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Neurolog;v
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Donald J. Sefcik, D.O.o M.S., FACOEP

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.

CME Resources Certification & Recertification Exam Review

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Certifrcation & Recertification Exam Review


CME Resources 2004 Neurology
Donald J. Sefcik, D.O., FACOEP

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.

Classic (but not pathognomonic lesions)

$ * c. Viruses

Neurofibrillary Tangles

intracytoplasmic filament bundles


(esp. cerebral cortex)

-f,au Q:f+gi S

Neuritic (senile) Plaques

swollen collections of eosinophilic nerve cell processes (amyloid protein cores)

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

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3.

a. b.

Signs and Symptoms

o r

c. d. e. f. g. h. lntellectual deciine i. Sleep disturbances

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Differentialdiagnosis ^, 1. Multi-infarctdem"#a - Zn-\ 2. Brain Tumor 4. Metabolic dishrbance

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cf

e)'t"^so'.

'

/i

F Q'iup'ol''* JZ"*t*t"

r o

Th)'roid
Renal

4. 5. 6.

Drug/Alcohol effects
Depression Any other cause of dementia

Labs and X-ray Findings

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.

c. Monitor for care giver "burnout" d. Consideralternatives-daycare, etc

Patienteducation a. Advise family and caregivers of progressive nature b. Advise about drug effects and side effects

Future Appointnents a. As necessary to follow progression b. Based on coexistent health problems


Emergency visits with signs of decompensation

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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.

Unknown etiology but may involve an autoimmune process or virus


Risk factors

2.
^d.) c'I,D t ',,"*tu(

a. Female>male b. Younger adults (16-40yo)

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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.
(y

c. European descent d' family historv r "=)

)6 i'. J b'c;c' un(: 'n ftrx4"o^ LA.lr,lZ a


defect)

--' .-J {'

Emotional lability Fatigue Inc o ordination/ataxia

SC'lo

grrc^=1

z Flz-nsuuf\\

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.

Brain tumor (CNS lymphomas) Neurosyphilis Systemic lupus erythematosus (SLE)

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

::f.frR?
Follow-up

r-\S

Patienteducation Variable and unpredictable coluse

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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Parkinson's Disease (paralysis agitans)


system of unknown Definition - A neurodegenerative disorder of tb neurons of the substantia nigra, cause that affects primarily the dopamine-containing resulting in a combination of motor dysfunction, often consisting of resting temor, rigidity, bradykinesia and postural instability. (Lewy bodies: eosinophilic inclusions)

Pathophysiology 1. Etiolory-unknown

2.

a. b. a.

Risk factors

Male > female 3:2


Age usually about age 55, (increases after 50, peaks at75)

3.

Signs and Symptoms

b.

c. Rigidity
d.
2)
1)

3) Micrographia R\brll B:i, -*o -.*i,. 4) Shuffling gait (small footsteps)


Cogwheeling

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*+

!DLrelD stress c a r&vhts :l$fnOf


Oe-rr^f r;\ r-rs1 4'"'-\ r\r^n^pas t' * '^*'

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

Increased tone in the involved exhemities (lead pipe)

Compensation - festination, rapid steps as if to run Decreased blinking

Depression

i.

HYPoPhonia

*'-ir^\k

ei'-'

P$

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
r

Wilson's disease (ceruloplasmin levels; patients younger than 40 years

6-l"irir..i.diT"'* 'T

sr:ru,-*. tqr.ls^

Diagnosis
1.
Clinical diagnosis

L4

a"to

'{ F 4 'ir:

lrrzl( old)

,(Q>1ur{u U{ ,Vro.

2. CT or MRI to rule out pathology-MRl may show degeneration of substantianigra 3. PET Scan

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Treatment Plan

i.

Lifestyle changes a. Hydration b. Smaller, frequent meals


Nondrug therapy a. PT, OT, Speech therapy b. Environmentalchanges

2.

3. Rx a. b.

Dopamine replacement

o Levodopa \ X . Levodopa/Carbidopa (SINEMET) "\4r^nc,rt-dz y


Dopamine agonists

mainstay oftreafuent

,.,

*V

o .

Bromocriptine(PARLODEL)
Pergolide (PERMAX)

c. MAO_B Tnhibitors . Selegiline @LDEpRyLl .\. Prqf$,bh


d. e.
Anticholinergics . Trihe:ryphenidyl (ARTANE) o Benzhopine (COGENTIN)
Amantadine (SYMMETREL)

\ 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:

a. Female; 20-{0 Years old b. Familial mYasthenia gravis d. e.

c.

Coexistent autoimmune disorders

Thyrnoma -* c
Thymus abnormal

e\\s -t I^ 4\"^6 '


n75% of patients

I^^V< Ll.3

3.

a. b.

Signs and SymPtoms: Muscular weakness

d. e.

c. Provoked bY exertion
Diplopia
Ftosis

Fluctuates through the daY

f.

