PANCE · PANRE · Board Prep Intensive

Neurology
Bootcamp Syllabus

Complete Neurology Bootcamp Syllabus — 18 modules, sequenced so the six core PANCE neurology topics come first: stroke, seizure disorders, headache syndromes, multiple sclerosis, meningitis and encephalitis, and Parkinson disease. The supporting domains — localization, cranial nerves, cognition, neuromuscular and peripheral nerve disease, and the neuro emergencies that turn up on every exam — follow. Built around the lesion-localization reasoning the PANCE rewards, not rote lists.

18Modules
11Clinical Domains
27Board Tables
10Don't-Miss Emergencies
25Must-Know Associations
Rajiv Choudhary, MD, MPH
Tier Key:
Tier 1 — Must Know
Tier 2 — Important
Tier 3 — Lower yield
◆ = Localize first, then diagnose
Core Topic 1 of 6 · Cerebrovascular Disease — Highest PANCE Weight
Stroke — Ischemic & Hemorrhagic
Before you beginStroke — Ischemic & Hemorrhagic3 questions
Answer these three before you read the module. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Question 1 of 3 · High Yield · Stroke · Initial Imaging (CT vs MRI)
A 68-year-old man presents with sudden-onset right-sided weakness and aphasia 90 minutes ago. What is the best initial diagnostic test?
Click to Reveal Answer
Correct answer: B — Non-contrast CT head
Non-contrast CT head is the first-line emergent imaging for suspected acute stroke. Its primary purpose is to exclude hemorrhagic stroke before considering thrombolytic therapy. It is fast, widely available, and highly sensitive for acute hemorrhage.
Why the other choices are wrong
  • MRI brain with diffusion-weighted imaging — Incorrect. MRI with DWI is more sensitive for early ischemic stroke but takes longer and should not delay treatment decisions.
  • CT angiography — Incorrect. CTA is important for identifying large vessel occlusion but is obtained after the initial non-contrast CT.
  • Lumbar puncture — Incorrect. LP is not indicated for stroke evaluation unless subarachnoid hemorrhage is suspected with a negative CT.
  • Carotid duplex ultrasound — Incorrect. Carotid studies stratify stroke risk during TIA workup; they have no role in the first minutes of an acute stroke.
Board pearlThe non-contrast CT is a gate, not a diagnosis. It answers one question — is there blood? — and nothing about reperfusion happens until that is answered. Remember that a normal CT does not exclude ischemic stroke; early infarct is often invisible on CT. DWI-MRI is the most sensitive test for acute infarction, but on the boards it is never the answer when the patient is inside the treatment window and CT is available.
Covered below under Module 1 — Stroke & Cerebrovascular Disease · imaging sequence
Question 2 of 3 · High Yield · Stroke · tPA Window
The CT head in the patient above is negative for hemorrhage. Symptom onset was 90 minutes ago. What is the best next step?
Click to Reveal Answer
Correct answer: A — Administer IV alteplase (tPA)
IV alteplase is indicated for acute ischemic stroke within 4.5 hours of symptom onset (3 hours in some guidelines for patients >80 or with certain comorbidities). This patient is well within the treatment window at 90 minutes. Time is brain — every 15-minute delay in treatment reduces the probability of a good outcome.
Why the other choices are wrong
  • Start aspirin 325 mg — Incorrect. Aspirin should not be given within 24 hours of tPA administration.
  • Obtain MRI before any treatment — Incorrect. Delaying treatment for MRI is inappropriate when the patient is within the tPA window and CT has excluded hemorrhage.
  • Observe for 24 hours — Incorrect. Observation without reperfusion therapy results in worse outcomes.
  • Proceed directly to mechanical thrombectomy — Incorrect. No large-vessel occlusion has been demonstrated and no CTA has been obtained. At 90 minutes with hemorrhage excluded, the lytic is the immediate step.
Board pearlThe clock starts at last known normal, not at the time symptoms were discovered — this is why wake-up strokes are usually outside the lytic window. Standard window is 4.5 hours; the 3–4.5 hour extension excludes age >80, prior stroke plus diabetes, current anticoagulation, and very severe deficits. BP must be brought to ≤185/110 before the needle, and no antiplatelet or anticoagulant for 24 hours afterward. Tenecteplase 0.25 mg/kg single bolus is an accepted alternative to alteplase.
Covered below under Module 1 — Stroke & Cerebrovascular Disease · tPA window
Question 3 of 3 · High Yield · Stroke · Hemorrhagic (SAH)
A 72-year-old woman presents with sudden severe headache ("worst headache of my life"), vomiting, and loss of consciousness. CT head shows hyperdense blood in the basal cisterns. What is the most likely diagnosis and best next step?
Click to Reveal Answer
Correct answer: B — Subarachnoid hemorrhage — obtain CT angiography
"Worst headache of my life" with acute onset and blood in the basal cisterns on CT is classic for subarachnoid hemorrhage (SAH), most commonly caused by ruptured cerebral aneurysm. CT angiography (or conventional angiography) should be performed urgently to identify the source for surgical clipping or endovascular coiling.
Why the other choices are wrong
  • Ischemic stroke — give tPA — Incorrect. tPA is contraindicated in hemorrhagic stroke.
  • Migraine — give sumatriptan — Incorrect. Sumatriptan is contraindicated in SAH and would not explain CT findings.
  • Meningitis — lumbar puncture — Incorrect. LP is unnecessary when CT already shows SAH; LP is used when CT is negative but clinical suspicion is high.
  • Hypertensive encephalopathy — give nicardipine — Incorrect. Hypertensive encephalopathy causes headache and confusion with severe hypertension, but it does not put blood in the basal cisterns.
Board pearlThunderclap headache follows a fixed sequence: non-contrast CT first; if CT is negative and suspicion remains, LP looking for xanthochromia; once SAH is confirmed, CTA or angiography to localize the aneurysm for clipping or coiling. Give nimodipine to reduce delayed cerebral ischemia from vasospasm (peak risk days 4–14). Any lytic is absolutely contraindicated.
Covered below under Module 1 — Stroke & Cerebrovascular Disease · SAH
Tier 1
Module 1
Stroke & Cerebrovascular Disease
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Time is brain · vascular territories · tPA window · thrombectomy · SAH
🩺 Opening Clinical Vignette
🔴 ADVANCED
A 71-year-old woman is brought in by EMS. Last seen normal 3 hours ago. NIHSS 14. CT head: no hemorrhage. BP 196/110. Her INR is 1.1, platelets 210K, glucose 118. The team wants to give tPA.
⏸ Pause & Discuss — Before Reading Further
Her BP is 196/110 — is tPA contraindicated? What must happen before the needle goes in, and what is the exact BP threshold?
✓ Answer
BP >185/110 is a contraindication to tPA — BUT it is a TREATABLE contraindication. Give IV labetalol or nicardipine to bring BP to ≤185/110, then administer tPA. Do not withhold tPA just because BP is high if it can be lowered. Post-tPA target: <180/105 for 24 hours.
💡 Teaching Pearl
The BP threshold for tPA is one of the highest-stakes PANCE facts in neurology. Students who memorize '185/110' without understanding it's a treatable contraindication will withhold tPA from eligible patients. Teaching the 'lower it then give it' sequence is the clinical pearl.
Transient Ischemic Attack
  • Transient deficit resolving within 24 h (most <1 h), no infarction on imaging.
  • Workup: MRI-DWI, vascular imaging (CTA/MRA), echo, telemetry, lipids, HbA1c.
  • ABCD2 score estimates short-term stroke risk.
  • High-risk TIA: dual antiplatelet (aspirin + clopidogrel) for 21 days, then single agent.
Ischemic Stroke — Vascular Territories
TerritoryKey Findings
MCAContralateral face/arm > leg weakness & sensory loss; aphasia (dominant); neglect (non-dominant); gaze toward lesion
ACAContralateral leg > arm weakness; personality change; urinary incontinence
PCAContralateral homonymous hemianopia with macular sparing; visual agnosia
VertebrobasilarCranial nerve deficits, crossed findings, ataxia, vertigo, diplopia, dysarthria
LacunarPure motor, pure sensory, ataxic hemiparesis, dysarthria-clumsy hand; HTN & diabetes
Board Pearl
Gaze deviation localizes: eyes look TOWARD the lesion in a cortical stroke, AWAY from the lesion in a pontine stroke.
Hemorrhagic Stroke
  • ICH — most common cause is hypertension (basal ganglia, thalamus, pons, cerebellum).
  • Lobar hemorrhage in the elderly → consider cerebral amyloid angiopathy.
  • Cerebellar hemorrhage → neurosurgical emergency if >3 cm or with hydrocephalus.
Subarachnoid Hemorrhage
SAH — Thunderclap 'Worst Headache of My Life'
  • Most common cause: ruptured berry aneurysm (anterior communicating artery most common site)
  • Dx: non-contrast CT (~95% sensitive <6 h) → if negative, LP for xanthochromia
  • Complications: rebleeding (day 1), vasospasm (days 4–14), hydrocephalus, hyponatremia (SIADH/cerebral salt wasting)
  • Mgmt: secure aneurysm (coil/clip), nimodipine for vasospasm prevention, ICU monitoring
Acute Ischemic Stroke — Reperfusion
IV Alteplase (tPA)
  • Window: within 4.5 h of onset / last known well
  • Tenecteplase 0.25 mg/kg as a single bolus is an accepted alternative to alteplase, and is often preferred when the patient is going on to thrombectomy
  • Key contraindications: active bleeding, recent surgery, platelets <100k, INR >1.7, BP >185/110 despite treatment
  • Extended (3–4.5 h) extra exclusions: age >80, NIHSS >25, anticoagulant use, diabetes + prior stroke
Mechanical Thrombectomy
  • Large-vessel occlusion (ICA or proximal MCA – M1)
  • Up to 24 h with favorable perfusion-mismatch imaging
  • Can be done with or after tPA
Secondary Prevention
  • Antiplatelet (aspirin, clopidogrel, or aspirin–dipyridamole).
  • Anticoagulation for atrial fibrillation — DOACs preferred over warfarin.
  • High-intensity statin; blood pressure control.
  • Carotid endarterectomy if symptomatic stenosis ≥70%.
Classic Board Trap
Do NOT aggressively lower blood pressure in acute ischemic stroke — permissive hypertension preserves penumbral perfusion. Only treat BP down to <185/110 if the patient is a tPA candidate.
Clinical Vignette
A 67-year-old is brought in 3 hours after sudden left-sided weakness and slurred speech. Non-contrast CT shows no hemorrhage; BP is 178/96.
Answer: Within the 4.5-hour window with hemorrhage excluded and BP below 185/110, evaluate for IV thrombolysis and screen for a large-vessel occlusion for possible thrombectomy. Do not drive the blood pressure down aggressively — permissive hypertension protects the penumbra.
Core Topic 2 of 6 · Episodic Disorders
Seizure Disorders & Epilepsy
Before you beginSeizure Disorders & Epilepsy3 questions
Answer these three before you read the module. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Question 1 of 3 · High Yield · Seizure · Classification & First-Line AED
A 24-year-old woman has had three episodes of a rising epigastric sensation followed by lip-smacking, unresponsiveness for 1–2 minutes, and post-ictal confusion. MRI shows left hippocampal sclerosis; EEG shows left temporal discharges. Which is the MOST appropriate first-line antiepileptic?
Click to Reveal Answer
Correct answer: C — Lamotrigine or levetiracetam
Aura plus automatisms plus post-ictal confusion with a temporal lesion is focal (temporal lobe) epilepsy from mesial temporal sclerosis. Classification drives drug choice: focal epilepsy responds to lamotrigine, levetiracetam, carbamazepine, or oxcarbazepine. In a woman of childbearing potential, lamotrigine and levetiracetam are preferred because valproate is the most teratogenic AED and carbamazepine induces hepatic enzymes that reduce oral contraceptive efficacy.
Why the other choices are wrong
  • Ethosuximide — Incorrect. Ethosuximide works only on absence seizures — it has no efficacy in focal epilepsy.
  • Valproic acid — broadest spectrum, so preferred in all women — Incorrect. Valproate is broad-spectrum and excellent for generalized epilepsy, but it is the most teratogenic AED (neural tube defects, reduced IQ) and is not first-line for focal seizures.
  • Phenobarbital — Incorrect. Effective but displaced by better-tolerated agents; sedation and cognitive slowing make it a late-line choice.
  • No antiepileptic — wait for a third documented seizure — Incorrect. Two or more unprovoked seizures meets the definition of epilepsy — treatment is indicated now.
Board pearlClassify first, then prescribe. Focal → carbamazepine, oxcarbazepine, lamotrigine, levetiracetam. Generalized → valproate, levetiracetam, lamotrigine. Absence only → ethosuximide. Carbamazepine and phenytoin can worsen absence and myoclonic seizures — that is the classic trap. For any woman who may conceive: avoid valproate, favor lamotrigine or levetiracetam, and start folic acid 4–5 mg/day.
Covered below under Module 2 — Seizures & Epilepsy · classification and drug selection
Question 2 of 3 · High Yield · Seizure · Absence Epilepsy
An 8-year-old girl has absence seizures characterized by staring spells lasting 5–10 seconds with no post-ictal confusion. EEG shows 3Hz generalized spike-and-wave pattern. Which is the MOST appropriate first-line treatment?
