Neurology Board Review. Nick Genes October 8, 2008. the inservice exam. Feb 25, 2009 Short term $$$ (moonlighting, Mets) Long term $$$$$$ (licensure, career in EM) But also: intro to EM practice Similar questions to ABEM Last year: 207 questions counted
Neurology Board Review Nick Genes October 8, 2008
the inservice exam • Feb 25, 2009 • Short term $$$ (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 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? • Basilar Artery Occlusion Locked-In Syndrome – severe quadriplegia… only upward gaze intact! • Subarachnoid Hemorrhage Where’s the headache? Nausea? Vomiting? • Lacunar Infarction Pure motor or sensory deficit, caused by chronic HTN • Middle Cerebral Artery Occlusion Most common stroke syndrome… face + arms > legs. Aphasia in dom. hem. • 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 • 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? • Middle Cerebral Artery No – face and arms > legs • Anterior Cerebral Artery Frontal, medial parietal and temporal lobes, legs > face, amnesia, confusion • Posterior Cerebral Artery Primarily visual, with homonymous hemianopia, also amnesia, tremor • Basilar Artery Locked-in state • 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 • 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? • Acute Labryinthitis • Acute vertigo, sure… but not going to cause Horner’s, dysphagia • 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 • 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 3 What is the most common etiology for the diagnosis revealed by the CT scan? • AVM It’s a possibility • Cavernous Angioma It’s a possibility • Mycotic Aneurysm It’s a rare possibility • Neoplasm More likely to cause hematoma, edema • 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 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? • Advanced Age Not an independent risk factor for ICH • Increased NIHSS In NINDS, one of 2 independent risk factors for ICH (with “infarct signs”) • Isolated global aphasia No – by itself, low NIHSS score but should be considered for tPA • Major surgery within 14 days No increased risk of ICH, but tPA means increased risk from noncomp sites • 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 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)
tPA 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 non-compressable site Glucose >400 or less than 50 Post MI pericarditis Patient with observed seizure at time of stroke onset Recent Lumbar Puncture 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? • CT and MRI are equivalent for detecting hemorrhagic transformation of an acute ischemic stroke MRI is superior at catching this. • CT is superior to MRI for detecting chronic hemorrhage MRI sees more small hemorrhages that CT misses, but determining age is tricky • 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. • MRI is superior to noncontrast CT for detecting acute hemorrhage Not superior. Equal. • 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: • Complex partial seizure Um… he’s alert and not shaking • Delirium Hallmark is inattention, fluctuating course, disorganization • Psychogenic amnesia Subgroup of “dissociative disorders” seen under stress, forget personal info • Transient global amnesia No new memories for a day! TIA? complex migraine? +/- headache, anxiety. • 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? • Anterior Cerebral Artery Embolism Sudden, maximal at onset. You’d expect leg weakness • Internal Capsule Intracerebral Hemorrhage Often HTN etiology, evolves from ischemic stroke, does not improve. • Posterior Cerebral Artery Rupture Well, sure, there’s a change in consciousness… Would be comatose. • Posterior Cerebral Artery Thrombosis Would cause fluctuating course, visual defects, ?hallucinations • 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 2 5-12 1 ________ ___13-15 0 ICH Vol >30 1 __________ _<30 0 IVH Yes 1 __________ _No 0 Infratentoral Yes 1 __________ _No 0 Age >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 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? • Dislocated Lens This is a cause of monocular diplopia • Tertiary neurosyphilis Restrictive gaze, vision loss. Unlikely by age 22… • InternuclearOpthalmoplegia 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. • Retro-orbital hematoma Another binocular diplopia, pressing on EOM, but same apart or conjugate. • 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? • Anxiety – discharge with psych f/u Dismissing medical complaints is almost never the answer • Gastroenteritis – if tolerating PO, D/C No, something’s changed… • Delirium – give haldol and call psych. Hallmark of delirium is inattention, not anxiety… • Med reaction -- give him Prochlorperazine No! Causes akathesia in 44% of ED N/V patients within 1h • 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 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: • Admit for pain control Fever must be worked up • CT scan Can’t visualize spinal canal, cord, or discs as well as MRI. • Discharge to pain clinic Much of his presentation suggests drug-seeking, but… • MRI Fever + back pain suggests epidural abscess or vertebral osteo. • 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 • IVDU • Chronic steroids • HIV • Osteoporosis • Pain > 6 weeks *American college of radiology “Red Flags”