Neurology Board Review

Nick GenesOctober 8, 2008

the inservice exam• Feb 25, 2009• Short term $$$ (moonlighting, Mets)• Long term $$$$$$ (licensure, career in EM)• But also: intro to EM practice

• Similar questions to ABEM• Last year: 207 questions counted

• Physician’s Evaluation and Educational Review VII• Las Vegas Board Review Course MP3s (2003?)

This lecture series

• Board review: Five months, 20 lectures… • Different than Dr. Cherkas sessions

• This year: • More engagement than 2005-6• More questions, buzzwords than last year• More repetition• More candy

Neurology

• 21 questions in PEER VII (out of 410, 5%)• Some overlap in HEENT, S&S

• Last year’s inservice: it was 11 out of 207• CV, GI, Pulm, Trauma each ~20• Likely emphasis: details that make or break ED

diagnosis or management

Neurology

• Today: Stroke, Other Stuff, Seizures

• No evidence, no nuance.

Question 1A 74 year old female with history of DM, HTN, presents with 2 hours onset right face, arm > leg weakness with an associated right hemisensory deficit. No left sided deficits. No cranial nerve deficits. What is the most likely diagnosis?

a)Basilar Artery OcclusionLocked-In Syndrome – severe quadriplegia… only upward gaze intact!

b)Subarachnoid HemorrhageWhere’s the headache? Nausea? Vomiting?

c)Lacunar InfarctionPure motor or sensory deficit, caused by chronic HTN

d)Middle Cerebral Artery OcclusionMost common stroke syndrome… face + arms > legs. Aphasia in dom. hem.

e)Posterior Cerebral Artery Occlusionwhere’s the diplopia? PCA stroke is primarily visual

Middle Cerebral Artery Occlusion• Lateral parietal, temporal, and

frontal lobes• Contralateral Motor/ and Sensory

Face and Arm > leg• Ipsilateral Hemianopsia • Aphasia/ Dysarthria (left sided

stroke)• Agnosia / Neglect, extinction of

double stimulus (right parietal lobe)- timing!

CT Finding with MCA Occlusion• Hyperdense MCA sign• Loss of cortical ribbon• Sulcal Effacement• Obscuration of the

grey/white junction

Question 2A 70 year old male presents to the ER with weakness in the leg upon waking this morning. His exam shows left leg 2/5 strength with ataxia of limb, 4/5 left arm strength, no facial droop. He keeps asking what time it is. Where is his lesion?

a) Middle Cerebral ArteryNo – face and arms > legs

b) Anterior Cerebral ArteryFrontal, medial parietal and temporal lobes, legs > face, amnesia, confusion

c) Posterior Cerebral ArteryPrimarily visual, with homonymous hemianopia, also amnesia, tremor

d) Basilar ArteryLocked-in state

e) Carotid ArteryHe’d have bigger problems…

Anterior Cerebral Artery Stroke

• Affects medial parietal, temporal, and frontal lobes

• Contralateral Motor and Sensory Leg > face and arm

• Dis-inhibition, perseveration, primitive reflexes

Basilar Artery Stroke• Bilateral sx• Coma• Locked in syndrome

Posterior Cerebral Artery Stroke• A variety of presentations involving amnesia, LOC,

perserveration, tremor, hallucinations. Primarily visual• Lesion on the right, past optic chiasm can’t see

images on the contralateral side of either eye

Cerebellar Infarct

• Sudden inability to walk or stand (drop attack)• Dizziness, nystagmus, ataxia• 1/3 will develop significant edema• Early neurosurg consultation• Rapid deterioation with hemorrhage, infarct

edema, watch for respiratory arrest

Question 2A 72 year old man presents with acute onset vertigo, nystagmus, dysphagia, and Horner’s syndrome. The most likely diagnosis is?a) Acute Labryinthitis

Acute vertigo, sure… but not going to cause Horner’s, dysphagia

b) Benign paroxysmal positional vertigo Vertigo… but not going to cause Horner’s, or dysphagia

c) Lateral Medullary Infarction what does this look like? well… does it matter?

d) Ophthalmoplegic Migraine Could cause CN III palsy, but not going to cause Horner’s

Lateral Medullary InfarctionAKA Wallenberg SyndromeAffects multiple areas:

