
compnste and rech a new homestatic level.
"LABOR A DELIVERY:"
OM is infrequently used durng the delivery itself; however, scrl pressure is
frequently comforting during labor and c be taught to the husband to be
prformed prioically or at his wife's request. The physician may elet to use
CV 4 tehnique in pstdate gravida women to induce uterine contraction 1 or to
overcome uterine inertia during labor.
"T RECOVERY A MAITENANCE STAGE:" Delver to 6 week
poparu - 2 visits:
o .. On the second day pstartum, the patient should be taken to the tretment
rom where a screning structural examination and indicated
manipulative tretment is prformed. The physician c us soft tissue,
muscle energy, indirect, Jones counterstrain, cranial methods and even
thrst manipUlation, as needed.
The effets of circulating materal hormones are still evident in the
articular and ligamentous structures making tretment methos esier.
Successful manipulation places the joints in goo fnctional psition as
the hormonal effet wers off and the ligaments begin to retur to their
normal tension and strength.
During this stage of tretment the physician is still interested in treting
the patient to improve lymphatic fow. Brest engorgement which
ocurs on the seond day in the multipara and on the third day in the
primipara is probably hormonal in etiology, but clinical exprience
indicates that patients with good lymphatic fow tend to have deresed
complaints of brest congestion and a reduced incidence of the
"pstartum blues. "
157
Careful chek of the scrum during this erly pstartum tretment
sssion is essntial. The mechanical progression of the infant through
the birth cal and the lithotomy psition of the patient during delivery
encourges ateror scral bas smatic dysfunction ad the extension
phas of the crioscral mehanism. It has ben obsred that
signifcant anterior scral bas smatic dysfunction is assoiated with
patient complaints of fatigue, depression, ad low energy. The
mehanical etiology of thes symptoms can be avoided if the physician
fnds and trets this somatic dysfunction ely and effectively.
o .. The usual fnal HOB" visit is at 6 weeks pstartum. The patient's progress
up to this pint is evaluated and a gyn/pap smer is repated. If the
obstetrical patient is treted as outlined, it is not common t fnd any
spcifc somatic dysfunction to tret and the patient presents herslf as
being well and happy. This is the time to make sure she has a
contraceptive program if desired, realizes the importance of slf-brest
exam and yerly gyn/pap smers, understands the imprtance of (and has
an appintment for) a follow-up visit regarding any chronic problems
that require further care. Osteopathic manipulative care is a part of the
total care of the obstetrical patient. Its inclusion makes the prenat time
and delivery more comfortable for the patient, enforces a quicker and
more complete recovery from delivery, and enhances this wonderful
miraculous event of life.
RFCE:
1. Gitlin RS, Wolf DL: Uterine contractions following osteopathic cranial manipUlation -- A
pilot study. JAOA 92(9): 1183, Sept 1992.
2. Zi JG, Lwsn WG: Pressur gradients in the ostepathic mipulative management of
the obstetrical patient. Ostepathic Anals May 1979; 7(5): 208-214.
3. Zi JG, Lwsn WG: An ostepathic structural examination and fctional interretation
of the sm. Osteopathic Annals De 1979; 7(12): 433-440.
4. Kuchera WA: Ostepathic considerations in the obstetrical patient. FAAO Tesis 1989.
5. Saunders JB et al: Te mjor determinats in norml ad pathological gait. Joural of
Bone and Joint Surger Jul 1953; 35-A(3): 543-558.
6. Pitkin R: Ament of nutritional status of mother, fetus, ad newbr. Te American
Joural of Clinical Nutrition Apr 1981; 34: 658-68.
7. Hekmn JD: Maaging musuloskeletal problem in pregnat patients, par I. Te Joural
Of Musculoskeletal Medicine June 1984: 14-24.
8. Dilts PV, Jr, Gerie, Sciar: Exercis ad physical activity during pregnacy, in Shrok P
(e) Gyeolo And Obstetrics. Philadelphia, Harr And Row, vol 2, rev e, 1985,
ch 8.
158
OSTEPATIC CONSIEATIONS
I RHEUATOWGIC DISORDES
I. IODUCTION
Ostepathic manipulative tretment (OM) is an extremely valuable compnent
in the cre of a patient with a rheumatologic condition. While the adjetive,
"rheumatologic", denotes a joint musculoskeletal disrder, many rheumatologic
disrders such as rheumatoid atis (RA) are chronic systemic diss. By
indiretly reducing the side effets of meications, diretly enhancing
homestatic mehaisms, and maimizing fnction within the patient's existing
structure, ostepathic palpatory diagnosis and manipulatve tretment play
spial roles in the maagement of chronic illnesses. This stion will fous
primarily on the rationale for OM in a patient with rheumatoid arthritis, but
the rationale c be extended to other rheumatologic conditions.
n. PATHOPHYSIOWGY
Articular cartilage is avascular,
therefore its nutrition needs to be
considered in any disussion of the
pathogenesis of rheumatologic
dis. Synovial fuid provides the
joint access to nutrients as well as
sring as a site for the dispsl of
metabolic wastes and immune
complexes. I addition, the effcacy
of any prescribed anti-infammatory
meications is depndent on their
concentration in the synovial fuids.
The transference of nutrients and
medications into the synovial fuid
and of immune complexes and other
wastes out is depndent on
diffusion. For this reson, factors
affeting diffusion such as blo
fow, concentration of nutrients and
waste proucts in the region, and
synovial membrne prmebility are
extremely relevant.
TPICAL JOINT
A
159
L
t
A - Aerial Supply
V . Venous Drainage
L - Lymphatic Drainage
On the basis of histologic studies, cartilage is best presered in those parts of
the joint where the articular surface is subjected to intermittent compressive
contact. This t of contact improves loal nutrition of the cartilage and
mobilizs immune complexes from the are. Accumulation of immune
complexes is assoiated with incresed joint destruction.
SYAmETICS:
In joints with rheumatoid arthritis, oxygen consumption is incresed up to
twenty times the amount used by a normal synovial membrane. Incred
sympathetic activity frther compromises blo fow t the involved joint(s) and
reduces the delivery of nutrients (including oxygen) and medication to the are
where it is needed the most. Tissue hypoxia may result in the rele of
plymorhonucler leukoytes which promote multilamination of the basment
membrane. This thickening further diminishes diffusion into and out of the
synovial fuid of the joint.
AUTONOMIC NERVOUS SYSTEM: ROLE IN RHEUMATOLOGY
(& Shunting)
Ru Bo R
1. Nu
2. t 02 Aa
3. t A Lls
To Hpthalamus
Substantia
Gelatinos z.d
1-jnelent Pain
T2-T8 Upper Eremities
Tl1-L Ler Eremities
Reducd Drainage
1. Fuids
2 . Proteins
3 . Immune Cmplexes
Baus structure and function are interrelated and beause rheumatoid arthritis
alters joint structure, it should not be surrising that arthritis leds to the
development of somatic dysfunction. Continuous afferent input to the cord
from a dysfunctional joint incites facilitation in those cord segments. The fare
up of a patient's arthritic joint with resultant segmental spinal cord facilitation is
160
often accompanied by dysfnction of the viscera that share sympathetic
inneration from thos cord segments. This relationship c als be reversed,
i. e. certain visceral diss are assoiated with atic complications. The
relationship of arthritis in the spine ad lower extremity in patients with colitis
is a common example of this relationship. The somatic inneration and somatic
afferent referral to the spinal cord from the lower extremities are loate from
TII-L2 while the sympathetic inneration to the colon is also found from TIO
L2. Likewis, incresed afferent input from uppr extremity joints to the T2-T8
stions of the spinal cord may refexly incre the sympathetic activity to the
uppr gastrointestinal tract (f5-9) leading to reuced tolerce of the non
steroidal ati-infammatory drugs (NSAIDs) use in the tretment of atis.
The sympathetic nerous system is capable of augmenting the symptomatology
and pathogenesis of rheumatoid arthritis. Increased sympathetic activity
snsitizs the patient's prception of pain both pripherally and centally and
plays a role in the musle spasm and contracture that limits rnge of motion and
intensifes deformity. Noxious somatic input refexly sets up pathophysiologic
change which bring about symptoms and signs which, carried to extreme, may
result in a diagnosis of refex sympathetic dystrophy (RSD) . The sympathetic
hyprctivity in this condition is also involved in initiating the bony erosion sen
in joints of patients with rheumatoid arthritis. It has been reported that there is
hyprsympathetic activity in patients with R, RSD and osteoporosis and that
bilateral sympathectomy often helps limit bony erosion signifcantly in these
patients.
Kelley's Toof R states that even in the most aggressive
c of R, only minimal reversible change ocurs until after the lesion
beomes chronic. "Chronicity" sems to te eight or more weks. This
information suggests a timeframe during which tretment direted toward the
sympathetic nerous system may result in prevention by addressing reversible
fnctonal changes before they beome structurl.
SOMTC SYST:
Somatic dysfunction plays a role in the pathogenesis of arthritic change. Por
psture, increase weight, ad/or mislignment of the spine or lower extremities
ech incre the mehanical stress placed upn a patient's joints. Short leg
syndrome is espially stressful to lower extremity joints and it has ben
assiated with incre incidence of hip osteoarthritis on the long leg side. It
has als ben implicate in tempromandibular joint dysfunction with
subsuent arthritic change. Lck of joint motion as will ocur with somatic
dysfnction, encourges degeneration and fbrosis. It has ben shown that
passive rge of motion c aid in cage regeneration. Like somatic
dysfunction, arthritic change is usually manifested frst in the minor motions of
a joint.
161
Arthritic patients and many of the patients that have ben improprly labele as
having "arthritis" have a gret del of myofascial somatic dysfnction. Travell
and Simons reprt that clinically there is a high incidence of myofascial
triggerints and tenderints in patients with joint problems. They have
demonstrated that pain and tenderess in the joints of thes "arthritic" patients
ofen improve or disppar if the adjacent trggerpints are treted. Tretment
of myofasial smatic dysfunction, including triggerint tretment, freuently
restores signifcat rage-of-motion (ROM) to thes joints. According to
Travell this even se ms to beneft joints that have appred to have ben
ankylos for yers. Signs and symptoms including infammation, effusion,
sf tissue swelling and synovial crepitus frequently disppr.
There is a strong assoiation between the somatic and the psychomotional
levels of patients who have myofascial triggerints. Sureys suggest that as
many as 10% of these patients seek psychiatrc care or think that they should.
Many psychic effects commonly seen in rheumatologic patients (including
depression and slf-centereness) have been repored to subside with treatment
of myofascial somatic dysfunction.
LYHATICS:
_ Ta
-. - (Faal Diaphragm)
-
Aomina
Diaphragm
1-Lpha1ic Vessl
Ruc Drainage
1.
+
Auids
2. + Protein
3. t Immune Cmplexes
The effects of the sympathetic
nervous system upn loal
circulation and the diffusion,
nutrition and removal of waste
proucts (including immune
complexes) from a rheumatic joint
have alredy ben presented. (Se
page 160.) The lymphatics,
however, are vital to the circulatory
link and are particularly important
in moving the immune complexes
out of the are before they can cause
damage to the joint. Manipulative
treatment to enhance lymphatic
homeostasis moves waste proucts
out of the joint are thereby
reducing diffsion gradients. This
treatment begins with opning
drainage pathways ad is an integrl
part of rational osteopathic care.
Tendon sheths are rich in lymphatic vessels and therefore lymphatic tretment
should be utilized in tenosynovitis. Failure to reduce or relieve lymphatic
162
congestion and the protein contained in the edematous fuid promotes fbrosis
and thickening of the tissues. This, in tum, reduces ROM, encourages the
formation of contactures around joints and subsequently frther compromises
lymphatic drainage.
It is kown that immune reactions involving local synovial cells produce by
proucts which are assoiated with joint destruction proprtional t their
concentrations i the synovial fuid. In some severe cases,
lymphoplasmaphoresis has ben effetively used to promote diffusion gradients
which are able t pull immune complexes out of the synovium. Expnsive and
dangerous surgical thoracic duct drinage has been found to b benefcial in
sme patients with systemic lupus erythematosus (SLE), myasthenia gravis,
glomerulitis and rheumatoid atis.
PARASYATTICS:
The parasympathetics play essentially no direct role in the musculoskeletal
symptomatology of the arthritic patient; but because the body is a unit and
rheumatologic disorders have chronic, systemic effects, consideration for
improving the function of the parasympathetic nervous system in rheumatic
patients is important because of its support of the visceral fnctions of the body.
OTR FACTORS:
Patients with chronic arthritis become toxic, either from disese, their chronic
use of medications, and/or from impaired excretion/metabolism. The physician
managing patients with rheumatologic conditions must remain alert for side
effets of medications or organ dysfunctions resulting from this toxicity. Total
management of any chronic disese involves eliminating all foci of infection and
visceral disese, supporting the patient's organs of detoxifcation and
elimination, ad supprting the known mechanisms of body homeostasis.
I. TREATT OF PATITS WIT RHUATOWGIC
DISORDES
In order to address the rheumatologic patient's physical and psychologic neds,
a rtional tretment protool must demonstrate the physician's understding of
the pathophysiology outlined above. General treatment goals include the
following:
o .. educate the patient regarding their disease process and the patient's
own responsibilities in carrying out progrms designed to
maintain maximal fnction
o .. provide psychologic support
o .. alleviate pain and the pain-spasm-pain cycle
163
o .. dere infammation
o .. improve joint nutrition
o .. enhance removal of synovial waste proucts
o .. maintn and/or increse joint fnction
o .. decres mehanical strain on affected joints
o .. correct existing deformity and prevent further deformity
OSTPATC MAT TCHQU:
Reognizing the multsystem involvement of many of the rheumatologic
disorders, assessment and tretment design in ech of the involved systems are
wa ted. Soft tissue techniques address periarticular tissues and osteopathic
manipulative tretments (OMT) reduce hyprsympathetic activity and improve
blo fow to the region. OMT direted toward removal of segmental
facilittion also helps alleviate pain and pain perception. Tender and infamed
joints often respnd best to indirect stacking or fascial unwinding manipulations,
espcially when prior structur changes may have roughened and modifed joint
surfaces. High velocity, low amplitude techniques (HVLA) are contraindicated
in the cervical region of patients with severe rheumatoid atis beause the
high incidence of weened cruciate ligaments is assoiated with ptential
pathologic subluxations.
In patients with infammatory rheumatic disese, OMT may cause a transitory
increse in joint pain; if this pain lasts more than 1-2 hours then either the
choice of activation for the manipulative technique was incorrect or the dosge
may have ben excessive for that patient. A more general aching in the soft
tissues may occur even with the most gentle activating forces (indirect). If this
general ache lasts more than 24 hours it usually indicates that the physician
attempted to prouce more changes than the patient's body was capable of
handling in a single visit and at that point in time. When this occurs, the OMT
dosge and typ should be evaluated and adjusted on the next visit.
After opning lymphatic drainage pathways and maximizing the patient's own
respirtory pump, gentle joint pump techniques have been shown to be
espcially benefcial in granting pain relief. Posterior axillary fold technique
(page 230) for patients with upper extremity congestion is particularly helpful.
The value of intermittent non-weight-being compression of joint surfaces has
been found to improve loal nutrition and crete benefcial histologic change in
rheumatologic joints. The mechanisms active in this fnding may explain the
clinical results seen following this type of osteopathic manipulative tretment.
It is not uncommon for moring stiffness, a hallmark sign in rheumatoid
arthrtis, to completely disppar after manipulative tetment is instituted and
renably provided as part of the maintenance management program. Propr
respiraton and exercises diretd toward maximizing respiratory abilities are
also helpful in maintning the lymphatic goals of tretment.
164
A variety of tehniques including compression, Fluor-Methane
R
spray and
stretch, counterstrain psitioning and injection have ben shown to be benefcial
in removing myofascial trggerints. It should be noted that the most common
underlying or prtuating factor assoiated with myofascia dysfnction is a
pstur disorder. For this reson and because pstural problems diretly and
biomehanically stress the joints, pstural analysis and tretment is ofen
necessy before any other conserative tretment program for rheumatologic
dis beomes effective. Postural correction may necessitate a sho lift,
Lvitor orthotic device, or an orthotic sho. Conserative tretment also
includes patient eucation, ostepathic manipulatve tretments, NSAIDs ad/or
other meications, exercis, and modifcations of activities-of-daily-living
(ADL).
Manipulative tretment of somatic dysfnction in the crnial region is fequently
employed because of its possible role in affecting the pituitary gland I s infuence
on the adrenal function, the essential steroidal hormones secrete by the adrenal
cortex, and the pure sympathetic activity effect on the adrenal medulla. It is
postulated that manipulation of somatic dysfunctions in the lower thoracic area
aso helps normalize hormona levels through diret infuence on adrenal
function.
A physician who understands viscerosomatic refexes and closely monitors the
musuloskeletal system with palpatory examination has a substantial non
invasive advantage in the discovery of clues to visceral dysfunction. In the
arthritic patient, musculoskeletl clues may be initiated by immune-complex
depsiton, toxicity from the medications used t tret chronic disease, or from
mehanical change. If discovered at a dysfnctional level, steps c often be
taken to prevent structural change. This connection is redily demonstrated
when monitorng Chapman I s refex points, the celiac ganglion and the mid
thoracic parspinal tissues in a patient taing NSAIDs. Erly dysfnctional
gastrointestinal signs wa t immediate intervention because structural changes
in the form of gastritis and/or ulceration are common side effects of medica
tretment for arthritis. Sometimes side effects wa t withdrwing certain
meications from an otherwise successful medical tretment progrm. The
fnding of a previously absent musculoskeletal somatic dysfnction suspected of
being viscerosomatic in nature, should prompt the physician to ask about new
stessors as well as to review curent medications. Ofen corecting the somatic
dysfnction and then re-educating the patient to tae their NSAIDs with fo or
discussing methods of stess management are adequate to reverse these erly
changes.
Tretment should be directed toward removal of factors contibuting to spinal
cord sgmental facilitation and also toward maximizing fnction in target organs
or in those orgas important in the excretion of the toxins (liver, kidney, and
165
bowel). It is kown that the liver plays an important role in the clearance of
soluble immune-complexes from the circulation and may play an important role
in preventing immune-complexes from being depsited in vessl walls elsewhere
in the boy. Liver pump and CV 4 tehniques are fequently utilized to aid the
boy in general detoxifcation.
OT MANAGE CONCENS:
Some exercises are designed to maintain fexibility and others are designed to
strengthen muscles where ligamentous support structures are inadequate.
Walkng programs as well as "aqua-cize" (water exercise) have both been shown
to be benefcial to patents with rheumatoid atis.
The role of a speifc dietary reommendation is nebulous at this time although
some general recommendations are pertinent. Certainly weight control in obese
patients is important in order to reduce biomechanical strain on joint structures.
Patients with osteoatis are ofen over-weight while patients with rheumatoid
atis are often under-nourished and warrant proper dietary education for
general health reasons. While most texts state that diet is ineffective in
managing arthritics, some patients are convinced that they experience arthritic
fares with intake of certain fods such as sugar, citrus fruit, milk, fermented
beverges, soium benzoate, white four, coffee and t. Some physicians
claim that there is a link betwen "food allergies" and atis. Some studies
suggest that linoleic acid may be benefcial. Physicians can legitimately
reommend a healthy diet as being appropriate for the patient regardless of any
coxisting rheumatologic condition.
In patients with osteoporosis, bone mass is frst lost in the anterior portion of
the thoracic vertebrae making this area particularly susceptible to compression
fractures. A loss of 30% of the bone mass is required before osteoporosis will
be evident on x-rays. It is prudent to avoid high velocity, low amplitude
tretments (HVLA) whenever osteoporosis is suspected. It is also best to
substitute another technique that will accomplish the desired goal for any
tehnique which places signifcant forward bending into the thoracic spine.
Patients with osteoatic changes may develop bony encroachment of the
neurl formena in the cervical or lumbar regions. Backward bending or
sidebending to the symptomatic side may increse the encroachment. Treatment
goals include reducing excessive lordotc cervical and lumbar pstural cures,
promoting venous and lymphatic drainage in the are of the intervertebral area,
and avoiding psitioning which might aggravate the neural symptomatology.
Structural interention is often neessy in patients with rheumatoid arthritis.
In patents with signifcant joint effusion, drainage may prevent stretch of
existing supprt structures and provide symptomatic relief for that patient.
166
Surgical interention for structural joint deformities is often helpful in
maintg the patient's fnctional capabilities. The expertise of the
rheumatologist and! or orthopdist ad a t approach to the patient's needs
c b extremely benefcial.
I patients with primary fbromyalgia syndrome who were already medicated
with appropriate doses of Flexeril or amytryptaline, counterstrain OMT to
tender pints and systemic OM t support homeostasis bot improved
subjective quality of life while reducing pain levels, but only the systemic OMT
protool was capable of reducing the number of tender points. After systemic
OMT, 25 % of patients in a KCOM study no longer ft the criteria for prmary
fbromyalgia establishe by the American College of Rheumatology. *
IV. SU ARY: SUGGFTIONS FOR TATNT DFIGN
PATHOPHYSIOLY OSTEOPATHIC CONSIDERTION
1. Passive ROM
Somatic 2. Correct Posture and
Arthritis <--> Dysfunction Alignment
3. Fascial Indirect OMT
4. Joint Pumps
Toxic 1. Lymphatic Drainage
2. Liver and GB Pumps
3. CV4
Poor Cartilage Nutrition 1. Soft Tissue
Periarticular Treatment
2. Indirect Stacking OMT
3. Joint Pumps
ANS Involvement 1. Treat Facilitated
Segments
2. Decrease SIV and VIS
Input
3. Rib Raising
4. Surg. or R Sympathetic
Blockade if Severe
Inflamation 1. Anti-Inflammatory R
2. Anti-Rheumatic R in
Severe Cases
3. Jnt. Pump and Lymphatic
Protocols
4. Use non-traumatic OMT
167
RUTOWGIC BfLIOGRHY:
*L KS, Kuchera ML, Preston SC, Jackson RW: Ostepathic manipulative
tretment i fbromyalgia syndrome. JAOA 92(9): 1177, Sept 1992.
(AOA article in review)
Stiles E: Osteopathic approach to rheumatoid arthritis. Osteathic Medicine
Aug 1977: 75-83.
Simkn P A: Synovial permebility in rheumatoid arthritis. Arthritis and
Rheumatism 1979; 22 (7): 689-96.
Rothschild and Masi: Pathogenesis of rheumatoid atis: A vascular
hypthesis. Seminars in Arthrtis and Rheumatism 1982; 12 (1): 11-31.
Palmosk and Brndt: Aspirin aggravates the degeneration of canine joint
cage caused by immobiliztion. Arthritis and Rheumatism 1982; 25
( 11).
Wallace DJ et a: Plasmaphoresis and lymphoplasmophoresis in the
management of rheumatoid arthritis. Arhritis and Rheumatism 1979; 22
(7): 703-10.
Cercere F et a: Evidence for the local production and utiliztion of immune
rectants in rheumatoid arthritis. Arhritis and Rheumatism 1982; 25
( 11): 1307-15.
Williams RC: Immunopathology of rheumatoid arthritis. Hospital Practice Feb
1978: 53-60.
Conditions of vessel wall depsition of immune complexes in immunologically
induced vascular diseses, in Deicher and Shulz (ed) Arthrtis--Models
ad Mechanism. Springer-Verlag, 1981.
Cohrane W et al: Absortive functions of the synovial membrane. Ann
Rheum Dis 1965; 24 (2): 2-15.
Levick JF: Contributions of the lymphatic and microvascular systems to fuid
absortion from the synovial cavity of the rabbit kee. J Physio 1980;
306: 445-461.
Weissmann G: Mediators of tissue damage in rheumatoid arthritis: Phagoytes
as secretory organs of rheumatoid infammation. Triangle 1979; 18
(2/3): 45-52.
Ennekng and Horowitz: The intra-articular effects of immobiliztion on human
kne. Joural of Bone and Joint Surger 1972; 54A: 973-85
Chrisman OD et al: The protetive effect of aspirin against degeneration of
human articular cage. Clinical Orhopaedics and Related Research
1972; 84: 193-196.
Mills and Sturrok: Clinical associations between atis and liver disease.
Annals of the Rheumatic Diseases 1982; 41: 295-307.
168
IEX OF APPENI
Mnipulation H the Pediatric Patient 171
The Musculoskeletal System. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171
The Immune System 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 172
The Nerous System 4 4 4 4 4 4 4 4 4 4 4 . . . 4 a 4 4 . . . 4 . . . 4 4 4 . . . . 4 . . . . 4 4 4 . .. . . 4 . . . 4 4 4 4 . 172
Overiew of The Pediatric Examination .4 4 4 4 4 4 4 4 4 . 4 4 4 4 4 . 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 173
Tretment Of The Pediatric Patient 4 4 4 4 4 4 4 4 . 4 4 4 4 4 4 4 4 4 4 4 4 . . . . 4 4 4 . . 4 4 4 4 . 4 4 4 176
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 178
Vision And Interest Of Infant From Birth to 12 Months ............. 179
Osteopathic Considerations H Pychiatry 181
Osteopathic Considerations H Imunology 182
Hyprympathetic Activity on Selected Tisue (Korr) 183
Autonomic Infuence on Selected Tissue 187
Osteopathic Manipulative Treatment In Systemic Dysfunction 189
Ventral Tehniques Indications and Contraindications 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 227
Anterior Chapman I s Refexes (Chart) 4 4 4 4 . . 4 4 4 4 4 4 4 4 4 4 4 . .4 4 4 4 . 4 . 4 4 4 4 4 4 4 4 4 232
Posterior Chapman I s Refexes (Chart) . . . . . . . . . 4 . . . . 4 . . . ... 4 4 4 4 . 4 . 4 4 4 4 4 4 233
Index For OMT In Systemic Disease 234
Jb9
NOT:
J7U
OSTEOPATlIC CONSIERATIONS I TE PEDIATRIC PATIT
The moem general practice of pdiatrics contains a large amount of preventive
medicine. It offers the physician the opprtunity to examine and begin a
program for a patient that is healthy; usually the mother brings her well baby to
you s that you c reommend and instruct her on mesures (including
nutrition, immuniztions, and structur sreening) that will optimize the health
of this newbor infant (birth to age 2 yes) or child (2 yes old to puberty) .
Diagnosis and manipulative tetment programs for infants or children are
different from those for adults; in a large part this diversity is due to certain
anatomical and functional characteristics peculiar to the pediatric patient.
I. MUSCUWSKELETAL SYSTEM:
Though it is often sid that the spine of the newbor is regionally fexed like a
large C-cure, the lumboscral angle actually begins to form as ely as the
fourth month of gestation age. The cerical curve has alredy begun to appear
at birth and will incre with the efforts of the infant to rise the hed and hold
it eret. Activities like raising from the for and crawling exercises develop
the erector spinae muscles and begin to coordinate patters of interaction
betwen the nerous and musculoskeletal systems. The lumbar curve, however,
dos not appar until upright weight bearing is assumed. Its normal backward
bending curvature gives spring to the spine and supprt of the plvis, which
then beomes the anchor for the hip extensors and rotators. Postural cures
develop with weight bearing during childhod and psturl abnormalities such
as soliosis c progress rapidly during growth spurts. Propr screning of
psture should detect all soliosis greater than 10 degrees; 1 scolioses mesuring
more than 20 degres should have the beneft of a spcialist' s consultation.
Seondary scoliosis c result from pstural compenstion for short leg
syndrome, congenital spinal asymmetries, or even cranial somatic dysfnction
which unlevels the eyes.
The musculoskeletal system of the infant and child is still developing. Most of
the bones are cartilaginous to begin with and ariculations between them are
very elastic and resilient. Fryette's motion characteristics do not apply to the
infant. Spinal motion patters are nonspecifc and restricted motion is usually
due t loal muscle contraction or fascial pull and not bony joint somatic
dysfunction. Te pdiatrc patient is surrisingly esy to tret. Although the
child thinks that the physician is playing a game with them, tretment is not just
haphazrd but designed to move restcted joints ad tissues through teir rges
of motion. Dysfunctions "work themselves out; " it is sldom necessry to us
thrusting typ manipulation. Prouctive tretment time is very short with actual
completion accomplished in about 2-3 minutes. Soreness as a rection to
tretment is rre.
11
l. SYSTE:
Since the immune system is just developing, its lymphatic tissues take every
opprtunity to respond to an antigen; lymphadenopathy is often pronounce
even with minor infetions. Infetious diseses are common in children. In
adults, viral adenopathy usually only involves the psterior cerical noes. In
children, viral lymphadenopathy c either involve anterior or psterior cervical
lymphatic chains and usually results in an immune respns that includes
formation of large, thickene, tender, congested lymph nodes and overlaying
skin that is moist, slick and hot. Anterior lymphadenopathy is often prouced
by bacterial infetion and thes noes are usually shotty, coarse, grainy and are
acutely tender to palpation.
It is clinically obsered that infants and children respond rapidly to osteopathic
manipulative treatment. Sometimes their temperature will incre a degree or
two for a very short time after the tretment, then the fever will lyse and the
temprature will drop to ner normal. Parents should be told that this will
happn. Children and infants get sick quickly but they also respond quickly to
propr tretment and supprt of homeostatic mehanisms.
M. TE NVOUS SYSTE:
In the newbor, cranial somatic dysfunction from 0 w6I0 forces or birth trauma
may result and should b evaluated during the initial physical examination. Any
obvious plagiocephaly or palpable cranial somatic dysfunction should be trete
as so n as pssible becaus both have ben assoiated with pdiatric otitis
meia,
2
attention defcit and leing disorders,
3
as well as colic, strabismus,
suckling disrders, and a host of other symptoms assoiated with cranial nere
dysfnction. Dysfunction or injury to the nerous system is the most common
srious consequence of a diffcult birth ad cranial OM is idely employed as
erly a pssible to assist in structural-functional relationships. The piatric
history should always consider a nartive of the birth and prinatal prio.
Neural connections are still developing so infants and children ofen rect
errtically, rapidly and very unpredictably to disese proesses. With an
infetion, a newbor ofen rects with decreased temprature and, ofen,
bradycrdia. In some newbors, the only symptoms of a svere infetion may
b eting p rly, regurgitating, beoming less active or more irritable or shaky.
On the other hand, children (age two to puberty) may get very high
temprtures with mild infetions, or ner norma tempratures with srious
infetons. Infants and children are also developing emotionally and soially.
Se page 179 for a graphic representation depicting some of this growth.
J7Z
I. OVERVIW OF TE PEITC EXAMATION:
At frst, infants and young children may be frightened, becaus the physician is
both a stranger and loks so big, tall, and thretening. Kneling or sittng on a
stol may help reduce their fers by making the physician more "their" size. It
helps to appar happy and to always be kind and honest with these little
patients. Some physicians do not wer a white coat beaus in the mind of the
child, this may trigger some previous unfortunate, uncomfortable or frightening
incident.
The frst prerequisite to successful clinical encounters with children is to gain
their confdence. It is essential that the physician knows the child's name and
repats it during questioning and converstion. The mother can promote
security and sfety by sitting clos or holding the child on her lap during the
examination; at other times, there are occasions when it is best to have the
parent in the rom, i.e. an overbearing parent or for an older child with a
prsonal need for non-judgmental advice or diretion. Afer greting the
mother and the patient, the very young child is best "ignored" while the history
is taken by questioning the mother, with only apparent casual glances given to
the child. He often dosn't understand the questions and, even if old enough to
talk, the answers cannot be entirely believed, especially if not supprted by
physical ad laboratory data. An adult often complains of pain and disbility
while a child notices inconveniences to playtime activity. The physician must
de more with objective signs as well as with the parent's anxieties about the
child's problem. It helps to ocasionally touch the infant on the fot, or briefy
us sme small talk during history taking. Avoid loking diretly into the
young child's eyes because this will usually produce a defnite and immediate
withdrwal respns and ofen sets the tone for the rest of the pediatric
patient/physicia encounter.
During the erly part of this visit, the physician ofen tries not to reveal a
primary interest in the young child; in fact, it is best for the physician t obtain
as much information as pssible while taking the history from the parent and
from casually obsering the child's stance, activity level, and respnss before
beginning t directly examine the patient. Usually by the time the history is
taken frm the parent or primary care-giver and even though the physician has
se me to b uninterested in the infant or child, with obsration and casual
palpation metatarsl varus and tibial torsion have been evaluated. Sometime
durng this erly encounter it is pssible to see that the child is able to move the
leg quickly and do s without pain.
Wile talkng with the mother it is often pssible to casually put a warm
stethoscop on the chest of the infant or child and pretend not to know the
stethoscop is there. He will lok at the stethoscope, then at the physician (who
is lokng at and talking to the mother), then at the stethoscop again; he relly
J73
is confusd as t whether the physician is relly doing anything @him or not.
