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 ofOsteopathic Medicine (CCON{), Midwestern University (MW{I), inDowners Grove, IL. He is a tenured professor and board certified in bothEmergency Medicine and Family Medicine. From June 1997 through May2000, Dr. Sefcik served as Medical Director for the Physician AssistantProgram, College of Health Sciences (CHS), at MWU. Dr. Sefcik is amember of the NCCPA's'Board of Directors. @r. Sefcik is NOTrepresenting NCCPA during any portion of this conference; he is lecturingbased 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 beeninvolved in the. clinical training of physician assistants since 1990. Prior tojoining Midwestern Universrty's faculty, Dr. Sefcik was a faculty member inthe Pharmacology Department at Butler University and in the NursingDepartment at Marian College, both in Indianapolis, Indiana. Dr. Sefcik hasa Bachelor of Science in Pharmacy (1981), a Master of Science inPha::nacology (1994), both from Butler University, ffid an MBA May2004) from Purdue University.

CME ResourcesCertification & Recertification Exam Review

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Certifrcation & Recertification Exam ReviewCME Resources

2004

NeurologyDonald 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 otheretiologies of progressive mental deterioration and dementia.A diagnosis of exclusion......The main cause of progressive brain function decline in old age.

1. Dementia: Alg"!""lliprogressive deterioration of cognitive function. Prognosisdepends on etiologf_.-

2. Delirium: Antacute\cognitive dysfunction secondary to some underlying medicalcondition. Acute confusional state, metabolic or toxic encephalopathy, acute organicbrain 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)

$ Neurofibrillary Tangles - intracytoplasmic filament bundles(esp. cerebral cortex) -f,au

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* Neuritic (senile) Plaques - swollen collections of eosinophilic nerve cellprocesses (amyloid protein cores)

c. Virusesd. Autoimmune processe. Aluminum toxicity

2. Risk factorsa. Female slightly > maleb. Age-50-90, mean onset 8i yearsc. Head trauma -Td. Familvilsdtv ,{srr exk'"t '(:" C\:.":rr.-.'*!O\e Z\, \Ct. tt\

3. Signs and Symptomsa. Initially - vague and nonspecific

o Early - short term memory problems, shallow and labile affectr Later - remote memory affected, may become lost and confused

b. Dyslexia and dysgraphiac. Dyspraxia (hears and understands task, but cannot perform)d. Occasional gait and extrapyramidal disturbancese. Personalitydisturbancesf. Amnesia and confabulationg. Dementiah. lntellectual deciinei. Sleep disturbances

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Differentialdiagnosis ^, ' /i

1. Multi-infarctdem"#a - Zn-\ rY'r<,si (u^71.Lt/\ Lctw!< cf e)'t"^so'.

2. Brain Tumor4. Metabolic dishrbance

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r Th)'roido Renal

4. Drug/Alcohol effects5. Depression6. Any other cause of dementia

Labs and X-ray Findings1. CBC/Chem-Z32. Vitamin 812 Level/Folate3. Thyroid Function4. CT SCAN - Head5. EEG @lectroencephalogram)6. Lumbar Puncture, Syphilis Testing7. ABG, ESR, HfV Testing, ANA8. DruglToxin Screens

Treatment Plan1. 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-upl. Patienteducation

a. Advise family and caregivers of progressive natureb. Advise about drug effects and side effectsc. Monitor for care giver "burnout"d. Consideralternatives-daycare, etc

2. Future Appointnentsa. As necessary to follow progressionb. Based on coexistent health problems

3. 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).