Trigeminal nucleusDescending sympatheticsLateral SpinothalamicVestibular nuclei

Ipsilateral face• Pain and Temperature (5)• Dysphagia• Dysarthria• Nystagmus (VN)• +/- limb ataxiaContralateral Limbs• Pain and Temperature (LS)

Posterior Circulation Strokes• The 6 D’s of Brainstem• Dysphagia• Dysarthria• Diplopia• Dystaxia• Dizziness• Drop attack (syncope)• Ipsilateral Face • Contralateral Extremity• Visual Field Deficits

Horner’s Syndrome• Miosis (constriction), ptosis, anhidrosis on affected side• Sympathetic fibers run upwards via cervical spine ganglia• Innervate pupillary dilators (dilation lag) and lids, sweat glands• Seen in migraine, brainstem CVA, Pancoast tumor, brachial plexus

trauma, Lung lesion (TB, HMX), neuronal lesion

Vertigo

Peripheral-Sudden-Tinnitus, Auditory-Severe n/v/dizzy-Horizontal Nystagmus-May be positional, recent

infections

Central-Insidious-No peripheral sx-Less severe n/v/dizzy-Vertical or Horizontal

Nystagmus-Not positional, may have

peripheral neuro deficits

Question 3

• A 43 year old female presents to the ER with her husband. Her husband states that his wife has been having the worst headache of her life and is “a bit off”. On exam she uncomfortable and confused without focal motor or sensory deficits.

• A CT scan is obtained.

Question 3What is the most common etiology for the diagnosis revealed by the CT scan?a) AVM

It’s a possibility

b) Cavernous AngiomaIt’s a possibility

c) Mycotic AneurysmIt’s a rare possibility

d) NeoplasmMore likely to cause hematoma, edema

e) Saccular Aneurysm“Berry” -- cause of 80% of non-traumatic SAH. 5% of us have these

Subarachnoid Hemorrhage• Collection of blood in subarachnoid space• Most likely causes are trauma, ruptured aneurysm, AVM• What makes a berry rupture? Age, HTN, smoking, drinking, coke• Mostly in age 40-60• 2-4% Patient visits for HA• 2-4% will have SAH; 12 % of pts with worst headache of life will

have SAH, increases to 25% if abnormal neurologic exam• Headache 100%, Nausea and emesis 77%, focal deficits 64%,

syncope 53%, neck pain 33%, photophobia, seizures in 25% of patients

• 20-50% have prior warning headache “sentinel bleed” days prior

Subarachnoid hemorrhage

• Hunt & Hess I-V grades severity, partially predicts rebleed, death

• Grade I has normal neuro exam, does very well (1/3)• Grade V presents in stupor or coma and always dies

• CT – 93% sensitive, drops with time• LP – xanthochromia• Treatment – nimodipine, neurosurgical consult,

aggressive BP control

Question 4Which of the following pretreatment patient characteristics has been associated with an increased risk of intracerebral hemorrhage following treatment with TPA for acute ischemic stroke?

a) Advanced AgeNot an independent risk factor for ICH

b) Increased NIHSSIn NINDS, one of 2 independent risk factors for ICH (with “infarct signs”)

c) Isolated global aphasiaNo – by itself, low NIHSS score but should be considered for tPA

d) Major surgery within 14 daysNo increased risk of ICH, but tPA means increased risk from noncomp sites

e) Rapid improvement of neurological signsNo – don’t give them tPA because (regular) risk of ICH outweighs benefits

Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group.

NEJM. 1995 333:1581-1587.

• Double-blind, randomized, placebo controlled• Pts tx with rTPA are 30% more likely to have minimal

to no disability at 3 months compared to standard care

• Increase risk of symptomatic ICH (6.4%) with increasing NIHSS

• American Heart Association, American Academy of Neurology, ACEP (if system in place)

tPAInclusion CriteriaAge > 18Diagnosis of stroke with measurable

deficitTime of onset < 3 hours before

treatment will begin

Relative ContraindicationsMajor surgery or serious trauma

within 2 weeksOnly minor or rapidly improving

stroke sxHistory of GI or GU hemorrhage

within 21 daysRecent arterial puncture as non-

compressable siteGlucose >400 or less than 50Post MI pericarditisPatient with observed seizure at

time of stroke onsetRecent Lumbar Puncture

Exclusion CriteriaEvidence of ICH on CTHistory of ICH or AVMSuspected SAH with normal CTActive internal bleedingPlatelets < 100,000Heparin within 48 hours with an

elevated PTTCurrent use of oral anticoagulant

with PT> 15secSBP > 185 or DBP >110 at time

treatment is to beginWithin 3 months any intracranial

surgery, serious head injury, or previous stroke (not TIA)