Bfore the child fgures out that the physician is gathering information about the
hert and lungs, the data has ben obtained and no crying interferes with this
imprtant evaluation.
B sure that the hed of the stethoscop is warmed. A rubber-rimmed
stethosop bell will be less cold to the infant. Even a warm stethoscop or a
stethosop with a rbber ring aound it apparently can fel col and startle a
child enough to make them cry. This suggested tehnique may improve chances
of obtaining go auscultatory data from an infant and will usually keep him
from crying: The physician's fngers are placed on the chest in about the
psition at which the stethoscop is to be placed; the infant or child dos not
sem to mind the touch of the hand, so the hand is placed on the chest with the
fngers in the ares where the heart and/or lungs are t be auscultated. Then,
one fnger at a time is lifed and immediately replaced by the hed of the
stethosop on the chest The infant is usually unable to tell when the fnger is
lifted and replaced by the stethoscop, so remains relaxed and dosn't cry. A
quiet infat or child improves the accuracy of auscultation.
Until a friendship has developd with you as the physician, never stare the
young child or infant eye to eye. It is very thretening to them ad they will try
to get away as son as the physician's eyes fous on theirs. It is neessry for
the physician to gain their confdence before they prmit eye contact. How this
is accomplished depnds upn the child's age and that undefnable "something"
that is presnt between the physician and ech of the young patients. After the
child has beome more accustomed to the physician, the cerical lymph glands
cn be evaluated by palpation. This can be prforme effetively in a short
prio of time. Mobility of the hyoid and the anterior cerical fascias can be
assssd at the sme time. The abdomen is gently squeezed several times,
loking for evidence of tenderess or masses. The ophthalmoscop is st at plus
8 diopters and at a distnce of about 1 112 or 2 feet from the eye the light is
fashed ("pek-a-bo") in the child's eyes loking for a red refex.
The ers are then examined. It is sfer and more information is quickly
gathered using the biggest er spulum in the diagnostic kit, even for the
newbor infant. Remember to pull the er down and back to opn the exteral
canal in an infant or young child. A single position of the spculum should
visuaize the entire tympanic membrane. Saying "pek-a-bo" makes the infant
or young child think it's a game and he may hold very still. Examine the nos
using the sme large er spculum. The diagnostic handle (light) must be held
in such a way that the physician has go control during the examination s that
any sudden, unexpcted motion of the child is followed instantly by the
otosopic or auroscopic spulum to avoid scratch or contact damage of the
cnal, drum, or mucos. Though it is not a scientifc word, "yuck" often makes
J74
the young child laugh and present the other er, nostril, or mouth to se if he
c get the sme respns from the physician.
Some otosopic diagnostic heds have a place to hold a tongue blade, but often
thes don' t diret the light to the right place. Frequently in the infant, the light
shines betwen their eyes insted of in the mouth. A spial diagnostic hed
usd only for holding the tongue blade ad directing the light diretly along the
blade and into the mouth, is very helpfl. If this spial holder is not a part of
your euipment, a bright pnlight, held and oprated on the tongue blade may
b usd. It allows the physician to control the light surce and the tongue blade
with one hand and have the other had fre to control the patient' s hed. If
pssible, have the child opn the mouth wide and "pat like a puppy dog. " The
tongue will automatically pull down, the soft palate will rs and it beomes
fairly esy to obtain a go view of the throat even without using the tongue
blade. Tongue blades tend to frighten children.
Again, it is helpful to make infants and young children think you are playing
with them. Sometimes the physician c hold the light up above the patient' s
head. When the child loks up at the light the mouth tends to open. Bring the
tongue blade down and touch the mouth sying, "ops". When the child smiles
or laughs, carefully but quickly slip the tongue blade over the tongue and lok
into the throat. A single gag, with you redy to quickly obsere the view of the
entire pharynx, often all the way to the epiglottis, is all that is usually required.
Children sem to understand the words, "all done, " even at an ely age; they
often won' t even cry. At that pint tum away telling the child how go he/she
was.
If the pdiatric patient c stand, have him do so and assess his psture. Then
have him bend over to touch his tos and lok for a rib hump due to
rotosoliosis. If presnt, have the patient swing his trunk off to the right and
lef while still forward bent. The functional compnent of the rotosoliotic
cure will reduce.
Infats and children don' t usually like to lie down in a physician' s offce. If
you ne to lay the infant down for some part of the examination such as
Ortlani' s test for a congenital hip disorder, do that proedure last, if at 8
pssible. Ofen, once you lay the infant or child down, any friendship that has
ben established is lost.
This stion dos not describe an entire examination but offers an approach
which considers the mind and spirit of the young child while beginning to
examine the by. Thes suggestions tend to work most, but not all, of the
time. Ocasionally, there is a child who just won' t coprate. In this c,
afer tng the history and makng a resonable attempt to beome friends, the
exam must pro d in a calm, frm but gentle fashion using the humane
IJ
restraints of the mother and/or nurs, and a calm ressuring voice of the
physician.
v. TEATT OF mE PEDIATRIC PATIT:
Like osteopathic tretment of any patient, ostepathic manipulative tretment of
a pdiatric patient is based upn the application of principles and not upn
formulae or techniques. Treting infants and children is ofen esy becaus they
rarely have fbrosis and or chronic fxations; don't overtret. Keep it simple
ad make it fun. Manipulative tretment is administered t the pdiatric patient
according t whether they are "pre-schol" or "schol age". Pre-shol
children only require articular mobiliztion and soft tissue. Schol-age children
may reuire moifed adult proedures.
Don't tret directly over infected lymphatic nodes; insted, treat around them
and supprt the boy systems that help the infant fght infetion and reover
from it effects. This mens rib raising to reduce sympathetic hypractivity
while moving fuids and fascial techniques to dome the diaphragm and st the
lymphatic pumps. Newbors and infants c be treate by placing them on the
physician's thigh or by placing them in a lateral reumbent psition of the table
(your kne on the table in front of them) and administering soft tissue to the
paraspinal tissues. The physician c also pick the child up and tret while
walking around. The newbor can also be held against the chest and treted. A
physician who has children c becomed experienced by treting his/her own
children.
Insuring that the child gets solid fods during the time of high fever and
anorexia is not a imprant as being sure that the child gets plenty of fuids.
Children normally have a larger percentge of fuids in their boies; many times
a child or infant must be admitted to a hospital because of dehydration and not
beaus of the diss proess. So increse fuids, deongest pripheral tissues
ad retur sequestered interstitial fuid back into the circulation by using
lymphatic and fascial thniques. "
Lymphatic pumps c be made fun for the child--"play with them". When the
infant gets a little fussy or tries to get away from a rhythmic chest pump,
suddenly stop and sy, "Do you want more?" While they are trying to fgure
out why they should want more, start it again; when he fusses again, you sy
the sme thing. Usually by the time he fgures out that it's not really a game,
the tretment is over; 8 done." Another approach to "tretment" is to grasp
fet and legs, lif their buttoks and their lower 2/3 of the boy off the tble,
then jiggle the lower extremities gently. Flex one leg and then the other onto
the chest, pushing ech one gently and then extend the legs again. The child
may be tured over by using the legs and then the physicia may "play
wheelbarrow" with them. This apparent play clinically promotes a typ of
J7b
lymph pump, fuid drainage, and movement of the boy tissues. The mother
c continue this "play-typ" mobiliztion at home.
Remembr, high veloity activation of osteopathic maipulative tehniques is
usually not require in infants and young children and becaus epiphysl plates
are still opn, may not be the best choice of tehnique in this age group. Sof
tissue tretment and articulatory methos of tretment are very effetive and
make it fn for the child. Again, do not over-tret. There is the "tick-tk
metho" of tretment, in which the physician holds the chest of the child under
the arms and roks him back and forth, from right t left, mobilizing the spine
and other tissues. The fascias of the thoracic inlet and the diaphragmatic are
should be trete. If the infant is getting an exanthema or proromal of an
infetious dis, tretment clinically results in less rsh, less fever and a
dere in the sverity of the dis. Pediatric patents beneft from
ostepathic diagnosis and manipulative tretment and both should be integrated
into pdiatric care.
Inform the parents that commonly after manipulative tretment, the temprature
will briefy go up in a pediatric patient before coming down. Also educate them
that fever is not neessrily bad. Incresed temprature is one of the boy's
ways of mobilizing defenses against an infection. Viruses multiply best at
temprtures slightly below normal. Fever hinders viral replication and is a
way of incresing circulation and getting the immune substances to the infected
ares, helping the infant's own homestatic mechanisms. It increses
metabolism and circulation and cretes an environment prly tolerated by
microrganisms.
Fever that is to high may cause convulsions and the threshold for convulsions
from fever varies from child to child; therefore, its level must be controlle. If
there is a febrile seizure history, then the physician must be more cautious in
instructing the parents in maintaining temprature control in the infant or child.
Aspirin may be assoiated with development of Reyes' Syndrome and therefore
it is not as go an atipyretic choice as acetaminophen. As a rle of thumb, a
fever under 101
0
F dosn't ned t be treted. Above I02
0
F a dose of
acetaminophen ( 1 grain pr age of life) could be given.
A physician knows that his/her management of a child has been successfl if a
mother brings in one of her children and sys, "Johnny cried beaus he wanted
t come in and se his dotor to." If you desire to red more on examination
of the child, red "How to examine a baby or a small child and how t kep
your col" written by retired pdiatrician, Robert Mercer, M.D.
4
You c fel
the joy he had in being able t care for infants and children. Dr. Mercer sys,
"The rel reward of a successful examination is when the small prson climbs
up on your lap for frther friendly play; then you know for sure that you have
done a go job and established a new friendship in the proess." When the
IJJ
child likes "the dotor," a stisfying patient encounter becomes even more
enjoyable.
RBFBRBNCB81
1. Kuchera W A, Kucher ML: Othic Princ in P. 2nd
eition. KCOM Press, Kirksville MO, 1992, Q 352.
children with a history of otitis media from kndergarten t third grade.
Med-Johnsn Fellowship Papr, 1993
3. Frymann V: Relation of disturbances of cranioscral mehanism t
symptomatology of the newbor: Study of 1,250 infants. JAOA
65: 1059-1075, 1966
4. Mercer V. How t examine a baby or a small child and keep your col.
Cleveland Clinic Ouarerly Fall 1983; 50: 255-261.
J78
PEITC GROWT (Aspufrm Wessl) 1
Hungry for companionship, staring is a baby's way of reaching out to others. Reching for
the closness neessy for healthy development. The infant progresses from the ability to
barely se to complex talents including cordination to se k, t remember,
and to imitate.
prefers complicated forms
to black and white reaches for toes and toys
close by, then those
hanging, then those in
center of room. Laughs,
coos, grunts when sees
watches
bright ob
jects on
ceiling in
front
I
1 Mo
smiles in
response
I
to smile
2 Mo
I knows mother
by sight and
may smile
surroundings more
important; stops
sucking to look at
father, a curtain
l or sunbeam on floor
I
favorite toy
1 1
I I I I
3 Mo 4 Mo 5 Mo 6 Mo
I
I smiles and
I
I dramatic development
coos to attract enjoy-ment for new
mother's atten- places, as long as
tion. When she mother is along side;
disappears gets trips are exciting
solemn and may and taken in stride;
cry but when back
begins to imitate facial
expressions and
home again, relaxes,
smiles, coos in delight
to be safe at home
again.
sees and
grabs hold
of his feet
7 Mo 8 Mo

looks carefully
at hands, navel,
toes as if they
were new
voice inflections
9 Mo
visual games: peek-a-boo, complex
and watch Momy pick it
10 Mo 11 Mo 12 Mo
I I
can interlock fingers, pull them
apart and repeat. Acts like is
discovering hands for the first
time
begins to imitate his favorite adult's
mannerisms. Interested in tiny details
in wallpaper, pictures or blocks;
studies mother's jewelry, clothing, etc.
1. Wessl, MA; From A Baby's Point Of View: Assoiate Professor Of Pediatrics At Yale University.
IJ9
Still-Hildreth Osteopathic Sanatorium
1914
Macon, Missouri
Dedicated to the Treatment and Care of Nervous
and Mental Patients
JBU
1939
OSTEOPATHIC CONSIERATIONS I PYCHIATY
BmLIOGRAPHY
Bradford, Spncer, G.; Role Of Ostepathic Manipulative Therapy In Emotional Disrders: A
Physiologic Hypthesis; JAOA; Vol. 6; No. 7; Jan 1965: 6-73
Dunn, Floyd E. ; Osteopathic Concepts In Psychiatry; JAOA; Vol. 49; No. 7; Mar 1950:
354-357
Espland, Darryl, and Peters, Christian; OMT And Substance Abuse Rehabilitation;
Ohic Annals; Vol. 13; Feb 1985: 26-30
Sadder, Arthur M.; Restricted Blo Flow In Brain Found In Some Schizophrenics; Meica
Tribune; Jan 11, 1984
Wods, John M. ; Wos, Rachel H.; A Physical Finding Related To Psychiatric Disorders;
JAOA; Vol. 60; Aug 1961: 988-993
I6I
OSTEOPATHIC CONSIEATIONS I IM NOWGY
BmLIOGRAPHY:
Amalftano, D.M.; The Osteopathic Thoracic-Lymphatic Pump: A Review of
the Historical Literature; J of Ostic Medicine; Apr-May,
1987: 20-24
Gundersn TG, Gordon V. A study of the infuence of spinal lesions on the
course of infections. IAOA 1932; 31: 390.
Mesl, I.W.; The Effect of Lymphatic Pump in the Immune Respns: .
Preliminary Studies in the Antibody Response to Pneumoocal
Polysccharide Assyed by Bacterial Agglutination and Passive
Hemagglutination; IAOA; 82 (1): 28-31
Mesel, I.W.; Introuction: Thoughts in Osteopathic Practice and Infetious
Disses; Ostthic Annals; 10 (3); Mar 1982: 7-11
Mesl, I.W., et. al,; The Effet of the Lymphatic Pump in the B and T Cells
in Peripheral Blo; Oepathic Annals; IAOA; 86 (9); Sep 1896: 68
Paul, R., et. al.; Interferon Lvels in Human Subjects Throughout a 24-hour
Perio Following Thorcic Lymphatic Pump Manipulation; IAOA; 86
(2); Feb 1986: 92-95
Purs FM: Clinical evaluation of osteopathic manipulative therapy in mesles.
IAOA 1961; 61: 274.
Thorp, R.; Ostepathic Manipulative Therapy for Infection; Oeopathic
Annals; 8 (9); Sep 1980: 30-34
The pro ings of an Interational Conference on this subjet will son be
available from the American Academy of Osteopathy. Conference c
chairrsons were Frank Willard, PhD and Michael Patterson, PhD.
J8Z
HYPERSYMATHETIC ACTIVITY ON SELECTE TISSUE
EXTRACTED FOM COLLECTED PAPES OF I.M. KORR, PH
1977-1989
Sympathetic hypractivity dos not introuce
any new qualities, only modifes the inherent
functional proprties of the target tissues.
SKELETAL MUSCLE:
o .. Augments contraction similar to inotropic effect on cardiac muscle, "Orbeli
effect"
o .. Facilitates neuromuscular transmission
o .. Increses contracture formation after spinal cord trauma
PERIHEAL SENSORY MCHANISM:
o .. Facilitation: increses rate of discharge and lowers threshold to fre (may
rech zr s tat fres without direct stimulation of reeptor)
o .. Exaggeration of respns: reprts a greter intensity of stimulation than is
actually ocuring; increses or exaggerates the perception of pain
o .. The snsory mehanisms that have been demonstrated to respond in this
manner include:
--muscle spindle --tactile receptors
--taste receptors --olfactory apparatus
--Pacinian corpuscles --retina and cohlea
--carotid sinus chemoreeptors
CENTAL NERVOUS SYSTEM:
o .. Strong infuential connection between hypersympathetic activity in suprior
cerical ganglion and subcortical activity, especially on the ipsilateral
side
o .. Primary infuence is on the mehanisms respnsible for generation of the
background electrical activity, te rhythm assimilation rection and the
sondary compnents of the induced rection to light
o .. Facilitating effets have been obsered in the reticular formation, general
brain, cerebellum and spinal cord
I63
COLLATERAL CICULATION:
o .. There is a decre in development of collateral circulation; sympathectomy
incres the development of collateral circulation in ares of oclusion
o .. There is dereased mortality and morbidity in exprimently induced
myodial infarction when sympathetics are cut
ADISE TISSUE:
o .. Sympathetics are requisite for liplysis indepndently from blo fow
(alpha for vasulature and beta for adipose tissue)
o .. Incres in glycogenolysis requires increased oxygen
ENDOCRI SYSTEM:
o .. Sympathetic signifcantly infuences the pineal gland and thereby infuences
other endorne systems; this is especially related to sexual development
and reprouction. Suprior cervical ganglion infuence on the pineal
gland through synthesis of melatonin
BONE GROWTH:
o .. Reduces the growth of longitudinal bone
RETICUWENDOTHELIAL SYSTEM:
o .. Increases circulating reticuloytes and normoblasts
SOM SPECIIC CLIICAL REACTIONS TO SYMATHICOTONIA:
ARTERIOSCLEROSIS:
Sustned stimulation of sympathetics produce histologic fetures of
arteriosclerosis and increses tendency towards thrombosis.
HYPETENSION:
High activity of the pripheral sympathetic nervous system is felt to be
an imprtant contributing factor in some forms of arterial hyprtension.
I84
HEART:
Incresd sympathetic activity increases oxygen demands which
contribute to the extent and degre of cardiac ischemia and angina.
Sympathicotonia incres the extent of myoardial damage following
an MI.
(Expriments with cts) Post-MI there is a higher discharge of
sympathetic activity at T3 ramus communicans, termed a cardio-cardiac
refex, which plays and imprtant role in incresed rate of dysrhythmia
and ventrcular fbrillation. Sympathicotonia als lowers threshold to the
development of etopic foi in the hert. Adrenergic blokade protets
the heart from thes effets especially in the few hours pst-MI and
lowers the mortality rates.
Incresed sympathetic impulses to the kidney is implicated in the
retention of Na and water in CHF patients.
PEI TICS:
Incresed sympathetic activity has been implicated in the long Q-T
interal assoiated with Sudden Infant Death Syndrome.
UETERAL CALCULI:
Ureteral calculi prouce ipsilateral facilitation of sympathetic activity.
Incre sympathetic activity is also implicated in poor ureteral
transprt of fuids, a factor in calculi formation. If calculi are present in
the ureter, sympathetic hypractivity decreses the prstalsis of the
ureters which hinders removal of the calculus from the ureter.
Suprmpsed emotions assoiated with increased sympathetic respnss
may are found to reduce glomerular fltration rate (GFR).
1 SKELETAL SYSTE:
Hyprsympathetic activity retards bone growth. Sympatholytic tretment
restores bone growth to a normal rate.
There is reduced rheumatoid and osteoarthrtic disease in the extremities
following sympathetomy.
I6
TE EXTTI:
Prolonged sympathetic activity in respns to signifcant or relatively
insignifcant trauma results in "refex sympathetic dystrophy", a
syndrome including heightened pain, trophic changes, osteoprosis,
connective tissue dis, and an extremity that is col, swety,
cyanotic, chronicly edematous, and has thickened nails. Often these
changes are respnsive to sympathetomy.
LIVE:
Sympathetic bombardment releses fatty acids from the priphery and
depsits them in the liver.
PANCREAS:
Sympathetic stimulation can convert a mild, nonlethal type of bile
induced pancreatitis into the necrotizing, hemorrhagic lethal form. This
is probably secondary to vasoonstriction and slight ischemia of the
pancreas.
OTER AREAS OF HYPESYMATIlETIC EFFECT:
Glaucoma, colitis, megacolon, pripheral vascular disese, pstoprative
paralytic ileus, Dupuytren's contracture, irritable bowel syndrome (S),
plvic congestion in women, etc.
I6b
A0TDNDNIC NBRVD08 8Y8TBN INFL0BNCB IN 8BLBCTBD ARBA8
8TR0CT0RB 8YNPATdBTIC PARA8YNPATdBTIC
Pupil M M M M M M M M M M M M M M M M M Dilation M M M M M M M M M M M Constriction
Ciliary Muscle M M M M M M M M M M M M
M M M M M M M M M M M M Contraction
Lacrimal Gland M M M M M M M
M M M M M M M M M M Secretory
Mucous Glands (N-Th) M M M M M Inhibition M M M M M M M M Secretory
Parotid Gland ............. lnhibition M M M M M M M M M Secretory
Submaxillary Gland M M M M M M lnhibition M M M M M M M M M M Secretory
Sublingual Gland M M M M M lnhibition M M M M M M M M M M Secretory
Blood Vessels (Skin) ...... Vasoconstriction ...... -
--
-
Pilomotor Muscles ......... Contraction ........... ------
Sweat Glands Secretory M M M M M M M M M M M
Common Carotid Artery M M Vasoconstriction M M M M M
Mucous Glands (phx-Iarx) M Vasoconstriction ...... Secretory

Thyroid Gland M M M M M M M M M M M M Vasoconstriction M M M
Heart ..................... Excitation ............ lnhibition

Bronchial Muscle M M M M M M M M Relaxation M M M M M M M M Contraction
Bronchial Glands M M M M M lnhibition M M M M M M M M M Secretory
Upper Body Vasculature M M M Vasoconstriction M M M M
Stomach M M M M M M M M M M M lnhibition M M M M M M M M M M Motor and Secretion

Liver M M M M M M M M M M M M M Glycogenolysis M M M M M M M Glycogen Synthesis
Spleen M M M M M M M M M M M M M M M M Vasoconstriction M M
Gallbladder and Ducts M M M M Relaxation M M M M M M M M M Contraction

Pancreas M M M M M M M lnhibition M M M M M M M M M Secretory
J6J
A0TDNDNIC NBRVD08 8Y8TBN INFL0BNCB IN 8BLBCTBD ARBA8 (cont)
8TR0CT0RB 8YNPATdBTIC PA8YNPATdBTIC
Kidney M M M M M M M M M M M M M M M M Vasoconstriction ......
Adrenal Medulla Q Q Q Q Q Q Q Q Q Q Adrenaline secretion ..
Intestinal Tract .......... Contraction M M M M M M Relaxation
Rectal Sphincter M M Contraction M M M M M Relaxation
vesicle Sphincter ......... contraction M M M M M M M Relaxation
Vesicle Body .............. Relaxation M M M M M M M M M M M Constriction
uterine Fundus ............ constriction M M M M M M M Relaxation
uterine Cervix ............ Relaxation M M M M M M M M M M M Constriction
Male Reproductive Organs .. Ejaculation M M M M M M M M M M Erection
Ovary and Testes M M Vasoconstriction M M M M (unknown)
RF PAI: Generally, visceral afferent neres from the viscera follow the sme pathway as
traveled by the sympathetic inneration of the organ. Impulses from visceral nere endings arrive
among the psterior hom cells as do impulss of somatic origin. Visceral referred pain will b noted
in the somatic segment(s) which share the sme dorsal hom lamina V of neurons. There may b
suprfcial skn changes, refex muscle spasm and vasomotor changes.
o .. Visceral referred pain may be gripping, cramping, aching, crushing, squeezing, tearing, stabbing
or buring.
o .. It is usually porly loalized.
o .. Referred pain may have rhythmic ocurrence to it.
From hollow viscus: gretest intensity in 20-30 s, lasts 2 minutes, quickly subsides, and
recurs again in minutes. From vascular ares: throbbing pain from infammation and
chemical mediators; it increses in severity and lasts an extended perio of time.
o .. Usually associated with other symptoms of visceral disease.
o .. People with viscerogenic pain get no relief from rest; they fnd more comfort if moving, trying
to fnd a position of comfort.
o .. Se pages 79-82 for diagrammatic depiction of pain progression.
I66
OSTEOPATC MULATIE TECHQUE
USE OF OSTEOPATC MULATIVE TREATMT
I SYSTEMC DYSFUNCTION
Dysfunction and dis change the loal and regional intercellular
environments. An increse in interstitial tissue fuids is one of the results of this
tissue dysfunction. Resulting congestion disturbs loal and regional biohemical
homeostasis. Dis and dysfnction also provoke receptors of visceral
afferent and/or smatic snsory neres which then fo their spinal cord ares
with neural impulses. Afferent (snsory) impulses usually follow the sme
fasial pathways as the sympathetic neres innerating the affeted organ or
organs. Ocasionally, as from the alveli of the lungs or from the cerix of the
uterus, viseral afferents follow the pathways of the organ I s parasympathetic
supply. In either case, constant bombardment by visceral afferent impulss
facilitates the spinal cord segments at their destination. This mens a reduction
in the threshold of the synapses in the neuronal pol of the dorsl hom in those
regions of the spinal cord. Bause there is "cross-talk" between these pols,
palpable smatic changes result from visceral dysfunction and viscerl
dysfunction c also result from somatic dysfunction. Once facilitated cord
sgments are established, stress of any kind (physical, mentl or emotional) will
initiate an outburst of sympathetic impulses to their assoiated viscera even if
that stress has no diret relationship to the low threshold segments.
Successful osteopathic manipulative tretment for patients with systemic
dysfunction or dis has thes common goals:
o .. Reduce the two main factors respnsible for initiating or sustning
facilitated spinal cord sgments, whether they be assoiated with somatic
and/or visceral dysfunction.
o .. Supprt homeostatic mehanisms by reducing somatic and visceral factors
that contribute to the maintenance of spinal cord facilitation. Reduction
of cord facilitation enables the boy to make more appropriat refex
respnss to proprioeptive input.
o .. Supprt biomehanical mehanisms respnsible for moving lymphatic fuids
from the interstitial spaces back to the circulation and for removing
metabolic by-products and medications from the intercellular
environment. This aids fuid homeostasis throughout the boy.
o .. Supprt the parsympathetic nerous system by treatment of fascial
restrictions and somatic dysfunction in the regions of the sphenopalatine
ganglion, the cranium, the OA or the scrum. These tretments promote
balance within the autonomic system and prepares the boy t retur
toward a homeostatic level which is more physiologic for that patient.
I69
o . . SUpprt the boy proesses and mechanisms which allow the boy to
metabolize and us the fo that is taken into the boy.
o . . Supprt the mental, spiritual and emotional neds of the patient.
It should b redily apparent why initial ostepathic manipulative tretment is
often direted tward reducing facilitation and promoting a more appropriate
sympathetic respns. The tretment program will usually progress toward
supprt of the boy's lymphatic system; ad fnally, toward effeting
parasympathetic balace. Ostepathic manipulative management is spifc for
ech patient, providing tretment indicated by the history of that patient, the
kown natural history of the disse proess, and the palpatory fndings on
examination of the patient. There are a vaiety of manipulative tehniques that
c b us to affet smatic dysfunction, the autonomic nerous system, and
the lymphatics. It must be re-emphasized that the manipulative prtion of a
management program is unique for ech patient and is planned according to
each patient's individual neds.
A basic plan for the effcient use of the patient's neuromusculoskeletal
system during the formulation of a differential diagnosis and tretment plan
is very helpful. The following fgure is a model for such a plan. It has been
found to be clinically useful in effectively and effciently formulating and
exeuting supprtive osteopathic manipulative treatment for a patient with
systemic disese.
Somatic Dysfunction
facil. seg.
Mid Cervicals
Tl - L2
Ribs
OA
Sacrum
Sympathetics Parasympathetics I
Chain Ganglia
Collateral Ganglia
Chapan's Reflexes
Treat.ant plan
Di.aa.e or
Dy.function
J
Cranial Nerves
III, VII, IX, X
Cranium,
OA, A, C2
1 Pelvic
Lymphatics I Splanchnic N.
mmmmm
Sacroiliac
Thoracic Inlets
Abdominal Diaphragm
Mesenteries
Pelvic Diaphragm
Lymphatic Pumps
I9U
ARMS
LEGS
SYMPATHETIC
NERVES
(T1-12)
SYMPATHETIC AND
PARASYMPATHETIC
INNERVATION
HEAD
PARASYMPATHETIC
SUPRASTERNAL
NOTCH
ANGLE OF
LOUIS
CRANIAL NERVES
III. VII. IX
PARASYMPATHETIC
CRANIAL NERVE
X
" _ a. UPPER GI TRACT
J9J
\
D, SMALL INTESTINES
RIGHT HALF COLON
_U"BIUCUS
LEF HALF COLON
PELVIC SPLNCHNIC
NERVE (S 2.3.4)
(PARASYMPATHETIC)

1
t
COMOSITE AUONOMIC INNERVATION CHART
PASYATHTIC
INERVATIONS
CRANIOSACRL
CRANIAL III
CRANIAL VII
CRANIAL VII
CRANIAL IX, X
CRANIAL X VAGUS
?
CRANIAL X VAGUS
?
VISCER
- PUPILS
- LACRIMAL AND
THORACO
LUMBAR
Tl-4
SALIVARY GLANDS-II Tl-4
- SINUSES
- CAROTID BODY
AND SINUS
- THYROID
- TRACHEA/BRONCHI
- M Y GLANDS
- ESOPHAGUS
LOWER 2/3
- AORTA
- HEART
Tl-4
Tl-4
Tl-4
Tl-6
Tl-6
Tl-6
- LUNGS AND
VISCERL PLEURA- Tl-6
TS-9L
TS-9
- STOMCH
- DUODENUM
- LIVER
GALL BLADDER
AND DUCTS
- SPLEEN
- PANCREAS
- RIGHT COLON
TSR
T6R
-
II
T7L
- T7R
- T10-ll
- OVARY AND TESTES -II T10-ll
CRANIAL X VAGUS 11- SMALL INTESTINES -II T10-ll
- KIDNEY
ENTIRE COLON
- APPENDIX
-
II
T10-ll
- T10-L2
T12
SYATHETIC INNERVATIONS
REGIONAL
AREAS
HEAD AND NECK
HEART
LUNGS
ENTIRE GI TRACT:
UPPER GI TRACT
SM INT./RHT COLON
APPENDIX
LEFT COLON/PELVIS
ADRENAL
KIDNEY
CORD
LEVEL
Tl-4
Tl-6
Tl-6
TS-L2
TS-9
T10-ll
T12
T12-L2
T10-ll
T10-ll
SPLANCHNIC
NERVES
GREATER
SPLANCHNIC
LESSER
SPLANCHNIC
LEAST AND
LUMBAR
SPLANCHNIC
COLLATERL
GANGLIA
(CERV. GANGLIA)
(CERV. GANGLIA)
CELIAC
GANGLION
SUP. MESENTERIC
GANGLION
INF. MESENTERIC
GANGLION
continued on next page

\
w
continuation of autonomic innervation chart:
COMOSITE AUTONOMIC INNERVATION CHART
PASYATHETIC SYATHETIC INNERVATIONS
INERVATIONS
VISCER THORACO- REGIONAL CORD SPLANCHNIC
CRANIOSACRAL LUMBAR AREAS LEVEL NERVES
PELV. SPLANCHNICS - LEFT COLON - T12-L2 UPPER URETER TlO-ll
(NONE) ADRENAL - T10-11 LOWER URETER T12-L1
VAGUS - UPPER URETER - T10-11
PELV. SPLANCHNICS - LOWER URETER - T12-L1 BLADDER T12-L2
W
- BLADDER (BODY) - T12-L2
BLADDER TRIGONE T12-L2
W
- AND SPHINCTER -
W
- UTERINE BODY - T12-L2
W
- PROSTATE - T12-L2
W
- GENITAL CAVERNOUS
TISSUES
(NONE) - ARS - T2-8
(NONE) - LEGS - Tll-L2

* PELVIC SPLANCHNIC S 2, 3, 4 (PARASYMPATHETIC)
COLLATERL
GANGLIA
I
I
(c)
1991
In order t use this plan, it is necessary to be familiar with sympathetic and
parasympathetic innerations for groups of organs. This is often where the plan
fails, beaus a physician may have trouble remembering the autonomic
innervations to organs. For this reson, sympathetic innerations of various
viser were reviewed in many anatomical and neurological texts where there
se med to be a wide and variable range of sympathetic inneration to any one
organ. Common visceral innerations were then group s that they could be
esily memorize while still maintaining their clinical relevance. The result was
the compsite chart of autonomic inneration on pages 192 and 193. This chart
retains credible correlation with all of the different rnges of sympathetic
inneration presnted by various authors, but is als much esier to memorize.