Pathophysiolory1. Unknown etiology but may involve an autoimmune process or virus

2. Risk factorsa. Female>male

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3. Signs and Symptoms: (Subjective >> Objective)a. Often parorysmal in natureb. Visual changes (optic neuritis = pain; af[erent papillary defect)c. Paresthesiasd. Clumsiness

Emotional labilityFatigueInc o ordination/ataxiaDepressionWeaknessNystagmus

Differential diagnosis1. Brain tumor (CNS lymphomas)2. Neurosyphilis3. Systemic lupus erythematosus (SLE)4. Spinocerebellar degeneration \5. Arnold-Chiari malformation I ir*.2; rat;\. .1.-.cn;L: ,.,'T\e- \6. Myasthenia gravis \?.A.,'\,;-irA )

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Labs and X-ray Findings (no test = diagnostic)1. Evidence of demyelinization

r VERs-visual evoked response-delayed in @ 80%r SSEPs-somato-sensory evoked potentials-delayed n @ 60%r BSEPs-brain stem evoked potentials-delayed n @ 40-50%

2. CSF analysisa. Elevated IgG (oligoclonal bands) ) J.^*,n€_ R e6(;dTLr,^b. Increased lymphocytes 'c. Normal or elevated proteinSyphilis test - RPR/VDRLEryttpgyle sedimentation rate (ESR)CT of nm,f {f the brain $dRI more sensitive = periventricular lesions onT2 sigrral)

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3.4.5.

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Treatment PIan1. Lifestyle changes

a. Avoid overwork and fatigueb. Rest periods during acute relapses

2. Nondrug therapya. Occupationaltherapyb. Self-catheterization for urinary retention

3. Rxa. Corticosteroids may offer some benefit

o Methylprednisolone 1 gram for three to five days; taperb. Amantadine (SYMMETREL)c. Amitriptyline(ELAVIL)d. Others

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Follow-up1. Patienteducation

a. Variable and unpredictable coluseb. Relapse rab3Ao/o within one yearc. May disable the patientd. Hot weather associated with relapses

2. Future appointments as needed3. Emergency visits with acute decompensation

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Parkinson's Disease (paralysis agitans)

Definition - A neurodegenerative disorder of tb system of unknown

cause that affects primarily the dopamine-containing neurons of the substantia nigra,

resulting in a combination of motor dysfunction, often consisting of resting temor,rigidity, bradykinesia and postural instability. (Lewy bodies: eosinophilic inclusions)

Pathophysiology1. Etiolory-unknown

2. Risk factorsa. Male > female 3:2b. Age usually about age 55, (increases after 50, peaks at75)

3. Signs and Symptomsa. Resting tremor (typically asymmetric in an upper extremity)

1) 3-5 cps (cycles per second)2) Distal exbemities, usually at res! increases with stress ! - :l$fnOf3) Damps with voluntary movement

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b. Bradykinesia1) Gait disturbance - slowness of movement2) Loss of facial expression3) Micrographia R\brll B:i, -*o -.*i,.4) Shuffling gait (small footsteps)

c. Rigidity

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1) Increased tone in the involved exhemities (lead pipe)2) Cogwheeling - qs 7ci:,rrl,)-{l-)o,n\ e,t$,r(\ ,.} gcJs .Jno,Jh .lten P'ujl

d. Loss of postural reflexes i)1) Retropulsion- falls baekwards easily 'T'gn 'hwb * e{? lft2) Compensation - festination, rapid steps as if to run

e. Decreased blinkingf. Depressiong. Dementiah. Droolingi. HYPoPhonia *'-ir^\k ei'-' P$

Differential diagnosis1. Exfapyramidal side effects of neuroleptic drugs2. Benign essential temor - head and UE (not LE), improved after alcohol ingestion3. Infectious, metabolic or toxin effects producing tremorr Thyroid 6-l"irir..i.diT"'* 'T sr:ru,-*. tqr.ls^ lrrzl( ,(Q>1ur{ur Wilson's disease (ceruloplasmin levels; patients younger than 40 years old) U{ ,Vro.