Click to Reveal Answer
Correct answer: B — Ethosuximide
Ethosuximide is first-line for pure absence seizures. It reduces 3Hz spike-wave activity via T-type calcium channel blockade. Carbamazepine is CONTRAINDICATED in absence seizures — it worsens absence and can precipitate absence status. Valproate is used if absence coexists with other generalized seizure types. Phenytoin has no efficacy for absence.
Why the other choices are wrong
  • Levetiracetam — Incorrect. Levetiracetam is a broad-spectrum agent that is safe in generalized epilepsy and is sometimes used adjunctively, but it is not first-line for pure absence seizures and is less effective than ethosuximide for this syndrome.
  • Phenytoin — Incorrect. Phenytoin is a sodium channel blocker effective for focal and generalized tonic-clonic seizures but ineffective for absence seizures, and it may aggravate generalized epilepsies.
  • Carbamazepine — Incorrect. Carbamazepine is actively CONTRAINDICATED in absence epilepsy — it can worsen absence seizures and precipitate absence status. This is the classic tested error for this presentation.
  • Valproate — Incorrect. Valproate is genuinely effective for absence seizures and is the main alternative, making this the strongest distractor. Ethosuximide is preferred first-line for PURE absence because head-to-head data showed comparable efficacy with fewer attentional adverse effects, and valproate carries teratogenic risk in a girl of childbearing potential.
Board pearlEthosuximide is first-line for pure absence, working through T-type calcium channels, and the EEG signature is 3 Hz generalised spike-and-wave with no post-ictal confusion. The drug trap runs the other way: carbamazepine and phenytoin can worsen absence and may precipitate absence status. Use valproate instead when absence coexists with generalised tonic-clonic seizures, since ethosuximide covers absence only.
Covered below under Module 2 — Seizures & Epilepsy · drug selection
Question 3 of 3 · High Yield · Seizure · Status Epilepticus
A 34-year-old woman has a witnessed generalized tonic-clonic seizure lasting 8 minutes in the ED. It is still ongoing. She received IV lorazepam 4mg 3 minutes ago without termination. What is the MOST appropriate next step?
Click to Reveal Answer
Correct answer: A — IV fosphenytoin or levetiracetam
Status epilepticus (seizure >5 min) protocol: 1st — benzodiazepine (lorazepam/diazepam). 2nd line after benzo failure — fosphenytoin, levetiracetam, or valproate IV. She received first-line benzo without effect; second-line IV agent is next. Do not give a second benzo before moving to second-line therapy.
Why the other choices are wrong
  • Oral levetiracetam via NG tube — Incorrect. Enteral dosing is far too slow for an actively seizing patient and carries aspiration risk. Status epilepticus requires IV therapy for immediate serum levels.
  • CT head first — Incorrect. Imaging is important once the seizure is controlled, but transporting an actively convulsing patient to CT delays second-line therapy. Ongoing status causes progressive neuronal injury — stop the seizure first.
  • Repeat lorazepam 4mg IV — Incorrect. A second benzodiazepine dose is reasonable practice if the first was underdosed, which makes this tempting — but she has already received an adequate 4mg without response. Guidelines move to a second-line agent rather than repeating a failed class.
  • Emergent EEG — Incorrect. EEG is essential for suspected NON-convulsive status or to confirm resolution, but this seizure is clinically visible. Waiting for EEG before treating a witnessed convulsion delays urgent therapy.
Board pearlStatus epilepticus is any seizure beyond 5 minutes, and the ladder is fixed: benzodiazepine first, then a second-line IV agent — fosphenytoin, levetiracetam, or valproate. The trap is stacking a second benzodiazepine after the first fails; that wastes time and adds respiratory depression without addressing the seizure. If second-line fails, move to anaesthetic infusion with intubation. Check glucose and give thiamine before glucose in anyone who may be alcohol-dependent.
Covered below under Module 2 — Seizures & Epilepsy · status epilepticus
Tier 1
Module 2
Seizures & Epilepsy
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Classification · absence vs focal · status epilepticus · ASM side effects
🩺 Opening Clinical Vignette
🟡 INTERMEDIATE
A 24-year-old man has a witnessed generalized tonic-clonic seizure lasting 8 minutes. He is postictal and confused now. No prior seizure history. Labs: Na 134, glucose 92, normal CBC. Brain MRI is normal. EEG shows normal interictal activity.
⏸ Pause & Discuss — Before Reading Further
This is an unprovoked first seizure with normal workup. Do you start an anti-seizure medication? Walk through the decision.
✓ Answer
Normal MRI + normal EEG after a single unprovoked seizure = low recurrence risk (~30% at 2 years). ASM is NOT automatically required. Start ASM if: abnormal MRI (structural lesion), abnormal EEG (epileptiform discharges), nocturnal seizure, prior brain injury, or patient preference (driving, occupation). Counsel on driving restrictions regardless.
💡 Teaching Pearl
Students reflexively start levetiracetam after any seizure. The PANCE tests whether they know ASM is a decision, not a reflex — and that a normal workup after a single seizure may not require medication. The driving restriction counseling is a separate must-do that's frequently missed.
Classification
TypeSubtypesKey Features
GeneralizedTonic-clonic, absence, myoclonic, atonicBilateral onset, loss of awareness
FocalSimple (aware), complex (impaired awareness), focal → bilateralUnilateral onset; aura common
Board-Tested Types
  • Absence: brief staring (3–20 s), 3 Hz spike-and-wave, childhood onset, provoked by hyperventilation; first-line ethosuximide (absence only) or valproate.
  • Tonic-clonic: tonic stiffening → clonic jerking → postictal confusion.
  • Focal with impaired awareness: temporal lobe; automatisms (lip-smacking, picking).
  • Todd paralysis: transient postictal focal weakness — mimics stroke.
Antiseizure Medications
MedicationIndicationKey Side Effects / Pearls
LevetiracetamBroad-spectrum, first-line for manyBehavioral changes, irritability; renal dosing
ValproateGeneralized, absenceTeratogenic (NTDs), hepatotoxic, pancreatitis; avoid in women of childbearing age
CarbamazepineFocalHyponatremia (SIADH), aplastic anemia, SJS; HLA-B*1502 testing in Asian patients
PhenytoinFocal & generalized TCGingival hyperplasia, hirsutism, zero-order kinetics, teratogenic
LamotrigineBroad-spectrumSJS (slow titration); relatively safe in pregnancy
EthosuximideAbsence onlyGI upset; does NOT treat tonic-clonic
Status Epilepticus
Seizure >5 min or ≥2 without return to baseline
  • 1. ABCs, IV access, glucose, thiamine
  • 2. First-line: IV benzodiazepine (lorazepam 4 mg IV or midazolam 10 mg IM)
  • 3. Second-line: IV fosphenytoin, levetiracetam, or valproate
  • 4. Refractory: continuous infusion (midazolam, propofol, pentobarbital) + continuous EEG
Board Pearl
Febrile seizures occur ages 6 months–5 years; simple febrile seizures are brief, generalized, and do not require antiseizure medication or neuroimaging.
Clinical Vignette
A patient has been convulsing continuously for 8 minutes in the ED with no return to baseline.
Answer: This is status epilepticus (>5 minutes). Give IV lorazepam first; if it continues, load fosphenytoin, levetiracetam, or valproate, then escalate to a continuous infusion with EEG. Treat immediately — mortality climbs with duration.
Core Topic 3 of 6 · Episodic Disorders
Headache Syndromes
Before you beginHeadache Syndromes3 questions
Answer these three before you read the module. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Question 1 of 3 · High Yield · Headache · Migraine Prophylaxis
A 29-year-old woman has migraine without aura on 8–10 days per month. Sumatriptan aborts most attacks, but she is now missing work. She has no vascular disease and is not pregnant. Which is the MOST appropriate next step?
Click to Reveal Answer
Correct answer: D — Start prophylaxis — propranolol or topiramate
Preventive therapy is indicated once attacks reach roughly 4 or more headache days per month, cause significant disability, or when acute therapy is failing or being overused. First-line options are propranolol or metoprolol, topiramate, amitriptyline, and valproate; CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab) and gepants are effective in patients who fail or cannot tolerate these.
Why the other choices are wrong
  • Continue as-needed triptans only — Incorrect. Acute therapy alone is insufficient once headaches are frequent and disabling — and at 8–10 days per month she is approaching the medication-overuse threshold.
  • Increase the triptan to daily dosing — Incorrect. Triptan use on more than 10 days per month causes medication overuse headache. Acute drugs are never scheduled prophylaxis.
  • Start a daily butalbital-containing compound — Incorrect. Butalbital carries high risk of dependence and medication overuse headache; it is not a preventive agent.
  • Obtain MRI brain before changing therapy — Incorrect. Neuroimaging is reserved for red flags — thunderclap onset, new deficit, papilloedema, new headache after age 50, immunosuppression, or a change in an established pattern. Typical migraine needs none.
Board pearlThe prophylaxis trigger is ≥4 headache days/month or disability; the overuse ceiling is <10 days/month for triptans, ergots, opioids, and combination analgesics (<15 for simple NSAIDs). Match the drug to the comorbidity: propranolol is out in asthma, topiramate causes paraesthesias, weight loss, kidney stones, and is teratogenic (cleft palate), amitriptyline helps coexisting insomnia, and valproate is avoided in anyone who may conceive.
Covered below under Module 3 — Headaches · prophylactic therapy
Question 2 of 3 · High Yield · Headache · Cluster
A 41-year-old man has 6 weeks of excruciating right periorbital pain with ipsilateral tearing, conjunctival injection, nasal congestion, and ptosis. Attacks last 45–60 minutes, wake him at the same hour nightly, and he paces the room in agitation. Which is the MOST appropriate acute treatment?
Click to Reveal Answer
Correct answer: B — High-flow oxygen and/or subcutaneous sumatriptan
Strictly unilateral periorbital pain with ipsilateral cranial autonomic features, attacks of 15–180 minutes, circadian clustering, and restlessness is cluster headache. Abortive therapy is high-flow 100% oxygen for 15 minutes and/or subcutaneous sumatriptan 6 mg — both act within minutes, which is what a 45-minute attack requires.
Why the other choices are wrong
  • Oral sumatriptan 100 mg per attack — Incorrect. Oral absorption is far too slow; the attack peaks and resolves before the drug works. Cluster headache requires the subcutaneous or intranasal route.
  • Indomethacin — Incorrect. A near-absolute response to indomethacin defines paroxysmal hemicrania — shorter attacks (2–30 minutes), many more per day. It is the distractor that tests whether you separated the two.
  • Oral verapamil — Incorrect. Verapamil is first-line preventive therapy for cluster headache, not an abortive agent.
  • IV ketorolac alone — Incorrect. NSAIDs are inadequate for cluster pain and act too slowly.
Board pearlBehavior separates the two big primary headaches: cluster patients are restless and pacing, migraine patients want dark and still. Cluster skews male, migraine female 3:1. Cluster management runs in three lanes — abort with oxygen plus SC sumatriptan, bridge with prednisone or an occipital nerve block, prevent with verapamil.
Covered below under Module 3 — Headaches · cluster headache
Question 3 of 3 · High Yield · Headache · Red Flags for Secondary Causes
A 48-year-old man with a history of migraines presents with a headache he describes as 'the worst of my life,' maximal at onset, while exercising. He is afebrile. CT head is negative.
Click to Reveal Answer
Correct answer: D — Lumbar puncture for xanthochromia
Thunderclap headache (maximal at onset) with a negative CT requires LP to rule out SAH. CT misses ~2% of SAH in the first 12 hours and more beyond 24 hours. Xanthochromia (yellow CSF) indicates blood breakdown and is diagnostic. The history of migraines does NOT change the workup when headache characteristics are atypical.
Why the other choices are wrong
  • Start sumatriptan and recheck in 2 hours — Incorrect. Treating this as migraine is the dangerous error. A known migraine history does not protect against subarachnoid hemorrhage, and triptans are vasoconstrictors that are inappropriate before SAH is excluded.
  • Prescribe NSAIDs and neurology follow-up — Incorrect. Outpatient management of an unexcluded thunderclap headache risks catastrophic rebleeding, which carries very high mortality. The negative CT is reassuring but insufficient at this point in the timeline.
  • Discharge with migraine medications — Incorrect. Discharge is the highest-risk option. Maximal-at-onset headache during exertion is a classic SAH presentation, and a negative CT does not exclude it — sensitivity falls progressively after the first 6 to 12 hours.
  • MRI brain with gadolinium — Incorrect. MRI is useful for many secondary headache causes but is not the standard next step for suspected SAH after a negative CT. LP directly detects xanthochromia and red cells, and is faster and more available.
Board pearlMaximal at onset is the phrase that changes the plan, and a known headache history does not soften it. CT sensitivity for subarachnoid hemorrhage is excellent within 6 hours but decays after that, so a negative CT with a thunderclap history still needs an LP looking for xanthochromia (or CT angiography where that pathway is used). Run the SNOOP red flags: systemic signs, neurologic deficit, onset sudden, older age, and a pattern that has changed.
Covered below under Module 3 — Headaches · SNOOP red flags
Tier 1
Module 3
Headaches
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Primary headache phenotypes · SNOOP red flags · GCA · IIH
🩺 Opening Clinical Vignette
🔺 TRAP LEVEL
A 54-year-old woman with a history of migraines presents with her 'usual' severe headache. She rates it 10/10 — 'the worst of my life.' It began suddenly 2 hours ago while gardening. She took her sumatriptan but it didn't help.