Reogniz that intens visceral afferent activity from certain clinical situations
may result in a spred of the facilitated cord segments up or down in the
thoracolumbar spinal cord are and result in an incresed range of palpable
somatic paraspinal involvement initiated by that organ system dysfunction. It
may even result in the expression of symptoms from other systems or organs
that happn to be innerated by sympathetic fbers from adjacent cord segments.
l. TEATMT SYMATHETIC NERVOUS SYSTEM
DYSFNCTION:
A. TREATMT GOAL AN GENRAL MANULATIVE
TEATMT PLAN:
Organs which are primarily or secondarily involved in dysfunction exhibit
characteristic changes or symptomatology of sympathicotonia. Diagnosis and
tretment c be direted to several anatomic-physiologic loations: The
thorcolumbar paraspinal chain ganglia, the collateral sympathetic (preortic and
cerical) ganglia, through the facilitated spinal cord sgments, or through
spcifc refex systems such as Chapman' s and Travell' s myofascial pints. The
spinal cord segments c be maintained in their facilitated state by being
bombaded by visceral or somatic afferent fbers from viscerl and/or somatic
dysfunctions.
Set Goals: Becaus the sympathetic chain ganglia are anatomically loated
anteror to the rib heds, any dysfunction that directly or indiretly and
"chronically" restricts fascia in this region may initiate and/or maintain
excessive sympathetic outfow to their reference organs. It naturally follows
that normal rib motion as well as reduced afferent input from paraspinal muscles
or the viscera, will help to reduce segmental cord facilitation.
I94
Abdominal collateral sympathetic ganglia are able t control loal and prhaps
sme regional autonomic respnss without reprting to the CNS. Thes
ganglia are also in the pathway of the visceral afferents that relay impulses of
GI or plvic dysfnction to the CNS.
Animal studies have reveed evidence that erly manipulation of smatic
dysfnction might act as a form of preventive medicine. Summarizing some of
his animal studies, Patterson 1 purrts:
o . . Persistent musuloskeletal dysfnction affecting a certain spinal cord
sgment c affect the function of an interal organ related to that sme
spinal cord segment.
o . . Removal of the musculoskeletal irritation prouced by dysfunction allows
the related interal organ to retur to its normal function.
o . . If the dysfunction of the musculoskelet system remains long enough, it
apparently "bums a memory patter" within the central nerous system
s that when the initial irritating musculoskeletal infuence is removed,
the original dysfunction not only continues but grows in severity.
B. R RIIG TECHQU:
Ribs should also move well to prmit painless, effortless brething. The
diaphrgm is the extrinsic pump of the lymphatic system. Go diaphragmatic
action is supprted by tretment of spifc rib somatic dysfnction and by rib
raising thniques that increse the depth of respiration. Tretment of somatic
dysfnction and the mechanical principles applied in "rib raising" techniques
provoke maximum excursion of the rib cage, encourage maximum inhalation
and the genertion of more effective negative intrathoracic pressure. This
incres lymphatic fow and also relaxes the patient. These techniques also
help to re-establish range-of-motion and thereby reduce excessive afferent input
to facilitated cord segments.
Rib raising is actually the primary manipulative metho by which the
ostepathic physician affets the hyrsympathetic activity initiated by
dysfnction or dis. Effetive rib raising tehniques lift and rotte the rib
heds; they, in tur, pull on the fascias that are common to a rib hed and its
sympathetic chain ganglion. This initially "stimulates" refex sympathetic
respnss in the related organs, an event which the physician usually wishes to
reuce and prevent, espcially a a long term circumstance. Refex
neurophysiologists explain that the sympathetic activation prouced by rib
raising is due to stimulation of fast and very fast efferent sympathetic fbers but
that this respns is fairly loalized and short lived. They also reprt that rib
raising tehniques will additionally stimulate slow and very slow efferent
sympathetic fbers in the sme ganglia and these fbers refex a high a the
I9
medullary centers. Thes latter refexes are reprted t be inhibitory to the
sympathetic system and also are long acting.
It is imprtant to reduce the sensitivity of the spinal ares demonstrating
incred facilitation frst, so that proprioeptor impulss prouced by tretment
of other ares will not prouce fring of these segments with lowered thresholds.
An optimal treatment protool strives t maximize the boy's own homestatic
ability to maintain rib motion -- thus, dysfunction of the thorcics, sterum,
diaphragm (including lumbar attachments and cericophrenic inneration), and
cranial elements might be considered and be appropriately treted. If a
physician applies the basic principles of rib raising tretment, a variety of
tehniques c be formulate for utiliztion in the management of patients who
are in a variety of psitions and who have a variety of medical conditions.
RI RAISIG FOR ACUTELY DEBIITATED PATITS: PATIT
SUPIE
o .. Purse(s):
o . . To decrease sympathetic facilitation
o . . To increse respiratory effciency and depth
o .. To incres lymphatic retur
o .. To reduce general stress and discomfort
o . . The oprator sits beside patient and inserts both hands under the patient
contcting the angles of the ribs with the fngers of both hands.
o . . The oprator must lift up (toward ceiling) suffciently t move the rib and
its rib hed (sterum should also rise) and pull slightly lateral to the
pint of tissue resistance--ese of performing the lif is gained by using
the dorsl surface of the MCP joints as a fulcrum against the bed or
table.
o . . Additional lymphatic and/or respiratory benefts may pssibly be gained by
using the hads and/or fnger pads t pressure the ribs towards inhalation
(pump handle inhalation encourgement requires a caudal diretion from
the fnger pads at the psterior aspt of the rib to bring the anterior
prtion supriorly; bucket handle rib motion requires a cephalad pull
from the psterior contact). The sympathetic effet of rib raising as
desribed is probably effective without any of this spcially directe
activity.
o .. When the tissues relax, the oprator should slowly repsition his or her
hands onto the next group of adjacent untreted rib angles and repat the
proedure. The other side of the rib cage is treted in the sme manner
until the entire rib cage has been treted.
J9b
R RAISIG TECHIQUE FOR LES DEBIITATED PATITS:
PATIT SUPIE
0 . . Purs(s): Same a above.
o . . The oprator stands at the hed of the patient.
o . . The patient is supine and reches up with both arms over hed to encourage
raising of te ribs and in some manner, affxes hands around the
psterior aspct of the oprator's waist or to a belt (or other material).
o . . The oprator contacts the patient's rb angles by sliding the hands under
ech side of the chest cage (approaching the rib angles from the sides of
the rib cage).
o .. The oprator must lift up (toward ceiling) and len backward suffciently to
move the ribs and their rib heds.
o . . As the oprator lifts ad lens backwards and downward, the pull through
the patient's arms stretches the ptoral and latissimus dorsi muscles,
encouraging the ribs into inhalation
o .. This lif from the hed of the bed or table is repeated until the ribs move
easily.
R RAISIG FOR A SEATED PATIENT:
This is an espcially helpful tehnique for patients that are uncomfortable or
unable to lie down.
o . . Patient is sted with arms crossed, the shoulders are fexed and the hed
rested on the arms
o . . Ortor stands at side of patient and supprts the crossed arms with one
uppr extremity; the other hand is placed across the patient's thoracic
spine contacting bilaterally a much of the rib as pssible
o . . The patient is instructed to rela their back and allow their weight to fall
forward onto the oprator's supprting arm
o . . The oprator lifts and allows the patient to transfer their weight farther
forard onto the supprting arm; the other hand is used to crete a
fulcrum in the thoracic spine for backward bending
o . . The proess above is applie t the entire rib cage a is comfortable to the
patient
J9J
MUSCLE USE I MUSCLE ENERGY R TECHIQU USE TO
ELEVATE OR DEPRES R SOMATIC DYSFNCTIONS (SD) :
mUSC0S US00 D 00V80 0xh88DD fD
C80p0S
.
..
DS 1
-
2
0CDf8S mpDf

DS 3,4,b(6)
0ff8US PD0fDf
DS 6,7,8,9, 1 0
L8SSmUS DfS DS 9, 1 0, 1 1 , 12
[wU80f8US LUmDDfUm] D 12 [D0f0Cy]
p0fCDS8S
[DfC00 Dh88D
p
mUSC0S US00 D 00f0SS Dh88DD fD
wU80f8US LUmDDfUm D 12 [0f0Cy]
g
D0fCDS8S
-
orce
0 0xh88DD
A. C80D0 MUSC0S
|DS 3,4,5
|DS 6,7,8
DS 9, 10
1 1 , 12
B. 0CDf8|S M|HDf MUSC0
L. 0ff8US PH0IDf MUSC0
. L8SSmUS D|S MUSC0
1 IEUS PREVENTION TEATMT: ("R RAISIG" AREAS
WITHOUT RIS)
Proucing the effects of rib raising in these segments could not b prformed
through rib heds. The following describes an inhibition technique for the LI to
L2 spinal are, but the sme technique c be used to tret the effets of
hyprsympathetic outfow in the thoracic are.
o . . The patient is supine and the physician is st at the side of the patient.
o . . The physician passs both hands under the back the patient to a pint where
the fnger tips are on one side and the thenar ad hypthenar eminences
are on the other side of the erector spinae mass (M.
o . . The hands are then closed, pulling the two erector spinae mass muscles
toward ech other between the fngers and the thenar/hypothenar
eminences of the oprator.
o = 4 This maneuver automatically lifs or backard bends the spinal region
OK above the hands. If the operator's hands were in an are of ribs,
this backward bending would be enough to prform effetive rib rising.
J96
o . . The pressure on the oprator' s fngers ad hel of te hands is equaiz by
altering the pressure on thes structures, resulting in a slight rotation of
the patient' s boy to the right or left.
o . . Further balance between the hands ad the patient' s back is adjusted by
pushing or pulling one fore away or toward the oprator' s boy until
the pressure on the two hands is about equal.
0 When pressures are balanced, the hands remain gripping the EM until
there is a sns of relaxation (usually about 690 seonds).
o . . Re-gripping the EM should revel less resistance of the tissues indicating
that there has been a favorable respnse to the tretment.
This is a description of the soft tissue tehniue called the "ileus prevention
tretment. " This technique has been proven in the clinical arena, preventing
and treting pstoprative ileus.
L. ABDOMAL COLLATERAL GANGLIA:
There are three main sympathetic
collateral ganglia in the abdominal
are; thes are the celiac, the
suprior mesnteric, and the inferior
mesnteric ganglia. Thes ganglia
are loated in the immediate
preortic are and psterior to an
imaginary line drawn from the
xiphoid proess to the umbilicus.
) CEUAC
SUPERIOR
MESENTERIC
INFERIOR
MESENTERIC
The celiac ganglion is usually separated into a right and a lef ganglion.
Functionally the celiac ganglion innerates the uppr GI tract (stomach,
duoenum, liver, gallbladder, pancres and spleen). The suprior mesnteric
ganglion is loated around the base of the suprior mesenteric artery and
innerates the entire small intestine below the duodenum, the right side of the
colon, and als the kdneys, adrenals and the gonads. The inferior mesnteric
ganglion, loate around the bas of the inferior mesenteric artery, supplies the
lef colon and the plvic organs (except for the gonads) .
I99
DIAGNOSIS OF FACIITATION OF AN ABDOMAL COLLATEAL
GANGLION:
o . . The extended fngers of both hands are placed over the midline of the
abdomen betwen the xiphoid proess and the umbilicus
o . . The longer fngers are bent slightly to prouce fngers of equal length and
therefore fngers that will make equal depth of pnetration when pressure
is applie
o . . Objetive snstion of a rapid incre in residence as pressure is direted
by extended fngers applied against the abdominal wall and diretly over
the ganglion
o . . Subjective complaint of increased tenderess with mild t moerate
pressure
o . . Positive respnss to questioning of the patient regarding signs and
symptoms related to the organ or organs innervated by the tender
ganglion
GANGLION IITION TEATMT TECHIQUE:
o . . The extended fngers of both hands are place over the midline of the
abdomen and over the tender involved (facilitated) ganglion
o . . The longer fngers are bent slightly to prouce fngers of equal length and
therefore fngers that will make equal depth of pnetration when pressure
is applied
o . . The patient takes a half-breth in against the operator' s fnger resistence and
holds it a long a pssible
o . . With exhalation, the oprator follows the tissues in until a new pint of
resistence is met; the brething cycle is repated
o . . Posterior pressure is applied and incresed to a pint where the resistance is
evident and the pressure is tolerable to the patient
o . . This pressure is held until the relaxation of resistance is exprienced by the
physician or the pressure has ben maintained for about 90 seonds.
o . . Rehek diagnostic pressure over the ganglion should indicate signifcant
reduction in subjetive complaint and a palpable reduction in tissue
resistance
D. CHAPAN' S REFEXE: DIAGNOSIS
Chapman' s refexes were reorded by Owen in a bok entitled Chama
R: Owen's Endorine Intt. The pints sem better related to
the sympathetic system than t the endorine system. Chapman chart anterior
and psterior myofascial pints where tenderess to mild to moerate pressure
was related to organ dysfunction in a predictable organ. (Se charts on pages
232 and 233). Like any diagnostic system, positive fndings in this non
invasive system of diagnosis must be corelated and interreted with other
ZUU
historical and physical fndings of visceral dysfnction. Their presnce should
als b correlated with other fndings of sympathetic hypractivity. Since the
anterior pints are more snsitive and more spred out than psterior pints,
they are usually us for diagnosis and the psterior pints are used for
tretment. A tender anterior Chapman pint indicates a pssible organ
dysfnction requirng further history and physical evaluation. The anterior
pints are als used to evaluate the success of tretment of that organ
dysfunction or dis.
Diagnostically, Chapman' s refex pints should be sught prior to any
maipUlative tretment which might moif their presence. Most physicians us
the anterior Chapman pints for an aid to diagnosis of systemic disses but do
not us the original Chapman tretment techniques.
CHAPAN' S REFEXE: TRATMT
In the original Chapman metho,
3
afer treting plvic somatic dysfunction, the
psterior pints were treted frst using a circular type of sof tissue
manipulation. The anterior pints were only used for tretment if the psterior
tretment was unsuccessful. Some physicians proposed that the tretment of all
pints related to the sme viscerl system be utilized to enhance homeostatic
function of that system.
Using the original tretment metho, psterior Chapman' s pints were treted
by prforming circular soft tissue tretment over the tender psterior pint for
20 t 30 sonds. The anterior Chapman' s points are usually K tender to treat
with this sf tissue proure. The anterior tibial bands (relating to the colon)
are an exception to this. Thes pints are very susceptible to circular sof tissue
or rpid mechanica pressure to prouce refex autonomic normaliztion in the
colon for such syndromes as irritable bowel syndrome, post-viral diarrhe and
ulcerative colitis.
Posterior myofascial pints by Chapman were treted with a circular sf tissue
tehnique to prouce refex changes in the viscera and improve organ fnction.
This is effetive, but the paraspinal sof tissue used by most ostepathic
physicians during their manipulative management of a patient prouces similar
results and could be directed to the ares of somatic change. Charts of
Chapman' s refexes are available through the Department of Ostepathic Thery
and Methos at the Kirksville College of Osteopathic Medicine.
E. 1 CEVICAL GANGLIA:
The cerical sympathetic ganglia are not in the thoracolumbar outfow and they
certainly do not ft into the rib raising mechanisms; but they are imprtant in
sympathetic respnses in the boy, espcially the heart and structures of the
ZUI
hed (sinuss) and neck. Eight original cerical paraspinal ganglia have
OC t form 2 or 3 cerical ganglia (the superior, middle, and smetimes
the inferior). They would be just like any other paraspinal ganglia except that
the cell bies for thes cerical ganglia are loated at spinal levels TI-4.
The inferior cerical ganglion lies on the
ventral surface of the head of the frst rib
and is frequently fuse with the frst
thoracic ganglion to form the stellate
ganglion. It sres C7, C8, and TI (and
smetimes C6). The middle cerical
ganglion lies approximately at the level of
the C6 vertebra ad has connections with
C5 and C6 (and sometimes C4 and C7).
The suprior cerical ganglion is a long
ganglion that lies anterior to the trnsverse
proesss of C2, C3, and C4 and sends
sympathetic fbers to cerical nerves CI-4.
Ech of the three cerical ganglia sends a
cardiac nere to one of the cardiac
plexuses.
"
Suprior Ganglion
\iddle Crc
Gaglion
- ..nl nnr Crc
Gaglion
Subavia Aer
The fascias around these ganglia are closely related to the cervical joints and the
fasial planes of the neck. The cervical ganglia and their activity c be
compromise by somatic dysfunction in the cerical joints or by abnormal
tensions in the cervical fascias. Sinusitis, e or eye dysfunctions, cardiac
tachyarhythmias, and other cardiac dysfunctions may be altered by freing
cervical pathways and treting cerical joint somatic dysfunctions. This is
espcially true in the CI-4 and the cervicothoracic junction ares.
M. TEATMT FOR LYMHATIC SYSTEM DYSFUNCTION:
A. BASICS: Goals of Treatment and General Manipulative Treatment
Plan:
o . . To promote the fre fow of lymph through its lymphatic vessels and fascial
pathways. Thes pathways extend from interstitial tissue spaces t the
venous circulation in the upper chest via the right and lef lymphatic
ducts.
o . . To improve function of the abdominal diaphragm, the extrinsic pump for
the lymphatic system.
o . . To reduce sympathetic outfow.
ZUZ
o . . The cericothoracic diaphragm is a common pathway in the cours of
lymph drainage from ay place in the boy. For tis ren, te
thoracic inlet is diagnosd for fascial rotational preference and treted as
indicate.
o . . Tensions in fascial planes and the other regional myofasial diaphrgms
loated at the junctions of structural change als hinder the fow of
lymph. For this reson, the other thre fascial and muscular diaphragms
may be diagnosed and treted as indicated (cranioerical, abdominal
and plvic).
The paraspinal musculature at the thoracolumbar junction is relaxed by
sf tissue, stretching, and/or myofascial tretments. The abdominal
diaphragm is then reome.
The plvic diaphragm works synchronously and passively with the
abdominal diaphragm to prouce optimal pressure gradients betwen the
thoracic and abdominal cavities.
o . . Lymphatic pump techniques are used to encourage lymphatic fow through
the pathways
o . . Rib raising in ares of major venous and lymphatic vessels is often
neessry beaus hyprsympathetic tone will constrict the larger veins
promoting congestion of tissues in that vein' s region of drainage;
hyprsympathetic tone also constricts the larger lymphatic vessls and
restricts the drainage of lymph from their regions.
B. SYMOMS OF FASCIAL DYSFUNCTION:
PSTUAL SYMOMS:
Whenever there is dysfunction or dis, the body' s tissues and systems must
participate in the establishment of a new homeosttic level for body function.
The typ, sverity and site of the stress determines which systems will ned to
compnste the most; the neuromusculoskeletal system is involve in all
dysfunctions and dis proesses.
Postural diagnosis provides an uncomplicated, non-invasive access to the
obvious expression of the function of the entire prson. Structurally, the AP
and lateral cures are affeted by gravity. Lteral cures may develop and are
particularly affeted by inequality of the scral base from such conditons as a
short leg or a scral sher, or from an unlevel cranial base as may ocur with
birth injury or certn smatic dysfunctions in this region. When no cause for
soliosis is found its etiology is termed idiopathic; Osteopathic reognition of
thes pstural causs allows re-classifcation of some previously diagnosed
idiopathic solioss. Rotational curatures are often maintained by regional
ZU3
fasial plane rotations or torsions. It is well known that the emotions may be
mirored in the psture of a prsn. It has ben clinically obsred that pstural
imbalance which initially affets any one of the thre cardinal planes of the
boy will also affet the remaining two boy planes ad the total psture of the
patient.
A " short leg" may result from a congenital developmental defet or it c b
prouced by a leg fracture, by muscle spasm, or by physiologic or
nonphysiologic joint smatic dysfunctions. Sometimes the myofascial
compnstion is s go that a spine apps to be straight even when there is a
very obvious short leg. With time, however, the prsn will develop lateral
soliotic curatures of the spine. Since sidebending motion of the spine is
always accompanied by rotation, these lateral cures are often sd to exhibit
rotosoliosis.
SYSTC CHAGE:
In the supine psition, normally the motion generated by quiet brething should
be obsred "down to the pubic symphysis. " Failure to observe this in a patient
suggests that the diaphrgm is not contracting from a well-domed starting
psition, is contracting p rly, or is demonstrating asymmetrical of contraction
between the right and left hemidiaphragm. Por respirtory function results in a
wide range of congestive symptoms which vary some depending upn which
tissues or system of tissues are congested. Healthy tissue and go function
depnds upn adequate circulation and removal of excessive interstitial fuids
from the tissues and their retur to the venous system and the heart. Venous
and lymphatic drainage depnd on goo abdominal diaphragmatic action and
effetive pressure gradients between the abdominal and thoracic cavities.
Examples of symptoms and signs from various ares of congestion are listed
below:
PEVIS LGS BE (CS)
hemorrhoids edema malaise
varicosities night cramps confusion
dizziness
SPIN ( CS) BOW nausea
irritability
Backaches constipation headaches
ZU4
Whenever fasias are subjete t prolonged abnormal physical or chemical
stress tey bome thickened ad reinforce by fbroblastic activity. The large
non-aqueus moleules of the interstitial eema will also stimulate
fbroprolifertion and subsuent fbrosis if it they are not proprly rebsorbed.
Fibrosis shortens the supprting tissues and impairs joint and general boy
motions. The chronic pull of shortened fascias on bony attachments may result
in excessive proliferation of bone called spurs which c be sen on x-ry.
Chronic congestion als results in contractures and/or calcifcation as well as
generlly compromising the intercellular environment of the tissues involved.
OTE SYMOMS AND SIGNS OF FASCIAL DYSFUNCTION:
fascial preference tissue congestion
tissue contracture restricted motion
tenderness shortness of breath
poor circulation myofascial points
limitation of motion trophic skin changes
"not breathing down to the pubes"
costal breathing by a relaxed person
thickened fascias
ticklishness
faulty posture
strains/sprains
muscle cramps
increased lumbar lordosis in the supine relaxed patient
pain on palpation over fascial dysfunction especially near
areas of fascial attachments, at points of fascial
calcification, and where forces of stress converge
general fatigue or malaise with no physical or laboratory
tests indicate disease.
C. DIAGNOSTIC ARAS IDICATIG
RGIONAL TISSUE CONGETION:
Baus of the argement of regional lymphatic and venous drainage
channels, fasial stress is reveed in boy fascial patters, preferences in
regional fascial plane motion and congestive changes in the sof tissues,
espially in spinal ares where there is a change in structure or function from
one region to the next.
Tissue congestion in certain key ares of the body provide a clue t congestive
dysfnction in designated boy regions. Regional congestion c b suspted
by palpating tssue texture changes at thes spcifc sites.
o . . Bgginess or eema in the supraclavicular are indicates evidence of tissue
congestion from p r lymphatic drinage and dysfnction somewhere in
the hed and neck.
ZU
o . . Fullness and tenderess on palpation of the psteror axillary fold indicates
congestion, pr lymphatic drainage, and dysfunction somewhere in the
uppr extremity.
o . . Bgginess in the epigastric are around the xiphoid proess mens
congestion, pr lymphatic drainage, and dysfunction somewhere in the
abdomen.
o . . Bgginess in the inguinal are mens congestion, pr lymphatic drainage,
ad dysfunction smewhere in the lower extremity.
o . . Bgginess in the pplitel space--problem is in the ke, leg, or fot.
o . . Bgginess just anterior to Achilles tendon or thickening of the Achilles
tendon itslf--problem is in the ankle or fot.
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Inhalation, with contraction of the abdominal diaphrgm, prouces negative
intrathorcic pressure and psitive intra-abdominal pressure because of fascial
compartmentaliztion. With diaphragmatic relaxation, intrathoracic pressure is
relatively incre and intra-abdominal pressure is relatively deresd. This
reipro action of the diaphragm prouces pressure gradients betwen the two
cvities of the boy and along with the one-way valves in the veins and large
lymphatic vessls, aids venous retur and provides an extrinsic pump
mehanism for the movement of lymph through the lymphatic vessels, back to
the central circulation and the heart.
ZUb
Diaphrgmatic action is most effcient when the diaphrgm is well domed, its
nere supply via the phrenic nere (C3, 4, 5) is not compromised, and the
lymphatic pathways are unhindered. Fascial restrictions and torsions of fascial
pathways and diaphragms can led to passive congestion and dysfunction of the
lymphatics, the lungs, and other boy systems and tissues.
Clinicl Pinciple: The most common site for relative obstruction t
lymphatic fow, no matter what tissue of the boy is congested, is the
fasial diaphragm at the thoracic inlet, the cericothoracic diaphragm
(Sibson' s fasia).
D. FASCIAL PATTERNS FOR DIAGNOSIS OF REGIONAL FASCIAL
DYSFUNCTION:
Fascias are affected by a prson' s structural and functional stresses even when
that prson believes that he/she is healthy. Gravity is one of the signifcant
natural stressors affecting upright boy posture; and the fascias can be examined
for evidence of compromised homeostatic mechanisms.
r
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. Gordon Zink, D. O. , FAAO, (formerly at the University of Ostepathic
Medicine and Helth Sciences at Des Moines, Iowa) ppularized the us of
fasial diagnosis and tretment. Zink had clinically studied pstural patters
ad obsre that amost 8 of the pple who thought that they were well had
alteratng fasial patters rather than the idel, in which no fasial preference
was palpated. Fascial diretion alterated at aatomical " transition" sites: the
ocipitoatlatal are, the cericothoracic area, the thoracolumbar are, and the
lumboscral are. Alteration of fascial patters is a homeostatic psturl
respns providing compnstion when the ideal cannot be reched.
Alterating patters are termed compnstory fascial patters. Zink then found
that 80% of the "well pple" had a particular compnstory patter in which
there was preference for its rotation t the lef at the ocipitoatlantal are, to the
right at the cericothoracic are, t the lef at the thoracolumbar are and to the
right at the lumboscral are (i. e. leftlrightlleftright or L,R,L,R). Bcaus this
patter was so common he named it the "Common Compenstory Patter
(CCP) " and the clinicians ofen add the words, "of Zink" in recognition of his
contribution.
Most of the 20% remaining who thought they were well also had a compnsted
fasial patter but it was just the oppsite of the Common Compnstory
Patter. The motion preference of the fascias at the four reference ares in
thes subjets was rightlleftlrightlleft (i.e. RlLIRlL). Dr. Zink termed this the
"uncommon compnstory patter.
II
Thos pople who do not have the ideal fascial patter and who are not
homestatically capable of reching one of the compenstory patters are sid to
have an uncompnsted fascial patter. This means that fascial preferences do
not alterate in direction from one reference are to the next. Non-compnste
patters ofen have a traumatic origin.
Rather than list the preferred fascial plane motion at ech are when reording
structural fndings on a physical examination or talking to someone about a
prsn I s fascial patters, the student or physician may write or state something
like one of the following:
o . . the fascial patter is ideal.
o . . the fascial patter is in the common compensatory patter of Zink.
o . . according to the Zink patters, the fascia is out of the CCP at . . . (and then
names the are or ares that do not ft the CCP. )
o . . the uncommon compnstory patter according to Zink is present. .
ZUB
Dr. Zink obsred that if a prsn' s fascias ft the idel patter (equal
preference to sidebending ad rotation right and left in all of thes boy ares or
had one of the compnstory patters identifed as the CCP of L,R,L,R
rotations resptvely or the uncommon compnstory patter of R,L,R,L), they
tolerate stress, smatic dysfunction, illness, and dis better, respnde to
meical cre more predictably, and reovered quicker and more completely than
prsns who had an uncompnsted fascial patter.
E. THE FASCIAL DIAPHAGMS, OTHER PATWAYS, 1
TEATMNTS:
SOF TISSUE DIAGNOSIS OF TE THORACIC IET:
The anatomical thorcic inlet is defned as being outined by the manubrium, the
right and lef frst rib and the frst thoracic vertebra. The functional thoracic
inlet is the clinical thoracic inlet and is defned as being the manubrium with the
angle of Louis, the frst two ribs on ech side and the frst four thoracic
vertebrae. When an osteopathic physician tk about the thoracic inlet he/she
almost always mens this functional thoracic inlet.
This diagram illustrates the thoracic inlet and illustrates the important sttic
landmarks that are used in the diagnosis of fascial rotational preference (torsion)
of the thorcic inlet.
L
Infacavla Sp
/ "
Lf
LRib HNe Ae
1st Rib
Right
R
The thorcic inlet is divided into two parts by the mediastinum with the
remaining spaces (one on ech side of the mediastinum) providing a opning
through which the apx of the right and lef lungs projet upward into the
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cerical are to a height of about 2. 5-3 cm above the clavicles. The apices of
the lungs and the thorcic inlet are covere by Sib son ' s fascia.
Thes thick cuplae are forme from fascias from the longus coli musle dep
in the cricothoracic are and from the fascias on the inner surfaces of the
salenus anticus, medius and psticus muscles laterally. Bth the left ad the
right lymphatic ducts of the boy must pass through this diaphrgm. The
rotational preference of thes fascias should be evaluated mehanically
whenever there is an upst of fuid homeostsis anywhere in the boy.
The thorcic duct (the left lymphatic duct) passes through the cericothoracic
diaphrgm once, travels 3-4 cm up into the neck to a level approximately laterl
to the lef transvers proess of the C7 vertebra, makes a U-tur, and comes
back down through this fascial diaphrgm the sond time into the thorcic cage
where it empties into the venous system at the junction of the left subclavian and
lef interal jugular veins. The rght lymphatic duct also passes through the
thoracic inlet, but only once. ([he site at which the lymphatic ducts empty into
the venous system may vary slightly. They enter into the region of the
brachioephalic vein.)
When palpating the thoracic inlet of a seated patient, the palpating fngers must
b clos enough to the vertebral column at Tl so that they are over the
costovertebral and costotransvers are of the frst rib. Is one side higher than
the other? If one rib hed sems to be elevated in relation to the other, it may
indicte smatic dysfunction of the frst rib. It may also men that the fascias
of the cericothoracic junction (the thoracic inlet) are holding the
cericothoracic region of the boy, sidebent and rotated to the side oppsite the
elevated rib. The frst thoracic vertebra may also exhibit a neutral typ smatic
dysfunction which will be sidebent to the opposite side and rotated to the sme
side. In all of these cases, the rib hed will be tender to the patient on the side
of the palpable "elevated rib hed; " differential diagnosis is then necessry.
If the infraclavicular spaces ne the manubrium are eual in depth, there could
b a elevate rib or the frst thoracic vertebra could be sidebent to the oppsite
side, proucing a secondary elevation of the frst rib hed. If the infraclavicular
space is more shallow on the sme side as the elevated frst rib hed then a
rotational fascial preference of the thoracic inlet is present.
Examples: (x = one direction and y is the opposite direction)
An elevated and tender frst rib on side x and a shallow infrclavicular
space on side x indicates that the fascial patter of the thoracic inlet is
sidebent and rotted y.
Z IU
An elevated and tender frst rib on side x with an equal depth to the
infraclavicular spaces on side x and y, indicates that this is not due to
fasial dysfnction of the thoracic inlet. Thes chages could me an
elevate frst rib on side x orland a neutral typ frst thoracic vertebral
smatic dysfunction with sidebending y.
As with all diagnoss of smatic dysfunction, motion testing is the fnal
and most reliable verifction.
The thoracic inlet of a patient whos general body fascias are in the Common
Compnstory Patter of Zink will have the left frst rib elevated and the right
infraclavicular space will b deepr (the left infrclavicular space ne the
sterum more shallow).
The apx of the coracolavicular angle on the left will be more anterior than on
the right. The following diagrm illustrates the fascial rotational preference of
the thorcic inlet a it would b found in a patient whose total boy fascial
patter agres with the CCP of Zink.
L
Infracavicla Sp
"
Lf Right
Shallo Depr
LkRib HN Ae
1st Rib Eate
,
R
It is imprtant to remember that the fascial patters from all of the four
junctional ares must b diagnos before one kows if any one fasial patter
is in agrement with a compnsted or uncompensted pattr. The following
diagram illustrtes fascial patters that are pulling the inlet into sidebending lef
and rotation left a would be found in a patient who had the other patters
compatible with the uncommon compnstory patter of Zink.
Z JJ
Faa E
Faa Drag -.
o Rib Reilienc C Rib Resistnc
L
MATIVE TREATMT OF THE THORACIC ILET
(CERVICOTORACIC DIAPHAGM:
MULATION OF THE THORACIC ILET WITH IDIECT
MOFASCIAL UNWIDIG TREATT:
o . . The patient may be sitting or supine.
R
o . . The oprator' s hands bridge ech shoulder with the fngers anterior and the
thumbs psterior.
o . . The tissues are followed in their preference for sidebending and rotation
and held in that psition as the patient breths in and out.
o . . The oprator follows the tissue preferences until the tissues approach the
midline again.
MULATION OF THE THORACIC ILET BY TWO-STEP DIECT
TECHIQUE:
o . . The patient is supine.
Z JZ
Step One (corretion of sidebending compnent) :
o . . The oprator' s MP joint of one hand is placed at the psterolateral
cericothoracic junction and will be used a a fulcrum for diret metho
sidebending.
o . . The hed and nek is taken a a unit and sidebent to the restrictive barrier.
o . . The patient' s hed is tured to the oppsite side to lok the cervical spine.
o . . Adjustment of the sgittal plae loizes the forces at the cericothoracic
junction and a thrust is caried through the fulcrum hand toward the
oppsite axilla while the cephalic hand counters the sidebending thrust.