Question 5Which of the following statements best describes the role of neuroimaging in a patient presenting with acute stroke symptoms?

a) CT and MRI are equivalent for detecting hemorrhagic transformation of an acute ischemic stroke

MRI is superior at catching this.

b) CT is superior to MRI for detecting chronic hemorrhageMRI sees more small hemorrhages that CT misses, but determining age is tricky

c) MRI and noncontrast CT are equivalent for identifying acute hem.Within 6 hours, yes, they’re just as good. Shouldn’t really impact our practice.

d) MRI is superior to noncontrast CT for detecting acute hemorrhageNot superior. Equal.

e) Unenhanced CT remains superior to MRI for detecting acute hem.Not superior. Equal.

Question 6A 47yoM with a history of DM2 and HTN presents with disorientation and repetitive questioning. He is amnestic to the events of the day and cannot provide details of his presentation. His long-term memory is preserved. His wife reports a sudden onset of symptoms this morning. He’s had no recent illness, med changes, travel, or drug use. FSBS is 115 mg/dL. No focal neurological deficits are seen, and he is alert and cooperative. The most likely diagnosis is: a)Complex partial seizure

Um… he’s alert and not shakingb)Delirium

Hallmark is inattention, fluctuating course, disorganizationc)Psychogenic amnesia

Subgroup of “dissociative disorders” seen under stress, forget personal infod)Transient global amnesia

No new memories for a day! TIA? complex migraine? +/- headache, anxiety. e)Transient ischemic attack

Possibly, but usually motor or sensory deficits. Unlike TGA, TIA can progress to stroke

Question 7An 84 year old man with h/o HTN, DM, Afib on coumadin presents with left sided hemiparesis and left sided hemisensory changes with left sided neglect. He has a GCS of 15. Thirty minutes into his assessment his GCS falls to 11 with profound confusion. What is the most likely cause?

a)Anterior Cerebral Artery EmbolismSudden, maximal at onset. You’d expect leg weakness

b)Internal Capsule Intracerebral HemorrhageOften HTN etiology, evolves from ischemic stroke, does not improve.

c)Posterior Cerebral Artery RuptureWell, sure, there’s a change in consciousness… Would be comatose.

d)Posterior Cerebral Artery ThrombosisWould cause fluctuating course, visual defects, ?hallucinations

e)Vertebral Artery OcclusionMaybe a Wallenberg syndrome or medial medullary syndrome

ICH

• Basal Ganglia 40-50%• Lobar: 20-50% (esp young,

increased sz activity)• Thalamus 10-15%• Pons 5-12%• Cerebellar 5-10%• Brain Stem 1-5%• Volume= (a+b+c)/2

ICHGCS 3-4 2 5-12 1________ ___13-15 0ICH Vol >30 1__________ _<30 0IVH Yes 1__________ _No 0Infratentoral Yes 1__________ _No 0Age >80 1__________ _<80 0

0-6

Intracranial Hemorrhage• 8-13% of all strokes• Only 20% of pts regain full functional independence • Increase incidence: AA, Asian, age >55, EtoH, Smokers• Trauma, HTN, altered homeostasis, hemorrhagic necrosis, venous

outflow obstruction• Causes brain injury via:

1. Increased Intracranial Pressure2. Increase edema, mass effect3. Decrease perfusion to local and adjacent tissue4. 35% ICH will expand sig (>33%) within 24 hours; majority within 6 hours

• Hemorrhagic transformation may occur during an apparent ischemic stroke

• Think of it with sudden change in consciousness • Reversal of anticoagulation

Question 8A 22 year old female presents with double vision. The symptoms disappear with either eye is covered. Extraocular movements are intact when tested individually. On conjugate gaze testing there is nystagmus in the left eye and limited adduction in the right eye. What is the most likely cause?

a)Dislocated LensThis is a cause of monocular diplopia

b)Tertiary neurosyphilisRestrictive gaze, vision loss. Unlikely by age 22…

c)Internuclear OpthalmoplegiaLesion of the MLF, which processes conjugate eye movements from cortex to VI and III. Eyes move

normally when tested separately because primary pathway intact. Often MS. d)Retro-orbital hematoma

Another binocular diplopia, pressing on EOM, but same apart or conjugate.e)Third Nerve palsy

Down-and-out. Another binocular diplopia, but same apart or conjugate.