⏸ Pause & Discuss — Before Reading Further
Why does the phrase 'worst of my life' change everything — even in a known migraineur? What is your immediate next step?
✓ Answer
Thunderclap headache = subarachnoid hemorrhage until proven otherwise — even in migraineurs. The sudden maximal onset ('sentinel bleed'), failure to respond to triptans, and severity mandate CT head immediately. A prior migraine history does NOT protect against SAH. If CT is negative → LP for xanthochromia.
💡 Teaching Pearl
This is one of the most dangerous cognitive biases in emergency medicine — anchoring on a known migraine diagnosis when the headache characteristics have changed. 'Worst headache of my life' + sudden onset = SAH workup regardless of history. This vignette could save a patient's life.
Primary Headaches
FeatureMigraineTensionCluster
QualityPulsating/throbbingPressing/band-likeBoring/stabbing
LocationUnilateralBilateralUnilateral (periorbital)
Duration4–72 h30 min–7 days15–180 min
AssociatedNausea, photo/phonophobia, auraMild nausea at mostIpsilateral lacrimation, rhinorrhea, ptosis, miosis, conjunctival injection
ActivityWorsenedNot worsenedRestlessness/agitation
PredominanceFemaleFemaleMale
Migraine Management
  • Acute: triptans (first-line moderate–severe), NSAIDs, antiemetics; avoid opioids/barbiturates.
  • Triptans contraindicated in CAD, uncontrolled HTN, hemiplegic migraine, basilar migraine.
  • Preventive (≥4 days/month): topiramate, propranolol, amitriptyline, valproate, CGRP mAbs.
  • Status migrainosus = migraine lasting >72 h.
Cluster Management
  • Acute: high-flow 100% oxygen (15 L/min), subcutaneous sumatriptan.
  • Preventive: verapamil (first-line); short prednisone taper as a bridge.
Medication-Overuse Headache
  • Rebound headache from frequent acute medication use — triptans or combination analgesics ≥10 days/month, or simple analgesics ≥15 days/month.
  • Presents as a daily or near-daily headache that worsens as each acute dose wears off.
  • Treatment: withdraw the overused agent and start a preventive; warn the patient that headaches transiently worsen before they improve.
Red Flags — SNOOP
Secondary Headache Red Flags
  • Systemic symptoms (fever, weight loss) or disease (HIV, cancer)
  • Neurologic signs (focal deficit, papilledema, AMS)
  • Onset sudden — thunderclap → SAH until proven otherwise
  • Older age — new headache >50 → temporal arteritis
  • Progressive or positional pattern
Giant Cell (Temporal) Arteritis
  • Age >50, new headache, jaw claudication, scalp tenderness, visual changes.
  • Labs: ESR (often >50) and CRP elevated.
  • Dx: temporal artery biopsy (gold standard); skip lesions cause false negatives.
  • Treat with high-dose steroids immediately — do NOT wait for biopsy; add aspirin.
  • Complication: permanent vision loss if untreated.
Idiopathic Intracranial Hypertension
  • Typical: obese woman of childbearing age.
  • Headache, pulsatile tinnitus, transient visual obscurations, papilledema.
  • Dx: elevated opening pressure on LP (>25 cm H₂O) with normal imaging.
  • Tx: weight loss, acetazolamide; optic nerve sheath fenestration or VP shunt if refractory.
Classic Board Trap
New headache after age 50 with jaw claudication and a high ESR is giant cell arteritis. Start steroids the moment you suspect it — the biopsy can wait, the eyesight cannot.
Clinical Vignette
A 74-year-old has a new temporal headache, jaw pain when chewing, and a brief episode of vision loss; ESR is 88.
Answer: Suspect giant cell arteritis and start high-dose corticosteroids immediately — do not wait for the temporal artery biopsy. Untreated, it threatens permanent, irreversible vision loss.
Core Topic 4 of 6 · Demyelinating Disease
Multiple Sclerosis
Before you beginMultiple Sclerosis3 questions
Answer these three before you read the module. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Question 1 of 3 · High Yield · MS · Optic Neuritis & MRI
A 27-year-old woman has 5 days of progressive blurred vision in the right eye with pain on eye movement. Exam shows an afferent pupillary defect and impaired red color saturation. Which is the MOST appropriate next step?
Click to Reveal Answer
Correct answer: A — MRI brain and cord with gadolinium
Painful monocular vision loss with an afferent pupillary defect in a young woman is optic neuritis, the presenting event in roughly 20% of multiple sclerosis. MRI of brain and cord with gadolinium is the key test: periventricular, juxtacortical, infratentorial, and spinal cord plaques establish dissemination in space, and simultaneous enhancing plus non-enhancing lesions establish dissemination in time under the 2017 McDonald criteria.
Why the other choices are wrong
  • Non-contrast CT head — Incorrect. CT is insensitive for white matter demyelination and cannot demonstrate the lesion distribution the criteria require.
  • Temporal artery biopsy — Incorrect. Giant cell arteritis causes painless vision loss in patients over 50 with jaw claudication, scalp tenderness, and a raised ESR/CRP — a different demographic and a different exam.
  • Visual evoked potentials — Incorrect. VEPs can support a demyelinating lesion but are not the primary diagnostic modality.
  • Oral prednisone alone — Incorrect. The Optic Neuritis Treatment Trial found oral prednisone alone offered no benefit and was associated with a higher recurrence rate. Treat with IV methylprednisolone, and image first.
Board pearlPain on eye movement + APD = optic neuritis until proven otherwise; get MRI with gadolinium. Two-thirds have a normal disc on fundoscopy (retrobulbar) — a normal-looking disc does not exclude it. CSF oligoclonal bands or an elevated IgG index can substitute for dissemination in time when the MRI is equivocal. Uhthoff phenomenon is symptom worsening with heat; Marcus Gunn pupil is the APD you elicit with the swinging flashlight.
Covered below under Module 4 — Demyelinating Disorders · diagnosis
Question 2 of 3 · High Yield · MS · Acute Relapse
A 31-year-old woman with relapsing-remitting MS develops 4 days of new right leg weakness and a sensory level. She is afebrile and urinalysis is negative. Which is the MOST appropriate treatment for this episode?
Click to Reveal Answer
Correct answer: E — IV methylprednisolone 1 g daily for 3–5 days
Acute MS relapses are treated with high-dose IV corticosteroids — methylprednisolone 1 g/day for 3 to 5 days — which shorten relapse duration and speed recovery. Before calling it a relapse, exclude a pseudo-relapse: fever, urinary tract infection, or any metabolic stressor can unmask old deficits, and the treatment for that is the infection, not steroids.
Why the other choices are wrong
  • Escalate her disease-modifying therapy to treat the relapse — Incorrect. DMTs reduce future relapses and new lesion formation. They do nothing for the deficit in front of you.
  • Plasmapheresis as first-line therapy — Incorrect. PLEX is second-line, reserved for severe relapses that fail corticosteroids.
  • NSAIDs and observation — Incorrect. NSAIDs have no role in relapse treatment and observation forfeits the faster recovery steroids provide.
  • Monthly IV immunoglobulin — Incorrect. IVIG is not standard therapy for either acute relapse or maintenance in RRMS.
Board pearlA true relapse is a new deficit lasting >24 hours, at least 30 days from the last one, without fever or infection. Steroids speed recovery but do not change long-term disability — only DMTs do, which is why every RRMS patient should be on one. Steroids for the attack, DMT for the disease: keep those two jobs separate on exam day.
Covered below under Module 4 — Demyelinating Disorders · relapse management
Question 3 of 3 · High Yield · MS · Subtype & DMT
A 48-year-old man has 3 years of steadily worsening spastic gait with no discrete attacks and no remissions. MRI shows periventricular and spinal cord plaques; CSF contains oligoclonal bands. Which subtype is this, and which DMT is FDA-approved for it?
Click to Reveal Answer
Correct answer: C — Primary progressive MS — ocrelizumab
Steady decline from onset with no discrete relapses defines primary progressive MS, which accounts for roughly 10–15% of cases, presents later, is more often male, and is dominated by progressive myelopathy. Ocrelizumab is the only DMT FDA-approved for PPMS.
Why the other choices are wrong
  • Relapsing-remitting MS — interferon beta — Incorrect. RRMS requires discrete relapses with full or partial recovery between them — this patient never had one.
  • Secondary progressive MS — natalizumab — Incorrect. SPMS begins as RRMS and only later converts to steady progression. A relapsing phase is a prerequisite and is absent here.
  • Clinically isolated syndrome — no DMT indicated — Incorrect. CIS is a single demyelinating episode lasting at least 24 hours, not 3 years of progression.
  • Neuromyelitis optica spectrum disorder — eculizumab — Incorrect. NMOSD causes severe or bilateral optic neuritis and longitudinally extensive cord lesions with AQP4-IgG positivity — and interferon beta makes it worse, which is why the distinction matters.
Board pearlRoughly 85% start as RRMS and most eventually convert to SPMS; PPMS is progressive from day one. The single testable drug fact: ocrelizumab is the only FDA-approved therapy for PPMS. Always test AQP4-IgG before committing to an MS diagnosis with cord-dominant disease — treating NMOSD as MS with interferon beta causes harm.
Covered below under Module 4 — Demyelinating Disorders · subtypes and DMTs
Tier 1
Module 4
Demyelinating Disorders
👁 Free Preview
MS · McDonald criteria · INO · optic neuritis · NMO (Devic)
🩺 Opening Clinical Vignette
🟡 INTERMEDIATE
A 28-year-old woman has a 3-day history of painful vision loss in the right eye. Exam shows decreased visual acuity, color desaturation, and a relative afferent pupillary defect (RAPD). MRI shows enhancement of the right optic nerve.
⏸ Pause & Discuss — Before Reading Further
What is the diagnosis, what is the acute treatment, and what do you tell her about her long-term risk?
✓ Answer
Optic neuritis — demyelination of the optic nerve. Acute treatment: IV methylprednisolone 1g/day × 3–5 days (speeds recovery but does not improve final visual outcome). Long-term risk: 50% of patients with isolated optic neuritis will develop MS within 15 years. Risk is higher if MRI shows other white matter lesions. Start disease-modifying therapy discussion if MRI shows additional lesions (McDonald criteria).
💡 Teaching Pearl
Optic neuritis is frequently the first presentation of MS and is a high-frequency PANCE scenario. The RAPD (Marcus Gunn pupil) is pathognomonic for an afferent lesion. Teaching that IV steroids speed recovery but don't improve final vision — and that MRI findings at this moment predict MS risk — prepares students for both the acute and longitudinal management questions.
Multiple Sclerosis
  • Autoimmune CNS white-matter demyelination; typical patient is a young woman (20s–40s).
  • Episodes disseminated in time and space.
  • Classic: optic neuritis, internuclear ophthalmoplegia, transverse myelitis, Lhermitte sign (shock with neck flexion), Uhthoff phenomenon (worse with heat).
McDonald Criteria & Workup
Dissemination in Space & Time
  • Space: ≥2 lesions in different CNS locations (periventricular, juxtacortical, infratentorial, cord)
  • Time: new lesions on follow-up MRI, or simultaneous enhancing + non-enhancing lesions
  • MRI: T2/FLAIR hyperintensities; gadolinium enhancement = active inflammation
  • CSF: oligoclonal bands (>90%), elevated IgG index
MS Types & Treatment
  • RRMS (~85%) discrete attacks with recovery; SPMS gradual worsening after RRMS; PPMS progressive from onset.
  • Acute relapse: IV methylprednisolone (3–5 days); plasmapheresis if steroid-refractory.
  • DMTs: interferon-beta, glatiramer, dimethyl fumarate, fingolimod, natalizumab, ocrelizumab.
  • Natalizumab → PML risk (check JCV antibody). Ocrelizumab approved for RRMS & PPMS.
INO & Optic Neuritis
  • INO: lesion of the medial longitudinal fasciculus → ipsilateral adduction deficit + contralateral abducting nystagmus. Bilateral INO in a young patient = MS until proven otherwise.
  • Optic neuritis: unilateral painful vision loss, afferent pupillary defect (Marcus Gunn). Often the first MS presentation. IV methylprednisolone speeds recovery.
Neuromyelitis Optica (Devic)
  • Severe optic neuritis + longitudinally extensive transverse myelitis (≥3 segments).
  • Aquaporin-4 (NMO-IgG) antibody positive.
  • More severe attacks, poorer recovery than MS.
  • Tx differs: rituximab, azathioprine, mycophenolate — interferon-beta may worsen NMO.
Clinical Vignette
A 28-year-old woman has painful monocular vision loss now and had transient right-hand numbness 6 months ago. MRI shows periventricular and spinal lesions.
Answer: Lesions disseminated in time and space indicate multiple sclerosis; CSF oligoclonal bands support it. Treat the acute relapse with IV methylprednisolone and start a disease-modifying therapy.
Core Topic 5 of 6 · CNS Infection
Meningitis & Encephalitis
Before you beginMeningitis & Encephalitis3 questions
Answer these three before you read the module. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Question 1 of 3 · High Yield · Meningitis · Sequencing
A 21-year-old presents with fever, neck stiffness, photophobia, and non-blanching petechiae. The team wants to do a CT head before LP. Which is the MOST appropriate sequence?