Difficultyswallowing

Differential dia gnosis

1. Thyrotoxicosis 2. Multiple sclerosis 3. Polymyositis 4. Depression 5. Any disorder associated 6. Penicillamine ingestion 7. Botulism
1.

with fatigue

Labs and X-ray Findings

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.

Lifestyle changes-diet and activity as tolerated Rx a. Pyridostigmine(MESTINON) b. Neostigmine SROSTIGMIN)

d. Azathioprine (IMIIRAN) e. Cyclophosphamide

c.

Prednisone

f.

g.

Immune Globulin Cyclosporine

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

Status Enilepticus (generalized convulsive seizure)


Concem

:7

l3'/* .f
c\

Ft'

!r

PL

?
Acidosis (respiratory and metabolic)

.,, rt Pr-c*z'* sYAcq>"\ ett"k

. o r r .

Evaluation (acutely): More helpful - Glucose, Electrolytes, Calcium, Magnesium Less helpful - CBC, Renal function, ABGs, Toxicological studies

c\57*

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L rn.nuj-eJ

Treatment: Lorazepam

(ATIVAN) [orDiazepam (VALIUM)]

Fosphenytoin(CEREBYX) o 15 - 20 phenytoin equivalents (PE)&ilogram

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Psychiatric Topics
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Ellen D. Mandel, MPA, MS, PA-C


Ellen Mandel is an Assistant Professor in the Department of Primary Care of the University of Medicine and Dentistry (UMDNJ) of NJ/School of Health Related Professions. Her education includes a Bachelor of Science in Foods and Nutrition and both a Master of Public Administration and a Master of Science in PA studies. In 1980, she completed a clinical dietetic intemship and became a registered Dietitian (RD). In recognition of her work as an RD, she was awarded the Recognized Young Dietitian of the Year award from the American Dietetic Association. Ellen is a leader in diabetes education and I also a Certified Diabetes Educator (CDE). Most recently, she has commenced her Doctorate in Medical Humanities from Drew University, NJ. Ellen's interest in behavioral medicine stems from her many years working in both in and out patient medicine. As a dietitian, she gained experience with eating disorders and other mental health issues related to obesity and disease management. She actively managed many mental health issues such as depression, ADD, substance abuse, anxiety and personality disorders as a Family Practice PA. She has both clinical andpractical knowledge of the pharmacological management and initial counseling approaches in psychology. Ellen lectures nationally on the topics of behavioral medicine, nutrition, diabetes/endocrine problems, and bladder disorders. She considers herself very fortunate to have the opporfunity to teach and work clinically as well as have the opportunity to teach and work clinically as well as have quality time to enjoy her family.

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Generic

Name

Trade

Name

Usual Dose Range (me/dav)

Typical (Conventional or Traditional) Antipsychotics


Chlorpromazine Fluphenazine Haloperidol Loxapine
Thorazine

Molindone Mesoridazine
Perphenazine Thioridazine Thiothixene Trifluoperazine

Prolixin Haldol Loxitane Moban


Serentil

100 to 800 mg Zto 20 mg 2to 20 mg l0 to 80 mg l0 to 100 mg

Trilafon Mellaril
Navane Stelazine

50 to 400 mg l0 to 64 mg 100 to 800 mg

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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Antideoressant Asents Generic Name Trade Name


Tricyclic Antidepressants Tertiary amines Amitriptyline
Doxepin Imipramine

Initial Dose (me/dav) Usual Dose Ranqe (me/dav)


50 50 50 50

Elavil
Sinequan

Trimipramine
Secondary amines

Tofranil Surmontil
Norpramin
Pamelor

to to to to

75 mg

75 mg 75 mg 75 mg

100 100 100 100

to to to to

300 300 300 300

mg mg mg mg
.

Desipramine

Nortriptyline Protriptyline Dibenzoxazepine Amoxapine Tetracyclic Maprotiline Mirtazapine Triazolopyridines Nefazodone


Trazodone

Vivactil
Asendin

50 to 75 mg 25 to 50 mg l0 to 20 mg 50

100 to 300 mg 50 to 150 mg


15

to 60 mg

to 150 mg

100 to 400 100 to 225 mg


15

Ludiomil
Remeron
Serzone

50 to 75 mg
15 mg

to 45 mg

200 mg
50

Desyrel

to 150 mg

300 to 600 mg 150 to 400 mg


300 to 450 mg (max 450 mg/day)
15

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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Serotonin/Norepinephrine Reuptake Inhibitor Effexor Venlafaxine

75 mg

75 to 375 mg

Mood Stabilizers: Dosing and Serum Concentrations

Acute Mania Initial dosing


Serum conoentrations

100 to 200 mg

BID

with meals

mglkg/d in divided doses with meals


900 mg/d or 15 0.8-1.2 rnEq/L

500-750 mg/d or 5-10 mglkg/d

in divided doses with meals


50-150 mcg/ml

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

Benzodiazenine Antianxietv Asents


N Alprazolam Chlordiazepoxide
Clorazepate Diazepam Halazepam Lorazepam Oxazepam Xanax

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

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