Internuclear Opthalmoplegia

• Occurs due to disruption in the medial longitudinal fasciculus (MLF)

• Coordinates conjugate eye movements• Most commonly due to MS• MS occurs in young women; deficits vary anatomically and

temporally

Diplopia

Monocular• Refractive error• Dislocated lenses• Iridodialysis• Malingering

Binocular• CN palsies• Brain lesions• HTN crisis• Cocaine• Wernicke’s • SLE• Retro-orbital

mass/hematoma

Question 9A 45 year old male presents with nausea, emesis, and diarrhea. He is given 2 liters of IVF and 12.5mg of promethazine. 15 minutes later he is anxious and wants to leave the ED immediately. What is the diagnosis and management?

a)Anxiety – discharge with psych f/uDismissing medical complaints is almost never the answer

b)Gastroenteritis – if tolerating PO, D/CNo, something’s changed…

c)Delirium – give haldol and call psych.Hallmark of delirium is inattention, not anxiety…

d)Med reaction -- give him ProchlorperazineNo! Causes akathesia in 44% of ED N/V patients within 1h

e)Med reaction – give him Benztropine This is akathesia

Akathesia• Acute dystonic reaction marked by anxiety,

restlessness• Other dystonic rxns include torticollis• Associated with high potency antipsychotic (haldol),

and any dopaminergic medications (promethazine, metoclopramide, prochlorperazine)

• Treatment includes anti-cholinergic medications such as diphenhydramine and benztropine (not to use in kids less than 3) – they restore the balance of dopamine-ACh receptors.

Question 10A 48 year old disabled physician presents with severe low back pain, screaming obscenities. After administering hydromorphone 8 mg IV, he is more cooperative but still rude.

Vitals are BP 190/105, HR 110, RR 22, Temp 101.3F, O2 Sat 99% RA. Exam reveals a disheveled man without signs of trauma, with a normal exam except for midline lumbar tenderness. No focal neuro deficits. UA, CBC, Chem 7 are normal. Plain lumbar films show moderate DJD.

Question 10Angry disabled physician with lumbar tenderness, HTN, tachycardic, febrile, screaming for opioids. The most appropriate next step in management is:

a) Admit for pain controlFever must be worked up

b) CT scanCan’t visualize spinal canal, cord, or discs as well as MRI.

c) Discharge to pain clinicMuch of his presentation suggests drug-seeking, but…

d) MRIFever + back pain suggests epidural abscess or vertebral osteo.

e) Consult psychiatryMuch of his presentation suggests drug-seeking, but…

Back Pain Red Flags

• Progressive neurological findings

• Constitutional symptoms (fever)

• History of traumatic onset

• History of malignancy

• Age under 18 years or over 50 years

• IVDU• Chronic steroids• HIV• Osteoporosis• Pain > 6 weeks

*American college of radiology “Red Flags”

Cauda Equina Syndrome• Ca, Infiltrative, Sarcoidosis,

Trauma, Infectious, Ank Spon

• Pain, radicular• Weakness- variable• Saddle sensory changes• Overflow incontinance

urine/stool• Neurosurgical consultation• Steroids + /-

Other causes

Sciatica• Radicular Pain• Lateral or post leg to foot• Straight leg raise (10-60),

crossed• Numbness, no weakness• NSAIDS

Epidural Abcess• Staph (MRSA) 63%; Gram Neg,

Strep, Anaerobes, TB (potts)• Multiple levels• Epidurals, Surgical, IVDU,

Cryptogenic• DM, ETOH, HIV• Pain, Fever, Weakness• MRI/ CT w/ gadolinium• Surgical Decompression

