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PAIN & PAIN PATHWAY

Presented by Dr. Santosh

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Introduction Definition of pain Classification of pain Pain pathways for each type of pain Visceral pain Referred pain Orofacial pain Theories of pain Pain modulation Prosthodontic consideration

INTRODUCTION
Pain is the most common symptom that compels patient to seek medical and dental therapy and constitutes a serious health and economic problem. problem. Dentist and dental specialists are concerned with two of the most common pain. pain. 1) Acute orofacial pain arising from the teeth and associated structures. structures. 2) Chronic orofacial pain which is believed to 40% problems. amount for 40% of an chronic pain problems. An understanding of the pathophysiology of pain is needed, particularly those which may have an important effect on patient management. management.

Pain is a protective mechanism of the body: it occurs whenever any tissues are being damaged and it causes the individual to react to remove the stimulus.

The international association for the study of pain defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in damage, terms of such damage

Reaction of Pain
Behavioral:Crying / moaning, on long standing, frustration and depression can be developed. 2) Muscular : Spasm of the skeletal muscles in the affected region. region. 3) Reflex response: A painful stimulus is usually response: associated with somatic reflexes. reflexes. 4) Inter relationship between threshold of pain and reaction: reaction: Reaction of the pain depends upon the environment. environment.
1)

Characteristics of Pain
1) 2) 3) 4) 5)

Threshold and intensity. intensity. Adaptation. Adaptation. Localization of pain. pain. Emotional accompaniment. accompaniment. Influence of the rate of damage on the intensity of pain. pain.

CLASSIFICATION OF NERVE FIBRES


Type A fibres: Alpha 70-120m/s, 70Beta 40-70m/s, 40Gamma 10-50m/s, 10Delta 6-30m/s, Type B fibres 3-15m/s, 12-20um. 125-12um 3-6um 2-5um <3um 0.4-1.2um 0.4-

Type C fibres 0.5-2.0m/s, fibres0.5-

Classification of Pain
Pain Visceral Eg. Angina pectoris / peptic ulcer intestinal coli

Somatic

Superficial From skin & subcutaneous tissues Eg. Superficial cuts, burns

Deep From Muscles/ bones / joints/ Eg. Fracture

PAIN

FAST PAIN SLOW PAIN

Fast pain occurs within 0.1 second of application of a pain stimulus, alternate names are sharp pain, pricking pain, acute pain and electric pain. Not felt Most of the deeper tissues

Slow pain begins only after a second or more of application of a pain stimulus , increases slowly over many seconds and sometimes-even sometimesminutes. Alternate names are burning pain, aching pain, throbbing pain, nauseous pain and chronic pain. Occurs in both skin and in almost any deep tissue or organ

The pain signals take 2 different pathways to the brain. PAIN PATHWAY

Neo Spinothalamic Tract

PaleoSpinothalamic Tract

NEOSPINOTHALAMIC PATHWAY
(Transnmission of fast pain)
The fast type a-delta apain fibres transmit mainly mechanical and acute thermal pain. pain. They terminate mainly in lamia I (lamina marginalis of the dorsal horns)

PALEOSPINOTHALAMIC PATHWAY
(Transmission of slow chronic pain)

The paleospinothalamic system transmits pain mainly carried in the peripheral slow-chronic type-C pain fibers, slowtypealthough it does transmit some signals from type A-delta Afibers as well. The peripheral fibres terminate almost entirely in laminas II and III of the dorsal horns, which together are called as substantia gelatinosa. gelatinosa.

Most of the signals then pass through one or more additional short fibres within the dorsal horn themselves before entering lamina V throughVI Here the last neuron in the series give rise to long axons that mostly join the fibres from the pathway passing through the anterior commisure to the opposite side of the cord and then upward to the brain in the same anterolateral pathway.

Projection of paleospinothalmic tract


The slow chronic paleospinothalmic pathway terminates widely in the brain stem. stem.

Only 1/10th of the fibres pass all the way to the thalamus. Instead they terminate principally in they one of the three areas. areas. 1. and 2. to 3. The reticular nuclei of the medulla, pons mesencephalon. mesencephalon. The tectal area of the mesencephalon deep the superior and inferior colliculi The periaqieductal gray region of surrounding the aqueduct of sylivius. sylivius.

From the brain stem pain area, multiple short fibres neurons relay the pain signal upward into the intralaminar and central lateral nuclei of the thalamus and into certain portions of the hypothalamus and other adjacent regions of the basal brain

Visceral Pain
Causes of pain are 1) Ischemia 2) Obstruction of a hollow viscous 3) Inflammation 4) Distension 5) Severe vasodilatation. vasodilatation. 6) Characteristic of visceral pain. pain.
a) b) c)

Visceral pain is referred pain. pain. Visceral pain is very often associated with vomiting and fall of B.P. Drugs required to alleviate visceral pains are often different from those required to alleviate the somatic pain. pain.