Click to Reveal Answer
Correct answer: D — Blood cultures → dexamethasone → antibiotics → CT head → LP
Correct sequence: (1) Blood cultures ×2, (2) IV dexamethasone 0.15mg/kg, (3) IV ceftriaxone + vancomycin — then CT if indicated, then LP. Dexamethasone must be given BEFORE or WITH first antibiotic dose to reduce cytokine-mediated neurologic damage. Never delay antibiotics for CT or LP results. Petechiae suggest meningococcemia — add rifampin prophylaxis for close contacts.
Why the other choices are wrong
  • LP immediately without CT — petechiae indicate meningococcemia not mass lesion — Incorrect. The reasoning about meningococcemia is clinically sound, and LP without CT is often appropriate — but the sequence still omits the critical early steps. Cultures, dexamethasone, and antibiotics must not wait for the LP.
  • Antibiotics → dexamethasone → blood cultures → CT → LP — Incorrect. Two ordering errors. Blood cultures should precede antibiotics to maximize yield, and dexamethasone must be given before or with the first antibiotic dose to blunt the inflammatory response to bacterial lysis.
  • CT head → LP → blood cultures → antibiotics → dexamethasone — Incorrect. This delays antibiotics behind two imaging and procedural steps. In bacterial meningitis, mortality rises with each hour of delayed antibiotics — treatment must not wait for imaging or LP.
  • Blood cultures → CT head → LP → antibiotics → dexamethasone — Incorrect. Cultures first is correct, but antibiotics and dexamethasone are then pushed behind CT and LP. Antibiotics should be given immediately after cultures, and dexamethasone must not come after the first antibiotic dose.
Board pearlThe order is the whole question: blood cultures, then dexamethasone, then antibiotics — and neither CT nor LP is allowed to delay the antibiotic. Steroids must go in before or with the first dose to blunt the cytokine surge; giving them afterwards loses the benefit. CT before LP is only needed for focal deficits, papilloedema, seizure, immunosuppression, or altered consciousness. Non-blanching petechiae point to meningococcus, which means droplet precautions and prophylaxis for close contacts.
Covered below under Module 5 — CNS Infections · empiric sequencing
Question 2 of 3 · High Yield · Encephalitis · HSV
A 62-year-old man has 3 days of fever, confusion, and word-finding difficulty, then a focal seizure. CSF shows 90 lymphocytes/µL, protein 85 mg/dL, normal glucose, and red cells that do not clear from tube 1 to tube 4. MRI shows temporal lobe hyperintensity. Which is the MOST appropriate next step?
Click to Reveal Answer
Correct answer: A — Start IV acyclovir now and send CSF HSV PCR
Fever, altered mental status, aphasia, focal seizure, a lymphocytic CSF with red cells, and temporal lobe involvement on MRI is HSV-1 encephalitis. IV acyclovir 10 mg/kg every 8 hours is started empirically the moment the diagnosis is suspected, before PCR returns. Untreated mortality approaches 70%, and every hour of delay worsens neurologic outcome.
Why the other choices are wrong
  • Await the HSV PCR result before starting antiviral therapy — Incorrect. Waiting is the fatal answer. PCR turnaround costs hours to days, and PCR can be falsely negative in the first 72 hours — treat first, repeat the PCR if suspicion persists.
  • IV ceftriaxone and vancomycin only — Incorrect. Adding empiric bacterial coverage while the picture is unclear is reasonable, but it treats the wrong organism. Antibiotics alone leave HSV untreated.
  • IV amphotericin B and flucytosine — Incorrect. That is cryptococcal therapy, which fits an HIV patient with a high opening pressure and a positive cryptococcal antigen — not temporal lobe encephalitis.
  • High-dose corticosteroids alone — Incorrect. Steroids may be used adjunctively for cerebral edema but have no antiviral activity.
Board pearlTemporal lobe + fever + aphasia or seizure = acyclovir now. Read the CSF as a pattern: bacterial gives neutrophils, glucose <40, protein >200; viral gives lymphocytes with normal glucose; HSV adds red cells and temporal localization. Bacterial empirics by age: neonate → ampicillin + cefotaxime; 1 month to 50 years → ceftriaxone + vancomycin; over 50 or immunocompromised → add ampicillin for Listeria; give dexamethasone with or just before the first antibiotic dose when pneumococcus is suspected.
Covered below under Module 5 — CNS Infections · HSV encephalitis
Question 3 of 3 · High Yield · HIV · Ring-Enhancing Lesion
A 38-year-old with HIV (CD4 45) presents with headache and confusion. MRI shows a SINGLE ring-enhancing lesion with mass effect. Which is MOST likely?
Click to Reveal Answer
Correct answer: C — CNS lymphoma (EBV-associated) — most likely with single lesion
Single ring-enhancing lesion in HIV = CNS lymphoma (EBV-associated). Multiple = toxoplasmosis. Workup: CSF EBV DNA, Toxoplasma IgG serology. May trial empiric toxo treatment × 2 weeks — if no radiographic/clinical improvement → brain biopsy to confirm lymphoma.
Why the other choices are wrong
  • Cryptococcoma — Incorrect. Cryptococcal CNS disease usually presents as meningitis with raised opening pressure rather than a solitary mass. Cryptococcomas are uncommon and would typically be accompanied by positive serum or CSF cryptococcal antigen.
  • Bacterial brain abscess — Incorrect. A pyogenic abscess produces a ring-enhancing lesion, so the imaging overlaps — but patients are usually acutely febrile with an identifiable source such as sinusitis, otitis, or endocarditis. The subacute course at CD4 45 points to an opportunistic process.
  • Toxoplasmosis — pyrimethamine + sulfadiazine — Incorrect. This is the key discrimination and the most tempting answer, since toxoplasmosis is common at this CD4 count. Toxoplasmosis characteristically produces MULTIPLE lesions, typically at the basal ganglia and gray-white junction; a SINGLE lesion favors CNS lymphoma.
  • PML — no treatment available — Incorrect. Progressive multifocal leukoencephalopathy produces non-enhancing white matter lesions WITHOUT mass effect. Ring enhancement and mass effect are inconsistent with PML, and antiretroviral therapy can improve it.
Board pearlCount the lesions in an HIV patient with CD4 under 100: a single ring-enhancing lesion suggests CNS lymphoma (EBV-associated), while multiple lesions suggest toxoplasmosis. Confirm with CSF EBV DNA and Toxoplasma IgG; a negative Toxoplasma IgG makes toxoplasmosis unlikely. The accepted pathway is an empiric two-week trial of toxoplasmosis therapy, with brain biopsy reserved for lesions that fail to improve radiographically.
Covered below under Module 11 — Tumors · ring-enhancing lesion differential
Tier 1
Module 5
CNS Infections
👁 Free Preview
CSF interpretation · empiric antibiotics · encephalitis · brain abscess
🩺 Opening Clinical Vignette
🟡 INTERMEDIATE
A 19-year-old college student has 6 hours of fever, severe headache, neck stiffness, and photophobia. He appears toxic. BP 96/60. Non-blanching petechiae are visible on his legs. CT head is being ordered.
⏸ Pause & Discuss — Before Reading Further
What must happen in the next 10 minutes — before the CT results are back?
✓ Answer
Blood cultures × 2 → IV dexamethasone 0.15mg/kg → IV ceftriaxone 2g + vancomycin — ALL before CT results. Non-blanching petechiae + meningismus + hemodynamic instability = meningococcemia/bacterial meningitis. Delay in antibiotics increases mortality ~7% per hour. CT is needed before LP only if papilledema or focal deficits. Antibiotics NEVER wait for imaging.
💡 Teaching Pearl
The treatment sequence in bacterial meningitis is the most tested temporal decision in neurology. The CT-before-LP rule trips students into delaying antibiotics. The correct sequence: cultures → steroids → antibiotics → THEN CT if indicated → LP after CT if safe. This sequence saves lives and is tested on every major board prep platform.
CSF Interpretation
FindingBacterialViralFungal / TB
Opening pressureElevatedNormal/mildElevated
WBC>1000, neutrophils<500, lymphocytes<500, lymphocytes
GlucoseLowNormalLow
ProteinElevated (>200)Normal/mildElevated
Empiric Antibiotics by Age
Age GroupEmpiric Regimen
Neonate (<1 month)Ampicillin + cefotaxime (or gentamicin)
1 month–50 yearsVancomycin + ceftriaxone
>50 or immunocompromisedVancomycin + ceftriaxone + ampicillin (Listeria)
Meningitis Management Rules
  • Dexamethasone before/with first antibiotic dose — reduces mortality & hearing loss in pneumococcal meningitis
  • Do NOT delay antibiotics for CT or LP if bacterial meningitis is suspected
  • CT before LP if: immunocompromised, CNS disease history, new seizure, papilledema, AMS, focal deficit
  • N. meningitidis close contacts: rifampin, ciprofloxacin, or ceftriaxone prophylaxis
Encephalitis & Brain Abscess
  • Encephalitis: fever + AMS + focal signs ± seizures; HSV-1 (temporal lobe); MRI temporal T2/FLAIR; CSF lymphocytic, HSV PCR. Start IV acyclovir empirically — do not wait for confirmation.
  • Brain abscess: headache, fever, focal deficits; ring-enhancing lesion. Tx: ceftriaxone + metronidazole ± vancomycin; drain if >2.5 cm.
  • Ring-enhancing differential: abscess, glioblastoma, metastasis, toxoplasmosis (HIV).
Core Topic 6 of 6 · Movement Disorders
Parkinson Disease
Before you beginParkinson Disease & Movement Disorders3 questions
Answer these three before you read the module. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Question 1 of 3 · High Yield · Movement · Parkinson vs Essential Tremor
A 68-year-old woman has a 2-year hand tremor that is worst when she holds a cup or writes, involves both hands, quiets after a glass of wine, and was present in her father. Tone, gait, and speed of movement are normal. Which is the MOST likely diagnosis?
Click to Reveal Answer
Correct answer: E — Essential tremor
A bilateral action and postural tremor with a family history, alcohol responsiveness, and no bradykinesia or rigidity is essential tremor. It is treated with propranolol or primidone. Parkinson tremor is the opposite in almost every feature: asymmetric, present at rest, damped by voluntary movement, and accompanied by bradykinesia and cogwheel rigidity.
Why the other choices are wrong
  • Parkinson disease — Incorrect. PD requires bradykinesia plus rest tremor or rigidity, and it starts asymmetrically. A pure bilateral action tremor with normal tone and gait does not fit.
  • Drug-induced parkinsonism — Incorrect. This follows D2 blockers such as metoclopramide, prochlorperazine, or antipsychotics, and produces symmetric bradykinesia and rigidity — there is no offending drug and no parkinsonism here.
  • Cerebellar tremor — Incorrect. Cerebellar disease produces a low-frequency intention tremor that worsens as the finger approaches the target, with dysmetria and ataxia.
  • Physiologic tremor — Incorrect. Physiologic tremor is fine and fast, provoked by caffeine, anxiety, or thyrotoxicosis, and is neither familial nor disabling.
Board pearlOne question sorts them: when is the tremor worst? At rest and asymmetric → Parkinson. With action, bilateral, familial, better with alcohol → essential. Treatment diverges accordingly: propranolol or primidone for ET, levodopa for PD. Reserve DaTscan for genuinely ambiguous cases — it separates PD from ET but is not part of a routine diagnosis, which remains clinical.
Covered below under Module 6 — Movement Disorders · tremor differential
Question 2 of 3 · High Yield · Movement · Parkinson First-Line Therapy
A 63-year-old man with newly diagnosed Parkinson disease has resting tremor and bradykinesia that now interfere with his work as a mechanic. Which is the MOST appropriate initial pharmacologic therapy?
Click to Reveal Answer
Correct answer: B — Carbidopa-levodopa
Carbidopa-levodopa is the most effective symptomatic therapy for Parkinson disease and is first-line once motor symptoms impair function. Carbidopa blocks peripheral dopa decarboxylase, which reduces nausea and delivers more levodopa to the CNS. MAO-B inhibitors such as rasagiline are reasonable monotherapy for very mild symptoms, and dopamine agonists are an alternative in younger patients — at the cost of impulse-control disorders, somnolence, and hallucinations.
Why the other choices are wrong
  • Benztropine — Incorrect. Anticholinergics can help tremor but cause confusion, urinary retention, constipation, and dry mouth — a poor trade in anyone over about 65.
  • Amantadine — Incorrect. Amantadine gives modest benefit and earns its place later, for levodopa-induced dyskinesia.
  • Quetiapine — Incorrect. Quetiapine treats PD psychosis. It does nothing for bradykinesia and does not belong as initial therapy.
  • Deep brain stimulation now — Incorrect. DBS is reserved for motor fluctuations or dyskinesias that persist despite optimized medical therapy, not for a newly diagnosed patient.
Board pearlRemember TRAP — tremor at rest, rigidity, akinesia/bradykinesia, postural instability — and treat with levodopa once function suffers. Expect wearing off and dyskinesia after roughly 5 years; the fix is fractionating doses or adding a COMT inhibitor (entacapone) or MAO-B inhibitor (rasagiline). And never hand a PD patient a D2 blocker: for psychosis use quetiapine, clozapine, or pimavanserin.
Covered below under Module 6 — Movement Disorders · pharmacologic therapy
Question 3 of 3 · High Yield · Movement · Drug Trap
A 62-year-old man with Parkinson disease develops nausea after increasing his levodopa/carbidopa dose. His physician prescribes metoclopramide. Two days later his tremor and rigidity are dramatically worse. What caused this deterioration?