(Rx sidebending compnent)
Step Two (corretion of rotational component):
o . . A flcrum is placed at the cervicothoracic junction (CT) on the oter side
and the hed and nek is rotated to the rotational barrier at the
cericothoracic inlet, without sidebending the neck.
o . . The sgittal plane and sometimes a slight sidebending adjustment is made to
loalize well and a rotational thrust is made through the rotational barier
at the CT junction.
MULATION OF TE TORACIC IET I SITTIG ONE STEP
TECHQUE:
o . . The patient is sitting.
o . . The oprator' s hand on the side of the patient' s somatic dysfunction is
place on the patient' s shoulder.
o . . The oprtor' s fot on the side oppsite the somatic dysfunction is placed
on the table next to the patient and the patient' s a on that side is
drapd over the oprator' s thigh.
o . . The oprtor' s thumb is placed on the spinous proess of TI , the oppsite
hand is place along side the patient' s hed and nek on the oppsite
side, and the patient' s hed is sidebent toward the side of the CT somatic
dysfunction; the hed is extended to loalize and the patient' s boy is
direted into a psterior and sidebent away psition by guidance through
the oprtor' s ke.
o . . When all forces are loalize there is a thrust with the thumb on the Tl
spinous proess away from the side of somatic dysfunction (this reverss
the rotation) and at the sme time, (beaus of psition of the patient' s
nek) sidebending is reversed.
Z I3
DIAGNOSIS TREATT OF TE ABDOMAL DIAPHAGM
DIAGNOSI OF THE TORACOABDOMAL DIAPHAGM (TE
EXTSIC PU FOR THE LYMHATIC SYSTE:
The thorcoabdominal diaphragm at the thoracolumbar region (TL) is the main
extrinsic pump for the lymphatic system. Diaphragmatic dysfunction is
suspted when respiratory effort dos not prouce movement of the abdominal
tissues down to the level of the pubic symphysis. Elements of this dysfunction
c b diagnosed indiretly through the fascias using one fat had in the
epigastric are and the psterior hand at the thoracolumbar junction t examine
for palpatory preference of rotation about an anterior/psterior (AP) axis.
Other elements c be diagnosd by diretly attempting to rotate the
thoracolumbar "tube" right and then left. Once the diagnosis of the myofascial
preference is known, tretment c be effectively applied. Lsting effect from a
redoming manipulative technique to the thoracoabdomina diaphragm often
depnds on removing dysfunction of its attchments and functional extensions.
This includes propr tretment of somatic dysfunction of LI-3, the lower six
ribs, and reduction of lumbar lordosis. The role of quadratus lumborum
dysfunction in inhibiting the effetiveness of these techniques should be note
and it is imprtant to remember that the diaphragm is innerated by the phrenic
nere, C3, 4, 5. It sems prudent to manipulate any somatic dysfunction found
in the lumbars, lower ribs, quadratus lumborum muscle, pelvis, and the
iliopsoas muscle frst.
MANULATIE TREATMT I PREPARATION FOR DIAPHAGM
REDOMG:
If there is incresed tone in the thoracolumbar paraspinal musculature and
incresd lumbar lordosis, utilize any and all methods of soft tissue kneding,
stretch, and/or myofascial tretment to relax the region.
TREATMT FOR QUADRATUS LUORUM SPASM OR LUAR
PARA VERTEBRAL MUSCLE SPASM:
The primary intent of tretment is to stretch the quadratus lumborum and re
establish normal 12th rib motion. The following example of a diret metho
tretment uses respiratory copration of the patient.
o . . The patient is prone; the a on the side of dysfunction is resting by the
side of the hed.
o . . The lower extremities are moved to the edge of the tble away from the
side of myofascial dysfunction.
Z I4
o . . The oprator stands on the side oppsite the dysfnction and contcts the
shaft of the 12th rib with the full length of the thumb on the cephalic
hand, to stabilize the rib.
o . . The plvis is grsp with the fngers of the cudal hand by curling the
fngers around the anterior suprior iliac spine (ASIS).
o . . The oprator' s contacts are sparated by lifting the plvis and carrying the
rib anterior and suprior.
o . . The patient is instructed to inhale as the oprator maintains tension at the
contacts. Musle energy is applied by having the patient pull the ASIS
toward the table against resistance.
o . . Traction/sparation is increased to take up slack when the patient exhales
and relaxes; the sme proedure with respiratory copration is repated.
Stretching of the quadratus lumborum c also be prformed with the patient in
the lateral reumbent psition. With the patient in this psition, the side of
dysfunction is up and there is a pillow under the oppsite side. Increased
stretch c be achieved by dropping the patient' s feet off the side of the table.
Sometimes, spray and stretch of quadratus lumborum myofascial trigger
pint(s), as described by Travell, is necessary in recurrent or recalcitrant
dysfunction.
T. IOPOAS RELEASE TREATT:
Se Jones Strain/Counterstrain indirect metho for treatment applicable to acute
situations. Example: The lower extremities of the supine patient are fexed
exterally rotated, and sidebent until 70% or more of the subjetive tenderess
over the iliacus counterstain pint is relieved. This position is held 90 sonds
and then passively retured to a neutral position. If not acute, diret stretch
using muscle energy and exercise is very approprate.
DIECT (STRETCH MTHOD TREATMT OF TE ABDOMAL
DIAPHAGM:
o . . The patient is supine and the oprator stands at the hed or at the side of
the table
0 The margins of the lower rib cage are gently grspd and pulled and/or
pushed to its rotation restriction and held as the patient deply brethes
in and out
o . . Sometimes a superior or inferior vector is added to the diret rotation of
the thorcic cage so that there is good palpable movement of both sides
of the diaphragm during dep brething, i. e. both leves of the
diaphragm are moving well.
Z J
o . . This psition is held for about three big breths so that the fascial
preference is eliminated and the respiratory effort has redomed the
diaphragm.
IDIECT MTOD OF TREATT FOR 1 ABDOMAL
DIGM:
o . . The patient is supine and the oprator stands at the side of the table.
0 . . The oprator' s caudal hand is placed on the abdomen with the fngers
immediately below the xiphoid proess (the anterior attachment of the
abdominal diaphragm); the cephalad hand contacts and bridges the
paraspinal regions from LI-3 (posterior attachment of the abdominal
diaphragm).
o . . The oprator' s caudal hand produces clokwis and counterclokwise
motion in the abdominal fascias to determine direction of fascial
freedom.
o . . The abdominal fascias are held in the direction of freedom with one hand
and the fascias of the paraspinal tissues at the thoracolumbar junction are
held in the oppsite diretion. The tissues are balanced in this psition
until reles is appreciated.
DIAGNOSIS MANIULATIVE TECHIQU OF THE PELVIC
DIAPHAGM:
The plvic diaphragm is diagnosed by pressing extended fngers into the lateral
side of the ischioretal foss; or placing the thumbs into the upper psterolateral
margin of the ischiorectal foss; or through evaluation of the muscles of the
plvic diaphragm during a retal or vaginal examination. The plvic diaphrgm
c b treted through the prineum, through the retum, or through the vagina.
Daily plvic coil or Kegel exercises by the patient at home helps to maintain
plvic tone after a successful manipulative tretment.
ISCHIORECTAL FOSSA TEATMT: (a fascial relese tretment)
o . . The patient is lateral recumbent with the foss to be treted away from the
table; or the patient could be supine. In either of thes psitions, the
patient has the hips and kes fexed 90 degres. The patient could be
prone but in that psition the hips could not be fexed 90 degres.
o . . The oprator stands behind the table or at the fot of the table, identifes the
ishial tuberosity and the cocyx, and then uses the extende fngers to
contact the lateral margin of that ischioretal foss (the interhalangeal
joints are fully extended and the metachalangeal joints slightly
fexed; the wrist is held rigid) .
o . . The oprtor sometimes sits on the table and braces the elbow aginst his/her
own ilium.
Z Ib
o . . The oprator' s cephalic hand may be placed on the patient' s hip for
counterforce.
o . . The fmgertips are gently insertd to compress the fat of the foss as far as
allowe by the fascias and as is tolerated by the patent.
o . . Tension (and diretion of tretment) will be slightly more ]0Sl6N0Iif retal
problems are presnt, more 0l6N0I (but still in the ishioreta foss) if
bladder problems are presnt, and just SR]6N0Iif ovarian and/or broad
ligament congestion is present.
o . . The patient is asked to brethe in and exhale; the fmgers drif more
supriorly as the fngers follow the diaphragm with exhalation; the push
of the plvic diaphragm is resisted when the patient inhales.
ITRAVAGIAL FASCIAL RELEASE:
o . . The muscle and fascia of the pelvic diaphragm and their ares of tension are
identifed by sweping laterally over the plvic wall.
o . . The fngers are spread in the transverse plane of the vagina to hold the
orifce opn
o . . The patient is then asked to cough shaly 2 or 3 times and the fascia and
plvic muscular diaphragm are automatically stretched by contact with
the oprator' s fngers.
o . . The plvic diaphragm is again palpated to evaluate the tretment' s effet on
the tens tissues.
.
ICTAL FASCIAL RELEASE: The principles for stretch of plvic
diaphrgm are similar to those use in the intravaginal tretment but are carie
out through the retum using a single gloved fnger and a go lubricant. The
plvic diaphragm is palpable through the rectal wall and the loation of tension
is mentally recorded. Cough is not used to activate; rather, the fngers press
frmly and steadily without hurting the patient, until relaxation of the plvic
diaphrgm is palpable.
MANIULATION OF THE CRANIAL DIAPHAGM:
Not all physicias are able to utilize cranial diagnosis and tretment; but
condylar deompression and muscle energy to stretch the OA fascia can be
prforme esily by any physician with manipulative sklls.
Diagnosis and crial tretment can be studied by takng spcifc undergrduate
or pstgraduate courss in this feld. An imprtant reference txt is Harold
Magoun' s bok, Ohin the Cal Field. Contact the Sutherland
Crnial Teching Foundation, the American Academy of Ostepathy or the
Cranial Academy for pstgraduate CME courses.
Z I7
- OTI SOF TISSUE TEATTS TO AI I LYHATIC
DRAIAGE
LYATIC PU TECHIQUF:
TE GOAL OF LYATC PU PROCEU:
o . . to accentuate negative intrthorcic pressure
o . . to incres venous and lymphatic retur
o . . to incre homestasis (immune function)
o . . to mobilize fuids
o . . to mobilize thick plugs of mucus (vibrtory tretment)
TREATT WITH USE OF LYHATIC PU:
TORACIC LYHATIC PU TEATNT: This works by
increasing the positive pressure in the chest through direct pressure on the chest
alterating with negative pressure which is increased by the relese of this chest
pressure.
o . . The patient is passively supine throughout the entire tretment with the
hed tured slightly aside t avoid brething in the oprator' s face.
o . . The oprtor stands at the hed of the patient and applies both hands t the
sides of the patient' s chest cage bilaterally (usually in the uppr ribs at
about the mid-clavicular line).
o . . A steady pressure is applied during the patient' s exhalation phase; this is
directed in a functional patter for the ribs to aid in exhalation. A
vibratory compnent may be added during exhalation to assist in moving
sretions.
0 . . The application and rele may be rhythmic at about 90-120 times pr
minute; or the oprator may hold pressure until shortly after the patient
initiates a breth and then suddenly reles the chest pressure (this last
metho is repated with ech exhalation/inhalation of the patient). The
oprtor must be sure that the patient dos not have gum, candy or lose
dentures in the mouth.
IRTANT: If the patient is very short of breth (as in COPD), their
own intrinsic rte of respirtion should not be disturbed. In more vital
patients, this proedure is optimally prformed with a rhythm or while
direting the patient through the exhalation and inhalation prtions of the
cycle.
PEDAL LYHATIC PU (DALYLE): This technique works
through fascial pumps and by the massge of the diaphragm (and indiretly the
lung bass) utilizing the intermittent movement of the abdominal contents up
Z I8
against the diaphragm. This "intermittent motion" aids in incresing the range
of psitivenegative pressure gradients.
o . . The patient is passively supine throughout the tretment
0 The oprator stands at the'patient' s feet and intermittently and rhythmically
applies activating force through the feet at a rate determined by watching
the rection of the patient' s abdomen. A rate of 90-120/min is common.
Dorsifexion of the feet with the oprtor' s had on the plantr surfaces
ad the fmgers over the tos stretches the psterior fasias of the leg and
is primarily directed into the lumbar and lumboscral regions.
Plant fexion of the fet stretches the anterior fascias and is direte
primarily to the thoracic region, ribs, and cerical ares.
PECTORL TRCTION: This works by helping to elevate the frst 6-7 ribs
during inhalation and thereby increasing the negative pressure during that phase
of respiration. Two minutes of pctoris traction treatment is believed t
provide as much assistance to lymphatic fow as fve minutes of thoracic pump
tretment.
0 The patient is supine with knes drawn up and hands on the abdomen.
0 . , The oprator is at the hed of the patient and gently grsps the anterior
aillary fold (torais muscles) with the fngers carefully conforming
t the patient and not gouging.
o . . Gentle traction is applied in a medial, anterior and cephalic diretion and
held for 1-3 minutes while the patient brethes normally or with slight
incres in volume. The grsp is repplied as needed to prmit patient
comfort.
Family members c b taught this metho of moving fuids with
relative sfety compared to some of the other techniques described in this
stion.
SPLENC PU:
This tehnique is effetive in patients with systemic infections and anemic
patients with low resistance t infetion. The spleen stores re and white cells
and srens the blo of damaged blo cells.
o . . The patient is supine; the oprator stands on the left side and places his/her
hands oppsite ech other on the lower lef rib cage.
o . . Gentle alterate compression and rele is applied until tissues relese.
The amount of pressure depnds upn the patient' s condition and the
judgement of the physician, A void in cases with fiable splenomegaly.
Z I9
LIVER PU:
This proure is prforme much the sme as the splenic pump except it is
applie over the liver. The liver has a rich bed of lymphatc vessls. Its
deongestion aids in detoxifcation and helps to relieve visceral congestion.
PSTERIOR AXILARY TECHQUE:
The goal is t reduce loal tenderess and induration H the myofascial tissues of
the psterior axillary fold; if the patient is able to sns the warmth that
accompanies go lymph fow, the desire is to tret s that the "warmth"
encompasss the entire arm to the fngers. Concomitant myofasial trigger
pints in the psterior axillary fold may also be addressed with this tehnique.
o . . patient supine and oprator facing the patient
o . . grasp suprior prtion of the psterior axillary fold with thumb anteriorly
and the index, middle and ring fngers psteriorly, both the thumb and
fngers are next to chest wall
0 . . apply stedy, gentle but frm squeeze pressure for 10-15 seonds and
inquire about "snstion of warmth in fngers or arm"
o . . if warmth is snse by the patient, it c b accentuate by having the
patient clench and unclench the fst to accentuate the pripheral muscular
lymphatic pumps.
WWER EXTREMTY FASCIAL PATWAY TEATT:
o . . patient is supine with the tretment leg off the table and kne bent
0 . . the oprator straddles the leg just above the ankle and grasps the patient' s
leg by clasping the hands together just below the knee joint (thumbs are
often rght over the medial and lateral margins of the joint space)
0 . . oprator lens backard applying gentle upward, outward, caudal and
rottional encouragement until the forces are centered (stacked in all
motions) at the femoroacetbular joint, kne and ankle. This tehnique
fres the fascial pathways of the leg, thigh, and hip and improves
lymphatic fow from the lower extremity.
o . . if the patient is able to sns the warmth that accompanies go lymph
fow, it should gradually move to the fot; if the warmth dos not
progress, spifc OM to that site would be benefcial.
Z ZU
VETAL ABDOMAL MULATIVE TECHQU:
ASCENDIG DECEDIG COWN MEC RELEASE:
The accessible parts of the colon are palpated to detet tension incres,
congestion, and/or restriction in the motion of their mesnteries. In thes
tehniques, the bowel is gently tken at right angles toward its mesnteric
attchments and to the extent allowed by its motion barrier. Gentle tension is
then applie to its attachments. The tehnique is activated by having the patient
take a shallow breth and hold it until a breth is need. When the patient has
to brethe again there will be a slight give to the mesentery. This thnique is
repate 2-3 times.
RELEASE OF A EPPE CECUM:
0 the patient is supine and the operator at the patient' s side
0 . . the patient' s knee is slightly bent on the right side to relax the abdominal
musculature over the ceum
o . . the oprator applies the hel of his/her right hand to the right lower
quadrant of the abdomen (RQ) of the abdomen
o . . the oprator attempts to gently lif the cecum from the plvic entrpment
and toward the hepatic fexure of the colon
0 . . the oppsite hand (optimal) may b used for inhibition to the
thoracolumbar junction where cecal sympathetic cell boies of the spinal
cord are loated
This tehnique is a slow maeuver allowing for rele of the ceum
from its entrpment in the plvis. The patient may complain of fllness
and sme pain in the ascending colon a well a the hepatic fexure a
the oprtor' s right hand releses the entrapment and moves the feal
mass and intestinal gas along the ascending colon.
ABDMAL MENTERIC FASCIAL RELEASE:
o . . the patient is supine; the oprator stands on the side of his dominant eye
and facing partially toward the hed of the table
0 stg at the right lower quadrnt (RQ) , the oprtor uss one had on
top of the other to gently move the abdominal wall and the underlying
intestine in the diretion of most ese and holds it until there is a relese.
This sme proedure is repted in the RUQ, the LUQ, and the LLQ, in
that order.
LI FI:
This proure is prforme to relese a liver "entrappd" by the diaphragm; it
fres the liver and aids in the deongestion of the right lung bas and the
Z Z I
suprior prtion of the liver. To vigorous an application or a friable liver are
contraindictions to this produre.
o . . The patient is supine; the oprtor stands on the right side of the patient.
o . . The oprtor' s lef hand is place under the right rib cage about the level
of the 6th, 7th ad 8th ribs psteriorly and the right hand is placed on
the anterior rib cage just suprior t the anterior-inferior margin of the
right rib cge at the mid-clavicular line.
o . . The patient is instructe to inhale deply and follow this with a full
exhalation; the oprator' s hand follows the rib cage down, compressing
over the rib cage as the patient exhales.
0 . . The compression is maintne as the patient is instructed to inhale deeply;
as the rib cage elevates with forced inhalation, the oprator suddenly
reles the compression with the right hand. (The patient must have
his/her mouth opn during this procedure.)
0 .. The proedure is repated 2-3 times
BASIC WCAL SOF TISSUE TREATMTS: kneading, stretching,
massge and wringing of soft tissues.
EFFLEURAGE: moderately light stroking of skin and subcutaneous tissues to
move lymph through their small vessels toward the heart. Treatment always
employs a strokng from dist to proximal.
FASCIAL RELEASE TREATMTS:
o . . Intrinsic Activation: determine direction of rottion of the tissues and then
hold them in that diretion until they relese (indiret metho); follow
tissue balance as dictate by palpation.
o . . Direct Metho Fascial Tretment: move tissues in the diretion of
restriction and hold the fascial plane at that barier. Traction is usually
used as the activator but if this is painful, compression is tred.
PETRISSAGE: (used to bre fascial adhesions)
o . . grasp skin and subcutaneous tissues in the region of the adhesions; lif and
twist them clokis and then counter clokwise
0 . at the resistance barrier in ech diretion, have the patient take a dep
breth and give a deep, explosive cough
(Continued with charts of ventral abdominal, fascial, and lymphatic tretments
on page 227. )
Z Z Z
. TREATMT FOR PARASYMATHETIC NERVOUS SYSTE
DYSFUNCTION:
The parsympathetics often se m to be overloked in osteopathic manipulative
maagement beus the hyprsympathetic and lymphatic dysfnctions sem to
b more clinically evident and demanding. als sems that there have ben
less rech and clinical reprts regading the results of moifying systemic
dis through manipulative infuence upn the parasympathetic system.
Parasympathetic infuence to the boy viscera is supplied by cranial neres III,
VII, IX, and X, ad by the parasympathetic outfow through the plvic
splanchnic neres from S2, 3, and 4. Parasympathetic fbers synaps in the
autonomic ganglia in the hed (ciliary, sphenopalatine, otic, submandibular,
submaxillary) , the cerical ganglia of the uterus, and the myenteric
(Auerbach' s) and submucosl (Meissner' s) plexuses of the GI tract.
The parsympathetic fbers from LIII supply the eye; LIX and L X
supply the carotid boy and carotid sinus. L VII synapses in the
sphenopalatine ganglion to supply the glands in the mucous membranes of the
sinuss, pharynx, Eustachian tubes, and the lacrimal glads. L X also
supplies the GI tract distally to the transverse or right colon. The plvic
splanchnic neres (S2, 3,4) supply parasympathetic fbers to the left colon and
plvic organs. A more complete chart is found on pages 192 and 193.
A. TREATMT THOUGH THE SPHENOPALATIE GANGLION:
The sphenopalatine ganglion is loated in the sphenopalatine foss of the skull.
It hangs from the maxillary division of the trigeminal nerve and cannot b
reched directly by the palpating fnger. It may be reched indiretly, through
the opn mouth of the patient by infuencing the fascias of the pterygopalatine
muscles. Thes fascias then manipulate the sphenopalatine (the pterygopalatine)
ganglion. Parasympathetic fbers reach this ganglion from the greater ptrosl
nere, a branch from the geniculate ganglion of the VII cranial nere.
o . . Purs: Tretment encourages establishment of a more normal cellular
rtio betwen the goblet and the ciliated columnar epithelial cells in the
nasl and sinus epithelium. Parasympathetic impulses reduce the goblet
cells and incre the proprtion of ciliated columnar cells to thick
mucus proucing goblet cells. Parasympathetic activity is a primary
infuence in the prouction of a thin saliva-like nasl seretions.
o . . The oprtor passes a cotted fnger over the molars of the upper jaw on one
side, then lateral and psterior to the maxillary rdge.
o . . Frm there the fnger is moved cephalad over the pterygoid plates (ust
psterior to the maxillary ridge) to the extent permitted by the buccal
mucos in the mouth.
Z Z 3
o . . The patient is then asked to no toward the palpating fnger. Two or thre
reptitions on ech side of the mouth will provide an adequat tretment
by indiretly applying pressure on the ganglion through the fascias of the
pterygoid muscles.
o . . Effetive tretment is signaled by unilateral "tering of the eye on the side
of tretment" prouced by effetive stimulation of the lacrimal glad
which shares the sme parasympathetic nere supply.
B. TEATMT TOUGH VAGUS NVE IFLUCE:
o . . Purs: t balance parasympathetic infuence t viscera of the nek, he,
lungs, kdneys, and the glands and OI tract (excluding the left colon).
o . . Sof tissue, condylar deompression, and manipulation of spifc somatic
dysfunction of the ocipitomastoid, OA, AA, and C2 joints will beneft
parasympathetic infuence through CN X.
o . . The vagus nere may pssibly be infuenced by inhibitory pressure over the
celiac and suprior mesenteric collateral ganglia.
C. TREATMT THOUGH PELVIC SPLACHIC IFLUCE:
o . . Purs: to balance parasympathetic infuence to the viscera (lef colon ad
plvic ares).
o . . Diret inhibition to the inferior mesenteric ganglia infuences
parasympathetic supply to the left colon and pelvis.
o . . With the patient prone, the oprator ca place one hand over the scrum
and enforce its application with the other had. Encouragement of the
motion of the scrum with respiration or the enhacement of the
cranioscral motion will help to balace scral splanchnic outut.
(Technique: Roking the scrum)
o . . With the patient supine, the oprator c place one hand under the scrum
with the fngers direted cephalad and the scral boy resting in the palm
of the oprator. The oprator senses the preference indicated by the
cranioscral motion and follows this motion. Sometimes the oprator's
cephalad hand and fore ae placed across the two ASIS s they c
be pulled toward approximation, to encourage separation of the
scroiliac joints and improve the reliztion and action of the
cranioscral impuls.
o . . Tretment of scral and innominate somatic dysfunction is also imprtant.
It is espially imprtnt to remove any non-physiologic scrl sher or
suprior innominate sher if present.
V. TEATT OF TE SOMATIC SYSTEM:
Spinal somatic dysfunction is espcially importnt in the Tl -L2 are. This is
true because dysfunction here can directly infuence the cord segments
ZZ4
containing the primary sympathetic cell bodies by establishing facilitation of
thos divisions. It should be recognized that if there is a facilitated sgment,
smatic dysfunction anywhere may prouce impulss that will caus that distant
sgment t fre. In general, the rotational compnent of the smatic dysfunction
related t viserl dysfunction will usually be toward the sme side a the organ,
espially if that organ is paire. If there is a non-neutral sgmental smatic
dysfnction in an are it is more likely to infuence or be connecte with
dysfunction of a organ conneted to the sympathetic inneration at that cord
level.
Tretment is designed to remove the somatic dysfunction and is based mainly
upn the problem, the condition of the patient, and the skill of the physician. It
must b stated that, clinically, high veloity, low amplitude methos of
activation (HVLA) are often unsuccessful, especially when palpation of the
paraspinal tissues has a "rubbery" texture.
VI. SUM Y:
In most viscerosomatic refexes, treatment of the visceral compnent with
medications, diet, surgery, or some other modality is utilized if the structural
compnent warts that level of interention. Tretment of the soma in a
viserosmatic refex arc is often helpful in breaking this refex cycle and is
benefcial for the functional component. Reduction of stressors at physical,
mental, spiritual, and environmental levels (etc. ) is a great beneft as well,
regardless of whether the primary problem is visceral or somatic.
In designing a manipulative approach in a patient with a facilitated segment,
strongly consider removing this "neurologic lens" prior to instituting any other
ostepathic manipulative tretment or introucing any other stressor. Reall
that any ostepathic manipulative tretment will initially rais sympathetic tone
slightly but will be followed by a clinically more important gradual, prolonged
deline. The degree of rise will depend upon the amount of neurologic input.
For this reson slet the propr technique for the patient' s condition.
Remember that high veloity, low amplitude techniques will often be ineffective
in removing somatic dysfunction that is secondary to visceral dysfunction and an
alterative activating force must then be chosen.
Z Z
RFCF:
1 . Pattersn MM: Moel mehanism for spinal segmental facilitation. JAOA
Sept 1976; 76: 121-131 .
ad Pattersn MM: The refex connetion: History of a middleman.
OhAnn Sept 1976; 357-367.
and Pattersn MM: Luis Bums memorial lecture 1980: The spinal cord-
Active proessr but not passive transmitter. JAOA Nov 1980; 80(3):
210-216.
2. Herrmann, Eward; The D. Ot 65; 163- 16
3. Owens C An Endorine InteIretation of Chapma's R. Carmel CA,
1963.
4. Kirksville College of Osteopathic Medicine; Department of Osteopathic
Theory and Methos; 80 West Jefferson Street, Kirksville, Missouri
63501
5. Simons D. O. , Travell JO: Myofascial origins of low back pain: Part 2.
Torso muscles. Postgraduate Medicine February 1983; 73(2): 85-89.
Z Z b
N
N
TABLE: VENR ABDMINA, FASCIA RELEASE; LYHATIC PUS VISCER TREATNTS P

TECHIQUE PHYSIOLOIC GOA ATTED INDICATIONS CONRINDI CAT IONS
V ADMINA B1
Liver Flip free diaphrag; decreased diaphragm motion; friable, enlarged liver
I
(p 221) milk right lung base rales in right lower lobe
Celiac Ganglion
Tension Release calm sympathetics TS-9 upper GI dysfunction aortic aneurysm
(pp 199-200) palpable subxiphoid tension open surgical wound
Superior Mesenteric calm sympathetics T10-l1 dysfunction of sm intestines aortic aneurysm
Ganglion Release below duodenum, right colon, open surgical wound
(pp 199-200) upper GU; palpable tension
midway between xiphoid and
umbilicus
Inferior Mesenteric calm sympathetics T12-L2 lower GI/pelvic dysfunction aortic aneurysm
Ganglion Release palpable tension just above open surgical wound
(pp 199-200) the umbilicus
Cecal Release improve bowel function complaints of constipation appendiceal inflamation
(p 221) (mechanical release) or RQ pain of mechanical open surgical wound
etiology; visceroptosis
Mesenteric Colon Release
(ASCending/Descending) improve bowel function complaints of constipation open surgical wound
(p 221) (mechanical release) of mechanical etiology colitis
Mesenteric Small improve bowel function abdominal cramping and/or open surgical wound
Intestinal Release (mechanical release) tenderness; altered stool
(p 221) texture
(continued)
N
h
0
TABLE: VENTR ABDMINA, FASCIA REEASE; LYMHATIC PUMS AD VISCERA TREATNTS continued
TECHIQUE PHYSIOLIC GA ATEMTED INDICATIONS CONRAINDI CAT I ONS
VER ABDOMINA OOD1+
Abdominal Fascial to decrease intra-abdominal abdominal tenderness; hernia open surgical wound
Release (p 221) pressure; improve bowel
function (mechanical)
Splenic Pump (p 219) improve imune function infection, fever enlarged spleen,
mononucleosis
Liver Pump (p 220) detoxification; passive hepatomegaly, friable liver
mobilize lymph epigastric lymphatic congest.
chronic toxic conditions
(Ischiorectal Fossa) improve pelvic diaphrag bloated feeling; hernia; perineal abscess
|
(pp 216-217) mobility; decongestion; re- lower extremity varicosities (patient incontinence)
duce intra-abdominal press.
FASCIA TREATMNTS:
Rib Raising improve lymphatic/venous visceral dysfunction; region of spinal fracture
(pp 195-198) return and imune function; respiration not extending to region of spinal surgery
calm sympathetic hyper- pubic symphysis; tight region of rib fracture(s)
activity; improve thoraco- paraspinal muscles; fever; (pleurisy)
abdominopelvic pump lymphatic congestion
Redoming Thoracic improve lymphatic/venous respiration not extending to tubes, incisions, etc.
Diaphragm return and imune function pubic symphysis; lymphatic
(pp 215-216) congestion (anywhere)
(continued)
b
b
W
TABLE: VENR ABDOMINA, FASCIAL RELEASE; LYMHATIC PUS VISCER TREATMNTS (continued) L
TECHIQUE PHYSIOLOIC GOA ATEMTED INDICATIONS CONRINDICATIONS
FASCIA TREATNTS OOD1+
Intravaginal/Intrarectal improve pelvic diaphragm spasm of pelvic floor on rectal or anal abscess
Fascial Release motion; decongestion; vaginal and/or rectal exam; rectal or anal malignancy
(pp 216-217) decrease pelvic floor vaginitis, prostatic spasm;
spasm if poor results with
ischiorectal fossa treatment
LYMHATICS/LYH PUMS:
Liver Pump (see section passive hepatomegaly;
"" of this table) detoxification; epigastric lymphatic friable liver
(p 220) mobilize lymphatic fluid congestion
rib fracture;
Lymphatic Pump (thoracic accentuate negative intra- rales and rhonchi; congestion too severe;
classic and rhythmic) thoracic pressure; productive cough; lymphatic incisions, subclavian
(p 218) increase lymphatic return congestion; fever, infection lines etc. COPD unless H
only at respiratory rate.
