Emergency Medicine EOR: Neurology (Smarty PANCE)

What is the mnemonic for the most common reversible causes of altered LOC/coma?

AEIOU TIPS: Alcohol, Epilepsy, Insulin (hypo/hyperglycemia), Opiates/Overdose, Uremia; Trauma, Infection, Psychiatric, Stroke/Structural

What GCS score defines coma?

GCS ≤8; Eyes: no opening (1), Verbal: no sounds (1), Motor: no movement (1) = minimum score 3

What are the components of the Glasgow Coma Scale?

Eyes (4 points): spontaneous/to voice/to pain/none

Verbal (5 points): oriented/confused/words/sounds/none; Motor (6 points): obeys/localizes/withdraws/flexion/extension/none; Max = 15

What is the immediate bedside workup for any patient with altered LOC?

Fingerstick glucose FIRST; then ABCs, O2, IV access, 12-lead ECG, BMP, CBC, LFTs, ammonia, TSH, tox screen, blood cultures, and consider head CT

What is the Doll's eye reflex (oculocephalic reflex) and what does abnormal finding indicate?

Eyes normally move opposite to head rotation (eyes stay fixed on a point) — indicates intact brainstem; absent reflex (eyes move with head) = brainstem dysfunction or herniation

What posturing indicates worse prognosis in coma: decorticate vs decerebrate?

Decerebrate posturing (arms extended, internally rotated, legs extended) = worse prognosis; indicates midbrain/upper pons injury; Decorticate (arms flexed, legs extended) = cortical or internal capsule injury

What metabolic causes of coma are immediately reversible and should be treated empirically?

Hypoglycemia → D50W IV; Opioid overdose → Naloxone 0.4–2 mg IV; Thiamine deficiency → Thiamine 100 mg IV BEFORE dextrose; Benzodiazepine overdose → Flumazenil (use with caution)

What brain herniation syndrome presents with unilateral fixed dilated pupil and contralateral hemiplegia?

Uncal (transtentorial) herniation — CN III compression causes ipsilateral mydriasis; Kernohan's notch phenomenon can cause ipsilateral hemiplegia (false localizing sign)

What is Bell palsy and what nerve is affected?

Idiopathic unilateral facial nerve (CN VII) palsy; most common cause of peripheral facial palsy; associated with HSV-1 reactivation

How do you differentiate Bell palsy (peripheral CN VII lesion) from a central stroke?

Bell palsy: affects ENTIRE ipsilateral face including forehead (cannot wrinkle forehead); Central stroke: forehead SPARED (bilateral upper motor neuron innervation to forehead)

What is the treatment for Bell palsy?

Prednisone 60 mg/day x 7 days (started within 72 hours = most effective); Valacyclovir added if severe (antivirals alone are insufficient); Eye lubrication/patching to prevent corneal abrasion

What is the prognosis of Bell palsy?

~85% recover fully within 3 months with treatment; incomplete eye closure (lagophthalmos) is the most concerning acute complication (corneal ulceration risk)

What conditions must be ruled out before diagnosing Bell palsy?

Ramsay Hunt syndrome (Herpes Zoster Oticus — look for vesicles in ear canal/pinna, worse prognosis); Lyme disease (bilateral palsy = Lyme until proven otherwise); Parotid tumor; Cholesteatoma; Stroke

What physical exam findings are present in Bell palsy?

Ipsilateral: inability to close eye, raise eyebrow, smile, or puff cheek; loss of nasolabial fold; hyperacusis (stapedius involvement); decreased taste anterior 2/3 tongue (chorda tympani)

What is the most common cause of viral encephalitis in the United States?

HSV-1 (Herpes Simplex Virus type 1) — most common and most deadly sporadic encephalitis; involves temporal lobes (temporal lobe hemorrhagic necrosis)

What is the classic triad of encephalitis?

Fever + Headache + Altered mental status (AMS); may also have seizures, focal neurologic deficits, and personality/behavioral changes

What is the gold standard diagnostic test for HSV encephalitis?

CSF PCR for HSV DNA — sensitivity ~98%, specificity ~99%; MRI brain (T2/FLAIR hyperintensity in temporal lobes) is the best imaging

What are the CSF findings in viral encephalitis?

Lymphocytic pleocytosis (10–500 WBCs), elevated protein (50–100 mg/dL), normal glucose (>60% serum); RBCs may be present in HSV (hemorrhagic)

What is the empiric treatment for suspected viral encephalitis before PCR results?