Referred pain: - Heterotropic pain that is felt in an area innervated by a nerve different from the one that mediates the primary pain.

In mammilian embryo body is divided into metamere A typical metamere consist of 1. Skin and subcutaneous tissue. 2. Skeletal muscles 3. Viscera

Each metamere contains one segment of spinal cord (corresponding) a. From anterior horn of segment motor nerve emerges and supplies skeletal muscles of this segment (MYOTOME) b. Autonomic fibres of this segment supply the viscera (VICEROTOME) C. Afferent fibres from the skin enter the dorsal horn of this segment. The area of the skin supplied by one dorsal root is called as DERMATOME

Vicerotome, Myotome and dermatome of each metamere are suppleied by the corresponding spinal cord segment. segment. In post natal life D, V, M of a given segement of the cord occupy geographically different area of the body ( NEURAL CONNECTIONS ARE RETAINED) E.G Dermatome of the T1 segement is inner side of the forearm and the corresponding vicerotome is part of the heart. heart.

Mechanism of referred pain. Following mechanism are responsible for the phenomenon of referral pain. 1. Convergence 2. Subliminal fringe effect

CONVERGENCE

Sympathetic afferent fibres carrying pain sensation from the viscus ends at the posterior horn of the spinal cord. Afferent somatic nerve, emerging from the pain receptor, of the corresponding dermatome of this viscus, viscus, enters the same segment and terminate on the same cell where the sympathetic nerve is terminating. ( i.e Two different neurons converge on the same next order neuron)

SUBLAMINAL FRINGE EFFECT

Subliminal fringe effect


The afferent sympathetic nerve bringing pain sensation from the viscus terminates on the second order neuron, It also gives a collateral which stimulate another second order neuron This second order neuron synapse with the somatic neuron of the corresponding dermatome. Therefore, when pain is felt by the patient he feel as if the pain is coming from the corresponding dermatome

Orofacial Pain Pathway


Somatic inputs from the face and oral structures do not enter the spinal cord by way of spinal nerves. Instead, sensory input from the face and mouth is carried by way of the fifth cranial nerve, the trigeminal nerve.

Trigeminal pathway is only one of the many pathways that carry orofacial nociception to the brain. Nociceptive impulses from the face and mouth may be mediated centrally by way of afferent neurons that pass through the 7th 9th and 10th cranial nerves as well and also visceral afferents that descend through cervical sympathetic chains.

The cell bodies of the trigeminal afferent neurons are located in the large gasserion ganglion. This region of the brain stem is structurally very similar to the dorsal horn of the spinal cord.

Semilunar Ganglion is located in meckels cavity. The ganglion is unipolar neuron forms central and peripheral processes. The peripheral branch form Opthalmic; Maxillary and Mandibular. Central branch leave the semilunar ganglion and enters the pons. Where they divide into ascending and descending fibers. The ascending fibers terminate in the upper sensory nucleus of the trigeminal nerve and convey the light touch, tactile discrimination. The main nucleus gives rise to dorsal trigeminothalamic tract; which ascends upwards. The spinal nucleus of the trigeminal nerve gives rise to ventral trigeminothalamic tract. Which extends caudally to the second cervical segment and crosses to opposite side ascends to the thalamus.

From the thalamus fibers continue to the cerebral cortex. cortex.  Convey pain and temperature from the entire trigeminal area. area.


Theories of Pain
Specificity theory (Von Frey (1890)) 1890))

He proposed that free nerve endings gave rise to pain sensation in brain. brain. This theory is concerned primarily with the sensory discrimination aspects of pain, its quality, location on skin, intensity and duration. duration.

Specificity theory cannot explain


a) Any

pathologic pain produced by mild noxious stimuli. stimuli. b) Referred pain that can be triggered by mil innocuous stimulation of normal skin. skin. c) Do not explain the paroxysmal episodes of pain produced by mild stimulation of trigger zone in trigeminal neuralgia. neuralgia.

Intensives or Summation theory (Gold Sheider)

 

He proposed that pain results from over stimulation of other primary sensations. sensations. He proposed that pain resulted when activity exceeded a critical level due to excessive activation of receptors resulting in convergence and summation of activity. activity.

Noordenbos sensory interaction theory

He proposed that rapidly conducting large fiber pathway inhibit or suppresses activity in slowly conducting small fiber pathway that conveys noxious information. information. A decrease in the ratio of large to small fiber activity results in central summation and an increase in pain and vise versa. versa. It explains different pathologic pain status. status.


Hyperalgesia following peripheral nerve injury. injury.