Lymphatic Pump: thoracic same as above but uses same; used in hopes of same; (COPD patients only
classic with vibratory vibratory component during loosening plugs of mucus at intrinsic respiratory
modification (p 218) pressure to loosen mucus rate)
Lymphatic Pump: thoracic same as above; but during same as above loose dentures, gum,
classic with accentu- patient's inhalation, there medication etc. in mouth
ation of negative is sudden release of
phase (p 218) thoracic pressure
Pedal lymphatic Pump accentuate negative intra- may be able to use when venous thrombosis;
(pp 218-219) abdominal pressure; thoracic pump can not; lymph lower extremity problems;
increase lymphatic return congestion; fever; infection abd. surgery (post-op)
(continued)

L
C
TABLE: VN ABDMINA, FASCIA REEASE; LYMHATIC PUS AND VISCER TREATS (continued) L
TECHIQU PHYSIOLIC GA ATTED INDICATIONS CONIND I CATIONS
LYHATIC/PUS OOD1+
Lymphatic Pump (seated) same as pedal pump same as pedal pump unable to sit
l
congestion (anywhere)
Pectoral Traction accentuate negative intra- (can be taught to tubes, lines, incisions
(p 219) abdominal pressure; in- a family member); lymphatic on the chest
crease lymphatic/venous congestion; fever; infection
return
Posterior Axillary Fold increase lymph drainage shoulder dysfunction; hand excessive ticklishness
(p 220) from upper extremity; calm and arm paresthesias; cool
sympathetics T2-6; H for and clammy hand
some myofascial points
Breast "Drainage" decrease lymphatic Fibrocystic breasts; post- mastitis;
congestion of breast partum breast engorgement; malignancy in the
breast tenderness breast
SPECIA CINICA (OTHER)
surgical wound or
Fascial Release: cough break superficial and deep scar tissue adhesions; incision not completely
activation (p 222) fascial adhesions restricted range of motion healed
Ileus Prevention treat- decrease sympathetic ileus or reduced bowel local infection;
ment: thoracolumbar hypractivity to GI and sounds; prevent ileus from incision;
inhibition (p 198) restore normal bowel funct. recent surgery or planned thoracolumbar fracture
___ -
(continued)
b
L
|
TAB: V ABDMINA, FASCIA RELEASE; LYHATIC PUS AND VISCER TREATS (continued)
TECB I QU
SPECIA CINICA OOD1+
Sacral Inhibition
(p 224)
Sphenopalatine Ganglion
Treatment (pp 223)
Supra-/Infra-Orbital
Treatment (p 28)
Myofascial Spray and
Stretch of Right
Pectoralis Major
(p 57)
Chapman's Reflex
treatment
(pp 200-201, 232-233)
PHYSIOLIC GA ATETED
improve parasympathetic
activity in left colon;
decongest uterus; calm
hyper-parasympathetic
activity; calm visceral
afferents from left colon;
reduce pain from cervical
dilation (in labor)
thin mucosal secretion
via parasympathetic
influence
decrease sensitivity of
visceral afferent receptors
from mucous membranes of
the head area
decrease input to SA node
from somatovisceral aff.
to decrease supraven
tricular tachyarrhythmias
decrease sympathetic tone
produced by afferent
visceral bombardment from
soma to associated
visceral tissues
INDICATIONS
Dysmenorrhea; make patient
more comfortable in second
and third stage of labor;
Diarrhea; (constipation)
thick nasal secretions;
nasal-lacrimal syndrome
sinus headache; sinusitis;
tenderness over the
innervation of the supra- or
infra-orbital nerves
supraventricular tachy
arrhythmias not responsive
to usual medications in a
patient with this trigger pt.
history of symptoms of organ
dysfunction; palpable
Chapman myofascial pint;
other physical confirmation
COHINDICTIONS
local infection;
local incisions
trigeminal neuralgia;
patient unable to cooper
ate, i.e. may bite you
neuritis of the supra
and infra-orbital nerves
if unable to rule out
primary cardiac disease
or if have not treated
the cardiac disease
L
CHAPMAN'S REFLEXES: anter|or po|nts
Hebm,
Cn|um~
N
~
"
6I
MddIeL
N Snus
Ph
TonsIs
Tongue
pp F
phagus, BronUus
Tyod, Mdum
UpperLung, Uppr Lmb
_Lower Lung
~~~~
Slom[aodq]
Lver H
Sloma [perslaI
Lver,GaIIBIadder
SpIeen, Pe
Inlbm-
pndb
Inwslne.
prsss
Prwleor
Uo Lgnl

Ogn [N00}
OT&MDpl.
HeTq, FeIIm
AdrenaIs
dn

BIadder
Abdomen
Oar|es
Urelhra
erus
Helum
CIon
232
AII pnare bIaleraI
plwherend
H for rghldor
Ie
CHAPMAN'S REFLEXES: poster|or po|nts
Hehna,
Cnjunma
CEHEBELLUM
MddIe ~~m
NASALSlNUSES
P,Tonqua
nu
,
"
s

CEHEBHUM
Ne
Eus, Brondus,
m
Thyrod
AHMS
UpprLung, dum
[aIso pemoraIs mnor]
Uppr Lmb
NEUHASTHENlA
LLung
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DDEXFOROSTOPAT CMIPUATETCHIQUS
SYSTMCDISEASE
CONTETS
Treatment Plan For The Of Osteopathic Manipulative Treatment m
Systemic Di................................................................. 8
Goals 189
A Diagrmmatic Illustration Of A Plan For OMT ................................. 19
Sympathetic/Parasympathetic Innervation Chart ............................. 19?
Treatment For Sympathetic Nervous System Dysfunction 4
Treatment Goals And General Manipulative Tretment Plans.................... 194
Rib Raising Techniques ........................... 4 ............................ 19
The Ileus Prevention Tretment (Rib Raising, Even For Areas Without
Ribs) ..................................... 198
Abdominal Collateral Ganglia ................................................... 199
Diagnosis ................................................................... ?
Tretment .......................................................... ?
Chapman's Refexes ....................... 4..................... ?
Diagnosis . . . ..... .... .. ............ .. ............................. ........ ..... .... ?
Tretment. . .. ..... ... .. ............. ................................ ...... .. ... .... ?1
Tretment Around Cervical Sympathetic Ganglia ............................... ?1
Treatment Of Lymphatic System Dysfunction Z0Z
General Goals And Tretment Plan ........................................... ??
Symptoms Of Fascial Dysfunction .......................... ?J
Postural Symptoms ............................................ ?J
Systemic Symptoms ........................................... ?4
Other Related Symptoms ................. ?
Anatomical Regions of Congestion ................................ ?
Fascial Patter Diagnosis ....................................... ?7
Fascial And Musculoskeletal Diaphragms ............................. ?
Thoracic Fascial Inlet............................................................ ?9
Diagnosis . . ... ....... ... ......................... ... .... ....... ... ... ..... .. ?9
Tretment. .......................................................... ?1?
Abdominal Diaphragm ................................................... ?14
Diagnosis .......4....................................... .... ?14
Preparation For Redoming ................................... ?14
Treatment. . ....................... .................. ........... ..... .. ... ... ?1
Pelvic Diaphragm ....w.............................. ?1
Diagnosis . . ................................................... ..... ..... .... ?1
Tretment. .................................................. ..... ...... ..... ?1
Cranial Diagnosis And Tretment.............................................. ?17
234
Lymphatic Pumps ....................................................................... ?18
Goals ?18
Tretment. . .......................... .................................. ............ ?18
Thorcic Lymphatic Pump ......................... ?18
Pedal Lymphatic Pump (Dalyrimple) ........................ ?18
Petor Traction ............................... ?19
Splenic Pump .......................................... ?19
Liver Pump .................................. ??
Other Soft Tissue Tretments For Lymphatic Drainage ............... p p ??
Axillary Fold Technique ........................ ??
Lower Extremity Fascial Pathway ............................................. ??
Ventral Abdominal Techniques .......................... ??1
Asending And Descending Colon Mesenteric Reless .......... p ??1
Entrappd Ceum Relese Tehnique .................................. ??1
Abdominal Mesenteric Release ....................... ??1
Liver Flip. . .... ..... ... .................................. .... ............ .. ??1
Basic Soft Tissue Treatments ................................................... ???
Effeurage .......................................... ???
Fascial Relese Tehniques.............................................. ???
Petrissage. . ................ ................................................. ???
Treatment Of Parasympathetic Nervous System Dysfunction ZZJ
Sphenopalatine Ganglion Infuence................................................... ??J
Vagal Nere Infuence Infuence ...................................... ??4
Pelvic Splanchnic Nere Infuence ............................... ??4
Treatment Of Joint Somatic Dysfunction ZZ4
Summar.. . . . . . . . . ............ . ......... . . ... . . ... . . . . . . ....... . .... ...... . .. . . . . . . . . . . . . .... . .. ZZ5
Cbarts LFascial Treatments .............................................................. ZZ7
2UD
THIS PAGE INTENTIONALLY LEFT BLANK
A
Abdomen 150, 151, 174
Abominal
- aeurysm 102
- bloating 104
- distension 97, 104, 109, 1 15-1 16, 1 17,
138, 139
- dysfnction 206
- guarding 86
- pain 104, 109, 1 10, 1 15, 1 16, 1 17,
120, 127, 132, 139, 141
- recurrent pain 11 0
- rigidity 86
- tenderess 227, 228
- wall 151
- surgery 101
Abruptio placentae 152
Abscess 102,228,229
Accidents 153
Accommodation spasm 4
Acetominophen 177
Acetylcholine 59
Ache 127, 164, 188
Achille's tendon 206
Acid secretion 93
Acidosis 95
Action potential 71
Activity level 173
Activity-of-daily-living (ADL) 57, 165
Adhesion 222, 230
- pharyngeal 10, 15
Adipose tissue 184
Adrenal 4, 65, 133, 151, 152, 155, 165,
188, 192, 193, 199
- Chapman's reflex 65 (diagram), 67
- corticoids 152
- fnction 65, 165
- hormones 151, 152, 155
Adrenaline 188
Adrenergic blockade 185
Aging 149, 151
- developmental stages (pediatric) 178-
179
- geriatrics 40
Air hunger 89
Albuminuria 123
Alcohol 78, 153
Aldosterone 62-63 (diagram), 65
Allergic factors 15
- allergen 1
- allergic etiology - EENT 16
- allergic manifestation 1, 24, 166
- antigen 171
- hay fever 48, 85
Altitude changes causing er pain 10, 15
Alveoli 189
- air scs 34 (diagram), 35, 38
- hyperinfation 48
- surfactant 36
Amblyopia 7, 14
Amebiasis 1 10
Amine compounds 1 15
Amoeba 1 10
Anal
- abscess 229
- cancer 229
- digital inhibition 105
- triangle 99
Analgesia 23, 138, 140
Anatomical disturbance 99
Anatomy 79, 107, 1 17, 171
Aemia 1 10, 219
Aneurysm 7, 102, 227
Angina 58, 60, 185
Angiography 59
Angiotensin 62 (diagram)
Angle of Louis 209
Ankylosis 162
Anorexia 176
Anovulation 132
Antacids 1 16
Anterior axillary fold 219
Anterior chest wall syndrome 57-58
Anterior cranial fossa 7
Anterior sacral base 151, 157
Anti-infamtory medication 13 1 , 159,
167
Antibiotic meication 15, 16,23,40,41,
42, 87, 106, 127, 135, 136
Anticholinergic medication 1 16
Antihistamine medication 15, 41
Antispasmotic medication 1 16
Anus 99
Anxiety 6, 1 10, 1 14, 1 16, 173
Aorta 85, 192
- aneurysm 227
Aphrodisiac 132
Appendix 192
Aqua-cize 166
Arm 59,193
Arousal 143
Arrhythmia 50,54,56,57,59,60
(diagram) , 61, 67-71,85, 172,
185
-bradyarrhythmia 59,67,68, 70, 85,
172
- etopic foci 50, 60, 185
-extrasystole 67
-mlignant arrhythmia 69
-paroxysmal atrial tachycardia 67
-paroxysmal ventricular tachycardia 67
- pathogenesis 71
-sick sinus syndrome 56, 72
-sinoatrial block 67
-supraventricular 50, 57 (diagram) , 23 1
-tachyarrhythmia 4, 50, 57 (diagram) ,
67,69,70,202,231
-ventricular 50, 60, 69, 70, 185
Artery/arteriole 50, 125, 149
- blood 89, 150
-carotid 187
-constriction 133
-inferior mesenteric 199
-lef circumfex coronary artery 69
-wall 71
Algia 136
Atis 161, 162, 167
-lower extremity 161
-morng stiffess 164
-spine 161
- se also Rheumatoid arthritis &
Osteoarthritis
- se also under Rheumatology
Articular cartilage 159
Articular mobiliztion 175
Articular surface 161
Ascending colon 1 1 1
- OMT: How to treat 221
Ascites 56, 66, 70, 73
Aspirin 1 1, 140, 177
Asthma 2, 5, 48, 49, 85
-length of hospital stay 49
-OMT 49
Atherosclerosis 50, 56, 71, 184
- pathogenesis 71
Atrial
-action potentials 71
- atrioventricular (A V) node 50, 55, 68
-atrioventricular block 67, 72
-atrioventricular conduction 72
-fbrillation 67
-futter 67
-sinoatrial block 67
Atrophic vagina 144
Atropine 1 16
Attention defcit disorders 172
Axillary folds
- anterior 219
-posterior 164, 206, 220, 230
-OMT 164, 220, 230
Auerbach's plexus 223
Autonomic
-activity 1 1 1,120
- balance 88, 95
- nerve plexi 120
- nervous system 66, 91, 142, 190
- Chart 187-188
-Extrinsic 1 17, 1 18, 121
-Intrinsic 120, 121
-Upper GI 83-85
-response 195
Azotemia 135
B
Backache 79, 128, 139, 204
- Se also Pain -Back
Bacteria 72, 80,95, 1 14, 134, 136, 137,
172
-bacteremia 136
-bacteriology prologue
- Campylobacer pylori 87
- endocarditis 72
-infection 68, 72
- proliferation 10, 25
-prostatitis 134
- secodary infection 3, 24, 25
- toxins 80
Barium GI study 1 10
Baroreceptors 62
Barral , IP 89, 102
Barrel chest 48
Bartholin gland 129
Basement membrane -Multilamination
161
Bed rest 40
Bedside m er 172
Bedwetting 129
Behavior modifcation 77
Belch 100, 1 15
Bell's palsy 7
Bicarbonate 84, 1 16, 1 17
Bile 186
Bile duct 93, 187, 192
Biohemical factor 109, 188, 189
-changes 6
-homeostasis 189
-kinins 24
-lactic acid accumulation 95
- mechanism 109
-rection 33
- str r 1 12
Biofeedback 66
Biological 155
Biological stress 152
Biomehanical dysfnction -Primary 82
-stress/strain 165, 166
- salso Physical stress , Trauma
Birth canal 157
Birth trauma 172, 203
Bladder (Urinary) 124, 126 (diagram) ,
129, 132, 137, 138, 188, 193, 217
- autonomic 126
-capacity 129
- dysfnction 132
- exteral sphincter 126, 133
-hyper-/ hypotonic 126
-incomplete emptying 125, 133, 134,
135
-infetion (Se cystitis)
-interal sphincter 126, 134
-irritation 132
-neurogenic 126 (diagram)
-sphincter 126, 133, 134, 193
-tone 133, 134
-wall 124, 125, 126, 133, 134
Blindness 14
Bloating 109, 141, 228
Blood 149
-cultures 40-41
- flow 55, 60, 91, 95, 1 15, 159, 161,
164, 181, 184
-pressure 54, 62, 64, 70, 124, 125, 133
-hypotension 68
-supply 123
-vessel 187
-volume 155
- Se also Artery, Circulation and specifc
topics
Blush 56
Body fuid shif 66
Body mehanics 123
Body unity iv, 12,93, 142, 152, 163, 175
Bogginess 205
Bone
- erosion 161
- growth 184, 185
-mass 166
- spurs 166
Bowel 165
-altered contractions 1 14
- changes 109, 1 10
- fuency 109
-fnction 227, 228, 230
- gas odor 1 15
-handling 10, 101
-hyperactivity 1 16
-irregular habit 109
-narrowing 1 14
- threshold to distension 1 14
- sounds 101, 230
- Se also GI contraction
Bradyarrhythmia 59,67,68,70,85, 172
Brain 1 12, 183
- s Central nervous system; Nerous
system
Breast
- cancer 230
-congestion 157, 230
- engorgement 157, 230
- examination 158
-hypertrophy 155, 156
-mamry gland 192
-OMT 230
-tenderess 28,230
Breathing 33, 34, 35, 38,43,44, 136,
195,204
-costal 205
-exhalation 33, 43 (diagram) , 198
- ineffective 205, 228
- inhalation 33, 35, 40, 43 (diagram) ,
4, 195, 198, 206
- intermittent positive-pressure brething
41
-rpid 38
- shallow 38
-splinted 4
- Se also Respiration, Chest motion,
Diaphragm
Broad ligament 1 30,217
-Chapman's reflex 125, 130, 232-233
Broncr 23,25,35,36,37,192
- constriction 50
-dilation 41, 50
-gland 187
-muscle/muscle tone 35, 48, 49, 187
-seretions 35
-spasm 48
Bronchitis -Chronic 48
Bronchodilators 40
Brunner's glands 84
Bruxism 8
BUN 135
Bug pain 81
Buring 100
C2 38,60,85
c
-Vagal connection 59, 85
C3- 5 34 (diagram), 35, 81, 124,207,214
Calcifcation 205
Calculus (GU) 123, 125, 134, 137
- calyceal 138
-silent 138
Campylobaeer pylori 87
Cancer 110, 114, 124, 229, 230
-colon 110, 114
-renal 124
Capillaries 149
Carfate 87
Carbon dioxide 117
Cardiac
-arrhythmia (See Arrhythmia,
Bradyarrhythmia,
Tachyarrhythmia)
- cardio-cardiac refex 60, 69, 70, 185
-chronotropic effect 54, 69
- conduction defcit 67
- dis/dysfnction 202, 231
-electrical instability 69
-fnction 57
-inotropic effect 54,69, 183
-inneration 54-55 (diagram)
-irritability 68, 71
-ischemia 185
- lymphostasis 71, 72
- muscle 183
-output 39,48, 57, 62, 66, 88
-pathology 59
-plexus 50, 202
- resuscitation 61
-workload 60, 68
- see also specifc disease or cardiac
condition
- s Myocardial infarction, Congestive
hert failure, Subacute bacterial
endoarditis
Cardio-cardiac reflex 60, 69, 70, 185
Cardiovascular system
- abstract sumries 68-73
- disorders 53-78
- fnction 50
- OMT 50,60,61,66,67,89
- parasympathetics 55
- shock 60 (graph)
Carotid
- artery 187
- body 34 (diagram), 35, 38, 54, 55,
192,223
- plexus 2
- sinus 34 (diagram), 54, 62, 67, 183,
192,223
- sinus massage 67
Carsickness 11
Cartilage 159, 161, 167, 171
- regeneration 161
Catecholamines 69
Cathie, Angus DO 17
Cause/effect 79
Ceum 111,221
-OMT: How to treat - Cecal relese 227
Celiac ganglion 80 (diagram), 90, 92,
107, 112, 165, 192, 199, 224
Cell bodies 225
Cellular level 88 ,98
- dysfnction 79, 95
-nutrition 98
Center of gravity 151
- See also Gravity, Posture, Postural
disorder
Central nervous system 80, 81, 150, 151,
152, 183, 195, 20
Central venous pressure 68, 73
Cephalgia 2,6,7, 14, 16, 17,40,44,85,
93, 104, 139, 204, 231
-occipital 85, 93
- sinus headache 16, 231
Cerebellum 183
Cerebrospinal distribution 81
Cerebrospinal tract 80
Cervical spine 154
-disk disease 2
- joints 202
-lordosis 166, 171
- lymph nodes 172, 174
- sndylosis 2
- strain 155
- sympathetic ganglion 2, 25, 26
(diagram), 50, 54 (diagram), 183,
184, 192, 194, 201, 202 (diagram)
- OMT 67
Cervical vertigo 2
Cerix 129, 132, 139, 188, 189
- ateverted 139
- dilation 231
- environment 144
- ganglion (Uterus) 223
Cericothoracic junction 202, 203, 207,
208, 210, 212, 213
- See also Sibson's fascia, Thoracic inlet
Chain ganglion 25, 194, 195, 202
Chapman's refex 3, 37, 82, 83, 90, 91,
92, 119, 134, 194, 200-201, 232-
233 (diagrams)
- adrenal 65, 77
- diagrams 65, 232-233
- bladder 125
-diagrams 125, 232-233
- broad ligament 125, 130
- diagrams 125, 232-233
- colon 96, 104, 119
- diagram 96, 232-233
- EENT 3, 17, 26
- diagrams 3, 232- 233
- GI 86, 90, 96, 165
- diagrams 90, 96, 232-233
- gonads 125, 130
- diagrams 125, 232- 233
- GU 125, 139
-diagrams 125, 232-233
-heart 37, 59
- diagram 37, 232-233
- kidney 125, 126
-diagrams 125, 232-233
-lung 37
- diagrams 37, 232-233
-OMT: How to treat 92, 104, 201
-prostate 125, 130
- diagrams 125, 232-233
- smll intestine 90, 119
- diagram 90, 232- 233
Charcot-Leyden crstals 48
Chek - Tingling 7
Chemical mediators 188
Chemical stress 205
Chemoreeptor 183
Chest 202
- barrel 48
- ge motion/excursion 38, 44, 48, 49
- compression 61
-incision 230
- pain 40, 44, 57, 58 (diagram)
- pressure, intermittent 102
- volume 156
Children 129, 171-175
- failure to thrive 7
- osteopathic considerations 171- 180
Chills 136, 13. 8
Cholecystectomy 87, 115
- post-cholecystectomy syndrome 87
Cholecytokinin 115
Cholelithiasis 82 (diagram), 110, 115
Cholinergic fbers 59
Chronic bronchitis 48
Chronic disese 123, 159
Chronic obstructive pulmonary disease
(COPO) 39, 48, 218, 229
-GMT 45, 48
ChTonicity 161, 163, 228
Chronotropic effect 54, 69
Ciliary ganglion 4, 223
Ciliary muscle 4, 5 (diagram), 187
Ciliated:goblet cell ratio (See
Goblet:ciliated cell ratio)
Ciliosplnal center 18
Circulation 88, 95, 120, 149, 151, 162,
165, 176, 184, 189, 202, 204,
205, 206
Cistera chyli 85
Clavicle 86
Clidinium 116
Clopping. 41
Cloudy swelling 95
Coccyx 216
Cochlea 183
Codeine 41
Cold (temperature) 8
Colic 82, 100, 172
Colitis 97, 98, 161, 186, 227
Collateral circulation 54, 56, 60, 68, 184
Collateral (sympathetic) ganglion 80, 82,
83 (diagram), 86, 91, 92
(diagrm), 107, 112, 118, 134,
192, 194, 195, 199 (diagram), 200
-diagnosis 200
- OMT: How to treat 20
- se also Celiac ganglion; Superior
mesenteric ganglion; Inferior
mesenteric ganglion
Colon 84, 85, 95, 96, 98, 99, 100, 104,
105, 107, 115, 143, 192, 193,
199,201,221,223,224,227,231
- acending 111,221
- cancer 110, 114
- colitis 97,98, 161, 186,227
Common cold 23-31,31 (chart), 48, 79
- OMT 25,29
Compensatory mechanism 63, 72, 121,
152, 153, 156, 204, 207
- Common compensatory patter 154,
156, 208, 209, 211
- compensatory fascial patter 207
(diagram), 208, 209, 211
- compensatory musculoskeletal problem
57
-uncommon compensator patter 208,
209,211
Complication 93, 139, 144
- post operative 46- 47
Compression 161, 164, 165, 219, 222
Compression fracture 166
Concentration of urine 127
Conception 144
Concussion 11
Conductive hearing defcit 10, 11
Condylar decompression 102, 105, 120,
217
Confsion 204
Congenital defect 204
Congestion 18,27,31,33,36,38,39,
42, 68, 88, 93, 95, 98, 99, 116,
118, 120, 131, 134, 135, 140, 149
(diagram), 150, 151, 155, 157,
162, 164, 186, 189, 203, 204,
205,206 (diagram), 207, 217,
221,228,229,230
- abdominopelvic 99
-congestive symptoms 149,204,206
- loal 24
-lymphatic 6, 8, 12, 40, 105, 116, 118,
120, 140, 149 (diaphragm), 151,
162,228,229,230
- passive 123, 207
-pelvic 105, 131, 186
- i pregnancy 149 (diagram), 155- 156
- terminal lymphatic regional sites 206
(diagram)
- venous 6, 70, 116, 118, 120, 140, 149
(diagram), 151, 152
Congestive hert failure 50, 56, 66, 71,
72,85, 185
- right-sided 48
Conjunctiva
- conjunctivitis 14
- reddening 8, 14
-vascular engorgement 8
Connective tissue 151
-dis 186
- pathway 89
Conservative treatment 165
-see also Rational osteopathic treament
Constipation 45, 93, 97, 98, 104, 105,
109, 114,204,227,231
- incomplete emptying 109
Contacts 13
Contracture 161, 1663, 183, 186, 205
Convulsion 177
Coordination 178
COPD (See Chronic obstructive pulmonary
disease)
Coracoclavicular angle 211
Cord memory 93, 112
Corea 6,7
Coronary
-artery 58, 59, 69
- lef cirumflex coronary artery 69
- artery dis 59, 61, 69
- artery occlusion 69
- blood flow 60
- vascular resistance 69
- vasospasm 54
- see also Myocardial infarction,
Myocardial ischemia
Corpora caveros 130, 193
Cortical infuence 142
Coryz 12
Cost 144
Costal examination 105
Costochondritis 58
Cough 2, 4, 36, 39, 40, 4, 45, 46, 48,
85, 127,229
-activation for OMT 222
-non-productive 45
-paroxysmal 48
- productive 46, 229
-reflex 2, 36
Counslling 139, 144
Counterurret exchange 127, 134
Cowper gland 129
Cramp (muscle) 20, 205
Cramping 81, 104, 105, 139, 188, 227
Cranial
- ba 60, 171 (See also OA, Occiput)
-cranioscral mechanism 140, 144, 154,
156, 224
- "diaphragm" 203
- dural strain/stress 7, 15, 172
- extension mechanics (CR) 48, 140,
157
- lambdoidal suture 120
- mobility 105
-occipitomastoid suture 6, 92, 120
- jugular foramen 84, 92, 105, 120,
150
- ocipitotemporal motion 105
- rhythmic impulse (CRI) 15
- strain patters 8, 15, 172
- se speifc bones; OMT -Cranial
Cranial nere
-dysfnction 7, 8, 9, 10, 172
- I (Olfactory) 7
- III (Oculomotor) 4, 7, 190, 192, 223
- IV (Trohler) 7
- V (Trigeminal) 5, 7, 9, 10, 15, 16,
28, 29
- VI (Abducens) 7
-VII (Facial) 7, 18, 31, 190, 192, 223
- geniculate ganglion 5 (diagram)
- superior salivator nucleus 5
- VIII (Vestibulocochlear) 7
- IX (Glossopharyngel) 7, 10, 15, 56,
190, 192, 223
- X (Vagus) 5, 7, 10, 11, 35, 38, 44,
48, 50, 55, 67, 68, 84, 85, 92, 93,
97, 98, 105, 107, 112, 120, 133,
141, 190, 192, 223
- XI (Spinal accessory) 9
-XII (Hypoglossal) 7
Crawling 171
Crteric muscle 127
Crepitus 162
Crohn's disease 97, 98, 110
Cross-talk 189
Crciate ligament 164
Cnshing pain 188
Cultural stress 137
Cultures 40-41
CV4 technique (See OMT - CV4 technique)
Cyanosis 186
Cystitis 134; 136
Cystosopy 129, 139
- basket extraction 139
D
Dalrymple tque (Pedal pump) 44,
46, 102, 218-219, 229, 230
Defess 15
Debilitated patient 196
Deongestat 23, 25, 135
Decongestion 34, 142, 176, 220, 221,
229, 231
- interstitial tissues 34
-uterus 14
Deformity 161, 164
Degeneration 161
Dehydration 176
Delivery 7, 153, 156-158
- diffcult 7
-labor 156- 157, 231
- pre-delivery care 156
- post-partum period 152, 157
- "blues" 157
- breast engorgement 230
- treatment 157
- uterine inertia 157
Demerol 138
Denervation 69
Dental
- dentures 8, 229
- trauma 7, 8
Depression 110, 116, 131, 139, 157, 162
Dermatome 101, 143
Detoxifcation 42, 45, 163, 166, 220,
228, 229
Developmental
- defect 204
- stages (pediatric) 178- 179
Diabetes mellitus 7, 130
Diagnosis
-abdominal collateral ganglion 20
- acumen - GI 10
- Chapman's reflexes 200-201, 232-233
- diaphragm 214
-fascial patters 207- 212
-pelvic diaphragm 216
- regional tissue congestion 205
- sf tissue 209
- somtic dysfnction 211
- system 20
- Se Somtic clues - Visceral dysfnction
Dialysis 135
Diaphragm 33 (diagram), 35, 81, 85,
10, 124, 127, 128, 130, 150,
151, 152, 156, 202, 203, 204,
20, 207, 214, 216, 218, 221, 227
-attachment 31, 38, 50, 104, 105, 156,
214, 216
- fattened 33 (diagram), 38, 39, 86, 156
-fnction 39, 48, 50, 99, 105, 152,
202, 204
- motion 38, 130
- OMT: How to treat 215-216
- redoming 43
- pump 123 (See also Extrinsic/intrinsic
pump)
- well domed 33 (diagram), 43, 90
(defned), 105, 156, 207
Diarrhe 93, 97, 98, 100, 104, 105, 109,
110, 139, 201, 210, 231
- idiopathic diarrhea 97
- post-viral 210
Diatolic pressure 65 (See also Blood
pressure, Hypertension)
Diet 13, 40, 50, 78, 116, 117, 121, 135,
139, 153, 165, 166, 172, 176, 225
- alcohol 78, 153, 166
- bulk in diet 116, 117
- non-absorbable 117
- chewing gum 8, 229
- citrus fruit 166
- coffee 153, 166
-considerations 13, 78, 166
-cranberr juice 135
- eting habit 153
- fasting state 113
- fat restriction 117
- fat storage 155
- four 166
