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Neurolog;v
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Donald J. Sefcik is the Associate Dean at the Chicago College of Osteopathic Medicine (CCON{), Midwestern University (MW{I), in Downers Grove, IL. He is a tenured professor and board certified in both Emergency Medicine and Family Medicine. From June 1997 through May 2000, Dr. Sefcik served as Medical Director for the Physician Assistant Program, College of Health Sciences (CHS), at MWU. Dr. Sefcik is a member of the NCCPA's'Board of Directors. @r. Sefcik is NOT representing NCCPA during any portion of this conference; he is lecturing based upon his experience as a clinician, medical school faculty member, and his student assessment research).
Dr. Sefcik has practiced witl physician assistants since 1988 and been involved in the. clinical training of physician assistants since 1990. Prior to joining Midwestern Universrty's faculty, Dr. Sefcik was a faculty member in the Pharmacology Department at Butler University and in the Nursing Department at Marian College, both in Indianapolis, Indiana. Dr. Sefcik has a Bachelor of Science in Pharmacy (1981), a Master of Science in Pha::nacology (1994), both from Butler University, ffid an MBA May 2004) from Purdue University.
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Learning Objeetives
Upon completion of this portion of the review course, the participant should be able to:
1. Compare and conhast the cenhal (CNS) & peripheral nervous system (PNS). 2. List and describe common dermatomes and nerve roots. 3. Compare and contrast delirium and dementia. 4. Define Alzheimer's disease. 5. Discuss the evaluation and management of Alztreimer's disease. 6. Describe tle manifestations/characteristics of multiple sclerosis. 7. Describe the manifestations/characteristics of myasthenia gravis. 8. Describe the manifestations of Parkinson's disease. 9. Describe the drug therapy of Parkinson's disease.
10. Compare and contrast fainting, seizures and cardiac syncope. 11. Present an overview ofstatus epilepticus.
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Alzheimer's Disease
Definition: A degenerative mental disorder, diagnosed after ruling out other
etiologies of progressive mental deterioration and dementia. A diagnosis of exclusion...... The main cause of progressive brain function decline in old age.
1.
2.
Dementia: Alg"!""lliprogressive deterioration of cognitive function. Prognosis depends on etiologf_.Delirium: Antacute\cognitive dysfunction secondary to some underlying medical condition. Acute confusional state, metabolic or toxic encephalopathy, acute organic brain syndrome.
Pathophysiology
1.
Etiology - unknown but may include: a. Loss ofneurons (cerebrocortical atrophy) characteristically in areas involved in cognition, memory and other thought processes (i.e., amygdala and hippocampus)
b.
$ * c. Viruses
Neurofibrillary Tangles
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d. Autoimmune process e. Aluminum toxicity 2. a. Female slightly > male b. Age-50-90, mean onset 8i years c. Head trauma -T d. Familvilsdtv ,{srr exk'"t '
Initially - vague and nonspecific
Early - short term memory problems, shallow and labile affect Later - remote memory affected, may become lost and confused Dyslexia and dysgraphia Dyspraxia (hears and understands task, but cannot perform) Occasional gait and extrapyramidal disturbances Personalitydisturbances Amnesia and confabulation Dementia Risk factors
3.
a. b.
o r
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Th)'roid
Renal
4. 5. 6.
Drug/Alcohol effects
Depression Any other cause of dementia
1. CBC/Chem-Z3 2. Vitamin 812 Level/Folate 3. Thyroid Function 4. CT SCAN - Head 5. EEG @lectroencephalogram) 6. Lumbar Puncture, Syphilis Testing 7. ABG, ESR, HfV Testing, ANA 8. DruglToxin Screens
Treatment Plan
1. Lifestyle changes - supportive mechanism (family, etc) 2. Nondrug therapy - safe environment caregiver, hydration, skin care...
3.
Rx-Tacrine (COGNEX)
Rivastigmine (EXELON) Donepezil (ARICEPT) Haloperidol (I{ALDOL)
Lorazepam (ATIVAN) Temazepam (RESTORIL)
Follow-up
l.
2. 3.
Patienteducation a. Advise family and caregivers of progressive nature b. Advise about drug effects and side effects
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Multiple Sclerosis
Definition: a disorder characterized by focal destruction of the myelin sheaths of nerve fibers throughout the white matter of the CNS. The presentation clinically often includes various sensory and motor disturbances (sometimes misinterpreted as hysteria).