Diagnosis L4 a"to '{ F 4 'ir:1. Clinical diagnosis2. CT or MRI to rule out pathology-MRl may show degeneration of substantianigra3. PET Scan

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Treatment Plani. Lifestyle changes

a. Hydrationb. Smaller, frequent meals

2. Nondrug therapya. PT, OT, Speech therapyb. Environmentalchanges

3. Rxa. Dopamine replacement - mainstay oftreafuent

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

b. Dopamine agonistso Bromocriptine(PARLODEL). Pergolide (PERMAX)

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

d. Anticholinergics. Trihe:ryphenidyl (ARTANE) \ ro Benzhopine (COGENTIN) d- TfenOt-

e. Amantadine (SYMMETREL)

4. Surgery-Thalamotomy

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Follow Up1. Patient Education

a. Advise about need for lifelong medicationsb. Advise on drug effects/side effectsc. Expected prognosis is cbronic, slowprogression

2. Future Appointments - Medication monitoring at appropriate intervals3. Emergency Visits - Acute decompensation

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lVlvasthenia Gravis

DefinitionA disorder of the neuromuscular junction resulting in a pure motor syndrome

characterized by weakness and fatigue on exertion, particularly of the extraocular'

pharyngeal, facial, cervical, proximal limb and respiratory musculature.

Pathophysiology1. Vtyasttrenia [iavis (MG) is a disorder of neuromuscular transmission characterized

bythe pr"s"nc" of a gamma globulin antibody (AChR-ab) directed against the

nicotinic acetylcholiie r"."pio. (AChR) of the neuromuscular junction, resulting in

reduction in postsynaptic response to ACh'

2. Risk Factors:a. Female; 20-{0 Years oldb. Familial mYasthenia gravis

c. Coexistent autoimmune disorders

d. Thyrnoma -* c e\\s -t I^ 4\"^6 I^^V< Ll.3e. Thymus abnormal n75% of patients '

3. Signs and SymPtoms:a. Muscular weaknessb. Fluctuates through the daY

c. Provoked bY exertiond. Diplopiae. Ftosisf. Difficultyswallowing

Differential dia gnosis1. Thyrotoxicosis2. Multiple sclerosis3. Polymyositis4. Depression5. Any disorder associated with fatigue6. Penicillamine ingestion7. Botulism

Labs and X-ray Findings1. Electrodiagnostic studies: repetitive nerve stimulation

2. CT orMRI for thymoma3. Muscle biopsy4. Acetylcholine receptor antibodies (AChR-ab)

5. Thyroid function tests

6. Edrophonium (TENSILON) test

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Treatment Plani. Lifestyle changes-diet and activity as tolerated2. Rx

a. Pyridostigmine(MESTINON)b. Neostigmine SROSTIGMIN)c. Prednisoned. Azathioprine (IMIIRAN)e. Cyclophosphamidef. Immune Globuling. Cyclosporine

3. Neurologist consultation

4. Surgical removal of thymus-thymectomy

Follow-up1. Patient education

a. variable courseb. medications-use and side effects

2. Future appointrnents-often when patient is unstable

3. Emergency visits-signs of decompensation, respiratory compromise

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Miscellaneous Points

Motor Sensory Reflex

L3 Hip flexion Anterior thigh

L4 Hip flexion Lateral thighMedial calf

Patellar

L5 ?*%ilffi,*{allux dorsiflexion

Lateral calfHallux

S1 Foot extension(Plantar flexion)

5ff toe Achilles

Last< 10 secondsAura (sometimes)Last - 2 minutes

F'?ostictal stateQuickly respond

Premonitory

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Status Enilepticus (generalized convulsive seizure)

Concem

. Acidosis (respiratory and metabolic)

Evaluation (acutely):

o More helpful - Glucose, Electrolytes, Calcium, Magnesiumr Less helpful - CBC, Renal function, ABGs, Toxicological studies

Treatment:

r 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 ofthe University of Medicine and Dentistry (UMDNJ) of NJ/School of HealthRelated Professions. Her education includes a Bachelor of Science in Foodsand Nutrition and both a Master of Public Administration and a Master ofScience in PA studies. In 1980, she completed a clinical dietetic intemshipand became a registered Dietitian (RD). In recognition of her work as anRD, she was awarded the Recognized Young Dietitian of the Year awardfrom the American Dietetic Association. Ellen is a leader in diabeteseducation and I also a Certified Diabetes Educator (CDE). Most recently,she has commenced her Doctorate in Medical Humanities from DrewUniversity, NJ.