- fuid intake 101, 102
- fod 190
- food allergy 166
- fod intolerence 10
- lactose/milk 117, 166
- linoleic acid 166
- meal 113, 116, 165
- precipitating pain 109
- sugar 166
- sodium benzate 166
- wheat bran 117
Differential diagnosis v, 11, 87, 88, 190
- cardiac 57
- EENT 7, 9(chart)
- GI 79, 90, 110
- GU 128, 131
- inguinal heria 129, 138
-ureterolithiasis 129, 138
- UTI 134
Diffsion 159, 161, 162
Diffsion gradient 162, 163
Digestion

112
- acids/enzmes 84, 111 (Se also
specifcs)
Digital m ge of prostate 136
Diplopia 14
Dis process 117, 172, 209 (See also
specifcs)
Diziness 2, 8, 11, 204
- differential diagnosis 11
Dorsal hom of spinal cord 24, 188, 189
- lamina V 188
Drainage
- cardiopulmonary system 56
- .colon 105
- decongestion 34, 142, 176, 220, 221,
229, - 231
- EENT 6-8
-GU 123
-lymphatic 6-8, 18, 25, 26, 27, 31, 33,
39, 43, 48, 50, 56, 86, 105, 120,
127, 139, 140, 156, 163, 164,
167, 176, 203, 204, 205, 206
-pathways 162 (See also speifc)
- surgical tubes 101
- thoracic 48
-venous 6-8, 2, 33, 43, 89, 140, 166,
204, 205
Dribbling 136
Drug u 153
Duodenum 84, 107, 192, 199
- duodenal ulcer 86, 110
Dupuytren's contracture 186
Dural strain/stress 7, 15 (See also listings
under Cranial)
Dysarthria 7
Dysmenorrhea 131, 132, 139-142, 231
- osteopathic approach to treatment 139-
142
Dyspareunia 143-144
-OMT 143
Dyspepsia 110
Dyspne 48
Dysuria 129, 134, 136, 137
E
E 5, 8, 9, 11, 12, 23, 174, 202
-abnorml sensation 8, 9, 11, 12
-dysfnction 11, 12, 202
-exteral canal 174
-hearing disorders 8, 9, 10, 12, 15
- conductive 10, 11
-deafess 10, 15
-decreased 11
-diminished 9, 10, 15
-high-pitched sound 9
-low-pitched sound 9, 12
-differential diagnosis 11
-sensineural 11
-middle er fnction 10
-wax plug 2
Ectopic foci -Heart 50, 60, 185
Ectopic pregnancy 152
Edem 4, 10, 13, 36, 38, 71, 73, 80,
105, 116, 150, 155, 162, 186,
20, 205
Edinger-Westphal nucleus 5 (diagram)
Education 144, 165, 166
EENT dysfnction 1-21
-OMT 18 (chart)
Efciency 121
Efeurage 13, 18, 31, 66, 93, 222
Ejaculation 130, 133, 143, 188
-disrder 130
-duct 129
EKG changes 56, 69, 72, 185
-long Q-T interval/syndrome 69, 185
-prolonged P-Q interal 72
-sick sinus syndrome 56, 72
Elavil 116
Electrolytes 127
- balace/imbalance 34, 40, 45, 56, 66,
101, 135
-electrochemical gradients 111
-eletrophysiologic mehanisms 111
- in hypertension 62 (diagram)
Embryologic
-development 171
-epiblastic origin 129
- fetal development/growth 144, 149,
153
-germ theory iv
-Mullerian duct 129
-origin 80, 124, 129
- Wolffan duct 129
Emergency treatment 79
Emotion 172, 181, 185, 189, 190, 204
-disorder 181
-factor 132, 142
-growth 172, 190
-instability 131
- stress 8, 69, 115, 125, 137, 138, 144,
189, 225
Empirical treatment 136
Endocardial
-endocarditis 68, 72
- fbroelastosis 72
-fbrosis 72
Endocrine system 184, 200 (See specifc
organs)
Endolymphatic
- channel/duct 6, 18
- hydrops 6
- pressure 18
Endothelium - Vascular 71
Energy 153
Enuresis 129
Environmental factors 15, 49, 61, 112,
113, 120, 225
-exteral environment 112, 114, 120
-smoking 15, 36, SO, 153
- See also Diet, Cold (temperature)
-interal environment 113
- host factors iv, 10, 15, 24, 69, 106,
113, 135, 177
- intracellular environment 205
-uterine environment 144
Enzymes 80, 84, 111
-cholecytokinin 115
-digestive enzymes 84, 111
- se also specifc enzymes
Eosinophils 48
Epigastric area 86, 206, 214, 227
- diagnosis of abdominal collateral
ganglion 200
- subxiphoid fllness/tension 86, 227
- see also Celiac ganglion
Epiglottis 175
Epiphoria 85
Epithelium
- bronchial 36, 42
- ciliated columnar 16, 23, 29, 223
- hyprplaia 25, 37, 38
- infa tion 24
- pseudostratifed ciliated columnar cells
35
- respirtory 24, 27, 28, 35
- sinus 223
- stratifed squamous 16, 24
Erben's refex 67
Eretile dysfnction 142-143
- erection 130, 142, 188
Erogenous zne 132
Esophagus 192
- esophageal heria 128
Essntial hypertension 55, 61, 70, 125
- blood pressure 54, 62, 64, 70, 124,
125, 133
- labile phase 62
- pathogenesis 64
Estrogen 151, 152, 155, 157
- cream 144
Ethmoid bone 16, 28
- pump 28
Eustachian tube 11, 17, 31, 223
- dysfnction 8, 9, 10, 11, 15
Exathema 176
Excitation 187
Excretion 124, 165
Exercise 13, 50, 140, 141, 164, 165, 166,
171, 215, 216
- Aqua-cize 166
- eye (Richardson) 13-14
- Kegel 216
- knee-chest position 141
- pelvic coil 216
Exophthalmic goiter 4
Expectorant 41
Extraocular muscle
- inneration 7, 14 (See also Cranial
nerves III, IV, VI)
- dysfnction 7
- strabismus 7, 14
- tone 14
Extremities 185, 186
Extrinsic pump 206, 214
Exudate 24, 25, 36
Eye 6, 18, 171, 174, 202, 223
- angle of the anterior chamber 6
- chart 13
- contact 173-174
- entropion/extropion 14
- exercise 13
- failure of lid to follow corea 4
- fatigue/strain 7, 14
- focus 13
- foreign body 13
- glaucom 6, 14, 18, 186
- acute closed angle 14
- chronic open angle 14
- narrow angle 4
- Horer's syndrome 3
- intraoular pressure 4, 14
- lens - innervation 4
- lymphatic drainage 6
- GMT: How to treat 13-14
-pain 8, 9, 14
- pressure 55, 67
- protrusion of eyeball 4
- symptoms 5, 8, 9
- visual disturbances
- blindness 14
- blurred 4, 7, 8, 14
- diminution of perceived light 4, 8
-diplopia 7, 14
- far-sighted/ner-sighted 13
- jumpy print 8
- visual development 178-179
- watery 5
- widening 4
F
Facial anhidrosi& 3
Facilitation 25, 44, 64, 130, 132, 143,
144, 164, 165, 183, 185, 189,
190, 196
- altered rection to stimulus 113-114,
117, 125, 138, 183
- deceased threshold 113, 183, 189, 196
- facilitated segment 3, 18, 26, 27, 31,
36, 37, 38, 4, 48, 50, 60, 64, 67,
80, 82, 83, 8, 88, 90, 91, 93, 95,
97, 101, 102, 107, 118, 130, 133,
141, 144, 164, 165, 167, 189,
190, 194, 195, 225
Failure to thrive 7
Fallopian tube 129, 131
- disorder 144
Falls 140, 153
- ice/roller skating 140
Family history 15, 153
Fasia 120, 123, 164, 171, 194, 195,
205, 207, 210, 219
- anterior/psterior by 219
- aterior cerical 174
- adhesions 230
- diaphragm 209
- pathway 89, 156, 189, 202
- patter 88, 89, 154, 203, 205, 207-212
- Compensate 208, 209, 211
- Ideal 208, 209
- Uncompensted 208, 209, 211
- plane 202, 203
- preference 203, 205
- restriction 207
- symptoms 203-203
- tension 92, 205
- torsion 86, 105149, 151, 204, 207
- treatment 208
- OMT 66, 90, 167, 176, 216, 230
- OMT (fascial release) 101, 102, 222
- OMT (fascial unwinding) 164
- upper GI 89-90
Fatigue 4, 40, 105, 157
Fatty acids 186
Febrile seizure 177
Feal mss 221
Feal movement 111, 113
Ferility 144
Fetus 151, 153
- growth & development 144, 149, 153
Fever 3, 40, 41, 45, 46, 110, 136, 138,
176, 228, 229, 230
- OMT 172
Fibroblastic activity 205
Fibroystic breast disease 230
Fibromyalgia syndrome 167
Fibroproliferation 205
Fibrosis 6, 18, 40, 72, 98, 161, 162, 175,
205
WFight or fightW 83
- se Sympathetic response,
Hypersympathetonia
Finger surgery 15
First rib 209-213
Fitt trimester 152, 153-155
Flan pain 127, 131
Flatulence 97, 104, 109, 114, 115
Flexibility 166
Floating kidney 123, 124
Flu epidemic of 1918 41, 42
Fluid 127, 139, 176, 210
- fuid intake 101, 102
- mobiliztion 140
- retention 70, 125, 131, 151, 152, 155
- volume 64
Fluori-Methane 165 (See Spray &
*etch; Trigger point
Focal point (lens) 4
Fracture 24, 58, 100, 166, 204, 228, 229,
230
- vertebral 100, 166, 228, 230
Frequency (See Urinary frequency)
Friable liver .222, 227, 228, 229
Friction 80
Friction rub 37
Frigidity 132, 143
Frontal bone 16
Frowning 8
Fryette motion 171
Functional
- change 161, 165
- defnition 109
- disorder 85, 109, 123, 142, 207
- obstruction - GI 113
- reaction 117
- retention of salt/water 125
- scoliosis 175
- structure-fnction interrelationship iv,
1, 12, 141 49, 50, 68, 93, 117,
131, 152, 161, 172, 175
Gag refex 175
Gait 57
G
Galbreath technique 17
Gallbladder 87, 93, 98, 116, 187, 199
- cholecystectomy 87, 115
- choleytokinin 115
- cholelithiasis 110, 115
- disorder 86, 87 (diagram), 93, 115
- pain 115
- post-cholecystetomy syndrome 87
- secretions 116
- study IH
Ganglion nodosum 85, 92, 105
Gas 109, 114, 116, 117, 221
- absorption 115
- bowel odor 115
- excessive (GI) 114-115
- fatulence 97, 104, 109, 114, 115
- hydrogen (GI) 114
- lung excretion 115
Gastric acid 24
Gatric ulcer 110
Gastrin 111
Gatritis 165
Gatrocolic reflex 111, 113, 116
Gastrointestinal (GI) tract 116, 161, 192,
199, 224
- bacteria 114
- cancer 229
- Chapman' s reflex (diagrams) 90, 96,
232-233
- contraction 111, 116
- gastrocolic reflex 111
- mass movement 111
- non-propulsive 111
- propulsive/retropulsive 111
- segmentation 114
- slow wave ratio 113
- dysfnction 79, 93 (chart), 165, 195
- fnction 109
- gas (Se Gas)
- glands 85
- greater omentum 81
- haustr 111
- headache 93
- hyperchlorhydria 84, 85
- hypermotility 85
- lesser omentum 80, 81
- lower GI disorders 92, 95-107
- mechanisms 87, 115-116
- motility 98
- OMT 79, 89-93, 95, 101-106
- perfortion 82
- polyps 110
- ulcer 86, 87, 110
- upper GI disorders 79-93
Geniculate ganglion 5 (diagram), 223
Genitoiliopsoatic syndrome 132
Genitourinary (GU) tract
- bladder fnction 126 (diagram)
- Chapman' s refex diagram 125, 232-
233
- disorder/dysfnction 123-147, 217,
227
- genital tissue 193
- genitoreproductive disorder 132, 143
- GYN examination 158
- infection li8
- neurologic fnction 126 (diagram)
- sphincter 188
- treatment 133-144
- (Se also spcifc disorders and
fnctions)
Geriatrics 40
- aging 149, 151
Germ theory iv
Glans penis i 31
Glaucoma 6, 14, 18, 186
- acute closed angle 14
- chronic open angle 14
- narrow angle 4
-OMT study 14
Glomerular fltration rate (GFR) 125,
133, 138, 185
Glomerulonephritis 135, 163
Glycogen
- glycogenolysis 184, 187
- synthesis 187
Gnawing pain 81
Goblet cells 3, 18, 23, 29, 31, 38
- goblet:ciliated cell ratio 23, 25, 29, 35,
38, 42, 223
Gonads 131, 199
- gonadal defciency 144
- gonadal tissue 130
Gravity 142, 149, 203, 207
Gripping pain 188
Groin pain 129, 131
Guarding 86
Gyinastics 140
GYN examination 157
- vaginal examination 100, 216, 229
Gynecologic dysfnction 132
H
H2 blocker medication 87
Habitual factors 61, 149, 153
Haemophilus infuenza 25
Hay fever 48, 85
Head 11, 153, 192, 202, 204, 205
- traum 11, 153
Headache (Se Cephalgia)
Healing process 118
- healing rate 19, 34, 40, 95, 98, 135,
209
Health v, 153, 171
Hering disorders 8, 9, 10, 12, 15
- conductive 10, 11
- defess 15
- dereased 11
- diminshed 9, 10, 15
- high-pitched sound 9
- low-pitched sound 9, 12
- loss 10
- snsineural 11
Hert 149, 150, 156, 173, 187, 192, 201,
204, 206, 222
- block 67, 72
- chronotropic effect 54, 69
- failure (See Congestive hert failure)
- inneration 54-55 (diagrams)
- inotropic effect 54, 69, 183
- muscle 69
- rate (See Bradyarrhythmia,
Tachyarrhythmia)
- rhythm (See Arrhythmia)
Het 40
Heel lif treatment 140, 165
- Se also Short leg syndrome, Postural
disorders
Hematuria 136, 138
Hemidiaphragm 204
Hemodynamics 101
Hemoglobin-oxygen dissociation curve 33
Hemophilus infuenza 15
Hemorrhage 72, 186
Hemorrhagic nerotizing pancreatitis 84
Hemorrhoid 204
Henshaw 46-47
Hepatic fexure 221
Hepatomegaly 56, 73, 227, 228, 229
Hereditary factor 1, 61
Hering-Breuer refex 38
Hera 128 (diagram), 129, 228
Hesitancy (Urinary) 137
Histology 161, 164, 184
History iv, 41, 79, 153, 154, 172-3, 177,
190
- family history 15, 153
- pediatric histor 172-3
- truma history 6, 153, 172
Hoarseness 2, 85
Homeostasis iv, v, 1, 6, 12, 15, 16, 19,
28, 29, 34, 38, 39, 42, 44, 46, 48,
49, 50, 56, 62, 65, 79, 84, 85, 87,
91, 93, 106, 117, 123, 135, 139,
149, 152, 153, 156, 159, 162,
172, 189, 196, 201, 203, 208,
210, 218
- cardiovascular 68
- mechanism 159, 177, 189, 207
Hormones 151, 152, 155, 156, 157, 165
- adrenal 4, 65, 133, 151, 152, 155,
165, 188, 192, 193, 199
- corticoids 152
- fnction 65, 165
- hormones 151, 152, 155
- adrenaline 188
- basis 131
- defciency 144
- influence 115
- mechanism 142
- pineal gland 184
- pituitary 4, 17, 144, 165
- pituitary-ovarian axis 144
- secretion 130
- steroids 165
Homer' s syndrome 3
Hospitaliztion 45, 176
- intensive care unit (lCU) 60
- length of stay 42, 49
- patient 49
Host factor iv, 10, 15, 24, 69, 106, 113,
135, 177
- host defenses . 136, 177
Humidifcation 23
Humoral factors 61
Hydrogen 93, 114, 116
Hydronephrosis 123, 124, 127
Hydrostatic pressure 71
Hyoid bone 15, 17, 31, 61, 174
- OMT 31
Hyperchlorhydria 84, 85
Hyperlordosis (See Lumbar hyperlordosis,
Cervical hyperlordosis)
Hypermotility of the intestines 85
Hyperparasympathetonia 231
Hypersympathetonia 44, 56, 64, 83, 84,
88, 91, 92, 104, 114, 118, 125,
135, 137, 138, 161, 176, 183-188,
194, 195, 198, 201, 203, 223,
228, 230, 231
- facilitation 25, 44, 64, 130, 132, 143,
144, 164, 165, 183, 185, 189,
190, 196
- altered reaction to stimulus 1 13-1 14,
1 17, 125, 138, 1 83
- deceased threshold 1 13, 183, 189,
196
- facilitated segment 3, 18, 26, 27,
31 , 36, 37, 38, 44, 48, 50, 60, 64,
67, 80, 82, 83, 84, 88, 90, 91 , 93,
95, 97, 101, 102, 107, 1 18, 130,
133, 141, 144, 164, 165, 167,
1 89, 190, 194, 195, 225
Hypertension 50, 55, 56, 61 , 64, 70, 1 84
- classifcation 61
- fxed 63
- mechanism diagrams 62, 64
- OMT 62-63
Hyperthyroidism 1 1
Hypogastric plexus 129
Hypoperfsion 95
Hypotension 68, 155
Hypothalamus 52, 69, 1 14
- hypothalamic "tuning" 1 14
Hypothyroidism 1 1
Hypoxia 40, 41 , 48, 161
I
Idiopathic diarrhea 97
Ileus 97, 100, 103, 104, 199, 230
- OMT 103, 198, 230
Iliac fossa 127, 1 31
Iliolumbar ligament 128, 129, 131
- pain patter diagram 128
- strain 128, 129
Iliopsoas tenderpoint 139
- Se Muscle - Iliacus, Psoas, Psoas
syndrome
- Se also OMT -Counterstrain
Iliotibial band 96, 104, 130, 201
- diagram 96
- Se also Chapman' s reflex (Colon,
Broad ligament, Prostate)
Illness 209
Immune system 172, 218, 228
- complex 159, 161 , 162, 163, 165, 166
- deposition 165
- fnction 218, 228
- reaction 163
- response 3, 177
Immuniztion 171
Immunology 1 82
Implantation 144
Impotence 130, 132, 134, 142-143
Incision 101, 102, 227, 228, 230, 231
Incontinence (Urinary) 127, 228
Induration 220
Inertial injury 2, 7
Infant 100, 171-175
Infection 6, 10, 24, 27, 34, 36, 40, 56,
72, 85, 88, 95, 98, 102, 1 10, 123,
127, 132, 134, 135, 144, 163,
172, 176, 177, 1 82, 219, 228,
229, 230, 231
- bacterial 24, 36, 68, 172
- bronchial 36
- EENT 16, 27
- focus 163
- lower respiratory tract 40
- measles 1 82
- nasal 10, 24
- OMT 172
- pharyngeal 6, 10
- predisposition 72, 85, 88
- prodrome 176
- prostate 136-137
- upper respiratory tract 23-31 , 48
- urinary tract 134-135
- viral 10, 24, 36, 41, 42, 172
Inferior cervical ganglion 202
Inferior mesenteric ganglion 92, 97, 104,
107, 1 12, 125, 129, 130, 192,
199, 224
Inferior thoracic outlet (Se Toracic
outlet)
Infertility 132, 144
- fallopian tube disorder 144
- genitoreproductive disorder 132, 143
- impotence 130, 132, 134, 142-143
- OMT 142
- spermatic count 144
- work-up 144
Infltration 80
Inflamtion vi, 14, 24, 36, 37, 72, 84,
98, 1 31 , 132, 134, 137, 163, 188
- EENT 27
- epithelium 24
- eye 14
- inflamtory arthritis 164
- inflamtory cells 137
Influenz 24, 41, 42
- epidemic (1918) 41, 42
- virus 24
Infraclavicular space 210, 21 1
Inguinal are 20
- hera 128 (diagram), 129, 228
Inherent fnctional property 1 83
- mechanism 121
Inhibition 1 87
Inhibition 88, 91 , 1 87
- pressure 42
- rfex 196
Injetion 165
Injury (See trauma)
Innominate somtic dysfnction (See
Somatic dysfnction - Innominate )
Inotropic effect 54, 69, 183
Insomnia 4
Intercellular environment 189
Intercostal
- muscle 39
- neuritis 58
- spaces 92
Interal jugular vein 86
Interstitial
- edema 71 , 205
- fluid 98, 149, 151, 176, 189
- pressure 134
- space 127, 149, 202
Intertransverse spaces 92
Intestinal tract (See Gastrointestinal tract)
Intra-abdominal pressure 127, 128
(diagram), 20, 228
Intracellular environment 205
Intralumenal pressure 1 16, 1 17
Intraocular pressure 4, 14
- Se Eye, Glaucoma
Intrapelvic pressure 128
Intrathoracic pressure 195, 206, 218
Intrinsic activation 222
Irritability 1 31 , 139, 204
Irritable bowel 85
- syndrome 97, 98, 109-122, 186, 201
- Diet 1 17
- medication 1 16-1 17
- OMT 1 17-121
- personality type 1 10
- tretment 1 16-121
Irritation
- bronchial epithelium 36
- intercostal nere 37
Ischemia 56, 84, 1 85, 1 86
- ishemic heart disease 69
Ishial tuberosity 216
Ischioretal fossa 99 (diagram), 10, 130
(diagram), 216; 229
- OMT technique 105, 136, 216-217
(how to tret), 228, 229
- pelvic for 99 (diagram), 128, 130,
134, 136, 143, 229
J
Joint 161
- arthralgia 136
- arthritis 161, 162, 167
- lower extremity 161
- spine 161
- cartilage 159
- damage/deformity 162, 166
- description 161
- destruction 163
- effsion 166
- fnction 164
- minor motions 161
. nutrition 162 (diagram), 164
- range of motion 162
- structure 166
- surface 159, 164
- tenderess 162
- see also Rheumatoid arthritis &
Osteoarthritis
- see also under Rheumatology
Jones' points
- iliopsoas 139
- See OMT - Counterstrain
Jugular foramen 84, 92, 105, 120, 150
- occipitomstoid suture 6, 92, 120
Jugular vein 6
K
Kegel exercise 216
Kidney 42, 55, 62, 65, 70, 123, 124,
126, 127, 133, 134, 138, 165,
1 85, 1 88, 192, 199, 224
- calyceal calculus 138
- damage 1 34
- fnction 65, 124
- glomerlar fltration rate (GFR) 125,
133, 138, 1 85
- glomerulonephritis 135, 163
- in hypertension 63
- infetion 134
- Lloyd' s punch test 127, 134
- nephrosclerosis 63, 64
- polycystic kidney dis 124
- ptosis 123, 124
- uremia 135
- Se also GU tract; Urine
K 24
Keding 214, 222
Kne 20
Kne-chest position 140, 141, 142
(diagram)
Korr, I. M. 1 83
Kyphosis 148, 151 , 155
Ll-2 132, 143
Lbia 127, 142
- pain 127
L
Lbr 156-157, 23 1
Lbratory data 1 10, 173, 205
Labyrinthitis 1 1
Lcrimal gland/ Lcrimation 5 (diagram),
8, 29, 1 87, 192, 223, 224
Lctase 1 17
Lctic acid accumulation 95
Lmbdoidal suture 120
Lmina V 1 88
Lrynx 55, 85
Leare refex patter 1 12
Learg disorder 172
Leg 155, 193, 204, 206, 219
- edem 155
- fracture 204
Lengt of stay 42, 49
- at 49
Levitor orhosis 165
- Se Lordosis, Postural disorders,
Gravity
Librium 1 16
Lifing 127, 128
Ligament 128, 129, 130, 140, 157, 164,
166
- iliolumbar 128 (diagram)
- strain 140
- tension 157
- weakened 151, 152, 155, 164
Ligamentum pectinatum 6
Light stroking of skin 222
Lightheadedness 1 1
Linoleic acid 166
Lipolysis 1 84
Lithotomy position 157
Liver 42, 81 , 98, 107, 123, 165, 166,
1 86, 1 87, 192, 199, 220, 221 ,
222, 227, 228, 229
- Glisson' s capsule 81
- hepatomegaly 56, 73, 227, 228, 229
- OMT (Liver fip) 221-222, 227
- OMT (Liver pump) 45, 86, 166, 167,
220, 228, 229
- portal venous congestion 70
- tenderess 73
Lloyd' s punch test 127, 134
Local environment 1 12, 120, 137, 144,
1 89
- control 1 1 1
- factors 137
- nutrition 164
Long Q-T interal/syndrome 69, 185
Lordosis
- cerical 148, 166
- lumbar 38, 1 15, 148, 151, 166, 171,
214
- byperlordosis 124, 139, 151
- Levitor orthosis 165
- See Posture, Postural disorders, Gravity
Low back pain 127, 132, 136
Low energy 157
Lower extremity dysfnction 206, 228,
229
- edem 155
- fracture 204
- leg 155, 193, 204, 206, 219
Lubrication 143, 144
Lumbar region 219
- See Lordosis
- lumbosacral angle 171
- lumbosacral junction 104, 105, 154,
208, 219
Lung 33, 34 (diagram), 86, 173, 1 89,
192, 207, 209, 210, 218, 224, 227
- ba 218, 221 227
- capacity 48
- hypoperfsion 37, 38
- inneration/reflexes 34 (diagram)
- See Respiratory tract
Lymphatic system 149, 150, 155, 172,
190
- change in pregnancy 151
- congestion 105, 1 16, 1 18, 120, 140,
151 , 162, 228, 229, 230
- E 8
- constriction/dysfnction 150, 223
- obstruction 152
- drainage 3, 18, 25, 26, 27, 31 , 33, 39,
40 (diagram), 43, 50, 56
(diagram), 86, 120, 127, 139,
140, 156, 163, 164, 167, 203,
204, 205, 20
- Colon 105
- EENT 6-8
- Eye 6
- GI 85-86, 89
- GU 127
- Heart 56
- Lungs 56
- Reproductive tract 130-13 1
- Thoracic 48
- duct 27, 56, 86, 202, 210
- Thoracic duct 56, 70, 73, 86, 99,
127, 210
- distension 66, 70, 73
- surgical drainage 163
- effect 18, 31 , 50, 93, 141
- Cardiovascular 68
- GU 134
- element 132, 135
- fow 18, 31 , 34, 50, 70, 71 , 72, 85,
86, 95, 99, 102, 1 17, 120, 127,
1 31 , 1 34, 150, 151, 156, 157,
195, 202, 203, 207, 219
- fow capacity 85
- rate 66
- renal hilar 127
- stasis 71 , 72, 1 31
- fuid 1 89, 229
- goals 164
- Rheumtology 162-163
- nodes 172, 174, 176
- cerical 6, 172, 174
- lymphadenopathy 172
- pathways 27, 28, 85, 88, 152, 164,
207
- production 70
- pump 13, 33, 39, 43, 4, 46, 105,
152, 156
- Extrinsic 120, 150
- retur 66, 124, 196, 218, 228, 229
- vessel 150, 151, 162, 202, 203, 206,
220
Lymphaticovenous communication 70,
71 , 86 (diagram)
- retur 3, 61
Lymphoid inflitration 4
Lymphoplasmaphoresis 163
Lysis of nasopharyngel adhesions 15
Lysozyme 23
M
Malaise 204
Manipulative treatment (Se OMn
Manubrium 105, 209, 210
Mass movement 1 1 1
Massage 222
Mastoid air cells 7
Materal homeostasis 149
Maxillary pain 12
Maxillary sinus 28
- pain 9, 16
- secretions 12
Mayo Clinic 82 (diagram)
Meal 1 13, 1 16, 165
- precipitating pain 109
Measles 1 82
Mehanical
- change 151
- decompensation 156
- 'stress/strain 151, 152, 155, 161, 164
Medial strabismus 7
Mediastinum 61 , 209
Medical treatment 14, 60, 67, 69, 86, 87,
93, 136, 153
- failure 86
- ineffective 40, 71 , 98-99
Medication 1 1 , 41 , 50, 79, 88, 10, 1 16-
1 17, 1 31 , 135, 138, 140, 159,
161 , 163, 165, 167, 1 89, 225, 231
- alcohol 78, 153
- amitriptyline 167
- antacids 1 16
- antibiotic 15, 16, 23, 40, 41, 42, 106,
127, 135, 136
- anticholinergic medication 1 16
- antidepressant medication 1 16, 167
- antihistamine medication 15, 41
- anti-inflamtor 131, 159, 167
- antipyretic 177
- antispasmotic medication 1 16
- antitussive 41
- aspirin 1 1 , 140, 177
- slicylate toxicity 1 1
- Crafate 87
- coeine 41
- concentration 3, 88, 99, 135, 136, 159
- demerol 138
- dextromethorpha 41
- dosage 48, 49
- drg u 153
- estrogen cream 144
- expectorant 41
- Flexeril 167
- H
2
blocker
- homeostasis and 79
- ineffective 231
- morphine 138
- NSADs 1 31 , 140, 165
- OMT and 79, 86, 88, 93
- penicillin iv
- pseudoephedrine 15
- side effect 1 1 , 159, 161, 163, 165
- sulfa compounds 1 15
- sulfamethoxazole 136
- sympathetic blocker 167
- sympathomimetic 41
- tranquilizers 1 16
- trimethoprim 136
Medulla 34, 35
- medullary center 34 (diagram), 196
Megacolon 1 86
Meissner' s plexus 223
Melatonin 1 84
Membrane permeability 159
Memory patter 195
Meniere' s disease 6, 1 1 , 15, 1 8
- OMT 15, 1 8
Meninges 150
Menstration 139, 144
- dysmenorrhea 1 31 , 132, 139-142, 231
- osteopathic approach 139-142
- irregular cycle 144
Mental factor 142
- mental helth 153
- mental need 190
- stress 144, 1 89, 225
Mesentery 80, 86, 89, 98 (diagram), 1 15,
1 16, 120, 221
- attachments 98 (diagram)
- congestion 1 16
- OMT (mesenteric lif, relese, stretch)
89 (how t treat), 93, 102, 107,
1 15, 190, 221 (how t tret), 227
Mesocolon 80
Metabolic
- acidosis 33
- changes 98
- dysfnction 79
Metabolism 95, 124, 151, 159, 163, 177,
190
- metabolites 155
Metallic taste 7
Metastatic dis 28
Metatarsal varus 173
Methane 1 14
Microorganism 177 (See Bacertia, Virus)
Micturition 126 (diagram)
Middle cervical ganglion 202
Middle cranial fossa 7
Middle ear fnction 10
Milk 1 17, 166
Mislignment
- lower extremities 161
- spine 161
- See also Postural disorders
Mitral stenosis 72
Mitral valve prolase 58
Morbidity 19, 54, 56, 69, 72, 184
Morg stiffess 164
Morphine 138
Morality 40, 41, 42, 50, 56, 60 (graph),
61 , 72, 84, 95, 184, 185, 186
Motion testing 154
Motor vehicle accident 7, 153
Mouth 174, 175
Mucolytic expetorant 41
Mucorrhea 1 17
Mucosa
- barrier 87, 93
- defenses 84
- mucous buffer 84
- GI 91
- mucous blanket 35, 36
- bowel 1 16
- irritation/ulceration 24, 27
- mucous membrane
- Defense mechanisms 3
- Driness 3
- Engorgement 5
- GI 84
- mucous gland 187
- Swelling 10, 27
- mucus plug 218, 229
- mucus seretion
- Excessive GI 1 14
- Thick 24, 28, 42
- T 24, 27, 28, 42, 231
- snsitivity 93
- sloughing 24
Mullerian duct 129
Mulleria orbital muscle 4
Multipara 157
Muncie Tehnique 1 5
Muscle
- contraction 1 71
- inhibitory pressure 42
- metabolism 69
- rigidity 1 31
- smooth muscle 138
- of bowel 1 1 1
- spasm 25, 86, 132, 161 , 204
- spindle 183
- strengthening 140 (See also Exercise)
- sympathetic effect on 183
- tone 101
- weakened 151, 152, 155
Musle - Speifc
- abdominal 86, 127, 1 31
- accessory respiration 48
- bronchial 35, 49, 1 87
- cardiac 1 83
- ciliary 4
- cremsteric 127
- digastric TP 9, 12
- erector spinae 42, 127, 171, 198, 199
- extraocular 7, 14
- hip 1 71
- iliacus/iliopsoas 214, 21 5
- Se slso Muscle - Psoas
- intercostal 35, 39, 198
- lateral pterygoid TP 7, 9, 16
- lateral retus 7
- latissimus dorsi 197, 198
- levator palpebrae 4
- longus coli 210
- m ter 1 1
- trigger point 8, 9, 12
- medial pterygoid 1 1 , 12, 17, 1 8, 31
- trigger point 9, 10, 12, 15
- Mulleria orbital 4
- ocipitalis 1 1
- occipitalis TP 8, 9, 12
- orbicularis oculi spasm 8
- orbicularis oculi TP 8, 9, 12
- parapinal 90, 92, 101, 102, 104, 1 31 ,
1 71 , 228
- pectoralis 197, 219
- Pectoralis mjor 4, 57, 23 1
- diagram 57
- Pectoralis minor 198
- pilomotor 1 87
- psoas 124, 128, 132 (diagram)
- OMT 215
- pterygoid 17, 29, 224
- trigger point 8, 9
- Se Musle - Lateral & Medial
pterygoid
- pterygopalatine 223
- quadratus lumborm 90, 124, 198
- OMT 214-215
- rectus abdominus 139
- rotatores 82
- scalene 39, 198, 210
- serratus anterior 198
- splenius cervicis TP 8, 9
- sterocleidmastoid, steral division TP
8, 9, 12
- sterocleidomastoid (Clavicular portion)
1 1
- trigger point 9, 1 1
- tensor veli palatini 12, 17
- trapezius TP 8, 9, 12
Musculoskeletal stress 153
- complaint 154