Acyclovir 10 mg/kg IV q8h immediately — do NOT wait for PCR results; also cover bacterial causes with ceftriaxone + vancomycin + dexamethasone until CSF results available

What encephalitis is associated with limbic symptoms, psychiatric features, and anti-NMDA receptor antibodies?

Anti-NMDA receptor encephalitis — most common autoimmune encephalitis; young women; presents with psychiatric symptoms, memory loss, seizures, dyskinesias, autonomic instability; associated with ovarian teratoma

What mosquito-borne viral encephalitides are high-yield for boards?

West Nile Virus: flaccid paralysis, anterior horn cells, crow deaths; Eastern Equine Encephalitis (EEE): highest mortality (~35%); La Crosse: most common arboviral encephalitis in children

What is the classic mechanism and vessel injured in epidural hematoma (EDH)?

Temporal skull fracture → rupture of middle meningeal artery (arterial bleed); most commonly from lateral skull trauma (pterion = thinnest skull)

What is the classic presentation of epidural hematoma?

Lucid interval: LOC → brief recovery → rapid neurological deterioration; ipsilateral fixed dilated pupil (CN III compression) + contralateral hemiplegia

What is the CT appearance of an epidural hematoma?

Biconvex (lens-shaped/lenticular) hyperdense hematoma; does NOT cross suture lines; usually temporal location

What is the definitive treatment for epidural hematoma with neurological deterioration?

Emergency surgical evacuation (craniotomy); temporizing measures: hyperventilation (PCO2 35-40), mannitol 1 g/kg IV, HOB 30°, avoid hypotension

What EDH findings on CT mandate immediate surgical evacuation regardless of neuro status?

Hematoma >30 mL, thickness >15 mm, or midline shift >5 mm; any EDH with neurological deterioration

What is the prognosis difference between EDH vs SDH?

EDH: better prognosis if treated early (younger patients, arterial bleed is faster but often no underlying brain injury); SDH: worse prognosis (venous, older patients, underlying brain injury common)

What vessel is injured in subdural hematoma (SDH) and what is the mechanism?

Bridging veins (cortex to dural sinuses) — torn by acceleration-deceleration; SDH crosses suture lines (unlike EDH)

What CT appearance distinguishes acute vs chronic SDH?

Acute SDH: crescent-shaped HYPERDENSE (white) collection; Chronic SDH (>3 weeks): HYPODENSE (dark) crescent; Subacute (1–3 weeks): isodense (may be missed)

Who is at highest risk for chronic subdural hematoma?

Elderly (cerebral atrophy stretches bridging veins), alcoholics, anticoagulated patients; often with trivial or no remembered trauma

What are the clinical features of chronic SDH?

Gradual headache, confusion, personality change, focal deficits over weeks to months; may fluctuate; elderly presenting with "dementia" → always consider chronic SDH

What is the treatment for symptomatic SDH?

Surgical drainage (burr hole or craniotomy) for symptomatic or large SDH; reverse anticoagulation; small asymptomatic chronic SDH may be managed conservatively with close monitoring

What midline shift on CT in SDH requires emergent surgical intervention?

Midline shift >5 mm or neurological deterioration → emergent surgical drainage

What is GBS and what is the pathophysiology?

Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) — autoimmune attack on peripheral nerve myelin; most common cause of acute flaccid paralysis in developed world

What is the classic clinical presentation of GBS?

Ascending symmetric flaccid weakness starting in legs, progressing to arms and potentially respiratory muscles; areflexia; preceded by URI or GI infection 2–4 weeks prior

What organism most commonly triggers GBS?

Campylobacter jejuni (GI infection) — most common trigger; also associated with CMV, EBV, influenza, COVID-19, and influenza vaccine (rare)

What CSF finding is pathognomonic for GBS?

Albuminocytologic dissociation: elevated protein (>45 mg/dL) with normal or near-normal WBC count (

What respiratory parameter indicates need for intubation in GBS? Use the "20-30-40 rule"

"20-30-40 Rule": FVC

What is the treatment for GBS?

IVIG 0.4 g/kg/day x 5 days OR plasmapheresis (equally effective); do NOT use corticosteroids (shown to be ineffective or harmful); supportive care + DVT prophylaxis

What variant of GBS presents with ophthalmoplegia, ataxia, and areflexia?

Miller Fisher Syndrome — anti-GQ1b antibodies; classic triad: ophthalmoplegia + ataxia + areflexia; descending pattern; generally good prognosis

What are the indications for immediate head CT in blunt head trauma (Canadian CT Head Rules)?