Ellen's interest in behavioral medicine stems from her many years workingin both in and out patient medicine. As a dietitian, she gained experiencewith eating disorders and other mental health issues related to obesity anddisease management. She actively managed many mental health issues suchas depression, ADD, substance abuse, anxiety and personality disorders as a

Family Practice PA. She has both clinical andpractical knowledge of thepharmacological management and initial counseling approaches inpsychology. Ellen lectures nationally on the topics of behavioral medicine,nutrition, diabetes/endocrine problems, and bladder disorders. She considersherself 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 havequality time to enjoy her family.

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Generic Name Trade Name Usual Dose Range (me/dav)

Typical (Conventional or Traditional) AntipsychoticsChlorpromazineFluphenazineHaloperidolLoxapineMolindoneMesoridazinePerphenazineThioridazineThiothixeneTrifluoperazine

Atypical AntipsychoticsClozapineOlanzapine

QuetiapineRisperidoneZiprasidone

100 to 800 mgZto 20 mg2to 20 mgl0 to 80 mgl0 to 100 mg50 to 400 mgl0 to 64 mg100 to 800 mg4to40mg5to40mg

ThorazineProlixinHaldolLoxitaneMobanSerentilTrilafonMellarilNavaneStelazine

ClozarilZyprexaSeroquelRisperdalGeodon

50 to 600 mg10 to 20 mg250 to 500 mg2to8mg40 to 160 mg

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Generic Name Trade Name Initial Dose (me/dav) Usual Dose Ranqe (me/dav)Antideoressant Asents

Tricyclic AntidepressantsTertiary aminesAmitriptylineDoxepinImipramineTrimipramineSecondary aminesDesipramineNortriptylineProtriptylineDibenzoxazepineAmoxapineTetracyclicMaprotilineMirtazapineTriazolopyridinesNefazodoneTrazodoneAminoketoneBupropionMonoamine oxidase inhibitorsPhenelzineTranylcypromineSelective Serotonin Reuptake InhibitorsCitalopramFluoxetineFluvoxamineParoxetineSerhalineEscitalopram

ElavilSinequanTofranilSurmontil

NorpraminPamelorVivactil

Asendin

LudiomilRemeron

SerzoneDesyrel

Wellbutrin

NardilParnate

CelexaProzacLuvoxPaxilZoloftLexapro

50 to 75 mg50 to 75 mg50 to 75 mg50 to 75 mg

50 to 75 mg25 to 50 mgl0 to 20 mg

50 to 150 mg

50 to 75 mg15 mg

200 mg50 to 150 mg

200 mg

15 mg20 mg

20 mgl0 to 20 mg50 mg20mg50 mgl0 mg

100 to 300 mg100 to 300 mg100 to 300 mg100 to 300 mg

100 to 300 mg .

50 to 150 mg15 to 60 mg

100 to 400

100 to 225 mg15 to 45 mg

300 to 600 mg150 to 400 mg

300 to 450 mg (max 450 mg/day)

15 to 90 mg20 to 60 rng

20 to 60 mgl0 to 80 mg50 to 300 mg20 to 50 mg100 to 200 mgl0 to 20 mg

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Serotonin/Norepinephrine Reuptake InhibitorVenlafaxine Effexor 75 mg

Mood Stabilizers: Dosing and Serum Concentrations75 to 375 mg

Acute ManiaInitial dosing

Serum conoentrations

Maintenance TherapyDose

100 to 200 mg BIDwith meals

4-l2mc{ml

400 to 1800 mgld

XanaxLibriumTranxeneValiumPaxipamAtivanSerax

0.8-1.2 rnEq/L

600 to 1800 mg/d

50-150 mcg/ml

15 to 45 mglkgld

900 mg/d or 15 mglkg/d 500-750 mg/d or 5-10 mglkg/d

in divided doses with meals in divided doses with meals

Serom conc€dati@s 4-12 mog/ml 0 6-1 0 mEq/L 50-125 tJlcglml

Benzodiazenine Antianxietv Asents

NAlprazolamChlordiazepoxideClorazepateDiazepamHalazepamLorazepamOxazepam

0.75-4 mglday25-100 mg/day7.5-60 mglday2-40 mglday20-160 mg/day0.5-10 mdday30-120 mg/day

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