Click to Reveal Answer
Correct answer: E — Dopamine antagonism opposing levodopa
Metoclopramide is a D2 receptor antagonist that crosses the blood-brain barrier and directly opposes dopaminergic therapy in Parkinson disease. It is CONTRAINDICATED in Parkinson patients. For nausea in Parkinson patients, use ondansetron (5-HT3 antagonist with no dopamine blockade) or trimethobenzamide.
Why the other choices are wrong
  • Cholinergic excess from metoclopramide — Incorrect. Metoclopramide does have prokinetic cholinergic effects in the gut, but its CNS action relevant here is dopamine D2 blockade. Cholinergic excess would produce salivation, bradycardia, and diarrhea, not worsening rigidity and tremor.
  • Levodopa toxicity from excessive dosing — Incorrect. Levodopa excess causes dyskinesias, hallucinations, and involuntary movements — not increased rigidity and tremor. The parkinsonian features got WORSE, which points to too little dopaminergic effect, not too much.
  • Disease progression unrelated to medication — Incorrect. Parkinson disease progresses over months to years, not over 48 hours. A dramatic decline with a clear temporal link to a new medication is a drug effect, not natural history.
  • Serotonin syndrome from drug interaction — Incorrect. Serotonin syndrome features hyperthermia, clonus, hyperreflexia, agitation, and autonomic instability. Metoclopramide is primarily a dopamine antagonist, and the picture described is worsened parkinsonism rather than serotonergic excess.
Board pearlAny central D2 antagonist will unmask or worsen parkinsonism: metoclopramide, prochlorperazine, promethazine, haloperidol, and the typical antipsychotics. For nausea in Parkinson disease use ondansetron or trimethobenzamide, which do not block dopamine. Run the same logic backwards too — when a patient develops new parkinsonism, review the medication list before diagnosing idiopathic disease, because drug-induced parkinsonism is typically symmetric whereas idiopathic Parkinson disease starts asymmetrically.
Covered below under Module 6 — Movement Disorders · drug-induced
Tier 1
Module 6
Movement Disorders
👁 Free Preview
Parkinson · essential tremor · Huntington · drug-induced · NMS
🩺 Opening Clinical Vignette
🟡 INTERMEDIATE
A 58-year-old woman with Parkinson disease develops severe nausea after starting levodopa/carbidopa. Her internist prescribes metoclopramide. Two days later her Parkinson symptoms are dramatically worse.
⏸ Pause & Discuss — Before Reading Further
Why did this happen, and what should have been prescribed instead?
✓ Answer
Metoclopramide is a dopamine antagonist — it blocks D2 receptors in the gut AND the brain, worsening Parkinson by opposing the therapeutic effect of levodopa. Never use in Parkinson patients. Safe alternatives for nausea: ondansetron (5-HT3 antagonist — no dopamine blockade), domperidone (doesn't cross BBB, not available in US), or trimethobenzamide.
💡 Teaching Pearl
The dopamine-blocking drugs in Parkinson is the single most dangerous drug trap in movement disorder management. Metoclopramide, prochlorperazine, promethazine, and most antipsychotics all worsen Parkinson. Students must have a reflex: 'Parkinson patient + nausea = ondansetron, not metoclopramide.' This exact scenario appears repeatedly on boards.
Parkinson Disease — TRAP
Classic Tetrad (bradykinesia is required for diagnosis)
  • Tremor — resting, pill-rolling
  • Rigidity — cogwheel
  • Akinesia / bradykinesia — the cardinal feature
  • Postural instability
  • Pathology: loss of dopaminergic neurons in substantia nigra pars compacta; Lewy bodies. Asymmetric onset; resting tremor improves with movement.
Parkinson Treatment
  • Levodopa/carbidopa: most effective; first-line for significant functional impairment.
  • Dopamine agonists (pramipexole, ropinirole): early use; impulse-control disorders, hallucinations.
  • MAO-B inhibitors (selegiline, rasagiline): mild benefit, early or adjunct.
  • COMT inhibitors (entacapone): extend levodopa effect.
  • Amantadine: levodopa-induced dyskinesias.
  • Long-term levodopa: wearing-off, on-off fluctuations, dyskinesias.
Essential vs Parkinson Tremor
FeatureEssential TremorParkinson Tremor
TypeAction/posturalResting
SymmetryBilateral, symmetricAsymmetric
Body partHands, head, voiceHands (pill-rolling)
AlcoholImprovesNo effect
OtherNo rigidity/bradykinesiaRigidity, bradykinesia
TreatmentPropranolol, primidoneLevodopa/carbidopa
Huntington Disease
  • Autosomal dominant; CAG repeat expansion on chromosome 4 (huntingtin).
  • Onset 30s–50s; chorea, psychiatric symptoms, cognitive decline.
  • Anticipation: earlier onset in successive generations; caudate atrophy on imaging.
  • Tx: tetrabenazine or deutetrabenazine for chorea.
Drug-Induced Movement Disorders
  • Acute dystonia (antipsychotics, metoclopramide) → diphenhydramine or benztropine.
  • Akathisia (inner restlessness) → reduce dose, add propranolol/benzodiazepine.
  • Tardive dyskinesia (chronic antipsychotics) → VMAT2 inhibitors (valbenazine, deutetrabenazine).
  • NMS: fever, lead-pipe rigidity, AMS, autonomic instability, elevated CK → stop agent, dantrolene, bromocriptine.
Classic Board Trap
Lead-pipe rigidity + fever + altered mental status + elevated CK after an antipsychotic is neuroleptic malignant syndrome — stop the drug and give dantrolene. Do not confuse with serotonin syndrome (which has hyperreflexia and clonus).
Domain 7 · Foundations — Localize Before You Diagnose
Neurologic Exam & Neuroanatomy
Tier 3
Module 7
Neurologic Exam & UMN vs LMN
The single most testable distinction in neurology — where the lesion sits dictates the differential
★★ High YieldLocalize First
🩺 Opening Clinical Vignette
🟢 FOUNDATIONAL
A 68-year-old man has right arm and leg weakness. On exam: increased tone, brisk reflexes, upgoing Babinski on the right, but normal sensation. He has no atrophy or fasciculations.
⏸ Pause & Discuss — Before Reading Further
Is this UMN or LMN? Where is the lesion — cortex, internal capsule, spinal cord, or peripheral nerve?
✓ Answer
UMN lesion — spastic weakness + hyperreflexia + Babinski = upper motor neuron. The right-sided involvement of both arm and leg with no sensory loss points to the left internal capsule or cortex (contralateral control). No atrophy or fasciculations exclude LMN.
💡 Teaching Pearl
The UMN vs LMN distinction is the foundation of all neurology localization. Teaching this as a physical exam framework — spastic vs flaccid, hyperreflexia vs hyporeflexia, Babinski present vs absent — gives students a tool they'll use every day in clinical practice.
Why the PANCE Tests This

Localization is the engine of every neurology vignette. Before naming a disease, the exam tells you whether the problem is cortex, brainstem, cord, root, nerve, neuromuscular junction, or muscle. The UMN vs LMN split is the highest-yield single concept.

UMN vs LMN Lesions
FeatureUMN LesionLMN Lesion
ToneIncreased (spasticity)Decreased (flaccid)
ReflexesHyperreflexiaHyporeflexia / areflexia
BabinskiUpgoing (positive)Downgoing (normal)
AtrophyMinimal / lateProminent / early
FasciculationsAbsentPresent
Weakness patternPyramidal distributionSpecific nerve / root
ClonusPresentAbsent
Localization Framework
Where Is the Lesion?
  • Cortex → contralateral deficits, seizures, aphasia, neglect
  • Brainstem → crossed findings (ipsilateral CN + contralateral body)
  • Spinal cord → bilateral findings below a level, bowel/bladder involvement
  • Peripheral nerve → specific nerve distribution
  • Radiculopathy → dermatomal pattern, level-specific reflex change
  • NMJ → fatigable weakness, no sensory loss
  • Myopathy → proximal weakness, no sensory loss
Exam Signs Worth Memorizing
  • Pronator drift — subtle UMN sign; the arm pronates and drifts downward.
  • Babinski — the most reliable single sign of UMN dysfunction.
  • Hoffmann sign — the upper-extremity UMN equivalent.
  • Romberg — positive = proprioceptive or vestibular dysfunction (NOT cerebellar).
Board Pearl
Romberg is a trap. A patient who is steady with eyes open but falls with eyes closed has a dorsal column / proprioceptive problem — not a cerebellar one. Cerebellar patients are unsteady with eyes open too.
Tier 2
Module 8
Neuroanatomy for Boards
Lobe syndromes · aphasia · brainstem syndromes · cord tracts — the localization atlas
★★ High Yield
Cerebral Lobe Syndromes
LobeKey FunctionsLesion Findings
FrontalMotor, executive, personality, Broca (dominant)Contralateral weakness, personality change, Broca aphasia, abulia, grasp reflex
ParietalSensory, spatial awareness, Gerstmann (dominant)Contralateral sensory loss, neglect (non-dominant), agraphia, acalculia
TemporalHearing, memory, Wernicke (dominant)Wernicke aphasia, memory loss, superior quadrantanopia ('pie in the sky')
OccipitalVisionContralateral homonymous hemianopia with macular sparing
Aphasia — Board Favorite
FeatureBroca (Expressive)Wernicke (Receptive)
LocationInferior frontal gyrusSuperior temporal gyrus
OutputNon-fluent, effortfulFluent but nonsensical
ComprehensionIntactImpaired
RepetitionImpairedImpaired
AwarenessAware & frustratedOften unaware
VesselSuperior MCA divisionInferior MCA division
  • Global aphasia = Broca + Wernicke both affected (large MCA stroke).
Brainstem Syndromes — PANCE Must-Know (2 Only)
SyndromeLocationClassic PresentationKey PANCE Fact
Wallenberg Syndrome
(Lateral Medullary)		PICA occlusion → lateral medullaIpsilateral face numbness + contralateral body numbness, dysphagia, hoarseness, vertigo, Horner syndromeCROSSED deficits = brainstem. Face and body on OPPOSITE sides.
Weber Syndrome
(Medial Midbrain)		PCA occlusion → cerebral peduncleIpsilateral CN III palsy (down-and-out eye, ptosis, dilated pupil) + contralateral hemiplegiaCN III + contralateral weakness = midbrain. The "eye and arm" syndrome.

🩺 PANCE Rule: You don't need to memorize all brainstem syndromes. Know the concept: crossed deficits (ipsilateral face + contralateral body) = brainstem lesion. Wallenberg is the most tested. Recognize it by the pattern, not the name.

Wallenberg (Lateral Medullary) Syndrome — PICA/vertebral
  • Ipsilateral: facial pain/temperature loss, Horner syndrome, ataxia, dysphagia, hoarseness
  • Contralateral: body pain/temperature loss
  • The classic 'crossed' sensory pattern — pain/temp split by side
Spinal Cord Tracts & Syndromes
TractLocationFunctionLesion Effect
CorticospinalLateral columnVoluntary motorIpsilateral UMN weakness below level
Dorsal columnsPosteriorVibration, proprioception, fine touchIpsilateral loss below level
SpinothalamicAnterolateralPain, temperatureContralateral loss (crosses 1–2 levels above entry)
SyndromePatternCommon Cause
Brown-SéquardIpsilateral motor + dorsal column loss; contralateral pain/temp lossPenetrating trauma
Central cordUpper > lower weakness; cape-like sensory lossHyperextension in elderly with cervical stenosis
Anterior cordMotor + pain/temp loss; dorsal columns sparedAnterior spinal artery occlusion
Posterior cordProprioception & vibration loss onlyB12 deficiency, tabes dorsalis
Cauda equinaLMN, saddle anesthesia, bowel/bladder dysfunctionDisc herniation, tumor
Conus medullarisEarly bowel/bladder, symmetric, less painTumor, trauma
Cerebellum — DANISH (ipsilateral signs, do NOT cross)
  • Dysdiadochokinesia · Ataxia · Nystagmus · Intention tremor · Scanning speech · Hypotonia
  • Hemiballismus = contralateral subthalamic nucleus lesion
Domain 8 · Cranial Nerves, Cognition, Tumors & Cord
Cranial Neuropathies, Cognition & Structural Disease
Before you beginCranial Nerves, Cognition & Cord3 questions
Answer these three before you read the module. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Question 1 of 3 · High Yield · Cranial Nerve · CN III Palsy
A 38-year-old woman presents with sudden onset ptosis and a fixed, dilated right pupil. The right eye is deviated down and out. She has a severe headache. CT head is negative for hemorrhage.
Click to Reveal Answer
Correct answer: D — Posterior communicating artery aneurysm — urgent CTA
A complete CN III palsy with pupil involvement (dilated, unreactive) is a surgical emergency — posterior communicating artery aneurysm compresses the outer parasympathetic fibers of CN III. Urgent CTA or MRA is mandatory. Diabetic/ischemic CN III palsy classically SPARES the pupil (central ischemia spares outer fibers). Severe headache further supports an aneurysmal cause.
Why the other choices are wrong
  • Diabetic CN III palsy — observe and monitor blood glucose — Incorrect. This is the critical discrimination. Ischemic microvascular CN III palsy characteristically SPARES the pupil, because the parasympathetic fibers run peripherally and are supplied by the pial circulation. A dilated, fixed pupil indicates external compression until proven otherwise.