High-risk features: GCS score < 15 at 2 hours post-injury, suspected open/depressed skull fracture, signs of basal skull fracture, vomiting ≥2 times, age ≥65; Medium-risk: amnesia ≥30 min, dangerous mechanism

What are the clinical signs of a basilar skull fracture?

Battle's sign (post-auricular ecchymosis), raccoon eyes (periorbital ecchymosis), hemotympanum, CSF rhinorrhea or otorrhea, cranial nerve deficits

What is the Monro-Kellie doctrine and why is it relevant to head trauma?

Cranial vault has fixed volume (brain 80%, blood 10%, CSF 10%); increase in one component must be offset by decrease in another; failure → rising ICP

What are the signs and symptoms of elevated ICP?

Cushing's triad: hypertension + bradycardia + irregular respirations (late, ominous sign); headache worse in morning, papilledema, vomiting, altered mental status

What is the target PaCO2 when using hyperventilation for elevated ICP?

PaCO2 35–40 mmHg (normocapnia); aggressive hyperventilation to < 35 mmHg is only a temporizing measure for acute herniation (causes cerebral vasoconstriction)

What medications are used to lower ICP in head trauma?

Mannitol 0.25–1 g/kg IV (osmotic diuretic) OR hypertonic saline (3% NaCl); elevate HOB 30°; avoid hypotension (MAP >80 mmHg); avoid hypoxia (O2 sat >95%)

What is the NEXUS criteria for cervical spine imaging in trauma?

Low-risk (no imaging needed) if ALL met: no midline tenderness, no focal neuro deficit, normal alertness, no intoxication, no distracting injury

What is a concussion and what are the diagnostic criteria?

Traumatic brain injury from biomechanical forces causing transient neurological impairment; NO structural abnormality on imaging; diagnosis is clinical

What are the classic symptoms of concussion?

HEADACHE (most common), confusion, amnesia (anterograde > retrograde), dizziness, nausea, photophobia, phonophobia, "foggy" feeling; LOC occurs in

What is the appropriate imaging workup for suspected concussion?

Head CT if red flag features (see Canadian CT/NEXUS rules); MRI brain preferred over CT for structural assessment; standard CT and MRI are typically NORMAL in concussion

What are the return-to-play guidelines after concussion?

No return same day; stepwise return: (1) rest, (2) light aerobic, (3) sport-specific, (4) non-contact drills, (5) full-contact practice, (6) competition; 24 hours between each step, symptom-free at each stage

What is second impact syndrome?

Rare but catastrophic — second concussion before full recovery from first; massive cerebral edema from loss of autoregulation; occurs predominantly in young athletes; ~50% mortality

What is post-concussion syndrome?

Persistence of concussion symptoms >3 months; headache, dizziness, cognitive difficulties, mood changes, sleep disturbance; treatment: rest, gradual return, cognitive behavioral therapy

What is a cerebral contusion and how does it differ from a concussion?

Contusion = bruising of brain parenchyma with hemorrhage into brain tissue — structural injury visible on CT; Concussion = functional disturbance with normal imaging

What is the most common location for cerebral contusions and why?

Frontal and temporal poles (coup-contrecoup mechanism); brain decelerates against rough orbital/sphenoid ridges; contrecoup injury opposite site of impact

What CT findings are seen in cerebral contusion?

Heterogeneous hyperdense (hemorrhagic) areas mixed with hypodense (edema) areas; "salt and pepper" appearance; may evolve and worsen over 24–72 hours (talk and die phenomenon)

What is "talk and die" phenomenon?

Patient initially appears well or has mild deficits, then rapidly deteriorates due to expanding contusion or hematoma; high-risk period is first 24–72 hours; requires close monitoring and serial CT

What is the management of cerebral contusion?

Neurosurgical consult; ICU monitoring; ICP management if elevated; surgical intervention for large contusions with significant mass effect or herniation; most are managed conservatively

What are the diagnostic criteria for migraine WITHOUT aura (5-4-3-2-1 rule)?

5 attacks, lasting 4–72 hours, with 3 of: unilateral, pulsating, moderate-severe intensity, aggravated by activity; 2 of: nausea/vomiting, photophobia, phonophobia; 1 exclusion of other cause

What is the first-line abortive treatment for migraine in the ED?

IV prochlorperazine (Compazine) 10 mg IV + diphenhydramine 25 mg IV (prevents akathisia) — most effective ED regimen; Sumatriptan (triptans) for outpatient use; ketorolac as adjunct

What is the classic presentation of cluster headache?

