Transcript Neurology Board Review

Neurology Board Review
Nick Genes
October 8, 2008
the inservice exam
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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
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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 1
A 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 Occlusion
Locked-In Syndrome – severe quadriplegia… only upward gaze intact!
b) Subarachnoid Hemorrhage
Where’s the headache? Nausea? Vomiting?
c) Lacunar Infarction
Pure motor or sensory deficit, caused by chronic HTN
d) Middle Cerebral Artery Occlusion
Most common stroke syndrome… face + arms > legs. Aphasia in dom. hem.
e) Posterior Cerebral Artery Occlusion
where’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
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Hyperdense MCA sign
Loss of cortical ribbon
Sulcal Effacement
Obscuration of the
grey/white junction
Question 2
A 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 Artery
No – face and arms > legs
b) Anterior Cerebral Artery
Frontal, medial parietal and temporal lobes, legs > face, amnesia, confusion
c)
Posterior Cerebral Artery
Primarily visual, with homonymous hemianopia, also amnesia, tremor
d) Basilar Artery
Locked-in state
e) Carotid Artery
He’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
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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 2
A 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 Infarction
AKA Wallenberg Syndrome
Affects multiple areas:
Trigeminal nucleus
Descending sympathetics
Lateral Spinothalamic
Vestibular nuclei
Ipsilateral face
• Pain and Temperature (5)
• Dysphagia
• Dysarthria
• Nystagmus (VN)
• +/- limb ataxia
Contralateral Limbs
• Pain and Temperature (LS)
Posterior Circulation Strokes
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The 6 D’s of Brainstem
Dysphagia
Dysarthria
Diplopia
Dystaxia
Dizziness
Drop attack (syncope)
Ipsilateral Face
Contralateral Extremity
Visual Field Deficits
Horner’s Syndrome
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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 3
What is the most common etiology for the diagnosis
revealed by the CT scan?
a) AVM
It’s a possibility
b) Cavernous Angioma
It’s a possibility
c) Mycotic Aneurysm
It’s a rare possibility
d) Neoplasm
More likely to cause hematoma, edema
e) Saccular Aneurysm
“Berry” -- cause of 80% of non-traumatic SAH. 5% of us have these
Subarachnoid Hemorrhage
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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 4
Which 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 Age
Not an independent risk factor for ICH
b) Increased NIHSS
In NINDS, one of 2 independent risk factors for ICH (with “infarct signs”)
c)
Isolated global aphasia
No – by itself, low NIHSS score but should be considered for tPA
d) Major surgery within 14 days
No increased risk of ICH, but tPA means increased risk from noncomp sites
e) Rapid improvement of neurological signs
No – 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 rtPA 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)
Inclusion Criteria
Age > 18
Diagnosis of stroke with measurable
deficit
Time of onset < 3 hours before
treatment will begin
Relative Contraindications
Major surgery or serious trauma
within 2 weeks
Only minor or rapidly improving
stroke sx
History of GI or GU hemorrhage
within 21 days
Recent arterial puncture as noncompressable site
Glucose >400 or less than 50
Post MI pericarditis
Patient with observed seizure at
time of stroke onset
Recent Lumbar Puncture
tPA
Exclusion Criteria
Evidence of ICH on CT
History of ICH or AVM
Suspected SAH with normal CT
Active internal bleeding
Platelets < 100,000
Heparin within 48 hours with an
elevated PTT
Current use of oral anticoagulant
with PT> 15sec
SBP > 185 or DBP >110 at time
treatment is to begin
Within 3 months any intracranial
surgery, serious head injury, or
previous stroke (not TIA)
Question 5
Which 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 hemorrhage
MRI 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 hemorrhage
Not superior. Equal.
e) Unenhanced CT remains superior to MRI for detecting acute hem.
Not superior. Equal.
Question 6
A 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 shaking
b)
Delirium
Hallmark is inattention, fluctuating course, disorganization
c)
Psychogenic amnesia
Subgroup of “dissociative disorders” seen under stress, forget personal info
d)
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 7
An 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 Embolism
Sudden, maximal at onset. You’d expect leg weakness
b) Internal Capsule Intracerebral Hemorrhage
Often HTN etiology, evolves from ischemic stroke, does not improve.
c)
Posterior Cerebral Artery Rupture
Well, sure, there’s a change in consciousness… Would be comatose.
d) Posterior Cerebral Artery Thrombosis
Would cause fluctuating course, visual defects, ?hallucinations
e) Vertebral Artery Occlusion
Maybe 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
ICH
GCS
3-4
5-12
________ ___13-15
ICH Vol
>30
__________ _<30
IVH
Yes
__________ _No
Infratentoral
Yes
__________ _No
Age
>80
__________ _<80
2
1
0
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1
0
0-6
Intracranial Hemorrhage
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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 Pressure
2. Increase edema, mass effect
3. Decrease perfusion to local and adjacent tissue
4. 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 8
A 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 Lens
This is a cause of monocular diplopia
b) Tertiary neurosyphilis
Restrictive gaze, vision loss. Unlikely by age 22…
c) Internuclear Opthalmoplegia
Lesion 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 9
A 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/u
Dismissing medical complaints is almost never the answer
b) Gastroenteritis – if tolerating PO, D/C
No, something’s changed…
c) Delirium – give haldol and call psych.