/Aspitation• Abx: Nafcillin (Vanc)+Flagyl+ Ceftazidime or Cefotaxime

Question 11A 32 year old man who lives in New England presents complaining of bilateral leg weakness. His symptoms began with paresthesias in his toes followed by progressive weakness in both legs. Cranial nerve exam is normal. Motor strength is 3/5 in both legs, 4/5 both arms and sensation to light touch is mildly decreased in both legs. DTR’s are absent in both legs and +1 in b/l arms. What is the most likely diagnosis?a)Amyotrophic lateral sclerosis

Involves UMN and LMN weakness, fasciculations, dysarthria, hyperreflexia

b)Familial periodic paralysisChannelopathy that can lead to severe symmetric extremity weakness.

c)Guillain-Barre SyndromeClassic presentation of ascending muscle weakness and loss of DTR. +/- sensory.

d)Myasthenia gravisAB against ACh receptor in NMJ. No sensory component.

e)Tick paralysisCan mimic GBS but is mediated by neurotoxin, never has sensory component

Guillain-Barre Syndrome

• Immune-mediated; motor, sensory, and autonomic dysfunction

• GBS the most common cause of acute flaccid paralysis in the United States

• Pure motor and motor + sensory subtypes. • 40-80% seropositive for Campylobacter jejuni• Haemophilus influenzae, Mycoplasma

pneumoniae, and Borrelia burgdorferi. CMV, EBV, HIV

• 85% of pts with normal recovery 6-18 months

Guillain-Barre Syndrome

• Ascending weakness from proximal thighs to trunk and upper extremities

• Cranial nerves, respiratory muscles (1/3rd)• Paraesthesias distal to proximal, Proprioception,

sensory• Autonomic dysfunction; HR, BP, Temp, Fecal and

urinary retention

Guillain-Barre Syndrome

• Clinical diagnosis supported by:• Elevated or rising protein levels on serial lumbar

punctures (90% pts) 1-2 weeks• CSF pleocytosis in HIV associated• Cauda Equina nerve roots enhance in 85%• ABG and FVC to assess respiratory function,

intubate for ventilatory failure• IVIG and plasma exchange tx (plasmapheresis)

MG and LEMyasthenia gravis-Autoantibodies against post-synaptic Ach receptors -Bulbar sx initially- ptosis, diplopia, dysphagia, 1% resp-Descending weakness-Thymoma 10-15%-Sx improve with rest

Lambart-Eaton Syndrome-Autoantibodies against voltage gated calcium channels in pre-synaptic

motor nerve terminal-Proximal lower extremity weakness (up from chair), months-Less common bulbar findings-Highly associated with cancer (50-70%)-Sx improve with movement

Other Paralytic DisordersFamilial periodic paralysis-Chanelopathy resulting in inexcitability of Na/Ca channels leading to

periodic flacid paralysis-Hyperkalemic and Hypokalemic subtypes-Worsened by heat, stress, high carbohydrate meals-Treatment: Give K (or take it away).

Tick paralysis-Caused by neurotoxin from salivary gland-Ascending paralysis 1-2 weeks-Rock Mountain wood tick (Dermacentor andersonii) and American

dog tick (Dermacentor variabilis) … not Idoxes (Lyme)-Treatment: Remove tick. Wait patiently.

Question 12A 43 year old male presents to the emergency room with 2 hours onset decreased movement of right side of face, ear pain, and thinks he might have had spoiled milk with his cereal this am because it tasted funny. What is the least important question for the diagnosis?

a) When was the milk’s expiration date?Come on (although botulism is associated with honey in infants)

b) Can he move his forehead?Distinguishes stroke from Bell’s Palsy (stroke = forehead spared)

c) Does he have a history of migraine?Attempting to pin this on complex migraine

d) Does he have clustered vesicles about the ear?looking for Ramsay-Hunt variant of Bell’s Palsy

e) Does he have peripheral motor weakness?Distinguishes stroke from Bell’s Palsy

Bell’s Palsy• Facial Nerve CN 7 palsy• Upper and lower facial

weakness• Post auricular pain• Hyperacusis (stapedius)• Hypoageusia (ant 2/3 tongue)• Decreased lacrimation

• Recovery: 30% pts w/ Crocodile tears, dysagusia, partial paralysis; 80-90% without sig deficit

Bell’s Palsy• GEORGE CLOONEY has revealed he

suffered from paralysing Bell's Palsy when he was a teenager. he muscle-weakening disorder left him with a temporary disfigured face, but Clooney has always had the perfect response for people who poke fun at his odd high school photos. He says, "People bring it up and they go, 'Look how goofy you looked,' and I go, 'I had Bell's Palsy; you feel bad now.'" And in a new interview with U.S. TV news show The Insider, the grey-haired movie hunk offered another big surprise from his past: "I was a blond."