- dysfnction 109, 151
- See also somatic dysfnction
Myalgia 136
Myasthenia gravis 163
Mydriasis 4, 1 8
Myenteric plexus 223
Myocardial damage 1 85
- infarction 50, 54, 59, 60, 66, 68, 70,
72, 1 84, 1 85
- Anterior wall 59, 68
- Inferior wall 59, 60, 68
- Morbidity 69
- Posterior wall 59, 70
- ischemia 70
- palpatory fmdings 59 (diagram)
- See also under listilgs Angina, Cardiac,
Coronary
Myofascial points 205
- Se under listings Trigger point,
Counterstrain
Myofaial trigger points (See Trigger
point)
Myotome 101
N
Nails - Thickened 186
Narrow angle glaucoma 4
Nasal
- congestion 24
- cycles 24
- discharge 85
- disorder 2, 16, 24
- mucosa 7
- passges 23, 24
- seretions 2, 3, 4, 5, 16, 223
- Thick 4, 16, 23 1
- T 5, 16
- sptal deviation 16, 24
- sinus fnction 16
- turbinates 23
Nasolacrimal syndrome 23 1
Nasopharyngeal
- adhesions 6
- mucosa 5
- nasopharyngitis 15
Natural defences 136
- host factors iv, 10, 15, 24, 69, 106,
1 13, 135, 177
Nause 81 , 85, 104, 138, 139, 204
Nek 192, 202, 205
- pain 5, 59
- Se also listings under Cervical and
OMT
- veins (distended) 73
Nephrosclerosis 63, 64
Nervous system 172
- central nerous system 150, 1 51 , 152,
172, 1 83, 195, 204
- cerebrospinal distribution 81
- spinothalamic tract 80
- endings 80
- fbers
- efferent fbers (sympathetic)
- lumbar sympath. splanchnic 83
- thoracic sympathetic 83
- pathways/plexi 1 1 1
- post-ganglionic fber 83, 129
- pregaglionic fber 125, 129
- ramus communicans 185
- somtic 50, 1 15
- snsory afferent 81 , 1 88, 189,
194
- speed (fast, very fast, slow, very
slow) 195, 196
- visceral afferent 2, 3, 24, 34, 35,
83, 89, 90, 95, 97, 1 1 1 , 1 15, 1 19,
1 26, 143, 1 88, 1 89, 194, 195, 231
- primitive 1 12
- receptors 62, 80, 81 , 183
- segmental 79
- See also Segmental facilitation,
Facilitated segment
- supply 95, 123
- thresholds 1 13 (See also Facilitation)
Nerous system - Specific Nerve
- abducens 7
- buccal (Trigeminal branch) 9
- cardiac 202
- deep petrosal 25
- facial S, 7, 190, 223
- genitofemoral 124
- glossopharyngeal 7, 10, 15, 190, 223
- greater petrosal 2, 5 (diagram), 223
- greater splanchnic 107, 192
- hypoglossal 7
- inferior laryngeal 5
- infraorbital 23 1
- OMT: how to affect 28
- intercostal 35, 37
- least splanchnic 107, 192
- lingual 56
- lumbar splanchnic 107, 192
- occipital 85
- oculomotor 4, 7, 190, 223
- olfactory 7
- pelvic parasympathetic 10
- pelvic splanchnic 84 (diagram), 93, 98,
100, 107, 1 12, 1 19, 126, 129,
133, 141, 190, 193, 223
- OMT: How to affect 224
- phrenic 27, 31 , 35, 46, 81 (diagram),
105, 124, 133, 196, 207, 214
- pterygoid canal 25
- pudendal 100, 106, 126, 127, 133, 142
- sciatic 132
- small petrosal 56
- spinal accessory 9
- splanchnic 80
- superior laryngeal 5
- supraorbital 231
- OMT: How to affet 28
- traum 172
- trigeminal 2 (diagram), 7, 9, 10, IS,
16, 28, 29, 223
- geniculate ganglion 5 (diagram)
- trohler 7
- vagus 2, 5, 7, 10, 1 1 , 35, 38, 44, 48,
50, 55, 67, 68, 84 (diagram), 85,
92, 93, 97, 98, lOS, 107, 1 12,
120, 133, 141, 190, 223
- OMT: How to affet 224
- Se also Vagal afferents, Vagal
connections, Vagal tone; Vagal
hyperactivity
- vestibulocochlear 7
- vidian 2 (diagram), 5 (diagram)
Neural
- control
- bladder 126 (diagram)
- EENT 6-8
- GI extrinisic/intrinsic 1 1 1-1 12
- pUlmonary 34 (diagram)
- element 135
- foramen 166
- fnction 156
- mehanism 142
- symptoms 166
Neuritis 23 1
Neuroanatomy 79
Neurogenic factors 61 , 132
- obstrction 137
"Neurologic lens" 144, 225 (See
Facilitated segment)
Neuromuscular
- splinting 101, 102
- transmission 1 83
- neuromusculoskeletal system 171, 190,
203
Neuronal pool 1 89
Neurophysiology 79
Neurovascular compromise 48
Nerousness 1 16, 1 31
Nerus erigens 56
Neurotic personality type 1 10
Newbor 171-2
Night cramPS 204
Nitrogen 1 14
Notural enuresis 129
Noturia 136, 137
Non-absorbable bulk 1 17
Normoblasts 1 84
Nose 174
- fracture 24
- pain 5, 1 2
- rhinitis IS, 1 6, 3 1 (chart)
- rhinomometry 16
- runny 5
- See also Sinus
Noxious somtic input 161
NSADs 131, 140, 165
Nutrient 93, 95, 161, 167
- concentration 159
- supply 3, 6, 25, 68
Nutrition 88, 95, 120, 141 , 149, 159,
161 , 164, 166, 167, 171
- See also Diet
Nystagmus 7
0
2
exchange 141
OA 154, 208
OA-AA 85, 105
Obstetrical
- cases 28
- patient 149-158
o
- OMT 157-158
Obstructive uropathy 134, 135
Occipital
- bone 6, 84
- compression 8
- headache 85, 93
- level 154
- occipitomastoid suture 6, 92, 120
- jugular foramen 84, 92, lOS, 120,
150
- occipitotemporal motion 105
Occlusal disharmony 8
Occult blood 1 10
Ocular
- oculocardiac refex 55
- oculocerical refex 2
- stroking 1 8
Olfactory apparatus 183
Omentum 80, 81
OMT (Ostepathic ManipUlative
Treatent) 40, 136, 1 89
[ote: Section subdivisions/or OMT
include:
OMT:AUTNOMIC FUNCTION
OMT:GENERAL EFFECT
OMT:GOALS
OMT:MANIPULTIVE
PRESCRITION
OMT:MOBILIZE FUIDS
OMT:RESERCH STUDIES
OMT:REGIONAL
APPLICATION
OMT:SOFTISSUES &
MUSCLES
OMT:SYSTEMIC COMPLAINTS
OMT:TECHNIQUE
DESCRIPTION
OMT: AUTONOMIC FNCTION
- OM: PARASYMPATHTICS 18,
3 1 , 50, 93, 107, 133, 140, 141,
190, 223-224
- to GI tract 92-93, 1 19-120
- Pelvic splanchnic infuence 224
- Se also OMT - Sacral , Sacroiliac,
S2-4
- Sphenopalatine ganglion 16, 17, 18,
3 1 , 49, 223, 224, 231
- Vagal influence 49, 224
- Se a OMT - OA-AA-C2,
Cranial, Occipitomastoid
- OM: SYMPATHTICS 18, 3 1 , 50,
93, 107, 1 18-1 19, 133, 141, 164,
190, 194-202
- Cerical ganglion 67
- Collateral ganglion (Ventral
abdominal) 91 , 93, 102, 107,
1 18, 120, 133, 141, 190, 200,
221-222, 224, 227-228
- Celiac ganglion 227
- Inferior mesenteric ganglion 133,
141, 20, 227
- Superior mesenteric ganglion 141,
227
- Ca ganglion 190
- Rib raising 18, 26, 27, 31 , 42, 44,
45, 46, 50, 67, 88, 91 , 93, 102,
104, 107, 1 18, 133, 138, 141 ,
176, 190, 195-199, 201 , 203, 228
- Chapmn' s refexes 17, 18, 31 , 50,
66, 67, 92, 93, 104, 107, 1 19,
133, 190, 201 , 231 , 232-233
OMT: GENERAL EFCT
- Circulation improvement 89
- Congestion relief 89
- Fever modulation 172
- Homeostasis 63
- Pain relief 88
- Preventative medicine 135
- Range of motion increae 175
OMT: GOALS 88, 10, 121, 133, 189,
194-195, 202, 227-23 1 (chart)
- Asthma 49
- Cardiovascular 61
- Congestive heart failure 66
- Ear 14-15
- EENT 6
- GI 87, 91
- GU 123, 138
- Irritable bowel syndrome 1 17-1 18
- Lower respiratory 45
- Lymphatic pump 218
- Myocardial infarction 60
- Obstetrics 153-158
- Physiologic goal addressed 227-231
(chart)
- Pneumonia 42
- Prevention 1 12
- Rheumatology 163-164, 167
- Systemic dis 88
- Upper respiratory tract 25
- Uterus 140
OMT: RESEARCH STUIS
- Asthma 49
- Cardiovascular 50
- Chronic bronchitis 48
- COPO 48
- Fibromyalgia 167
- Glaucoma 14
- Historical 41-42
- Hypertension 65
- Lymphatic pump 28
- Meniere' s dis 15
- Nos 16
- Pneumonia 41-42
- Post-operative ileus J03
- Postoperative respiratory complication
46-47
- Renal disease 135
- Uterine contractions 157
OlIT: MANIPULATIVE
PRESCRIPION 121
- Choice of technique 164, 225
- Dosge 154, 164, 175
- General 1 , 152
- Indicatiors for 227-231 (chart)
- Ineffetive 17
- Length of treatment 91
- Mechanisms postulated 66 (chart)
- Modifcations needed 101
- OMT ad medication 79, 86, 88, 93
- OMT" by family member 157, 176,
219, 230
- Order of treatment 44, 60, 91 , 201
- Hypersympathetonia treated frst
- (Relative) contraindications 6, 13, 41,
79, 102, 139, 152, 164, 166, 176,
219, 222, 227-231 (chart)
- Side effets 164, 171
- Therapeutic trial 144
- Treatment frequency 101
- When t star 88
OMT: MOBIIZE FLUIS
- OMT: MAXIZE THORACO
ABDOMIO-PEL VIC PUMP
- Thoracoabdominal diaphragm 13,
18, 27, 3 1 , 43, 50, 67, 85, 90, 93,
101, 105, 107, 120, 133, 141,
176, 190, 214-216
- Abdominal fascial release 228
- Diaphragm redorg 61 , 105,
120, 176, 214, 228
- Thoracic cage
- Costal 18, 31 , 44, 50, 61 , 66, 90,
93, 107, 133, 141, 190, 198
- Sterum 50, 61 , 90, 102
- Pelvic diaphragm 107, 190, 216-217
- Intrarectal relese 105, 229
- Intrvaginal 105, 217, 229
- Ishioretal fossa 105, 136, 216-
217, 228, 229
- OMT: LYMPHATIC PUM
- Lymphatic pumps 18, 28, 31 , 46,
49, 50, 66, 67, 88, 93, 102, 120,
133, 141, 176, 182, 190, 203,
21 8-219, 229-230
- Dalrymple (Pedal pump) 44, 46,
102, 21 8-219, 229, 230
- Thoracic pumps (various
modifcations) 28, 176, 229, 230
- Lymphatic techniques 120, 162,
167, 176, 202-222, 218-222, 229-
230
- Pectoral traction 28, 44, 61 , 102,
156, 219, 230
- OMT: LOCAL TISSUE
MOBIIZATION
- Ascending colon release 227
- Brest drainage 230
- C.al rele 227
- Descending colon relese 227
- Eustachian tub 15, 17
- Gallbladder pump 167
- Hyoid 3 1
- Liver fip (lung bases) 221-222, 227
- Liver pump 86, 166, 167, 218, 219,
220, 228, 229
- Mandibular drainage technique 17
- Mesenteric lif 89, 102
- Mesenteric release 89, 93, 107, 190,
221 , 227
- Mesenteric stretch 1 15
- Ocular muscle energy 14, 1 8
- Ocular stroking 14, 1 8
- Posterior axillary fold 164, 220, 230
- Ruddy technique 14
- Small intestine mesenteric release 89,
227
- Small intestine mesenteries 89
- Splenic pump 219, 220, 228
- Somatic component 1 1 8
- Supportive 104-106
- Symptom relief 87
OMT: REGIONAL APPLICATION
- OMT: ACTIVATIG FORCES
- Diret 90, 105, 222
- HVLA 43, 49, 82, 164, 166, 171,
176, 225
- Muscle energy 14, 18, 49, 157,
198, 215, 217
- Muscle energy for eyes 14
- Pillow technique 154
- Resistive duction (Ruddy) 1 8
- Indirect 43, 49, 60, 61 , 90, 101,
102, 105, 157, 164, 167, 212,
215, 222
- Counterstrain 139, 157, 165, 167,
215
- Stacking 164, 167
- Joint pump 164, 167
- Myofasciallfascial unwinding 164,
212, 214, 222
- Fascial release 101, 102, 222
. Respiratory cooperation/force 89,
215
- OMT: CERVICAL
- Suboccipital 92
- OA 13, 18, 31 , 44, 46, 50, 66, 67,
88, 93, 104, 120, 133, 141, 190,
224
- A-C2 18, 31 , 44, SO, 61 , 67, 88,
93, 104, 107, 120, 133, 141, 190,
224
- C3-5 18, 31 , 190
- Cervical 12, 44, 46, 101, 102
- OMT: CRANIOSACRAL 144, 224
- Condylar decompression 16, 30, 92,
102, 105, 120, 217, 224
- Cranial 7, 13, 14, 16, 18, 28, 31 ,
50, 67, 77, 88, 92, 93, 105, 107,
133, 140, 144, 157, 165, 190, 224
- CV4 46, 49, 61 , 66, 102, 140, 157,
166, 167
- Frontonasal suture spread 28
- Infraorbital nerve 16, 28, 231
- Occipital decompression 30
- Occipitomastoid suture 66, 104, 224
- Supraorbital nerve 16, 28, 23 1
- OMT: SACRAL
S2-4 93, 107, 133, 141, 190
- Sacral inhibition 140, 23 1
- Sacral rocking 1 19, 140, 224
- Sacroiliac 93, 107, 1 19, 133, 135,
141, 142, 190
- OMT: THORACIC
- Thoracic inlet 12, 18, 31 , 46, SO,
67, 93, 101, 107, 133, 141, 176,
190, 212
- Tl-12 31, 190
- Tl-4 12, 18, 31 , 46
- Tl-6 50, 67
- T5-9 93, 107
- TlO-ll 93, 107, 133, 141
- OMT: THORACOLUMBAR
- Tl2-L2 93, 107, 133, 141
- Thoracolumbar junction 18, 27, 31 ,
50, 66, 67, 90, 93, 1 18, 120, 135,
140, 141 , 230
OMT: SOF TISSUES & MUSCLE
- Fascia 66, 90, 167, 176, 216, 230
- Anterior cervical fascia 17, 46
- Anterior/posterior body 219
- Cerical fascia 17, 18, 46
- Muscles
- Iliopsoas 215
- Medial pterygoid 18, 31
- Paraspinal 88, 90, 101, 102, 104,
138, 201 , 214
- Quadratus lumborum 214-215
- Sof tissue 18, 27, 31 , 43, 45, 46,
90, 91 , 104, 105, 1 18, 1 19, 120,
157, 164, 167, 175, 176, 201 ,
214, 218, 222, 224
- Clopping 41
- Compression 165
- Efeurage 1 8, 31 , 93, 222
- Inhibition 43, 46, 91 , 101, 102,
104, 138, 224
- Kneading 104
- Vibratory 218
OMT: SYSTEMIC COMPLAITS
- Asthma 49
- Cardiovascular 67 (chart)
- Common cold 25-29
- Dysmenorrhea 139-142, 141 (chart)
- Dyspareunia 143
- EENT 18 (chart)
- GI dysfnction 95
- Colon dysfnction 101-106, 107
(chart)
- Ulcer 79
- Upper GI dysfnction 89-93, 94
(chart)
- GU dysfnction 133 (chart)
- Hypertension 62-63
- Ileus 103 (chart)
- Ileus prevention 198, 230
- Infection 172
- Obstetrical patient 158
- Postpartum patient 157
- Pediatric 171, 175-177
- "Tick-tock" method 176
- Pulmonary dysfnction 31 (chart), 34,
SO (chart)
- Rheumtology 163-167
- Sexual dysfnction 142
- Sinus dysfnction 16
- Systemic dysfnction 1 89-233, 190
(chart)
- Urologic disorders 133-134
- See also Rational osteopathic tretment
plans
OMT: TECHIQUE DESCRIPION
(How to tret)
- Abdominal diaphragm 215, 216
- Diret stretch 215-216
- Indirect 216
- Asending colon mesenteric release
221
- Ceal release 221
- Chapmn' s refexes 65, 92, 201
- Colon 104
- Collateral ganglion inhibition 20
- Dalyrimple technique 218-219
- Descending colon mesenteric relese
221
- Eye exercises 13-14
- Faial release 222
- Ileus prevention 198-199
- Infraorbital nerve 28
- Intrarectal releae of pelvic floor 217
- Intravaginal release of pelvic floor 217
- Ischiorectal fossa 216-217
- Liver fip 221-222
- Liver pump 220
- Lower extremity unwinding 220
- Lymphatic pump 218, 219
- Thoracic 218
- Petoral traction 219
- Pedal 218-219
- Mandibular drainage 17
- Mesenteric release/lif 89, 221
- Ocular 14
- Pectoral traction 219
- Peal pump 218-219
- Pediatric 176
- Pelvic diaphragm 216-217
- Pelvic splanchnic nerves 224
- Petrissage 222
- Posterior axillary fold 220
- Quadratus lumborum 214-215
- Rib raising 42, 196, 197
- Debilitated patient 196
- Seated patient 197
- Supine patient 197
- Rib Twelve (R12) 214-215
- Sphenopalatine ganglion 223-224
- Splenic pump 219-220
- Supraorbital nerve 28
- Toracic inlet (Indiret) 212
-" Thoracic inlet (Direct, 2-step) 212-213
- Thoracic inlet (Seated) 213
- Vagal infuence 224
Oocotic pressure 134
Ophthalmoscope 174
Oral fuids 101
Orbeli effect 1 83
Orbital tenderess 231
Organ fnction 150
Organ hypertrophy 151
Organic disorder 88, 109, 142, 144
Orgasm 1 30, 143
Ortalani ' s test 175
Orthodontic tretment 140
Orthosis 165
- heel lif 140, 165
- Levitor orthosis 165
- shoe 165
Orthostatic albuminuria 123
Osmotic gradient 127
Osteoarthritis 166, 185
Osteopathic considerations vi, 152
- GU tract 123-147
- irritable bowel syndrome 109-122
- obstetrical patient 149-158
- pediatric patient 171-180
- rheumatology 159-168
- treatment plan model 18, 31 , 50, 93,
107, 133, 141, 190
- See also Rational osteopathic treatment
- See also OMT for patients with
SYSTEMIC COMPLAINTS
Osteopathic mnipUlative treatment (Se
OMT)
Osteopathic principles application (See
Rational osteopathic tretment)
Osteoporosis 28, 161, 166, 1 86
Ostial occlusion 16
Otalgia 10, 15
Otic ganglion 223
Otitis media 10, 15, 172
Otologic examination
- abnormal 10
- otoscope 174
Ova & parasites 1 10
Ovarian
- congestion 217
- cyst 1 31
- inflamtion 132
- ovaries 130, 132, 141, 188, 192, 217
- ovulatory cycle 139, 144
Oxygen 33, 34, 38, 40, 48, 88, 93, 95,
98, 1 14, 120, 141, 161 , 1 84, 1 85
- consumption 161
- saturation 48
- oxygenation 88, 98, 120, 155
p
Pacinan corpuscle 80, 183
Pain 86, 162, 164, 173, 1 83, 1 86, 1 88
Pain factors/qualities
- amplifcation 161
- characteristics 81
- excrciating 139
- fbrs 85
- mechanisms 80-81 (diagram)
- meication 138 (Se Analgesics,
Specifc R)
- pain-insensitive structures 81
- pain-spasm-pain cycle 163
- perception 161, 164, 1 83
- precipitated by meals 109
- quality 1 88
- rdiation 1 31
- receptors 80, 81
- location 80
- reduction/relief 104, 163, 231
- swallowing 12
- threshold 141
- visceral 80-81 (diagram)
Pain location
- abdominal 109, 1 14, 1 15, 1 16, 1 17,
120, 127, 132, 138, 139
- abdominal distension 1 15-1 16
- arm 59
- back 138, 139
- low back 127, 132, 136
- cerical 59
- chest 40, 44, 57, 58 (diagram)
- colon 105
- er 5, 9, 10, 1 1 , 15
- with altitude changes 10, 15
- eye 8, 9, 14
- eyebrow 7
- fallopian tube 131
- fa 13 1 , 138
- gallbladder 1 15
-01 104, 109
- compression (01) 1 16
- contraction (G1) 1 16
- groin 129, 1 31
- head (See Cephalgia)
- iliac fossa 13 1
- iliolumbar ligament 1 31
- localiztion 80, 81 , 1 88
- maxillary 12
- maxillary sinus 9, 16
- menstral 139
- neck 5
- nose 5, 12
- orbit 8
- pelvic 105, 1 31 , 132, 137
- penis 1 31
- perineum 136
- phrenic 81
- pleuritic 37
- post-auricular 12
- prostate 137
- rectum 1 31
- retro-orbital 5, 8
- right-sided abdominal 1 16
- sacral 1 31
- shoulder pain 59, 81
- sinus 7, 9, 12, 28
- somatic 81
- somatic localiztion 81
- substeral 57
- suprapubic 138
- temple 5
- thigh 1 31 , 138, 139
- thoracolumbar 127, 138
- throat 12
- urinary bladder 129
- uterus 131
- vascular 1 88
- visceral 80, 81
Pain patter 79, 82, 86, 132
- cardiac 58, 81 (diagram)
- cardiovascular system 58
- duodenum 81 (diagram)
- gall bladder 81-81 (diagram)
- iliolumbar ligament diagram 128
- Mayo 01 surgical diagram 82
- peptic ulcer 82
- peritoneocutaneous reflex (Morley) 81
- somatic 83
- ureterolithiasis 138
- visceral 81-82 (diagram)
- viscerosomatic 80 (diagram), 87
Pain referred 8, 9, 81 , 87, 129, 188
- cardiovascular patter 58, 81
- segmental 1 31 (See Facilitated
segment)
- se also Pain patter
Painfl urethral syndrome 137
Palate shape 48
Pallor 81
Palpation 121, 154, 165
- accuracy 59
- change 127, 1 31 , 138
- examination 41, 82, 154, 190, 225,
231
- prostate 136, 137
- "rbbery" 225
- tissue texture change 82, 83, 91 , 102,
172, 188, 205, 225
- touch 173
Palpitations 4
Pancreas 93, 107, 1 16, 1 86, 1 87, 192,
199
- pancreatitis 84, 86, 1 13, 186
Panic 1 14
Pap smear 157
Paralytic ileus 100
Paraspinal inhibition 60
Paraspinal tissues 225 (See also Muscles -
paraspinal)
Parasympathetic characteristics
- activity 23 1
- balance 190
- dominance 104-105
- efect 18, 3 1 , 50, 93, 141
- Cardiovascular 68, 70
- Lower GI 104-105
- see also specifc organs
- hyperactivity 98, 23 1
- hypoactivity 98
- imbalance 139
- infuence 1 16
- infuence - Chart 187-188
- nere ending 1 1 1
- reflex 85, 126, 142, 144
- supply 1 89
- symptoms 104-105 (See also effect)
- tone 130
Parasympathetics 1 18, 190 (diagram),
191-193 (chart), 194, 223-224
- cardiovascular 60
- diagr 5, 55, 84, 97
- EENT 4-6, 28, 223
- Eye 223
- GI 48, 84 (diagram), 85, 89, 97
(diagram), 98, 10, 1 12-1 13, 1 19,
120, 223
- GU 124, 126
- mucous membrane 223
- OMT (Se OMT: Autonomic)
- pelvic organs 1 12, 1 19
- respiratory 23, 27, 29, 35, 38, 44, 48
- rheumatology 163
- sinuses 28
Paresthesia 230
Parietal peritoneum 80
Parotid gland 56, 1 87
Paroxysml atrial tachycardia 67
Paroxysml ventricular tachycardia 67
Passive range of motion 161
Patlogen 1 36, 137
Patnogenesis
- arthritic change 161
- GI dis 87 (diagram), 109
- GU calculi 139
- rheumatoid athritis 161
- rheumatologic dis 159, 161
Pathophysiologic changes 135, 161
- cardiac 59
- GI 87 (diagram), 1 13
- pathology 109, 11 1 , 164
- pathophysiology v, 2, 38, 50, 79, 99,
1 18, 124, 163, 167
- cardiovascular 50
- extraocular muscle disorder 7
- eye 14
- GU 133-134
- respiratory 24, 36
- rheumatology 159-160, 167
- upper GI 79-87
- syndromes 85
Patient
- comfort 87, 1 17 (s also symptomatic
care)
- education 163
- patient-physician relationship 155,
172-177
- rapport 153
Patterson, Michael 93, 193
Petoral traction See OMT 44, 61 , 102
Petoralis trigger point 57, 58, 59, 67,
23 1
Pedal pump 46
Pediatric
- EENT 15, 172
- growth (Chart) . 17 8
- immune system 171-172
- nervous system 172
- OMT 171-2, 175-177
Pelvic 140, 154, 192, 204
- coil exercise 216
- congestion 1 31 , 1 86
- diaphragm 99, 100, 105, 123, 127,
128, 130, 137, 143, 216-217, 228,
229
- dysfnction 92, 195, 227
- for 99 (diagram), 128, 130, 134,
136, 143, 156, 229
- p. flor tension myalgia 128
- organ 98, 10, 107, 140, 143, 199,
223, 224
- pain 105, 1 31 , 132, 137, 139
- tone 216
Penicillin iv
Penis 56, 130, 1 31 , 143
Peptic ulcer disease 82 (diagram), 86
Percussion hammer 1 19
Perforated viscus 82
Periarticular tissues 164, 167
Pericarditis 58
Perineum 10, 129, 216, 228
- abscess 228
Perineural edema 105, 106
Peripheral arteriolar vasculature 55
Peripheral edem 56, 66, 73
Peripheral resistance 62-63 (diagram), 64
Peripheral vascular disease 186
Peristalsis
- GI 90, 93
- ureter 125, 126, 133, 134, 135, 139,
1 85
Peritoneocutaneous reflex of Morley 81
(diagram)
Peritoneum 80, 81 , 124
- irritation 134
Periumbilical palpatory change 125
Perpetuating factor 8, 57, 134, 144, 165
Personality type
- in irritable bowel syndrome 1 10
- neurotic 1 10
Petrosphenoidal ligament 7
Pharmacologic tretment 1 16-1 17, 121,
124, 127
- pharmaceutical by-product 124, 127
Pharynx 23, 223
- dysfnction 17
- hypresthesia 4
- seretions 2-5
- pharyngitis 16, 31 (chart)
Philosophy iv, xvi, 149
- of treatment 87
Photophobia 4, 5
Phrenic
- nerve 27, 46
- pain 81
Physical examination 154, 165, 172, 208
- kidney 124
- pediatric 172-172
- physical fnding 201
Physical needs 163
Physical stress 1 12, 1 89, 205, 225
Physiological
- basis prologue, 109
- change 151
- fnction 144
- massage 1 36
- mechanism 99, 10, 109, 132, 142,
144
- reaction 1 17
- relief 121
- stress 151, 152, 153
Physiology 1 17, 149, 189
- GI tract 1 1 1-113
Pilomotor muscle 1 87
Pineal gland 1 84
Pituitary 4, 17, 144, 165
- pituitary-ovarian axis 144
Plagiocephaly 15, 172
Placenta 151
Pleura 192
- pleural friction rub 37
- pleurisy 58, 228
- pleuritic pain 37, 38
Pneumonia 38, 40-46, 85
- bronchial 45
- hospitalized patient 45
- lobar 45
- viral 85
Pneumotaxic center 34 (diagram)
Polycarbophil tablet 1 17
Polycystic kidney dis 124
Polymorphonuclear leukocytes 161
Polyps - GI 1 10
Popliteal space 206
Portal venous congestion 70
Post-concussion syndrome 1 1
Post-nasal drainage 16
Post-operative
- complication 46-47
- conditions 28
- ileus 103, 199
- patient 95, 229
- postcholecystectomy syndrome 87
- protool - OMT 101-102
Post-partum situation
- "blues" 157
- brest engorgement 230
- OMT 157
- prio 152, 157
- tretment 157
Posterior axillary fold 164, 206, 220, 230
Posterior pharynx 23, 24
Postural clopping 41
Postur 167, 171, 175, 204, 207
- Posturl analysis 165
- autonomic nervous system 139
- cerical lordosis 166
- crossover 57
- diagnosis 171, 175, 203
- iliac crest level 154
- lumbar lordosis 38, 1 15, 151, 166,
171, 214
- patter 208
- shoulder level 154
- symptoms 203-204
- thoracic kyphosis 57, 151
- tretment 165
- heel lif 140, 165
- Lvitor orthosis 165
- trochanteric level 154
- Postural disorder 8, 57, 1 18, 123, 128,
1 32, 137, 139, 144, 149, 161,
165, 167, 171, 203, 204, 205
- lumbar hyperlordosis 124, 139, 151
- short leg syndrome 128, 132, 140,
154, 161 , 171, 203, 204
Preortic region 199
- preaortic ganglion 194
- preortic nodes 127
Predissing factor 10, 15, 134, 135
- otitis media 10, 15
Preelampsia 152
Pregnancy 144, 149-158
- congestive stage 149 (diagrm), 155-
156
- contraindications to OMT 152
- etopic 152
- labr and delivery 157
- mUltipara/primipara 157
- OMT 152, 157-158
- prelampsia 152
- premture rupture of membranes 152
- preparatory stage 156
- structural stage 153-154
Premature ejaculation 133, 143
Premature labr 152
Premature rupture of membranes 152
Premenstrual syndrome 1 31
Prenatal care 151, 156, 158
Pressure 80
- change - intermittent 86
- gradient 33 (diagram), 38, 39, 105,
150, 151, 152, 156, 195, 203,
204, 206, 218, 229, 230
- ear 10
- intermittent compression 161
- oncotic pressure 134
Preventative meicine 93, 103, 1 12-1 13,
135, 139, 157, 166, 171, 195
Primary vs secondary 82
Primipara 157
Prognosis 87, 136
Prolonged P-Q interVal 72
Proprioceptive input 1 89, 196
Prostaglandins 87, 1 31 , 140
- prostaglandin inhibitor R 131 (Se
also list under Medication)
Prostate 128, 129, 130, 1 31 , 132, 133,
136, 137 (diagram), 193
- congestion 134
- digital mssage 136
- dysfnction 132
- physiologic massage 136
- prostatitis 128, 134; 136-137
- prostatodynia 136, 137
- refux 133
- secretion 136, 137 (diagram)
- spasm 229
- wall 136
Protective reflex 36, 127
Protein 162
- balance 66
Pseudoephedrine 15
PSIS level 154
Psoas
- contracture 124
- spasm 124, 128
- See also Muscle - Iliopsoas, Psoas;
OMT - Iliopsoas; Trigger point -
Iliopsoas
Psychiatry
- care 162
- depression 1 10, 1 16, 1 31 , 139, 157,
162
- illness 1 10
- neurosis 1 1 0
- prsonality type 1 10
- psychogenic disturbances 49
- shizphrenia 1 81
Psychologic factor vi, 109, 1 12, 132,
1 37, 142
- neds 163
- support 156, 163
- psychoemotional level 162
Pterygoid plate 223
Pterygoid venous plexus 17
Ptosis 3, 8
Pubic bone 130
Pubic symphysis 204, 214, 228
Puboprostatic ligamnet 129
Pubovesicular ligament 129
Pulmonary branches of vagus 55
Pulmonary
- Chapman' s refex 37, 232-233
- dysfnction 50 (chart), 85
- OMT 34
- eema 56, 72
- embolism 58
- hypertension 48
- lymphatic system 72
- mucosal irritation 36
- staging 45
- toilet 40
- postural clopping 41
- vascular resistance 48
Pupil 1 87, 192
- constricted 3, 4
- dilation 4
- Homer's syndrome 3
- inneration 4
Pyelonephritis 135
Pylorus 98
Q-T interal 1 85
Q
Quadratus lumborum spasm 124, 214
R
Rales 48, 227, 229
Range of motion 161 , 162, 163, 167,
1 71 , 195, 205
Rash 176
Rational osteopathic treatment protocol
163
- Arrhythmia 67-8
- Asthma 48-49
- Cardiovacular 67-68
- Common cold 25-29
- Congestive hert failure 66
- COPD 48
- Dysmenorrhe 141
- Ear 14-15
- EENT 12-19
- EENT Sumry 1 8
- ENT Unit 17
- Eye 13-14
- General prologue, v, 19, 29-30, 50
- GI dysfnction 93, 107
- GU dysfnction 133
- Hypertension 61-66
- Myocardial infarction 60-61
- Nose 16, 31
- Pharyngitis 31
- Pneumonia 40-46
- Post-op pulmonary complications 46-
47, 101-102
- Respiratory 25-29, 48, 50
- Rheumatologic 163
- Sinuses 16-17, 31
- Throat 17
- Pediatric 175-177
Receptor
- baroreceptor 62
- chemoreceptor 1 83
- pain 80, 81
Rectosigmoid region 99, 1 13, 1 31 , 216
- abscess 229
- bleeding 1 10
- cancer 229
- examination 10, 216, 229
- sphincter 1 88
- ulceration 1 10
Red blood cell 124
Red refex 174
Reference organs 194
Referred pain 8, 9, 81 , 87, 129, 188
- arm 58
- cardiovascular 58
- gallbladder 87