Hallmark of delirium is inattention, not anxiety…
d) Med reaction -- give him Prochlorperazine
No! 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 dopamineACh receptors.
Question 10
A 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 10
Angry disabled physician with lumbar tenderness, HTN, tachycardic,
febrile, screaming for opioids. The most appropriate next step in
management is:
a) Admit for pain control
Fever must be worked up
b) CT scan
Can’t visualize spinal canal, cord, or discs as well as MRI.
c) Discharge to pain clinic
Much of his presentation suggests drug-seeking, but…
d) MRI
Fever + back pain suggests epidural abscess or vertebral osteo.
e) Consult psychiatry
Much 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
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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 11
A 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 paralysis
Channelopathy that can lead to severe symmetric extremity weakness.
c) Guillain-Barre Syndrome
Classic presentation of ascending muscle weakness and loss of DTR. +/- sensory.
d) Myasthenia gravis
AB against ACh receptor in NMJ. No sensory component.
e) Tick paralysis
Can 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 LE
Myasthenia 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 Disorders
Familial 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 12
A 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 greyhaired movie hunk offered another
big surprise from his past: "I was a
blond."
Bell’s Palsy
Causes
HSV 1,2
VZV
Mycoplasma pneumoniae
Borrelia burgdorferie
HIV (b/l)
Adenovirus
coxsackievirus
Ebstein-Barr virus
Hepatitis A, B, and C
Cytomegalovirus
Treatment
Prednisone 60mg/day X 10 days
?Acyclovir 800mg 5X/day for 7 days
?Valacylovir 1000mg TID for 7 days
Artificial 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 13
A 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 CVA
Pain less likely, Horner’s fits but no other lesions?
b) Cluster Headache
Time course is wrong, pain behind eyes for minutes a day, O2 therapy
c) Bell’s Palsy
Pain doesn’t fit
d) Tick Bite
Not even a diagnosis… Not Lyme, not Tick Paralysis, not RMSF…
e) Carotid artery dissection
Unilateral 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
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Trauma
Chiropractic manipulation
Sports, yoga
CTD
HTN
Smoking
Oral contraceptives
Diagnosis and Treatment
• Angiography gold
• Anticoagulation with
standard
heparin to prevent
thromboembolic
• MRA optimal if available
complications
• CT angiogram evolving,
• If can’t, consider ASA
esp for trauma pts
• Neurosurgical
consultation
Question 14
Clinical features of delirium include:
a) Apraxia
A decreased ability to carry out motor activities? More likely in dementia
b) Auditory hallucinations
Usually visual
c) Disordered attention
The hallmark of delirum. Unlike dementia! Worth investigating and reversing.
d) Insidious onset
Delirium is abrupt, involve fluctuations over the day. Dementia is stable.
e) Sustained delusions
Usually poorly organized, rarely sustained. Dementia has fixed, false beliefs.
Question 15
Pharmacologic causes of parkinsonism include:
a) Barbiturates
Sedative-hypnotic with no extrapyramidal effects
b) Benztropine
Cogentin – actually helps parkinsonism (anticholinergic for dystonia)
c) Bromocriptine
Actually helps parkinsonism (dopamine agonist)
d) Bupropion
This is Wellbutrin/Zyban. Overdose is associated with seizures.
e) Butyrophenones
Haldol, Droperidol antagonize dopamine, disinhibit cholinergic response.
Parkinsonism
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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 16
Which of the following statements regarding idiopathic
intracranial hypertension is correct?
a) A head CT will show markedly enlarged ventricles
Ventricles are actually small, cisterna magna is large.
b) Acetazolamide is an accepted medical treatment
Reduces CSF production
c) LP is contraindicated
LP is diagnostic and therapeutic (pressures > 20 cm H20, the rest is WNL).
d) Requires prompt neurosurgery to prevent herniation
Delirium 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)
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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:
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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 17
A 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 18
A 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 seizure
No abrupt onset – this was a progression from a focus
d)
Psychomotor seizure
Bad catch-all term that encompasses complex partial seizures
e)
Temporal lobe seizure
Often preceded by aura, complex partial… involves behavioral changes, hallucinations
Nonconvulsive
(absence)
Seizure types
Generalized
No inciting focus
Begin in both
hemispheres
Abrupt LOC
Often, no aura
Convulsive
Tonic clonic (Grand Mal)
Clonic only, tonic only,
atonic, myoclonic
Partial (focused)
Simple: No LOC or AMS
Simple: Motor, sensory,
autonomic
Complex: 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
Question 19
38 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 B6
No reason to suspect INH toxicity
d)
Fosphenytoin load
This is the appropriate second-line agent for status epilepticus
e)
Succinylcholine and etomidate with ETT
What, 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 12
A 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 Craniotomy
no
c)
Serial lumbar punctures
no
d)
Magnesium Sulfate IV
no
e)
Heparin
yes
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 5
A 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 hypotension
This is very important
c)
Hyperventilate to pC02 25-30 mmHg
No!
d) Raise head of bed to 30 degrees
This is fine
e) Consider mannitol or hypertonic saline for deterioration in
neurologic status
This 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 (Defasciculating 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