Bell’s PalsyCausesHSV 1,2VZVMycoplasma pneumoniaeBorrelia burgdorferieHIV (b/l)AdenoviruscoxsackievirusEbstein-Barr virusHepatitis A, B, and CCytomegalovirus

TreatmentPrednisone 60mg/day X 10 days?Acyclovir 800mg 5X/day for 7

days?Valacylovir 1000mg TID for 7 daysArtificial Tears

Ramsey-Hunt Syndrome

• Herpes Zoster Oticus; HSV1, HSV2, VZV• Triad of auricular pustules, ear pain, ipsilateral

facial paralysis• +/- Hypoaguesia and hyperacusis• Worse prognosis

Bell’s Palsy- Treating Ourselves?• Cochrane Database 2004- trials of antivirals with or without

steroids -- insufficient evidence for support of antivirals• Valcyclovir and prednisolone treatment for Bell's palsy: a

multicenter, RCT Otol Neurotol. 2007 Apr;28(3):408-13. N=221; 6-8% improvement in severity and complete remission

• “low-cost steroids can yield a 9% absolute reduction in risk for residual paralysis.” 1 mg/kg of prednisone or prednisolone daily in two divided doses for 10 days.

• If steroids are contraindicated, the spontaneous recovery rate of 85% by 9 months is reassuring to both doctor and patient.

Question 13A 25 year old male presents with 1 day of severe right sided head and neck pain with blurred vision. He states he went to his chiropractor in the morning before symptom onset. On exam he has right sided miosis and ptosis with normal motor function and sensory function. What is his most likely diagnosis?

a) Right brainstem CVAPain less likely, Horner’s fits but no other lesions?

b) Cluster HeadacheTime course is wrong, pain behind eyes for minutes a day, O2 therapy

c) Bell’s PalsyPain doesn’t fit

d) Tick BiteNot even a diagnosis… Not Lyme, not Tick Paralysis, not RMSF…

e) Carotid artery dissectionUnilateral facial / neck / orbital pain, usually after manipulation

Carotid Artery Dissection• Unilateral

facial/neck/orbital pain• Hypoageusia• Transient blindness,

amaurosis fugax• 50% w/ partial Horners

syndrome• 25% pulsitle tinnitus• Neck swelling, bruise• May progress to CVA with

dense hemiparesis

• Trauma• Chiropractic manipulation• Sports, yoga• CTD• HTN• Smoking• Oral contraceptives

Diagnosis and Treatment

• Angiography gold standard

• MRA optimal if available

• CT angiogram evolving, esp for trauma pts

• Anticoagulation with heparin to prevent thromboembolic complications

• If can’t, consider ASA• Neurosurgical

consultation

Question 14Clinical features of delirium include:

a)ApraxiaA decreased ability to carry out motor activities? More likely in dementia

b)Auditory hallucinations Usually visual

c)Disordered attentionThe hallmark of delirum. Unlike dementia! Worth investigating and reversing.

d)Insidious onsetDelirium is abrupt, involve fluctuations over the day. Dementia is stable.

e)Sustained delusionsUsually poorly organized, rarely sustained. Dementia has fixed, false beliefs.

Question 15Pharmacologic causes of parkinsonism include:

a)BarbituratesSedative-hypnotic with no extrapyramidal effects

b)BenztropineCogentin – actually helps parkinsonism (anticholinergic for dystonia)

c)BromocriptineActually helps parkinsonism (dopamine agonist)

d)BupropionThis is Wellbutrin/Zyban. Overdose is associated with seizures.

e)ButyrophenonesHaldol, Droperidol antagonize dopamine, disinhibit cholinergic response.