Pathophysiolory
1.
2.
^d.) c'I,D t ',,"*tu(
f, Lrr+l'irrr'f e 3. Signs and Symptoms: (Subjective >> Objective) a. Often parorysmal in nature b. Visual changes (optic neuritis = pain; af[erent papillary c. Paresthesias d. Clumsiness of pi
f.
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h.
i.
Depression Weakness
j.
Nystagmus
Differential diagnosis
2. 3. 4. Spinocerebellar degeneration \ 1trrGI -'a 7 ,^.ri1;^*"'r\ 5. Arnold-Chiari malformation I ir*.2; rat;\. .1.-.cn;L: ,.,'T\e- \ 6. Myasthenia gravis \?.A.,'\,;-irA ) Prrv^tr:'"Jr- &t s '
Labs and X-ray Findings (no test = diagnostic)
1.
1.
2.
Evidence of demyelinization VERs-visual evoked response-delayed in @ 80% SSEPs-somato-sensory evoked potentials-delayed n @ 60% BSEPs-brain stem evoked potentials-delayed n @ 40-50%
r r r
a. Elevated IgG (oligoclonal bands) b. Increased lymphocytes )' J.^*,n_ c. Normal or elevated protein
Syphilis test - RPR/VDRL
CSF analysis
R e6(;dTLr,^
3. 4.
5.
Eryttpgyle sedimentation rate (ESR) CT of nm,f {f the brain $dRI more sensitive = periventricular lesions onT2 sigrral)
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Treatment PIan
1.
2. 3.
Lifestyle changes a. Avoid overwork and fatigue b. Rest periods during acute relapses Nondrug therapy a. Occupationaltherapy b. Self-catheterization for urinary retention Rx a. Corticosteroids may offer some benefit o Methylprednisolone 1 gram for three to five days; taper b. Amantadine (SYMMETREL)
c. d.
1.
Amitriptyline(ELAVIL)
Others
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Follow-up
r-\S
2. 3.
a. b. Relapse rab3Ao/o within one year c. May disable the patient d. Hot weather associated with relapses
Future appointments as needed
Emergency visits with acute decompensation
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Pathophysiology 1. Etiolory-unknown
2.
a. b. a.
Risk factors
3.
b.
c. Rigidity
d.
2)
1)
Resting tremor (typically asymmetric in an upper extremity) 1) 3-5 cps (cycles per second) 2) Distal exbemities, usually at res! increases with as's wrur 3) Damps with voluntary movement 4) Often begins unilaterally Bradykinesia 1) Gait disturbance - slowness of movement 2) Loss of facial expression
-SD
-1o7o
FA*+
Loss of postural
g. Dementia h. Drooling
f.
e.
2)
- qs 7ci:,rrl,)-{l-)o,n\ e,t$,r(\ ,.} gcJs .Jno,Jh .lten P'ujl i) reflexes * 'T'gn 'hwb e{? lft 1) Retropulsion- falls baekwards easily
Depression
i.
HYPoPhonia
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Differential diagnosis
2. 3.
1.
Exfapyramidal side effects of neuroleptic drugs Benign essential temor - head and UE (not LE), improved after alcohol ingestion Infectious, metabolic or toxin effects producing tremor
r Thyroid
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Diagnosis
1.
Clinical diagnosis
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a"to
'{ F 4 'ir:
lrrzl( old)
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2. CT or MRI to rule out pathology-MRl may show degeneration of substantianigra 3. PET Scan
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Treatment Plan
i.
2.
3. Rx a. b.
Dopamine replacement
mainstay oftreafuent
,.,
*V
o .
Bromocriptine(PARLODEL)
Pergolide (PERMAX)
\ r d- TfenOt- -U
R6nl,t
4.
1.
Surgery-Thalamotomy
Follow Up
Patient Education Advise about need for lifelong medications Advise on drug effects/side effects Expected prognosis is cbronic, slowprogression Future Appointments - Medication monitoring at appropriate intervals Emergency Visits - Acute decompensation
2. 3.
c.
a. b.
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lVlvasthenia Gravis
Definition A disorder of the neuromuscular junction resulting in a pure motor
syndrome extraocular' characterized by weakness and fatigue on exertion, particularly of the pharyngeal, facial, cervical, proximal limb and respiratory musculature.