Unilateral periorbital/retro-orbital SEVERE pain, 15–180 min duration, clusters over weeks; ipsilateral autonomic symptoms: lacrimation, rhinorrhea, ptosis, miosis (Horner's), conjunctival injection; restlessness (pacing); men >women

What is the abortive treatment for cluster headache?

100% O2 via non-rebreather mask 15 L/min x 15–20 min (most effective, most rapid); Sumatriptan 6 mg SQ; intranasal zolmitriptan; preventive: verapamil

What are the features of tension-type headache?

Bilateral, band-like/pressure quality, mild-moderate intensity, NOT worsened by activity; NO nausea/vomiting; possible mild photophobia OR phonophobia (not both); most common primary headache

What are the red flag features of headache requiring emergent workup? Use mnemonic SNOOP4

S: Systemic symptoms/signs; N: Neurologic deficits; O: Onset sudden (thunderclap); O: Older age (>50, new headache); P: Positional change; P: Precipitated by Valsalva; P: Progressive worsening; P: Papilledema

What is the treatment for tension headache?

NSAIDs (ibuprofen, naproxen) or acetaminophen — first line; avoid opioids and frequent analgesic use (rebound headache); TCAs (amitriptyline) for prevention

What is medication overuse headache (rebound headache)?

Headache ≥15 days/month in patient using acute headache medications ≥10–15 days/month for >3 months; treatment = withdrawal of offending medication

What is the most common cause of spontaneous intracerebral hemorrhage?

Hypertensive hemorrhage (chronic HTN causing lipohyalinosis of small penetrating arteries); most common locations: putamen (most common) > thalamus > pons > cerebellum

What is the clinical presentation of ICH vs ischemic stroke?

ICH: sudden onset, headache, vomiting, altered mental status, rapid progression; hypertension prominent; Ischemic: more gradual onset, no headache typically, normal LOC early

What CT findings are seen in acute ICH?

Hyperdense (bright white) intraparenchymal collection; surrounding edema (hypodense halo); may have intraventricular extension; spot sign on CTA = active bleeding, worse prognosis

What blood pressure target should be used in acute ICH management?

Systolic BP target 140–150 mmHg (AHA guideline); use nicardipine or labetalol IV; avoid excessive lowering

What anticoagulant reversal agents are used in ICH?

Warfarin: Vitamin K + 4-factor PCC (Kcentra) — preferred over FFP; Dabigatran: Idarucizumab (Praxbind); Rivaroxaban/Apixaban: Andexanet alfa or 4-factor PCC; Heparin: Protamine sulfate

What surgical intervention is considered for cerebellar ICH?

Cerebellar hematoma >3 cm with neurological deterioration or brainstem compression → emergent surgical evacuation; brainstem compression can cause rapid death

What is the ICH Score and what does it predict?

Scores GCS (0-2), ICH volume >30 mL (1), IVH present (1), infratentorial location (1), age >80 (1); Score 0 = ~0% 30-day mortality, Score 5-6 = ~100% 30-day mortality

What is the differential diagnosis for acute change in mental status in an elderly patient?

AEIOU TIPS + medications (polypharmacy), urinary/septic source, pain, constipation, dehydration; always check urinalysis, BMP, CBC, blood cultures, head CT, and medication list

What distinguishes delirium from dementia?

Delirium: ACUTE onset, fluctuating course, impaired attention, often reversible; Dementia: insidious onset, stable course, memory predominantly affected, generally irreversible

What is the CAM (Confusion Assessment Method) criteria for delirium?

Diagnosis requires: (1) Acute onset + fluctuating course AND (2) Inattention AND either (3) Disorganized thinking OR (4) Altered level of consciousness

What are the most common causes of delirium in the ED?

Infection (UTI, pneumonia, sepsis), metabolic (hypo/hyperglycemia, electrolyte disturbances, renal failure, hepatic encephalopathy), medications (anticholinergics, opioids, benzos), hypoxia, intracranial pathology

What medication class is most associated with causing delirium and should be avoided in elderly?

Anticholinergic medications — Beers Criteria; also benzodiazepines, opioids, and corticosteroids; use STOPP/START criteria

What is the first-line pharmacologic treatment for agitated delirium in the ED?

Low-dose haloperidol (antipsychotic) — preferred; avoid benzodiazepines EXCEPT in alcohol/benzo withdrawal delirium; dexmedetomidine for ICU patients

What is the most common acute cause of cerebellar ataxia in adults presenting to the ED?

Alcohol intoxication/acute ethanol toxicity — always check blood alcohol level; other: cerebellar stroke, cerebellar hemorrhage, Wernicke's encephalopathy

What cerebellar signs are elicited on physical exam?