Parkinsonism

• 80% idiopathic (called Parkinson’s disease)• Other causes: drugs, trauma, malignancy, degen• Insiduous onset• Motor deficiencies are assymetric• Cogwheel rigidity on passive ranging, shuffling gait• Falls

Question 16Which of the following statements regarding idiopathic intracranial hypertension is correct?

a)A head CT will show markedly enlarged ventriclesVentricles are actually small, cisterna magna is large.

b)Acetazolamide is an accepted medical treatmentReduces CSF production

c)LP is contraindicatedLP is diagnostic and therapeutic (pressures > 20 cm H20, the rest is WNL).

d)Requires prompt neurosurgery to prevent herniationDelirium is abrupt, involve flucuations over the day. Dementia is stable.

e)Severe weight loss is a prominent part of the HPI??? Obesity is associated with pseudotumor

Pseudotumor Cerebri (Benign Intracranial Hypertension)

• Young obese female, irregular menses• At risk: high vit A or chronic steroids• Impaired CSF absorption• Elevated CSF pressure without mass or obstruction• Serious outcome – visual loss• Visual complaints, headache, no focal signs• CT – slit like ventricles, no mass effect• LP- high pressures• Treatment – repeat LP, steroids, acetazolamide

Acetazolamide• Not something commonly given in the ED• It comes up in (at least) three places on the inservice:

– Acute Mountain Sickness (only FDA approved agent!) – Pseudotumor– Glaucoma (but don’t give it if they’re sicklers)– No lit to support in HACE (give steroids, O2, descend)

• Carbonic anhydrase inhibitor• Makes you piss away bicarb metabolic acidosis

increased ventilation, oxygenation• Also decreases CSF volume, relieves ICP, IOP• Makes soda taste funny

Question 17A pediatrician calls AMAC with a greet: “PRIVATE PATIENT EN ROUTE BY CAR. MOTHER SAYS CHILD (MALE) IS JERKING, FEELS HOT. NO PMHX, NO MEDS. SUSPECT SIMPLE FEBRILE SEIZURE.” Assuming that the PMD is right, which of the following most likely describes this patient and his ED encounter? a)2 weeks old, afebrile, well-appearing, had a generalized seizure that lasted 10 minutes

Too young (must be 6 months – 5 years)b)4 months old, febrile, had a generalized seizure at home that lasted 10 minutes, UTI diagnosed in ED

Too young. Would need LP. Also at this age, more likely to recur. c)19 months old, febrile, well-appearing, had a generalized seizure at home that lasted 10 minutes

Right age, right seizure. No chance of occult meningitis. LP? d)23 months old, well-appearing, had 2 gen. seizures 5 min each

Simple Febrile Seizures can only occur once per 24 hours. LP him! e)9 years old, febrile, generalized seizing on arrival, had one hand twitching at home x10 minutes.

Too old! Must be under five years. Also, this is a complex partial seizure. CT,LP.

Question 18A 44yoM presents following a witnessed seizure that lasted 2 minutes. He has no history of a seizure disorder, and has otherwise been in his usual state of health. Thirty minutes later he has another seizure that begins in the right arm and progresses to 1 minute of jerking of the extremities followed by a post-ictal confusion. This event is most accurately classified as:

a)Absence seizure Um… he’s shaking (absence seen in kids 4-12, sometimes with fine facial tics)

b)Complex partial seizure Most accurate classification … simple partial with secondary generalization

c)Grand mal seizureNo abrupt onset – this was a progression from a focus

d)Psychomotor seizureBad catch-all term that encompasses complex partial seizures

e)Temporal lobe seizureOften preceded by aura, complex partial… involves behavioral changes, hallucinations

Seizure types

GeneralizedNo inciting focusBegin in both

hemispheresAbrupt LOCOften, no aura

Partial (focused)Simple: No LOC or AMSSimple: Motor, sensory,

autonomicComplex: Altered

Consciousness

New onset seizures in adults are most often these simple seizures with secondary generalization… due to a focal finding on CT or MRI

ConvulsiveTonic clonic (Grand Mal)Clonic only, tonic only,

atonic, myoclonic

Nonconvulsive (absence)

Question 1938 y/o female with a history of epilepsy presents with multiple seizures without return to consciousness for 30 minutes. Her finger stick is 100 and her blood ICON is (-). She has been given 4 mg of ativan x2 but continues to seize. What is your next step?a)4 mg midazolam

A short-acting benzo is not “the next step”

b)8 mg lorazepam We’ve already tried 8 mg of ativan…

c)Vitamin B6No reason to suspect INH toxicity

d)Fosphenytoin loadThis is the appropriate second-line agent for status epilepticus

e)Succinylcholine and etomidate with ETTWhat, and take away our neuro exam?