Gate Control theory Melzack and Wall (1965)

 

The term gate refers to relative amount of inhibition or facilitation. facilitation. The gating mechanism is modulated presumably S.G. layer of spinal cord. cord. The gating mechanism is influenced by the relative activity in large diameter (AF)fibers activated by low (AF threshold non noxious stimuli. stimuli. Small diameter (A-delta + C) fibers (Aactivated by intense noxious stimuli. stimuli.

 

Activity in large fibers tends to close the gate. gate. Small fiber activity tends to facilitate transmission. transmission.

Large fibers in particular, are postulated to activate, central control mechanism related to cognitive processing, which intern modulate gating mechanism. mechanism. When the output of the transmission cell exceeds a critical layer activates the two major systems. systems.


Sensory discriminative system, involving neospinothalamic fibers projecting into the ventroposterior thalamus and the somatosensory cortex. cortex. The descending control exerted by neocortical activity is thought to modulate activity is sensory discriminative and motivational affective systems. systems.

All this systems ultimately influence the motor mechanisms responsible for behaviour elicited by noxious stimuli. stimuli.

MODULATION
The concept of modulation is extremely important in understating the patients experience of pain .It is based on the principle that neural impulses ,rising to the higher centers that are termed painful can be altered by a process called as inhibition

The following areas of orofacial pain modulation are as follows : 1. Pain modulation in the trigeminal spinal tract nucleus 2. Transcutaneous electrical nerve stimulation 3. Pain modulation in reticular formation 4. Pain modulation of the descending inhibitory system

PAIN MODULATION
IN THE TRIGEMINAL SPINAL TRACT NUCLEUS Tip of dorsal horn of the spinal cord is called as substantia gelatinosa substantia gelatinosa neurons were proposed to inhibit transmitter release from primary afferent neurons, thus inhibiting the impulse carried by the primary afferent neuron .

The myelinated afferents were proposed to excite the inhibitory interneurons This in turn reduce the activity of pain transmission neuron

TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION [TENS] The chief product of the gate control theory was the introduction of transcutaneous electrical nerve stimulation as a therapeutic modality The rationale of TENS is based on the antinociceptive effect of stimulating cutaneous sensory nerves

An interrupted periodic current of very low intensity at a frequency of 50 to 100Hz is used The stimulation is usually below what is required to activate A-delta and C Anociceptive fibers

The effect is immediate and usually disappears rapidly Pain relief is localized to the segment stimulated, Serotonin and dynorphin are released when superficial cutaneous nerve are stimulated Instinctive act of grabing, holding ,pressing or rubbing exemplifies this effect Pain reducing remedies are of this category e.g.: massage analgesic balms ,counter irritants mustard plasters, hot and cold compresses, vibration,hydrotherapy,and vapocoolant therapy

PAIN MODULATION IN RETICULAR FORMATION


Reticular formation is a portion of the brain stem that contains a number of nuclei that can either excite or inhibit the incoming impulses Reticular formation controls the overall activity of the brain Pain signal in particular , increase the activity in this area and strongly excite the brain to attention

PAIN MODULATION OF THE DESCENDING INHIBITORY SYSTEM


The neuronal mechanism in the brain stem that appears to balance the continuous barrage of sensory input is called the descending inhibitory system Fibers descend from the brain stem and terminate on the substantia gelatinosa rolandi Stimulation of these fibers leads to pain inhibition

These fibers at their terminals , secrete either serotonin or enkephalin as neurotransmitter and they are called as serotogenic or enkephalinergic neurons.

Serotogenic or enkephalinergic neurons synapse with the A delta and C fiber terminals which bring pain from periphery in the posterior horn of the spinal cord

Stimulation of these descending tracts causes synaptic inhibition or block at the SGR Spinothalamic tract is no more stimulated in spite of the presence of the stimulus for pain in the periphery

The large diameter fibers, which carry touch sensation from the skin to the brain ,also play a strong role to inhibit the pain sensation

When touch conveying fibers of the same dermatome [from which the pain is arising ] are stimulated, the intensity of the pain is reduced (A phenomenon called as Gate Control)

MODULATING EFFECT OF ENDORPHINS AND ENCEPHALINS Endorphins revealed the inherent presence of an endogenous antinociceptive system that normally modulates pain Endorphins play a part in emotional states, such as child birth ,schizophrenia is matters of addiction and in physiological activities Endorphins and encephalins are the two substance which are produced within the human body and act like opium alkaloids

Two types of encephalins:


METHIONINE ENCEPHALINS LEUCINE ENCEPHALINS

Endogeneous opioid peptide combine with their receptors There are three receptors, mu, kappa, delta Mu receptors are present most abuntantly in the PAG and other brain areas Kappa are present particularly in the substantia gelatinosa rolandi [SGR] Combination of enkephalin or endorphin with mu and kappa leads to inhibition of pain perception

Diagnosis
The most important aid to the diagnosis of pain is the 1) History, followed by clinical examination & appropriate 2) Investigation which includes radiographs, a computerized or magnetic resonance scan. scan.