Pathophysiology 1. Vtyasttrenia [iavis (MG) is a disorder of neuromuscular transmission characterized bythe pr"s"nc" of a gamma globulin antibody (AChR-ab) directed against the junction, resulting in nicotinic acetylcholiie r"."pio. (AChR) of the neuromuscular reduction in postsynaptic response to ACh'
2.
Risk Factors:
c.
Thyrnoma -* c
Thymus abnormal
I^^V< Ll.3
3.
a. b.
d. e.
c. Provoked bY exertion
Diplopia
Ftosis
f.
Difficultyswallowing
1. Thyrotoxicosis 2. Multiple sclerosis 3. Polymyositis 4. Depression 5. Any disorder associated 6. Penicillamine ingestion 7. Botulism
1.
with fatigue
2. 3. 4. 5. 6.
Electrodiagnostic studies: repetitive nerve stimulation CT orMRI for thymoma Muscle biopsy Acetylcholine receptor antibodies (AChR-ab) Thyroid function tests Edrophonium (TENSILON) test
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Treatment Plan
i. 2.
c.
Prednisone
f.
g.
3.
Neurologist consultation
Surgical removal of thymus-thymectomy
4.
1.
Follow-up
Patient education variable course medications-use and side effects Future appointrnents-often when patient is unstable Emergency visits-signs of decompensation, respiratory compromise
2. 3.
a. b.
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Miscellaneous Points
Motor
L3
Sensory
Reflex
Hip flexion
Anterior thigh
L4
Hip flexion
Lateral thigh
Patellar
Medial calf
L5
?*%ilffi,
*{allux dorsiflexion
Foot extension
(Plantar flexion)
Lateral calf
Hallux
5ff toe
S1
Achilles
Last
- 2 minutes
Aura (sometimes)
Last<
10 seconds
Quickly respond
F '?ostictal state
Premonitory
:7
l3'/* .f
c\
Ft'
!r
PL
?
Acidosis (respiratory and metabolic)
. o r r .
Evaluation (acutely): More helpful - Glucose, Electrolytes, Calcium, Magnesium Less helpful - CBC, Renal function, ABGs, Toxicological studies
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Treatment: Lorazepam
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Psychiatric Topics
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Generic
Name
Trade
Name
Molindone Mesoridazine
Perphenazine Thioridazine Thiothixene Trifluoperazine
Trilafon Mellaril
Navane Stelazine
4to40mg 5to40mg
Atypical Antipsychotics
Clozapine Olanzapine Quetiapine Risperidone Ziprasidone Clozaril Zyprexa
Seroquel Risperdal Geodon 50 to 600 mg 10 to 20 mg 250 to 500 mg
2to8mg
40 to 160 mg
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Elavil
Sinequan
Trimipramine
Secondary amines
Tofranil Surmontil
Norpramin
Pamelor
to to to to
75 mg
75 mg 75 mg 75 mg
to to to to
mg mg mg mg
.
Desipramine
Vivactil
Asendin
50 to 75 mg 25 to 50 mg l0 to 20 mg 50
to 60 mg
to 150 mg
Ludiomil
Remeron
Serzone
50 to 75 mg
15 mg
to 45 mg
200 mg
50
Desyrel
to 150 mg
Aminoketone Bupropion Wellbutrin Monoamine oxidase inhibitors Phenelzine Nardil Tranylcypromine Parnate Selective Serotonin Reuptake Inhibitors Citalopram Celexa Fluoxetine Prozac Fluvoxamine Luvox Paroxetine Paxil Zoloft Serhaline Escitalopram Lexapro
200 mg
15 mg
to 90 mg
20 mg 20 mg l0 to 20 mg
50 mg
20 to 60 rng 20 to 60 mg l0 to 80 mg 50 to 300 mg
20mg
50 mg
l0 mg
20 to 50 mg 100 to 200 mg l0 to 20 mg
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75 mg
75 to 375 mg
100 to 200 mg
BID
with meals
4-l2mc{ml
400 to 1800 mgld
Maintenance Therapy
Dose Serom
600
to
1800 mg/d
15 to 45
mglkgld
concdati@s
4-12
mog/ml
0 6-1 0
mEq/L
50-125 tJlcglml
Librium
Tranxene
Valium
Paxipam
Ativan
Serax
0.75-4 mglday 25-100 mg/day 7.5-60 mglday 2-40 mglday 20-160 mg/day 0.5-10 mdday 30-120 mg/day