  • Myasthenia gravis — acetylcholine receptor antibodies — Incorrect. MG causes fluctuating, fatigable ptosis and ophthalmoparesis but NEVER affects the pupil — pupillary function is not mediated by the neuromuscular junction. A fixed dilated pupil excludes MG.
  • Cavernous sinus thrombosis — CT with contrast — Incorrect. Horner syndrome produces the opposite pupillary finding — a small, MIOTIC pupil with mild ptosis and anhidrosis. It does not cause a down-and-out eye or a dilated pupil.
  • Horner syndrome — MRI of the lung apex — Incorrect. Cavernous sinus pathology usually involves several nerves together, producing CN III, IV, VI and V1 findings with proptosis, chemosis, and often fever. An isolated pupil-involving CN III palsy points to a posterior communicating artery aneurysm.
Board pearlThe pupil decides the urgency in a third nerve palsy. Pupil-involving means compression from outside — the parasympathetic fibers run on the surface — so think posterior communicating artery aneurysm or uncal herniation and image the vessels now. Pupil-sparing points to microvascular ischemia, typically diabetic, because the infarct sits centrally and spares the outer fibers. Down-and-out with ptosis plus a severe headache is an aneurysm until angiography says otherwise.
Covered below under Module 9 — Cranial Nerve Disorders
Question 2 of 3 · Medium · Dementia · NPH
A 74-year-old man is brought by family for 'memory problems' and incontinence. Exam shows a wide-based shuffling gait with very short steps, inability to lift feet ('magnetic gait'). Head CT shows enlarged ventricles out of proportion to cortical atrophy. What is the MOST likely diagnosis and treatment?
Click to Reveal Answer
Correct answer: C — Normal pressure hydrocephalus — trial LP, then VP shunt
Normal pressure hydrocephalus (NPH): classic triad = Wet (incontinence) + Wobbly (gait apraxia — most prominent/first symptom) + Wacky (dementia). CT: enlarged ventricles out of proportion to atrophy. Diagnosis confirmed with high-volume LP (30–50 mL CSF) improving gait. Definitive treatment: ventriculoperitoneal shunt. Gait responds best; cognition and continence less reliably.
Why the other choices are wrong
  • Vascular dementia — control cardiovascular risk factors — Incorrect. Vascular dementia typically shows stepwise decline with focal deficits and infarcts or extensive white matter disease on imaging, not ventriculomegaly out of proportion to atrophy with a magnetic gait.
  • Parkinson disease with dementia — start levodopa/carbidopa — Incorrect. This is a genuine clinical mimic because both cause a shuffling gait. Parkinson disease features asymmetric rest tremor, cogwheel rigidity, and bradykinesia, and the gait does not have the wide-based magnetic quality — nor does PD explain the ventriculomegaly.
  • Frontotemporal dementia — behavioral management — Incorrect. FTD presents with early personality change, disinhibition, or progressive aphasia, with frontal and temporal atrophy on imaging. Gait apraxia and incontinence as the leading features do not fit.
  • Alzheimer disease — start donepezil — Incorrect. Alzheimer disease begins with episodic memory loss, and gait disturbance and incontinence appear late rather than first. Imaging shows hippocampal and cortical atrophy rather than disproportionate ventricular enlargement — and Alzheimer disease is not reversible, whereas NPH may be.
Board pearlNormal pressure hydrocephalus is the reversible dementia, so it has to be excluded rather than assumed. The triad is wet, wobbly, and wacky — and the order matters: gait comes first and responds best to shunting, while cognition and continence improve less reliably. Imaging shows ventricles enlarged out of proportion to cortical atrophy. Confirm with a high-volume tap that improves gait before committing to a ventriculoperitoneal shunt.
Covered below under Module 10 — Dementia & Cognitive Disorders · NPH
Question 3 of 3 · High Yield · Cauda Equina · Emergency
A 44-year-old man with low back pain presents with new urinary retention and perianal numbness. Exam shows bilateral leg weakness, diminished patellar and Achilles reflexes, and saddle anesthesia. What is the MOST appropriate next step?
Click to Reveal Answer
Correct answer: E — Emergent lumbar MRI, then surgical decompression
Cauda equina syndrome: saddle anesthesia + urinary retention + bilateral leg weakness/numbness = surgical emergency. Emergent MRI (not CT — better soft tissue visualization) then immediate neurosurgical decompression within hours. Delay beyond 24–48h is associated with permanent bladder, bowel, and sexual dysfunction. Foley catheter is appropriate but never instead of emergency decompression.
Why the other choices are wrong
  • CT myelogram — less expensive than MRI — Incorrect. Cost is not a relevant consideration in a surgical emergency, and MRI provides far superior visualisation of the cauda equina, disc, and soft tissue. CT myelography is invasive and reserved for patients who cannot have MRI.
  • Oral NSAIDs and physical therapy referral — Incorrect. This is conservative management for uncomplicated mechanical back pain. Saddle anesthesia with urinary retention are red flags that mandate imaging and surgery — delay risks permanent bladder, bowel, and sexual dysfunction.
  • IV methylprednisolone for suspected inflammatory etiology — Incorrect. Steroids are used for malignant cord compression to reduce edema, which is why this seems plausible. Cauda equina syndrome from disc herniation is a mechanical compression requiring decompression, and steroids do not substitute for surgery.
  • Foley catheter insertion and outpatient MRI within 1 week — Incorrect. A catheter manages the retention symptomatically while leaving the compression untreated. Outcomes depend heavily on time to decompression, so a one-week delay risks permanent deficits.
Board pearlCauda equina syndrome is saddle anaesthesia + urinary retention + bilateral leg weakness with reduced reflexes, and it is a surgical emergency measured in hours — MRI then decompression, with delay past 24 to 48 hours risking permanent bladder, bowel, and sexual dysfunction. Contrast it with conus medullaris and with cord compression, which are upper motor neuron and hyperreflexic. Urinary retention with an elevated post-void residual is the most reliable early sign; a catheter is supportive care, never the treatment.
Covered below under Module 12 — Spinal Cord Disorders · cauda equina
Tier 2
Module 9
Cranial Nerve Disorders
CN III palsy · trigeminal neuralgia · Bell palsy · vestibular schwannoma
🩺 Opening Clinical Vignette
🟡 INTERMEDIATE
A 62-year-old hypertensive man wakes up with right-sided ptosis. On exam: the right eye is 'down and out,' the pupil is 6mm and unreactive to light. He has no headache. His blood glucose is 312 mg/dL.
⏸ Pause & Discuss — Before Reading Further
What is the diagnosis and what dangerous structural cause must be ruled out immediately — and what feature of this exam paradoxically reassures you?
✓ Answer
CN III palsy. The 'down and out' eye + ptosis = CN III. A dilated, unreactive pupil = SURGICAL emergency — posterior communicating artery aneurysm compressing CN III externally (parasympathetics run on the outside). However: diabetic CN III palsy classically SPARES the pupil (ischemia affects the central fibers, sparing the peripheral parasympathetics). This patient has both risk factors — do CTA head urgently.
💡 Teaching Pearl
Pupil-involved vs pupil-spared CN III is one of the highest-stakes distinctions in neurology. Pupil dilated = aneurysm until proven otherwise → CTA/MRA immediately. Pupil spared + diabetes/HTN = ischemic CN III palsy = observation. This distinction is almost certain to appear on the PANCE.
CN III Palsy — Compressive vs Ischemic
FeatureCompressive (aneurysm)Ischemic (diabetes)
PupilDilated, fixed ('blown')Spared (normal)
MechanismPComm aneurysm compresses surface parasympathetic fibersMicrovascular ischemia of central fibers
UrgencyEmergency — CTA/MRA nowUsually self-limited, resolves in weeks
CN III Palsy Findings
  • Ptosis, 'down and out' eye position, mydriasis (if pupil involved)
  • Pupil-involving CN III palsy = posterior communicating artery aneurysm until proven otherwise → emergent vascular imaging
Trigeminal Neuralgia (CN V)
  • Sudden, severe, lancinating facial pain in V2/V3.
  • Triggered by chewing, talking, touching the face, wind.
  • Tx: carbamazepine (first-line), oxcarbazepine.
  • MRI to exclude structural cause (MS in young patients, tumor).
Bell Palsy (CN VII)
FeatureBell Palsy (LMN)Central (UMN) facial weakness
ForeheadInvolved (can't raise brow)Spared (can raise brow)
PatternEntire ipsilateral faceLower face contralateral to lesion
OtherHyperacusis, taste changesOther neurologic deficits
  • Bell palsy tx: oral corticosteroids within 72 h; eye protection (artificial tears, night taping).
  • ~85% recover fully; no improvement by 3–4 months → reconsider diagnosis.
  • Bilateral facial weakness → consider Lyme, sarcoidosis, Guillain-Barré.
Vestibular Schwannoma (CN VIII)
  • Unilateral sensorineural hearing loss, tinnitus, imbalance.
  • Dx: MRI with gadolinium (IAC protocol).
  • Bilateral acoustic neuromas = neurofibromatosis type 2.
Classic Board Trap
Forehead sparing separates a central (stroke) facial palsy from Bell palsy. The forehead has bilateral cortical input, so a UMN lesion spares it — if the whole half of the face including the forehead is weak, the lesion is peripheral (CN VII).
Tier 1
Module 10
Dementia & Cognitive Disorders
Delirium vs dementia · Alzheimer · vascular · Lewy body · FTD · NPH
🩺 Opening Clinical Vignette
🔺 TRAP LEVEL
A 74-year-old man with Lewy body dementia becomes agitated and is given haloperidol 1mg IM in the emergency department. Within 12 hours he is profoundly rigid, febrile, and barely arousable.
⏸ Pause & Discuss — Before Reading Further
What happened, what is the mechanism, and what antipsychotic carries the lowest risk if one is truly needed in LBD?
✓ Answer
Neuroleptic hypersensitivity reaction in Lewy body dementia. LBD patients have severe sensitivity to dopamine-blocking antipsychotics — even low doses can cause irreversible parkinsonism, marked sedation, and death. Mortality rate of this reaction is ~50%. Mechanism: LBD has reduced dopaminergic neurons → blockade causes catastrophic motor and autonomic deterioration. Safest antipsychotic if absolutely required: quetiapine (lowest D2 affinity) or clozapine.
💡 Teaching Pearl
This is the most dangerous drug error in dementia management and appears reliably on the PANCE. The teaching must include WHY — the neuropathology of LBD means these patients have minimal dopamine reserve, so any blockade triggers a disproportionate response. 'Dementia + Parkinsonian features + visual hallucinations' = suspect LBD = never give haloperidol.
Delirium vs Dementia
FeatureDeliriumDementia
OnsetAcute (hours–days)Insidious (months–years)
AttentionImpaired (hallmark)Preserved early
CourseFluctuatingProgressive
ConsciousnessAlteredClear until late
ReversibilityUsually reversibleUsually irreversible
Dementia Subtypes
TypeKey FeaturesDistinguishing Findings
AlzheimerMost common; memory → language → visuospatial → executiveHippocampal atrophy; amyloid plaques, neurofibrillary tangles
VascularStepwise decline; stroke risk factorsFocal signs; white matter changes on MRI
Lewy bodyVisual hallucinations, parkinsonism, fluctuating cognition, REM sleep behavior disorderAvoid antipsychotics (severe sensitivity); Lewy bodies
FrontotemporalPersonality/behavior change or progressive aphasia; younger (50s–60s)Frontal/temporal atrophy; Pick bodies
NPHTriad: gait apraxia, urinary incontinence, dementia ('wet, wobbly, wacky')Ventriculomegaly out of proportion to atrophy; improves with large-volume LP
Workup & Treatment
  • Screening: MMSE, MoCA. Reversible-cause labs: TSH, B12, RPR/VDRL, CBC, CMP, HIV.
  • Imaging: MRI (preferred) or CT; LP if infection, NPH, or atypical.
  • Alzheimer: cholinesterase inhibitors (donepezil, rivastigmine, galantamine) mild–moderate; memantine moderate–severe.
  • Lewy body: cholinesterase inhibitors may help; avoid typical antipsychotics & anticholinergics.
  • Vascular: risk-factor management; no specific proven pharmacotherapy.
Classic Board Trap
Visual hallucinations + parkinsonism + fluctuating cognition is Lewy body dementia — and giving a typical antipsychotic can cause a life-threatening neuroleptic sensitivity reaction. Recognize it specifically so you don't reach for haloperidol.
Clinical Vignette
An older man has fluctuating confusion, recurrent vivid visual hallucinations, parkinsonism, and acts out his dreams. The team wants haloperidol for agitation.
Answer: This is dementia with Lewy bodies — typical antipsychotics can trigger a severe, even fatal, neuroleptic sensitivity reaction. Avoid them; a cholinesterase inhibitor is more appropriate.
Tier 2
Module 11
Tumors
Primary brain tumors · increased ICP · herniation syndromes
Primary Brain Tumors
TumorKey Features / Board Pearl
Glioblastoma (GBM)Most common primary malignant brain tumor in adults. Ring-enhancing, 'butterfly' across corpus callosum. Poor prognosis. ring-enhancing; poor prognosis
MeningiomaMost common primary overall; extra-axial, dural-based, calcified; 'dural tail'; more common in women
SchwannomaCN VIII, cerebellopontine angle; NF2 = bilateral
Pituitary adenomaBitemporal hemianopia; prolactinoma most common (cabergoline/bromocriptine)
MedulloblastomaMost common malignant in children; posterior fossa; hydrocephalus
CraniopharyngiomaSuprasellar, calcified; children/young adults; bitemporal hemianopia
Oligodendroglioma'Fried egg' cells, calcified; 1p/19q co-deletion; better prognosis
EpendymomaFourth ventricle in children; hydrocephalus
  • Metastases are more common than primary tumors — lung (most), breast, melanoma, renal, colon; multiple lesions at gray-white junction.