The history should include 1) Its character, eg. Sharp, dull, thrombing, burning or eg. stabbing. stabbing. 2) The site or sites from which it arises, and to which it travels. travels. 3) Its timing, when did the first attack occur its frequency & duration. duration. 4) The provoking factors. factors. 5) The relieving factors. factors. 6) Associated phenomena eg., swelling, discharge, eg. bruxism, trismus. trismus. 7) Does the patient suffer from anxiety or depression? 8) The current and previous general medical history and drug therapy. therapy.

CLASSIFICATION OF OROFACIAL PAIN

Methods of Pain Control

Following are methods of pain control 1) Removing the cause 2) Blocking the cause 3) Raising the pain threshold 4) Preventing pain reaction by cortical depression. 5) Using a psychosomatic methods. 1 and 2 affect pain perception. 4 and 5 affect pain reaction. 3 affect pain perception and pain reaction.

Blocking the cause




 

Nerve block: Depositing a suitable local block: anesthetic solution within a close proximity to a main nerve trunk. trunk. Field block: Deposition a solution in proximity block: to the large terminal nerve branches so that area to be anesthetized. anesthetized. Local infiltration: Deposition a solution in infiltration: proximity to the small terminal nerve branches so that area to be anesthetized. anesthetized. Intra ligamentary technique: For single tooth technique: anesthesia. anesthesia. Topical analgesia renders the free nerve endings in accessible structure in capable of stimulation. stimulation.

Action of anti-inflammatory analgesics anti-

HOW TO MEASURE PAIN




Pain measurement is a complex and controversial psycho physiologic subject

There is no simple method of measuring pain. Pain intensity can be measured by using ratings such as VISUAL ANALOG SCALE (VAS).

A VAS consists of a 10cm line on which 0 no pain 10 pain as bad as it can get

The VAS are sensitive to treatment effects, can be incorporated effects, into pain diaries and can be used with children. Disadvantage: the multidimensional aspects of pain are not well measured

Prosthodontic Considerations
Myofacial pain dysfunction syndrome Its a chronic dysfunction where the transition from a functional to a structural disturbance maybe quite prevalent. prevalent. Pain are well localized to the affected joint and provoked by movement, especially chewing. chewing. Emotional tension, bruxism, lack of occlusion support bruxism, due to either unreplaced teeth or old ill fitting dentures may provoke the pain. pain. Treatment 1) Antiinflammatory analgesics 2) Correction of occlusion with adequate denture in those patient with missing teeth. teeth. 3) Open surgery smoothing of the condylar head, repair of perforated meniscus.
1)

2) Somatopsychic problems Its over reaction of dental procedure to more aggressive conditions. Anxious, depressed state of conditions. mind will amplify the pain and create agitation after what appears to be a normal dental procedures. procedures. The procedure may be fitting of new denture. denture. Treatment New dentures must be carefully adjusted replicas of the previous set or if possible of the natural teeth. teeth. Costens syndrome Clinical feature - Pain usually unilateral and is described as a dull ache in ear or preauricular area which may radiate to angle of mandible - Muscular tendernes - Clicking of TMJ

Etiology Masticatory muscle spasm: a) Muscular over extension b) Muscular over contraction Treatment 1) Anti inflammatory drugs 2) Correction of occlusion and replacement of old denture with new one. Atypical Odontalgia Patient may present with pain without any obvious cause. The pain is severe and throbbing in character and the teeth are hypersensitive to any stimulus. Some time appears to have been precipitated by a dental procedure. Such as fitting of a bridge or an extraction but they are made worse by any further active treatment.

Treatment a) Pulpal and periodontal inflammation must be excluded b) Reassurance is important it response well to the explanation. c) Medication must be combined with regular reviews to provide reassurance and to active drug compliance. compliance.

Burning mouth syndrome An intraoral pain disorder unaccompanied by clinical science or idiopathic causes in which the main symptoms, being described as a burning, painful or etching sensation. sensation. There is a decreased pain tolerance of oral mucosa, tongue. tongue Treatment 1) Correction of malocclusion 2) Muscle relaxants such as diazepam 3) Treatment of systemic disease such diabetes mellitus. mellitus. 4) Topical analgesics

Conclusion
Not only is understanding the neurological mechanism of orofacial pain is vital but also it equally important & or to consider the psychosocial manage and psychophysiosocial control the diverse

dimension of pain & THEN proceed to manifestation of the pain ACCORDINGLY. ACCORDINGLY.

References
Guyton Textbook of Medical Physiology.  Monheim Local anesthetic and pain control.  DCNA  Timothys Miles Clinical Oral Physiology  Malcolm Harris Clinical Oral Science  Bells Oro facial pain.  Chaudhari Concise Medical Physiology.


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