DANISH: Dysdiadochokinesia, Ataxia (gait), Nystagmus, Intention tremor, Slurred speech (dysarthria/scanning speech), Hypotonia

What is Wernicke's encephalopathy and what is the classic triad?

Acute thiamine (B1) deficiency (alcoholics, malnutrition); triad: ophthalmoplegia (nystagmus, CN VI palsy), ataxia (cerebellar), confusion (encephalopathy); treat with thiamine 500 mg IV TID x 3 days BEFORE glucose

What is Korsakoff syndrome?

Chronic thiamine deficiency sequel of Wernicke's; anterograde > retrograde amnesia with confabulation; caused by mammillary body damage; largely irreversible

What is the most dangerous cerebellar cause of acute ataxia to rule out immediately?

Cerebellar stroke or hemorrhage — posterior circulation (PICA/AICA/SCA territory); may be missed on CT (posterior fossa poorly visualized); MRI DWI preferred

What is the gait pattern in cerebellar ataxia vs sensory ataxia?

Cerebellar: wide-based, lurching, cannot tandem walk; Romberg NEGATIVE (ataxia same eyes open/closed); Sensory: Romberg POSITIVE (worse eyes closed, uses vision to compensate)

What is transient global amnesia (TGA) and what is the presentation?

Sudden onset of anterograde amnesia lasting 1–24 hours; patient repetitively asks same questions; no loss of identity or procedural memory; benign, self-limited; precipitated by Valsalva, physical exertion, sexual activity, cold water

What is the difference between anterograde and retrograde amnesia?

Anterograde: inability to form NEW memories after the event (most common in head trauma); Retrograde: inability to recall events BEFORE the event

What is the most common cause of acute anterograde amnesia in the ED?

Concussion/head trauma; benzodiazepine/alcohol intoxication; also consider TGA, seizure (post-ictal), stroke

What type of stroke most commonly causes acute amnesia?

Posterior cerebral artery (PCA) or posterior communicating artery territory; also thalamic strokes (bilateral thalamic infarcts = severe amnestic syndrome — artery of Percheron)

What is the classic triad of bacterial meningitis?

Fever + Neck stiffness (nuchal rigidity) + Headache; altered mental status in ~75%; only ~44% have all three; nausea, photophobia, phonophobia also common

What are Kernig's and Brudzinski's signs?

Kernig's: flex hip 90° → resistance/pain with knee extension (meningeal irritation); Brudzinski's: passive neck flexion → involuntary hip/knee flexion; both have low sensitivity (~5%) but high specificity

What is the most common cause of bacterial meningitis in adults?

Streptococcus pneumoniae (most common overall in adults); Neisseria meningitidis (most common in college students/young adults — petechial/purpuric rash); Listeria in elderly/immunocompromised

What is the empiric antibiotic regimen for suspected bacterial meningitis?

Ceftriaxone 2g IV q12h + Vancomycin 15–20 mg/kg IV q8–12h + Dexamethasone 0.15 mg/kg IV q6h x 4 days (given BEFORE or with first antibiotic dose); add Ampicillin if age >50 or immunocompromised (Listeria coverage)

When should head CT be performed BEFORE lumbar puncture?

Papilledema, focal neurologic deficits, new seizure, immunocompromised, altered mental status, history of CNS disease; BUT do NOT delay antibiotics for CT or LP — treat FIRST

What are the CSF findings in bacterial vs viral meningitis?

Bacterial: turbid, WBC >1000 (PMNs), protein >200, glucose

What is the opening pressure in bacterial meningitis?

Elevated >20 cmH2O (normal 6–20 cmH2O); markedly elevated in fungal meningitis (Cryptococcus)

What is the management of meningococcal meningitis contacts?

Ciprofloxacin 500 mg PO x1 OR rifampin 600 mg BID x 2 days OR ceftriaxone 250 mg IM x1 for close household/daycare contacts

What is the dermatomal distribution of most clinically important nerve roots?

C6: thumb/index; C7: middle finger; C8: ring/little finger; L4: medial leg/foot; L5: dorsal foot/great toe; S1: lateral foot/sole; remember "C6 is thumbs-up"

What distinguishes peripheral neuropathy from radiculopathy?

Peripheral neuropathy: stocking-glove distribution, bilateral symmetric, distal > proximal; Radiculopathy: dermatomal distribution, radiation from spine, associated back/neck pain

What are the most common causes of peripheral neuropathy?

Diabetes (most common overall), alcohol, B12 deficiency, hypothyroidism, uremia, medications (INH, metronidazole, vincristine, HIV meds)