Increased ICP & Herniation
  • Symptoms: morning/Valsalva headache, vomiting, AMS, papilledema, CN VI palsy (false localizing).
  • Cushing triad (late): hypertension, bradycardia, irregular respirations.
  • Emergency mgmt: head of bed 30°, mannitol or hypertonic saline, short-term hyperventilation (PaCO₂ 30–35), dexamethasone for vasogenic (tumor) edema, neurosurgery.
HerniationKey Findings
Uncal (transtentorial)Ipsilateral CN III palsy (blown pupil) → contralateral hemiparesis → coma
Subfalcine (cingulate)ACA compression → contralateral leg weakness
TonsillarBrainstem compression → cardiorespiratory arrest
CentralProgressive rostral-to-caudal deterioration
Board Pearl
Uncal herniation — an ipsilateral fixed, dilated pupil is the earliest sign. (Kernohan notch can produce ipsilateral hemiparesis, a classic false-localizing sign.)
Tier 1
Module 12
Spinal Cord Disorders
Cervical myelopathy · cauda equina · cord compression · transverse myelitis
🩺 Opening Clinical Vignette
🔺 TRAP LEVEL
A 68-year-old man with known prostate cancer presents with 2 days of worsening low back pain and now reports that his legs feel 'heavy.' On exam: bilateral leg weakness, hyperreflexia, upgoing Babinski signs bilaterally, and a sensory level at T10. He reports difficulty initiating urination.
⏸ Pause & Discuss — Before Reading Further
What is the diagnosis, what is the first drug to give — before imaging — and what determines whether he walks again?
✓ Answer
Malignant spinal cord compression at T10. Give IV dexamethasone 10mg IMMEDIATELY — before MRI, before calling neurosurgery. Steroids reduce edema and preserve neurologic function. Then: urgent MRI whole spine. Then: radiation oncology + neurosurgery. Prognosis depends on neurologic status at time of treatment — ambulatory patients at start of treatment have ~80% chance of remaining ambulatory. Non-ambulatory have ~30%. Time from weakness onset to treatment is the key variable.
💡 Teaching Pearl
Malignant spinal cord compression is a true oncologic emergency and a high-yield PANCE topic. The teaching is twofold: (1) dexamethasone before imaging — this is the life-altering intervention, (2) ambulatory status is the single most important prognostic factor. Students who wait for MRI before giving steroids cost the patient neurologic function.
Cervical Myelopathy
  • Most common cause: cervical spondylosis.
  • Progressive gait difficulty, hand clumsiness; UMN signs in legs, LMN signs at the level in arms; Lhermitte sign.
  • Dx: MRI cervical spine. Tx: surgical decompression for progressive/moderate-severe disease.
Cauda Equina Syndrome — Surgical Emergency
New back pain + urinary retention + saddle anesthesia = cauda equina until proven otherwise
  • Compression of cauda equina roots (usually below L1–L2); most common cause large central disc herniation
  • Saddle anesthesia, urinary retention (most consistent), fecal incontinence, bilateral leg weakness, decreased rectal tone, absent ankle reflexes
  • Dx: emergent MRI lumbar spine; Tx: emergent surgical decompression (within 24–48 h)
Cauda Equina vs Conus Medullaris
FeatureCauda EquinaConus Medullaris
LevelBelow L1–L2At conus (L1–L2)
OnsetGradual or acuteOften sudden
PainSevere, radicularLess prominent
MotorAsymmetric LMNSymmetric, mild
BladderLate, retentionEarly, retention/incontinence
ReflexesAbsent (LMN)Variable (may have UMN signs)
Cord Compression & Transverse Myelitis
  • Cord compression: metastatic disease most common (lung, breast, prostate). Back pain → weakness, sensory level, bowel/bladder dysfunction. Dx: emergent MRI of the entire spine. Tx: high-dose IV dexamethasone immediately + radiation/surgery.
  • Transverse myelitis: acute bilateral weakness, sensory level, bowel/bladder dysfunction; MRI T2 lesion over 1–2 segments (≥3 → consider NMO). Tx: IV methylprednisolone.
Syringomyelia — PANCE Recognition
  • What it is: Fluid-filled cavity (syrinx) within the spinal cord
  • Classic cause: Chiari I malformation most common. Also post-traumatic, tumors
  • Classic presentation: Cape-like bilateral loss of pain and temperature in arms/shoulders (anterior commissure compression) with preserved touch/vibration. Weakness and atrophy of hands/arms.
  • Diagnosis: MRI spine (T2 hyperintense central canal)
  • Treatment: Treat the cause (decompress Chiari). Neurosurgery referral.

🩺 PANCE Pearl: "Cape distribution" sensory loss = syrinx. The dissociated sensory loss (pain/temp lost, touch preserved) distinguishes it from cord compression.

Domain 9 · Neuromuscular & Peripheral Nerve
Junction, Motor Neuron & Nerve Disease
Before you beginJunction, Motor Neuron, Nerve & Vertigo3 questions
Answer these three before you read the module. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Question 1 of 3 · High Yield · Neuromuscular · MG vs LEMS
A 55-year-old male smoker has 4 months of proximal leg weakness. His grip strength actually IMPROVES slightly after repeated testing. EMG shows incremental response with high-frequency stimulation. CXR shows a hilar mass.
Click to Reveal Answer
Correct answer: D — Lambert-Eaton syndrome — workup for SCLC
Lambert-Eaton myasthenic syndrome (LEMS): proximal weakness that IMPROVES with repeated activity (facilitates), incremental EMG response, autonomic features, associated with SCLC in 60%. Anti-voltage-gated calcium channel antibodies. Unlike MG (decremental response, fatigable weakness). The hilar mass strongly suggests SCLC — this is a paraneoplastic syndrome.
Why the other choices are wrong
  • ALS — EMG confirms motor neuron disease — Incorrect. ALS produces mixed upper and lower motor neuron signs with fasciculations, and its EMG shows denervation with fibrillations — not an incremental response to high-frequency stimulation. Improvement with repeated effort also argues strongly against ALS.
  • Polymyositis — check CK and anti-Jo-1 antibodies — Incorrect. Polymyositis causes proximal weakness, so the pattern overlaps — but it produces markedly elevated CK and a myopathic EMG without incremental facilitation. Weakness in myositis does not improve with repetitive activity.
  • GBS — administer IVIG — Incorrect. GBS presents subacutely over days with ascending weakness and areflexia, not over 4 months. The incremental EMG response and improvement with use are not GBS features.
  • Myasthenia gravis — start pyridostigmine — Incorrect. This is the key discrimination. MG weakness FATIGUES with repetition and shows a DECREMENTAL EMG response, while this patient facilitates with an incremental response. The smoking history also points toward an underlying small cell lung cancer driving LEMS.
Board pearlThe direction of fatigue separates the two junction diseases. Myasthenia gravis worsens with use — fatigable ptosis and diplopia, ocular onset, a decremental EMG response, anti-AChR antibodies, and an association with thymoma. Lambert-Eaton improves with use — proximal legs first, autonomic dryness, an incremental response at high-frequency stimulation, anti-voltage-gated calcium channel antibodies, and small cell lung cancer in roughly 60%. A smoker with proximal weakness and a hilar mass makes LEMS a cancer hunt.
Covered below under Module 13 — Neuromuscular Disorders · MG vs LEMS
Question 2 of 3 · Medium · Peripheral Nerve · GBS Pattern
A 35-year-old man has progressive weakness over 5 days. He had a respiratory illness 2 weeks ago. Which CSF finding pattern BEST supports Guillain-Barré syndrome?
Click to Reveal Answer
Correct answer: A — WBC 4 cells/μL, protein 95 mg/dL, glucose 58 mg/dL
Albumino-cytologic dissociation = elevated protein with normal or minimally elevated cell count. This is pathognomonic for GBS (and also seen in some other neuropathies). The elevated protein reflects nerve root inflammation without pleocytosis. High WBC suggests infection (meningitis). Normal CSF (option E) would argue against GBS.
Why the other choices are wrong
  • WBC 450 cells/μL (neutrophil predominant), protein 40 mg/dL, glucose 30 mg/dL — Incorrect. This is a bacterial meningitis profile — high neutrophil count with low glucose from organism consumption. GBS produces essentially no pleocytosis.
  • WBC 200 cells/μL (neutrophil predominant), protein 110 mg/dL, glucose 22 mg/dL — Incorrect. The high protein is compatible with GBS, but 200 neutrophils and glucose of 22 indicate bacterial infection. Albumino-cytologic dissociation requires elevated protein WITHOUT the cells.
  • WBC 2 cells/μL, protein 18 mg/dL, glucose 62 mg/dL (normal) — Incorrect. This is an entirely normal CSF. The cell count fits GBS but the protein is normal, and it is the elevated protein reflecting nerve root inflammation that supports the diagnosis.
  • WBC 80 cells/μL (lymphocyte predominant), protein 60 mg/dL, glucose 40 mg/dL — Incorrect. Lymphocytic pleocytosis with mildly elevated protein suggests viral or aseptic meningitis. The cell count is too high for the dissociation pattern that characterizes GBS.
Board pearlAlbumino-cytologic dissociation — high protein with a normal cell count — is the CSF signature of Guillain-Barré, reflecting nerve root inflammation without pleocytosis. It may be normal in the first week, so a normal early tap does not exclude it. Clinically the pattern is ascending, symmetric, areflexic weakness after a respiratory or GI illness. The thing that kills is respiratory failure, so trend forced vital capacity and negative inspiratory force rather than pulse oximetry, which falls too late.
Covered below under Module 14 — Peripheral Neuropathies · GBS
Question 3 of 3 · High Yield · Vertigo · Central vs Peripheral
A 59-year-old man has sudden severe vertigo. He cannot walk without falling. Neurologic exam shows direction-changing nystagmus that does not suppress with fixation, mild left-sided dysmetria, and dysarthria. Vital signs are normal.
Click to Reveal Answer
Correct answer: C — Central vertigo — obtain MRI brain urgently
This is central vertigo with multiple red flags: inability to walk, direction-changing nystagmus not suppressed by fixation (peripheral nystagmus suppresses with fixation), cerebellar signs (dysmetria, dysarthria). This is a posterior fossa stroke until proven otherwise. MRI with DWI is essential — CT misses posterior fossa infarcts in first 24–48h.
Why the other choices are wrong
  • BPPV — perform Epley maneuver — Incorrect. BPPV produces brief positional vertigo lasting seconds with fatigable upbeat-torsional nystagmus, and patients can walk. Direction-changing nystagmus and cerebellar dysmetria are incompatible with BPPV.
  • Vestibular neuritis — prescribe meclizine and reassure — Incorrect. Vestibular neuritis is the most dangerous misdiagnosis here because it is common and would justify discharge. It produces unidirectional nystagmus that suppresses with visual fixation and preserved gait — the opposite of this presentation.
  • Ménière disease — recommend low-sodium diet — Incorrect. Ménière disease features episodic vertigo with fluctuating hearing loss, tinnitus, and aural fullness over months. There is no hearing complaint here and no cerebellar signs in Ménière.
  • Labyrinthitis — prescribe oral steroids — Incorrect. Labyrinthitis is vestibular neuritis accompanied by hearing loss and remains a peripheral process. It does not cause dysmetria or nystagmus that fails to suppress with fixation.
Board pearlPeripheral vertigo gives unidirectional nystagmus that suppresses with visual fixation and a patient who can still walk. Central vertigo gives direction-changing nystagmus that does not suppress, inability to walk unaided, and any cerebellar or brainstem sign — dysmetria, dysarthria, diplopia, dysphagia. Treat that combination as posterior circulation stroke and get MRI with diffusion, because CT misses posterior fossa infarcts in the first day or two.
Covered below under Module 15 — Dizziness & Vertigo · central vs peripheral
Tier 1
Module 13
Neuromuscular Disorders
Myasthenia gravis · Lambert-Eaton · ALS
🩺 Opening Clinical Vignette
🔴 ADVANCED
A 44-year-old man has 6 months of ptosis and diplopia that worsens throughout the day, especially after prolonged reading. He has no limb weakness at rest. A CT chest shows a 3.2 cm anterior mediastinal mass.
⏸ Pause & Discuss — Before Reading Further
What is the diagnosis, what does the CT finding mean, and what test confirms the diagnosis?
✓ Answer
Myasthenia gravis with thymoma. Fatigable ocular weakness (worse with use) + anterior mediastinal mass = MG + thymoma until proven otherwise. 10–15% of MG patients have thymoma; 30–50% of thymoma patients have MG. Confirm: AChR antibody (positive in 85% of generalized MG), repetitive nerve stimulation (decremental response), ice pack test for ocular MG. Management: pyridostigmine + thymectomy (improves MG even in non-thymoma patients if age <60).