- groin 129
- jaw 58
- neck 58
- sgmental referred 1 31 (See Facilitated
segment)
- shoulder 81
- ureterolithiasis 138
- viserosmtic 87, 188
Refex 1 89
- Cardio-cardiac 60, 69, 70
- Cardiocardiac 1 85
- Chapm's 37, 82, 83, 90, 91 , 92,
1 19, 1 34, 194, 20-201
- Chapmn' s (adrenal) 77
- Chapman' s (bladder) 125
- Chapman' s (broad ligament) 130
- Chapman' s (colon) 104
- Chapman' s (GI) 86, 165
- Chapmn' s (gonads) 130
- Chapman' s (GU) 139
- Chapman' s (heart) 59
- Chapm's (kidney) 126
- Chapm' s (prostate) 130
- Cough 36
- Erben's 67
- Gag 175
- Gastroolic 1 1 1 , 1 16
- Hering-Breuer 38
- Intraprostatic 137
- Ouloardiac 55
- Oculoerical 2
- Parasympathetic 48, 85, 126, 142, 144
- Protetive 36
- Red 174
- Somatosomatic 34
- Somatovisceral 26, 34, 36, 49, 57,
10, 1 12, 1 15, 1 1 8, 1 19, 167, 231
- Sympathetic 142
- Uterus 1 31
- Visceromotor 125, 127, 165, 167, 225
- Viserosensory 127
- Viserosomatic 33, 35, 36, 37, 38, 49,
79, 83, 86, 90, 10, 101, 109
1 15, 1 1 8
- Viscerovisceral 25, 33, 69, 70, 85
- Vicious cycle 1 1 8
Refex parameters
- activity 135
- center - Rostral 125
- connections - EENT 2
- cycle 225
- dysfnction 88
- mehanisms vi, 19, 36
- neurophysiology 79
- pathway 93
- patter
- Genitoreproductive 1 31
- Leared 1 12
- response 195
- symptom
- EENT 16
Refex sympathetic dystrophy 161 , 1 86
Refux
- gastric 58
- urinary 125, 133, 135
Refractory period 71
Regional fascial dysfnction 207-212
- See Fascial patters, Compensation
Regurgitation 172
Relaxation 27, 66, 87, 88, 121, 195, 214
Renal
- blood fow 138
- calyces 138
- capsular lymphatics 127
- capsule 127
- circulation 135
- colic 138
- damage 139
- disease/dysfnction 132, 135, 138
- failure 135
- fat pad 123, 124
- fnction 70
- parenchyma 127
- renal pelvis 127, 138
- See also Kidney
Renin 64
- Renin-Agiotensin 66
Reproduction 1 84
- fnction 144
- organ 188
- tract 129-132
Residual urine 129
Resistance - Host 10
- resistace to infection 88
Respiration 26, 33-35, 38, 42, 50, 70, 86,
90, 130, 164, 228
Respiratory
- acidosis 33, 35
- alkalosis 33
- axis of sacrum 105
- center 38
- complication 46-47
- depth 196
- disorders/dysfnction 33-52
- effciency 196
- effor 150
- epithelium (See Epithelium)
- fnction 66, 204
- infetion 40
- inneration 34 (diagram)
- interal/exteral 26 (diagram)
- mucosl fnctions 23-24
- plexus 25
- pump 164
- symptom 40 (See also Specifc
symptoms)
- terapy 40
- postural clopping 41
Restricted motion 171 (See Somatic
dysfnction)
Retention - SaltlWater 1 85
Reticular formation 183
Reticuloendothelial system 26, 184
- Reticulocytes 1 84
Retina 1 83
Retrograde ejaculation 133
Retroorbital pain 5
Rheumatoid arthritis 159, 161, 164, 166,
1 85
Rheumatic fever 72
Rheumtology
- diagrams 160, 162
- OMT 163-166
- pathophysiology 159-160
Rhinitis 15, 16, 31 (chart)
Rhinomanometr 16
Rhinovirus 24
Rhonchi 229
Rhythm assimlation reaction 183
Ribs 91 , 123, 156, 195
- fracture 58, 228, 229
- head 91 , 194, 195
- hump 175
- motion 194, 196
- bucket handle 196
- rb 1 105
- rb raising - effect 42-44
Richardsn eye exercises 13-14 (chart)
Risk fctor 135
- cardiac 69
- gallbladder 93
- hypertension 78
Rotatores muscles 82
Rotoscoliosis 154, 204 (See scoliosis)
"Rubbery" palpatory fnding 225
Ruddy resistive duction technique 14, 18
s
Sl-3 1 19
S2-4 98, 10, 1 12, 1 19, 124, 126, 129,
130, 133, 135, 136, 140, 142,
143, 193, 223
Sacral 154, 224
- axis 105
- base anterior 140, 157
- base unleveling 203 (See also: shor leg
syndrome)
- diagnosis 157
- Sacral shear 140, 154, 203, 224
- Sacral somatic dysfnction (See
Somatic dysfnction - Sacrum)
- rocking 1 19
- sacroiliac joint 1 19
- sacroiliac strain 140
Salicylate toxicity 1 1
Salivary gland 192
- salivation 7
Salt retention 62, 70
Scar tissue 40, 98, 230
- scarring 40, 98
Schizophrenia 1 81
Sclera 6
Scoliosis 57, 154, 171, 175, 203, 204
Screening examination 157
Scrotal pain 127
Seasickness 1 1
Second trimester 155
Secretion 18, 31 , 50, 1 87, 223
- secretion rate - GI glands 85
- secretions - Thick 48
Sedimentation rate 1 10
Segmentation 79, 1 14
Seizure 152, 177
Self-breast examination 157
Self-centered 162
Self-regulatory mechanisms 152 (See
homeostasis)
Seminal vesicle 129
Sensation of "warmth" 220
Sense of smell 7
Sensineural hearing loss 1 1
Serosa 8 1
- stretch 1 15
Serum laboratory measurements
- aldosterone levels 65
- serum lipid 71
- srum pC0
2
33, 35, 48
- srm pH 33, 34
Sexual
- aphrodisiac 132
- desire 132
- development 1 84
- dysfnction 142-144
- OMT 142
- fnction 142, 143 (diagram)
- intercourse 142
Shallow breathing 38
Shock 60
Short leg syndrome 128, 132, 140, 154,
161 , 171, 203, 204
- heel lif 140, 165
Shortness of breath 205, 218
Shoulder dysfnction 230
- pain 81
Sibson's fascia 207, 210 (See Thoracic
inlet)
Sigmoid colon 1 1 1
- sigmoidoscopy 1 10
Sinoatrial (SA) node 50, 55, 68, 71 , 231
- automatism 71
- block 67
- bradyarrhythmia 55, 67, 70
- tachyarrhythmia 67, 70
Sinobronchial syndrome 17
Sinus 5, 192, 202, 223
- attack 12
- disorder 2
- drainage 28
- headache 16, 231
- infection 28
- OMT 16
- pain 7, 9, 12, 16, 28
- sinusitis 12, 15, 16, 202, 23 1
- acute 16
- chronic 16
Sitz bath 136
Skin 1 87, 222
- change 205, 188
- clammy hand 230
- Se Tissue texture change
Skull 223
- base 150 - Se also Cranial
Sloughing 36
Slow wave activity 1 1 1
- slow wave GI contraction ratio 1 13
Small intestine 84, 89, 107, 1 14, 1 15,
1 17, 192, 199
- dysfnction 227
- mesentery 89
- small bowel study 1 10
- Se also OMT
Smoking 36, 50, 153
Smooth muscle 138
- bowel 1 1 1 , 1 12
- cyclic activity 1 1 1
- GU 130
- spasm 81
- stretch 81
Sneezing 10, 1 6, 127
Social growth 172
Sodium benzoate 166
Sodium resorption 64
Sof palate 175
Soft tissue 155
- swelling 162
- See also OMT; Tissue texture change
Solitary nucleus 34, 35
Somatic afferent referral 161
Somatic and cardiovascular system 57-59
Somatic clues v, 1 , 25, 28, 37, 59
- Cardiovascular 59
- Colon dysfnction 104
- Congestion 205-207
- EENT 28
- General 152
- GI 90
- GU 138
- Lower GI 97
- Lower respiratory tract 44
- Lung dysfnction 37
- Visceral dysfnction 82, 83, 85, 86,
1 18, 130, 165, 1 89, 225
- See also Visceromotor patters
Somatic complaints 1 10
Somatic component 100, 144
Somatic dysfnction v, 18, 3 1 , 50, 93,
107, 1 1 8, 123, 125, 133, 141,
161, 167, 171, 1 89, 190, 194,
195, 209, 225
[See also Somatic Dsunction
Subdivisions -
SD:CERVICAL REGION
SD:CRANIUM
SD:EXTREMITIES
SD:GENERAL FACTORS
SD:LUMBAR ARE
SD:SACRAL & PELVC AREAS
SD:THORACIC & CHEST CAGE
Somatic dysCunction:
CERVICAL REGION
- Subccipital 104
- OA 1 1 , 27, 44, 55, 66, 85, 92, 120,
1 89
- A 10, 55, 92, 120
- C 55, 59, 85
- C3-5 46-47, 105
- Cervical 2, 4, 27, 44, 58, 59, 92, 202
- Hyoid 17, 61
CRANIUM
- Cranial 7, 8, 10, 14, 15, 48, 49, 120,
165, 171 , 172, 1 89, 203
- Cranial nerve involvement 7, 9
- Extraocular muscles 14
- Lmbdoidal suture 120
- Occipitomastoid 66, 92
- Sphenobasilar symphysis 10, 49
- Temporal bone 8, 9, 10, 1 1 , 15
EXTREMTIS
- Lower extremity 206
- Posterior axillary fold 206
- Upper extremity 206
GENERAL FACTORS
- Diagnosis of Somatic Dysfnction 21 1
- Fascia 105, 1 89, 205
- Fascial patter 207-212
- Fascial symptoms 203-205
- Joint 204
- Lymphatic 205, 207
- Myofascial 162, 165
- Non-neutral 82, 225
- Non-physiologic 154
- Predisposing factor 135
- Primry 1 12
- Contributing factor (GI) 109
- Reurrent 82, 153, 154
- Regional tissue congestion 205
- Segmental 86, 134, 154
- Sidedness 80
- Seondary 82
LUMAR AREA
- Ll-3 214
- Lumbosacral 105
- Psoas 214
- Quadratus lumborm 214
SACRAL & PEL VIC AREAS
- Innominate 105, 154, 224
- Pelvic foor 134
- Pelvis 1 32, 144, 201 , 214
- Pubic symphysis 129, 134, 154
- Sacral 105, 1 19, 132, 139, 140, 157,
1 89, 224
- Sacral shear 1 19, 140, 154, 203,
224
- Superior innominate shear (upslipped)
1 19, 224
THORACIC & CHST CAGE
- Collateral ganglion 200
- Diaphragm 66, 196, 214
- Rib 36, 38, 39, 44, 49, 58, 66, 82,
124, 195, 198, 210, 21 1 , 214
- First rib 39, 154
- Steral 58, 196
- Thoracic 4, 38, 58, 82, 196, 210, 21 1
- Thoracic cage 43, 66
- Thoracic inlet 27, 43, 61 , 105
- Thoracolumbar 66, 124, 143, 144
Somatic elements
- effect of viscerosomtic reflex 1 15
- efferent fbers 83
- innervation 161
- input 142
- pain 81 , 83
- pain localiztion 81
- predisposing to dysfnction 10, 15,
135, 172 (See also specifc
factors)
- segmental distribution 81
Somatic system
- EENT 8-12
- Genitoreproductive 132
- Lower respiratory 38
- Renal 127-129
- Rheumatology 161-162
- Upper GI dysfnction and 86-87
Somatosomatic refex 34
Somatovisceral refex 167, 231
Somatovisceral refex 26, 34, 36, 49, 57,
100, 1 12, 1 15, 1 1 8, 1 19
Sonic disruption 139
Soreness 171
Spam 132, 161, 204
- bwel 1 15, 1 17
- intercostal muscle 58
- orbicularis ouli 8
- pain cycle 163
- paraspinal 101, 228
- plvic diaphragm/floor 99, 128, 143,
229
- psoa 124, 128, 132
- quadratus lumborum 124, 214
- reeptors 80
- refex 138
- smoth muscle 81, 138
- sphincter (GU) 129
- vagina 143
Spasmogenic action 140
Spastic colon 85
Spastic constipation 1 14
Spermtic count 144
Sphenoid bone 7
Sphenopalatine fossa 223
Sphenopalatine ganglion 16, 18, 25, 28,
3 1 , 49, 223
- diagrams 2, 5, 29
- sphenopalatine syndrome 5
Sphincter 124, 126, 127, 133, 134, 1 88,
193
- tone 127
Spike potential 1 1 1
Spinal
- cord 1 12, 143, 150, 183, 1 89, 194,
195
- leng 195
- membrnes 151
- motion patter 171
Spinothalamic tract 80
Spiritual factor 142
- spiritual need 190
- spiritual stress 225
Splachnic nere 80
Splen 81 , 1 87, 192, 199, 219, 228
- slenic pump 45
- splenomegaly 219, 228
Sprain 205
Spray and stretch technique 165, 215, 231
- Se also Trigger points; Fluori-Methane
Spurs 205
Sputum - Frothy 48
Squinting . 8
Stabbing pain 1 88
Staging - Pulmonary disease 45
Stance 173
Staphlococcu pogen 25
Staphylcoccu bacteria 25, 95
Stellate ganglion 69, 70, 202
Sterum 105, 196
Steroids 165
Stethoscope 173, 174
Stiffess 164
Stiles, E study 60 (diagram)
Still, AT quote prologue, xvi, 53
Stimulus
- altered reaction to 1 13-1 14, 1 17, 125,
138, 183
- bronchial tree 24
- cardiac 69
- cervical somatic dysfnction 10
- cranial somatic dysfnction 10
- dermatomal 143
- emotional 1 14
- "erogenous" 132
- esophagus 10
- exteral/interal 1 17
- U-2 143
- lung
2, 36, 44
- penis 143
- renal sympathetic 1 25
- sinus 24
- somatic 88
- teeth 10
- thigh 132
- TMJ 10
- tongue 10
- tonsils 10
- tympanic membrane 2
- upper Gl 2
- upper respiratory tract 25
- ureter 125
- visceral 3
- visceral afferent 82, 231
Stirrups 129
Stomach 24, 84, 98, 107, 1 1 1 , 1 87, 199
- See also Specifc disorders or
dysfnction
Stool 1 16, 1 17
Stool changes 227
- stool laboratory tests 1 10
Strabismus 7, 14
- medial 7
Strain 128, 129, 205
Strept pneuonia 15
Stress/stressor 8, 24, 49, 50, 61, 64, 66,
69, 85, 88, 90, 98, 109, 1 12, 1 1 8,
1 21 , 125, 132, 138, 139, 144,
149, 153, 155, 165, 1 89, 196,
203, 205, 207, 209, 225
- emotional 8, 49
- environmental 49
- pathogenesis of hypertension 64
(diagram)
- physical 49
- pregnancy 1 51 , 152
- reduction 50, 64
- stress-relaxation response 66
- visceral pathology 1 1 1
Stretch 1 15, 166, 214, 222
- receptors 80
- stretching 104
Structural
- abnormality 154
- balace 156
- change 1 35, 1 51 , 161, 164, 165
- component 225
- effect 155
- examination 157, 1 71 , 208
- factor 139
- (s also somatic dysfnction,
postural disorder)
- scoliosis 175
- stress 144, 1 51 , 207
Strcture-fnction interrelationship iv, 1 ,
12, 14, 49, 50, 68, 93, 1 17, 1 31 ,
152, 1 61 , 172, 175
- Cardiovascular 68
Subacute bacterial endoarditiis 68
Subclavian line 229
Subclavian vein 86
Subcortical activity 183
Subcutaneous tissue 222
Sublingual gland 1 87
Subluxation 164
Submdibular ganglion 223
Submxillary ganglion 223
Submxillary gland 56, 1 87
Submucosl plexus 223
Subccipital
- headache 93
- OMT 92
- strain 155
Substance abuse 1 81
Substeral pain 57
Subxiphoid fllness/tension 86, 227
Suckling disorder 7, 172
Sudden death 69
Sudden infat deth syndrome 185
Sugar 166
Sulfa compounds 1 15
Sulfamethoxazle 136
Superior cerical gaglion 183, 184, 202
- diagrams 2, 26
- OMT 67
Superior mesenteric ganglion 90, 92, 107,
1 12, 125, 192, 199, 224
- OMT 141 , 227
Superior transverse axis of sacrum 105
Superior vena cava 150
Superoxide 95
Supraclavicular
- edema 205
- region 6
Supraventricular tachyarrhythmia 50, 57,
23 1
- treatment (See Trigger point - Pectoralis
major)
Surgical treatment 14, 16, 17, 46-47, 69,
72, 87, 95, 100, 101, 102, 106,
1 12, 129, 136, 139, 163, 166,
167, 225, 228, 230
- cholecystectomy 87, 1 15
- complications 46, 47, 87, 103, 199
- Congestive heart failure 72
- GI 46-47
- post-operative OMT 46-47, 101-103,
198, 230
- site 101
- sympathectomy 161 , 184, 185, 186
- tubes 228, 230
- wound 101 , 102, 227, 228, 230, 231
Swallowing 10, 15
- disorder 7, 9
- pain 12
Sweat 1 86
- sweat gland 1 87
- sweting 4, 81
Sympathetic supply 83 (diagram), 1 18,
162
- Adipose tissue 1 84
- Bladder wall 124
- Blood vessel 1 84
- Bone 1 84
- Bronchial tree 26
- Cardiovascular 53-55
- Central nervous system 183
- Collateral circulation 1 84
- Colon 104, 161
- EENT 2-4
- Endocrine 1 84
- Extremity 1 86
- Fallopian tube 129
- Genitoreproductive 129, 130
- GI 83-84, 89
- GU 1 85
- Hert 1 85
- Liver 1 86
- Lower respiratory 36, 42, 49
- Nasal mucosa 26
- Pancreas 1 86
- Pediatric 1 85
- Penis 130
- Peripheral sensory mechanism 1 83
- Reticuloendothelial system 184
- Rheumatology 160-161
- Sinuses 26
- Skeletal 1 85
- Skeletal muscle 183
- Structural involvement 3
- Thoracic duct 56
- Urinary tract 124, 125-126
Sympathetics
- activity 165
- blokade 167
- cell bdies 221
- chain ganglion 90, 91
- dominance 104
- effet 18, 50, 93, 1 14, 141
- Cardiovascular 68, 70
- GU 133
- Kidney 70
- Lower GI 104
- fbers 83
- gaglion
- diagrams 26, 91
- (See Sympathetic chain ganglion;
Collateral ganglion; and specifc
ganglia by name)
- ganglion block 1 85
- hyperactivity 68 (Se
Hypersympathetonia)
- imbalance 139
- influence - Chart 1 87-188
- salso Sympathetic supply
- inneration 101, 192-193 (chart), 194
- s also Sympathetic supply
- mechanism 137
- nerve ending 1 1 1
- nervous system - general 37
- OMT (See OMT: Autonomic)
- outfow 194, 202
- refex 142
- reflex patter 90
- response 143, 190
- segments 161 (See Facilitated
segments)
- stimuli 62
- tone 225
- venous response 55
Sympathetic-parasympathetic hyperactivity
coexisting 70
Sympathomimetic drug 41
Symptomatic care 15, 19, 23, 25, 29, 41,
42, 45, 87, 88, 10, 1 16, 1 17,
121 , 129, 134, 139, 140, 152, 166
Symptomatology v, vi, 40, 44, 45, 85,
188, 204
- Genitoreproductive tract 132
- GI 109
- GU 138
- Respiratory 40, 4
Synapse 1 1 1 , 125, 189
Synovial
- cell 163
- crepitus 162
- fuid 159, 161, 163
- membrane 159, 161
- synovium 163, 154
Systemic disese/dysfnction 79, 106,
109, 159, 1 89
- OMT 1 89-233
- systemic effets 163
- systemic infection 1 35, 219
- systemic involvement 164
- systemic toxicity 40, 41 , 43, 44, 45
Systemic lupus erythematosus 163
Systolic pressure 65 (See Blo pressure;
Hypertension; etc)
T
Tl-12 35, 38, 45, 166
Tl-4 2 (diagram), 3, 24, 25, 59, 105,
192, 202, 209
Tl-6 24, 25, 34 (diagram), 36, 37, 38,
42, 50, 59
T2-8
T3
T5-9
161, 193
1 85
82, 83, 84, 90, 91 , 92, 107, 1 12,
1 61 , 165, 192, 227
TlO- 1 1 83, 84, 90,91 , 92, 107, 1 12, 130,
1 31 , 192, 227
TlO-12 135
TlO-L2 161
Tl 1-12 129
T1 1-Ll 135
Tl2-L2 92, 1 12, 107, 124, 125, 126, 130,
136, 140, 193, 227
Tachyarrhythmia 4, 50, 57 (diagram), 67,
69, 70, 202, 231
- Paroxysmal atrial tachycardia 67
- Paroxysmal ventricular tachycardia 67
Tachypnea 38, 40
Tactile receptor 183
Target organ/tissue 125, 1 83
Taste - Metallic 7
Taste receptor 1 83
Tea 166
Team approach 167
Ters 5, 14, 29, 224
Teth - Clenching 8
Teeth - Wor 8
Temperature - Decre 172, 177
Temperature - Increased (See Fever)
Temperomadibular joint 7
- temperomandibular joint dysfnction
161
- temporomandibular joint syndrome 8
Temporal bone 6, 7, 14, 84
Tender points 162, 167
Tenderess to palpation 82, 172, 205,
206, 220
Tendon sheath 162
Tenosynovitis 162
Tentorium cerebelli 7
Terminal lymphatic drainage 86
- diagram 206
- dysfnction 205-207
- lymphatic ducts 27
Testes 1 30, 188, 192
- ache 128
- dysfnction 132
Therapeutic trial v, 1 , 14, 19, 144
Thickening - Achilles tendon 206
Thigh pain 1 31
Third trimester 1 51 , 152, 154, 155-156
Thoracic
- cage (thorax) 123
- mehanical impediments 42
- duct 56, 70, 73, 86, 99, 127, 210
- distension 66, 70, 73
- surgical drainage 163
- ganglion 202
- inlet 27, 86 (diagram), 89, 154, 156,
203, 207
- defned 209
- diagrams 27, 209, 21 1 , 212
- See OMT
- kyphosis 57, 151
- outlet (Inferior) 89
- outlet (Superior) 48
- pain 59
- pump 219
- See OMT, Lymphatic pump
- thoracoabdominal pump efcacy 156
- thoracoabdominopelvic pump 228
- See OMT for thoraco-abdomino-
pelvic pump
Toracolumbar junction 38, 100, 104,
105, 1 15, 127, 130, 140, 154,
156, 194, 201 , 208, 214, 230
Threshold 183, 1 89, 196
- decreased 1 13
- See Facilitation
Throat pain 12
Throbbing pain 1 88
Thrombosis 1 84, 229
Thyroid 4, 1 1 , 1 87, 192
- dysfnction 17
- hyperthyroidism 1 1
- hypothyroidism 1 1
- innervation 5, 6
- secretion 4
- thyrotropic hormone 4
Tibial torsion 173
Tic douloureux 7
Ticklishness 205, 230
Tietze' s syndrome 58
Time efcacy iv
Tinnitus 4, 6, 7, 8, 9, 10, 1 1 , 12, 14, 15
- differential diagnosis 1 1
Tissue
- congestion 93, 95, 98, 135, 141, 149,
155
- damage 1 39
- defense 135
- hypoxia 161
- tissue response to OMT 154
Tissue texture change 82, 83, 91 , 102,
172, 188, 205, 225
- See Somtic dysfnction; specifc
changes
Tobacco 15, 36, 50, 153
Tongue 56, 174, 175
- tongue blade 174-175
Tonsilletomy 10
Total peripheral resistance 55, 60, 61 , 62,
63 (diagram)
Touch 173
Toxemia of pregnancy 152
Toxicity 40, 41 , 43, 4, 45, 163, 165,
167, 228
Toxins 80, 120, 165
Trachea 36, 192
Traction 80, 222
Tranquilizer medication 1 16
Transition zones 208
Transverse colon 1 1 1
Trauma 6 , 1 1 , 95, 100, 1 12, 1 1 8, 140,
153, 1 83, 186, 203, 208
- falls 140, 153
- head trauma 1 1 , 153
- history 6, 153
- motor vehicle accident 7, 153
- pst-concussion syndrome 1 1
- whiplash injury 2, 7
Travell 10, 162 (See Trigger point)
Tretment
- General goal 1 16
- See also Rational osteopathic
tretment
- Medical (Se Medical treatment)
- See OMT
- Surgical (See Surgical treatment)
- Tender points 162
- See also Spray & stretch; Fluori-
Methane; OMT; Inhibition
Tretment plan 18, 31 , 50, 93, 107, 133,
141, 190
- Cardiac dysfnction (Chart) 67-8
- Common cold 31
- Dysmenorrhea 141
- EEN 18
- GI dysfnction 93, 107
- GU 133
- Pharyngitis 3 1
- Pulmonary dysfnction 50
- Rhinitis 31
- Upper respiratory tract infection 31
- See also Rational osteopathic treatment;
OMT
Treatment protocol 163, 196
Treatment response 135
Tricyclic medication 1 16
Trigeminal neuralgia 7, 231
Trigger point 10, 15, 67, 86, 132, 162,
165, 194, 220
- Abdominal 10, 129, 132
- Digastric 9, 12
- Ear symptoms 12
- EENT symptom 8, 9 (chart)
- Lteral pterygoid muscle 7, 9, 16
- Masseter 8, 9, 12
- Masseter (Deep) 1 1
- Medial pterygoid 9 , 10, 1 1 , 12, 15
- Occipitalis 8, 9, 1 1 , 12
- Orbicularis oculi 8, 9, 12
- Pectoralis major 57, 58, 59, 67, 231
- Pectoralis minor 58
- Pterygoid 8, 9
- Quadratus lumborum 215
- Rectus abdominus 132, 139
- Splenius cervicis 8, 9
- Spray and stretch technique 14
- Fluori-Methane 165
- Steralis 58, 67
- Sterocleidomastoid
- clavicular portion 9, 1 1
- steral division 8 , 9, 12
- Trapezius 8, 9, 12
Trigone 124, 193
Trimethoprim 136
Trophic change 85, 88, 1 86, 205
Tumors - GI 1 10
Twelfth rib 214
Tympanic membrane 174
- abnormal light refex/retraction 10
- fuid level 10
- perforation 15
- poor insufation 10
u
Ulcer 82 (diagram), 86, 87 (diagram),
1 10
Ulceration 84, 165
Ulcerative colitis 1 10, 1 13, 201
Umbilicus 89, 92, 97, 104, 1 15, 1 18,
125, 155, 199, 200, 227
Uncommon compensatory patter 208,
209, 21 1
Unsteadiness 4
Upper extremity 48, 164, 206
- afferents 161
Upper GI tract 161
- dis 85, 87 (diagram)
- s Specifc dysfnction, Inneration,
etc
Upper respiratory tract (Chart) 31
- ifetions 23-3 1, 48
- symptoms 17
Uremia 135
Ureter 124, 126, 133, 137, 138, 1 85, 193
- kinked 123
- dysfnction 132
- fow 1 85
- fnction 124
- obstruction 127, 134
- orifce 124
- peristalsis 125, 126, 133, 134, 135,
1 39
- refux 133
- stone 123, 125
- ureterocolic 127
- ureterolithiasis 137-139
- ureterospasm 125, 133, 138 (diagram)
Urethra 124, 129, 137
- dysfnction 132
- hyprtonia 137
- sphincter 126
- tone 137
Urinary
- culture 136
- dribbling 136
- frequency 128, 1 31 , 134, 136, 137,
138, 139
- hematuria 136, 138
- hesitancy 137
- incontinence 127
- obstrction 125
- output 133, 135
- pH 135, 139
- stasis 123
- stream - weak 137
- urinary tract infection (UTI) 128, 134-
135, 136
- OMT 133-134
- urgency 128, 129, 136, 137
Urine 124, 127
- concentration 134
- fow 133
- fortion 127
- volume 125
Urogenital diaphragm 129, 130, 131
- (Se also Pelvic diaphragm)
Urogenital triangle 99, 130 (diagram)
Uropathy 134, 135
Uterus 129, 140, 141, 142, 155, 188,
189, 231
- contraction 140, 141, 157
- fndus 139, 188
- growth 155
- hypertrophy 151
- inertia 157
- inhibition 140
- pain 1 31
Uvula 175
- asymmetrical elevation upon phonation
10
v
Vagal (See also Cranial nerve X (Vagus
- aferents 2
- See Nerve - Visceral afferent
- hyperactivity 60, 68
- vagal tone - Techniques to modif 67
- See OMT, OA-AA-C2,
Occipitomastoid
- vagal-C2 connection 59, 85
Vagina 129, 142, 143, 144, 216
- examination 10, 157, 216, 229
- leukorrhea 131
- vaginitis 229
Val salva manuever 67
Valves - One way 206
Varcosity 204, 228
Vas deferens 129
Vasa recta 127
Vascular factors 61
- dis 1 86
- element 132, 135
- mechanism 142
- occlusion 1 84
- tone 93
- vasculatur 1 87
Vasoconstriction 3, 15, 18, 25, 31 , 37,
50, 54, 55, 64, 68, 84, 125, 140,
141, 186
- venoconstriction 62
Vasodilation 54, 55, 140
Vasmotor tone - change 48, 1 88
Vasovasorum 71
Vegetative nervous system 1 12
Vein 89, 203
- agos 150
- bracbioephalic 210
- communicating 150, 152
- hemiazygos 150
- inferior vena cava 155
- interal jugular 86, 150
- jugular 150
- lef interal jugular 210
- lef subclavian 210
- lower extremity 155
- one-way valves 206
- renal 127
- spinal membrane 152
- subclavian 86, 127
- valveless vertebral plexus 150, 152
- vertebral 150, 152
Venous
- anastomosis 150
- capacity 68
- change 151
- circulation 202
- congestion 6, 70, 1 16, 1 1 8, 120, 140,
151 , 152
- drainage 6-8, 25, 33, 43, 89, 140, 166,
204, 205
- EENT 6-8
- fow 152
- plexus 150, 206, 218, 228
- retur 66, 124
- stasis 1 31
- system 149, 150, 155, 204, 210
- thrombosis 229
Ventricular
- arrhythmia 50, 60, 69, 70, 185
- fbrillation 50, 60, 69, 70, 185
- output 54
- repolariztion 69
- subndocardial hemorrhage 72
- tachycardia 70
Vertebral column 150, 151
- factre 10, 166, 228, 230
Verigo 2, 4, 6, 7, 8, 9, 10, 1 1 , 14, 15
- differential diagnosis 1 1
Vessel wall 64, 71 , 166
Vicious cycle 1 18, 123, 163
Viral infection 23, 24, 41 , 42, 85
- lymphadenopathy 172
- measles 1 82
- pneumonia 85
- post-viral diarrhea 201
- replication 177
- upper respiratory tract 24
- virus 24, 172, 177, 201
- inflenz virus 24
- rhinovirs 24
- varicella (heres) zoster 58
Viscera 1 88, 192-193 (chart), 194
Visceral
- afferents (See Visceral afferent under
specifc nerves)
- component 144, 225
- dysfnction 82, 83, 95, 10, 109, 1 18,
1 19, 152, 161, 163, 165, 1 89,
194, 201 , 225, 228
- secondary 93, 1 12
- fnction 89, 163
- innervation 83, 194
- irritation 95
- manipUlation 89, 200, 220-222
- pain 80 (diagram), 81 , 188
- peritoneum 81
- pleura 192
- serosa 81
- stimulus effet 3
Visceromotor refex 125
- Cardiac 58
- Genitoreproductive 131
- GI 79-82, 10
- GU 127, 1 31
- Uterus 1 31
Visceroptosis 120, 123
Viscerosensory patter
- diagram 80
- GI 79-82, 100
- GU 127
- Genitoreproductive 1 31
- Gonads 1 31
- Uterus 13 1
Viscerosomatic dysfnction 82
- pain diagram 80
Viscerosomatic reflex 33, 35, 36, 37, 38,
49, 79, 83, 10, 101, 109, 1 15,
1 18, 165, 167, 225
Viscerosomatic-Somatovisceral cycle 103
Viscerovisceral reflex 25, 33
Vision
- Blindness 14
- Blurred 7, 8, 14
- Diminution of perceived light 8
- Diplopia 7, 14
- Disturbance 8, 9
- Far-sighted 1 3
- Jumpy print 8
- Ner-sighted 13
- Visual development 178-179
Vomiting 81 , 85, 100, 104, 138, 172
Y
Walking 166
Warm slide preparation for amoeba 1 10
Waste product 98, 120, 124, 127, 159,
162, 164
- removal 88, 95
Water retention 62, 70
Wax plug (ear) 2
WBC increase 45
Weight control 166
Weight gain 1 31 , 153, 161
Weight loss 1 10
Well-baby 171
Whet bran 1 17
Whiplash injury 2, 7
White blod cells 95
Wolffan duct 129
Work absence 79
A
X Ray 41 , 166, 205
Xiphoid 92, 104, 105, 1 18, 155, 199,
20, 206, 227
y
Yawning 10, 15
Z
Zi, J. Gordon 154, 208
- salso Fascia - patter; Compensatory
mechanism - Common
compensatory patter
ISBN 1 -57074- 154-9
GREEN

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Kuchera - Osteopathic Considerations in Somatic Dysfunction

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Osteopathic Considerations

Common Carotid Artery M M Vasoconstriction M M M M M

Mucous Glands (phx-Iarx) M Vasoconstriction ...... Secretory

Heart ..................... Excitation ............ lnhibition

Stomach M M M M M M M M M M M lnhibition M M M M M M M M M M Motor and Secretion

Gallbladder and Ducts M M M M Relaxation M M M M M M M M M Contraction

TABLE: VENR ABDMINA, FASCIA RELEASE; LYHATIC PUS VISCER TREATNTS P

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