Status Epilepticus

• Status Epilepticus• 30 minutes of seizure activity without return of

consciousness• If seizure >4-5 minutes consider status; neuronal

injury- must wake up!• If considering Non-convulsive SE, get EEG!

• Treatment of SE based on universal guidelines and institutional protocol

• Treatment and investigation parallel

Status Epilepticus• 1/3rd new onset• 1/3rd epilepsy• 1/3rd:

• Idiopathic• Hyper/hyponattremia• Hypercalcemia• Hypoglycemia• CVA• Trauma• Infectious• Mass• HE

Toxins• INH • Tricyclics (AVR, QRS)• Theophylline • Cocaine• Sympathomimetics• Alcohol withdrawal • Organophosphates

(strychnine)• DM medications

(glucose)

Status Epilepticus

1st Line: Ativan 4 mg over 2 minutes q5 min X2• If no access 20mg diazepam pr, 10mg midazolam IM• 2nd Line: IV Fosphenytoin (20mg/kg at 150mg/min;

may add 10mg/kg)• May give IV Keppra, Valproic Acid, Phenobarbitol if

pt is on it• 3rd Line: Pentobarbitol, Intubation with continuous

drip of midazolam or propofol• Other: Vitamin B6 (70mg/kg up to 5 )

THE END

Bonus slides

Question 12A 35 year old female 1 week post-partum presents with 1 day of severe headache, nausea and vomiting. She is slightly confused and lethargic. She is afebrile, normo-tensive, with a negative UA. Given the clinical picture, what is the treatment of choice? a)PCC or FFP

no

b)Emergent Craniotomyno

c)Serial lumbar puncturesno

d)Magnesium Sulfate IVno

e)Heparinyes

Venous Sinus Thrombosis

• Headache, nausea, emesis, ams, focal deficits; pesudotumor cerebri

• Women, peripartum, hypercoaguable states, systemic inflammatory conditions

• CT head, MRV• Atypical ischemic or

hemorrhagic region• Tx: Heparin

Question 5A 23 year old patient presents is BIBEMS being bagged with a GCS of 3. His friend is with him and states that while doing “a lot” of cocaine his friend developed severe headache with sudden loss of conciousness. Which of the following considerations in further management is incorrect?a) Pretreat with lidocaine and consider fentanyl and vecuronium

This is fine (especially with the “consider”)

b) Do not allow single episode of hypoxia or hypotensionThis is very important

c) Hyperventilate to pC02 25-30 mmHgNo!

d) Raise head of bed to 30 degreesThis is fine

e) Consider mannitol or hypertonic saline for deterioration in neurologic statusThis is fine (note: “consider”)

Maintain pCO2 between 35-40, not any lower!

Pretreatment• Oxygen NRB• Lidocaine 1.5mg/kg 3

minutes before• Fentayl 2ug/kg• Vecuronium .01mg/kg (De-

fasciculating Dose)• Intubation by most

experienced MD; single episode of hypoxia associated with poor outcome

Ventilation*Short term hyper-ventilation

for neurologic deterioration*Maintain pCO2 35-40 *Long term hyper-ventilation

not Rx

Management of elevated ICP

• CPP=MAP-ICP• Maintain cerebral perfusion• Do not lower BP by > 20%• General rule is to maintain

systolic between 160-180• A single hypotensive

episode is assoicated with worse outcomes

• Tx hypotension with IVF

• Treatment of Increased ICP includes:

-Mannitol-Raise Head of bed 30 D-Hypertonic Saline (future)-Hyperventilation-Surgical evacuation

• Orphan Slide• Cranial Nerve 6 (abducens)

palsy; lateral rectus; ACOM• Cranial Nerve 3

(occulomotor) palsy; ptosis, medial, superior, inferior gaze, pupillary constrictors; PCOM

• Subhyaloid Hemorrhage