💡 Teaching Pearl
The MG + thymoma association is testable in two directions: a MG patient needs CT chest, and an anterior mediastinal mass raises MG. Teaching the fatigability concept (weakness worsens with sustained activity, improves with rest) is the key clinical discriminator from other causes of ptosis and diplopia.
Myasthenia Gravis
  • Autoantibodies against postsynaptic AChR at the NMJ.
  • Fatigable weakness — worse with activity, better with rest.
  • Ptosis, diplopia (ocular); bulbar (dysarthria, dysphagia); proximal limb weakness.
  • Dx: AChR antibodies (~85%), anti-MuSK if seronegative; edrophonium test; repetitive nerve stimulation (decremental); single-fiber EMG (most sensitive).
  • Tx: pyridostigmine; immunosuppression (prednisone, azathioprine); thymectomy (especially thymoma); IVIG/plasmapheresis for crisis.
  • Avoid: aminoglycosides, fluoroquinolones, beta-blockers, magnesium, neuromuscular blockers.
Lambert-Eaton (LEMS)
  • Antibodies against presynaptic voltage-gated calcium channels.
  • Paraneoplastic — small cell lung cancer (~60%).
  • Proximal weakness that improves with repeated use; autonomic dysfunction (dry mouth); hyporeflexia improving after exercise.
  • Dx: VGCC antibodies; incremental response on repetitive nerve stimulation.
  • Tx: treat malignancy; 3,4-diaminopyridine; IVIG.
MG vs LEMS — Board Favorite
FeatureMyasthenia GravisLambert-Eaton
WeaknessOcular → bulbar → limbsProximal limbs; ocular less common
FatigabilityWorse with useImproves with use
ReflexesNormalDecreased (improve post-exercise)
AntibodyPostsynaptic AChRPresynaptic VGCC
CancerThymomaSmall cell lung cancer
RNSDecrementalIncremental
Amyotrophic Lateral Sclerosis
  • Combined UMN + LMN signs with no sensory involvement.
  • Progressive weakness, fasciculations, hyperreflexia, spasticity, atrophy; bulbar onset has worse prognosis.
  • Dx: EMG/NCS widespread denervation; El Escorial criteria.
  • No sensory loss, no bowel/bladder involvement (distinguishes it).
  • Tx: riluzole (modest survival benefit), edaravone; multidisciplinary + respiratory support.
  • Median survival 3–5 years from onset.
Board Pearl
ALS is the classic 'UMN and LMN signs together with completely normal sensation.' Hyperreflexia in a wasted, fasciculating limb — with no numbness anywhere — is the giveaway.
Clinical Vignette
A 30-year-old woman has drooping eyelids and double vision that are mild in the morning and worse by evening, with fatigue chewing dinner.
Answer: Fatigable ocular and bulbar weakness points to myasthenia gravis (postsynaptic AChR antibodies). Confirm with AChR antibodies and image the chest for a thymoma; pyridostigmine is symptomatic therapy.
Tier 1
Module 14
Peripheral Neuropathies
GBS · CIDP · diabetic neuropathy · high-yield mononeuropathies
Guillain-Barré Syndrome
  • Acute inflammatory demyelinating polyradiculoneuropathy (AIDP, most common variant).
  • Preceding infection — Campylobacter jejuni most common (also CMV, EBV, Zika).
  • Ascending symmetric weakness, areflexia, possible respiratory failure; autonomic instability.
  • Dx: CSF albuminocytologic dissociation (high protein, normal cells); NCS demyelinating.
  • Tx: IVIG or plasmapheresis (equal) — do NOT use corticosteroids.
  • Monitor FVC (20/30/40 rule); intubate for declining respiratory function.
  • Miller Fisher variant: ophthalmoplegia, ataxia, areflexia; anti-GQ1b antibodies.
CIDP — 'Chronic GBS'
  • Progressive or relapsing over >8 weeks; symmetric proximal + distal weakness with sensory loss.
  • Dx: NCS demyelinating, CSF high protein, nerve biopsy if needed.
  • Tx: IVIG, corticosteroids, or plasmapheresis — unlike GBS, steroids ARE effective.
Diabetic Neuropathy
  • Most common peripheral neuropathy overall.
  • Distal symmetric polyneuropathy: stocking-glove pain/numbness, feet → hands.
  • Autonomic: gastroparesis, orthostatic hypotension, ED, neurogenic bladder.
  • Diabetic amyotrophy: acute painful proximal leg weakness, often asymmetric.
  • Mgmt: glycemic control; gabapentin, pregabalin, duloxetine, or TCAs.
High-Yield Mononeuropathies
NerveSiteMotor DeficitClassic Finding
MedianCarpal tunnel (wrist)Thenar atrophy, weak thumb oppositionTinel/Phalen; most common entrapment
UlnarCubital tunnel (elbow)Interossei/hypothenar atrophy'Claw hand'; Froment sign
RadialSpiral groove (humerus)Wrist drop, finger dropHumeral fracture; 'Saturday night palsy'
PeronealFibular head (knee)Foot drop, weak dorsiflexion/eversionLeg crossing, cast compression; most common LE mononeuropathy
Board Pearl
Carpal tunnel is diagnosed clinically and confirmed by NCS/EMG (the gold standard). Phalen test (wrist flexion) is more sensitive than Tinel (tapping).
Clinical Vignette
Two weeks after a diarrheal illness, a patient develops ascending leg weakness with absent reflexes; CSF shows high protein with a normal cell count.
Answer: Guillain-Barré syndrome — treat with IVIG or plasmapheresis and monitor forced vital capacity for respiratory failure. Do NOT give corticosteroids; they are ineffective here.
Tier 2
Module 15
Dizziness & Vertigo
Peripheral vs central · BPPV · vestibular neuritis · Ménière
🩺 Opening Clinical Vignette
🟢 FOUNDATIONAL
A 67-year-old woman has sudden severe vertigo, nausea, and vomiting that started this morning. She cannot walk without falling. She has horizontal nystagmus that does not suppress with fixation, mild dysarthria, and difficulty with finger-to-nose testing on the left.
⏸ Pause & Discuss — Before Reading Further
Is this peripheral or central vertigo? What imaging do you order and why is this urgent?
✓ Answer
Central vertigo — posterior fossa stroke. Red flags: cannot walk (peripheral vertigo usually allows walking), direction-changing nystagmus that doesn't suppress with fixation, cerebellar signs (dysarthria, finger-to-nose ataxia), acute onset. MRI brain with DWI immediately (CT misses posterior fossa strokes in first 24–48 hours). This is a cerebellar or lateral medullary infarct until proven otherwise.
💡 Teaching Pearl
The central vs peripheral vertigo distinction is the highest-stakes triage decision in dizziness management. The teaching rule: if the patient cannot walk or has any additional neurologic finding → central until proven otherwise → MRI. BPPV patients can walk, have positional brief nystagmus, and no other findings. This vignette teaches the exam-based differentiation, not just the feature list.
Peripheral vs Central Vertigo
FeaturePeripheralCentral
OnsetSudden, episodicGradual or sudden
SeveritySevereMild–moderate
NystagmusHorizontal/rotatory; suppressed by fixation; fatigableAny direction (vertical = always central); not suppressed; non-fatigable
Hearing lossMay be presentUsually absent
Neuro signsAbsentPresent (diplopia, dysarthria, dysphagia, ataxia)
CausesBPPV, vestibular neuritis, MénièreStroke, MS, tumor
Classic Board Trap
Vertical nystagmus is central until proven otherwise — get urgent neuroimaging. A peripheral cause cannot produce purely vertical nystagmus.
Common Peripheral Causes
  • BPPV: most common cause of vertigo; brief positional episodes; Dix-Hallpike positive; treat with Epley maneuver.
  • Vestibular neuritis: acute sustained vertigo after viral illness, no hearing loss.
  • Ménière disease: episodic vertigo + fluctuating sensorineural hearing loss + tinnitus + aural fullness; low-salt diet, diuretics.
Domain 10 · Don't-Miss Emergencies
Neuro Emergencies — Rapid Review
Tier 1
Module 16
Emergencies Card
🩺 Opening Clinical Vignette
🔴 ADVANCED
A 32-year-old man on haloperidol for schizophrenia develops high fever (40.2°C), severe generalized muscle rigidity, diaphoresis, tachycardia, and confusion over 24 hours. CK is 18,400 U/L.
⏸ Pause & Discuss — Before Reading Further
What is the diagnosis, how does it differ from serotonin syndrome clinically, and what are the immediate interventions?
✓ Answer
Neuroleptic malignant syndrome (NMS). Caused by dopamine blockade (antipsychotics). Key findings: LEAD pipe rigidity (vs clonus in SS), hyperthermia, autonomic instability, CK elevation, encephalopathy. Treatment: STOP the antipsychotic immediately + ICU + IV fluids + cooling + dantrolene (muscle relaxant) + bromocriptine (dopamine agonist). Serotonin syndrome distinction: SS has hyperreflexia + clonus + tremor (not lead-pipe rigidity) + onset within hours (NMS develops over days).
💡 Teaching Pearl
NMS vs serotonin syndrome is one of the highest-yield drug reaction comparisons on the PANCE. The distinguishing exam finding is rigidity type: lead-pipe (NMS) vs clonus/hyperreflexia (SS). Teaching the mechanism for each — dopamine blockade vs serotonin excess — makes the clinical differences logical rather than memorized.
Status epilepticus
Seizure >5 min or ≥2 without recovery → benzodiazepine → fosphenytoin/levetiracetam/valproate → infusion. Treat immediately; mortality rises with duration.
Acute ischemic stroke
Time is brain. Non-contrast CT to exclude hemorrhage → tPA within 4.5 h; thrombectomy for LVO up to 24 h. Permissive hypertension unless tPA candidate.
Subarachnoid hemorrhage
Thunderclap headache → CT → LP if negative. Secure aneurysm, nimodipine, watch for vasospasm (days 4–14).
Bacterial meningitis
Do not delay antibiotics. Dexamethasone before/with first dose. Vancomycin + ceftriaxone (+ ampicillin if >50).
HSV encephalitis
Fever + AMS + temporal lobe signs → start IV acyclovir empirically before PCR results.
Cauda equina syndrome
Back pain + urinary retention + saddle anesthesia → emergent MRI → decompression within 24–48 h.
Spinal cord compression
Back pain + sensory level + weakness → high-dose IV dexamethasone now + emergent whole-spine MRI.
Epidural hematoma
Temporal fracture, middle meningeal artery, lucid interval, biconvex CT → emergent craniotomy.
Uncal herniation
Ipsilateral blown pupil → intubate, hyperventilate, osmotic therapy, neurosurgery.
Giant cell arteritis
New headache >50 + jaw claudication + high ESR → high-dose steroids immediately to save vision.
Tier 2
Reference
Epidural vs Subdural Hematoma
Two trauma bleeds the boards always contrast
🩺 Opening Clinical Vignette
🟡 INTERMEDIATE
Two patients arrive after head trauma. Patient A (age 28, MVC) has a brief LOC, lucid interval, then rapid deterioration. CT shows a biconvex hyperdense lens-shaped collection. Patient B (age 82, ground-level fall) has gradual confusion over 3 days. CT shows a crescent-shaped hypodense collection crossing suture lines.
⏸ Pause & Discuss — Before Reading Further
Name both diagnoses, explain the different mechanisms, and state the urgency for each.
✓ Answer
Patient A: Epidural hematoma — torn middle meningeal artery (arterial, rapid). Biconvex = does NOT cross suture lines. Lucid interval pathognomonic. Surgical emergency — burr hole within hours. Patient B: Chronic subdural hematoma — bridging vein tear (venous, slow). Crescent-shaped = crosses suture lines. Elderly + anticoagulants + atrophy (stretches bridging veins). Surgical if symptomatic/large; small ones may resolve with observation + stopping anticoagulation.
💡 Teaching Pearl
The epidural vs subdural contrast is one of the most reliable PANCE neurology vignettes. Teaching the imaging shapes (biconvex vs crescent), vessel source (arterial vs venous), and speed (hours vs days/weeks) as a three-way comparison is more durable than memorizing facts individually. The lucid interval is pathognomonic for epidural — boards test it every cycle.
Side by Side
FeatureEpiduralSubdural
SourceMiddle meningeal artery (arterial)Bridging veins (venous)
CT shapeBiconvex (lens)Crescent
Crosses suturesNoYes
OnsetRapid; lucid intervalAcute, subacute, or chronic
PopulationYoung (trauma)Elderly, anticoagulated, alcohol, atrophy
  • Chronic subdural: hypodense on CT weeks–months after minor trauma; burr-hole drainage.
  • Epidural: emergent craniotomy.
Domain 11 · Trauma, Pediatric & Additional Topics
TBI, Concussion & High-Yield Add-Ons
Tier 1
Module 17
Traumatic Brain Injury & Concussion
GCS severity · concussion & return-to-play · when to CT · post-concussive syndrome
Why the PANCE Tests This

Head injury is one of the most common presentations in primary care, sports medicine, and the ED. Boards test concussion recognition, the rules for when imaging is required, return-to-play decisions, and the catastrophic complication — second-impact syndrome.

TBI Severity by Glasgow Coma Scale
SeverityGCSKey Point
Mild (concussion)13–15Most TBI; normal structural imaging by definition
Moderate9–12Admit, serial neuro checks, CT
Severe≤8Intubate (GCS ≤8 = protect airway); ICU, ICP management
Concussion (Mild TBI)
  • Trauma-induced transient alteration of brain function — confusion, headache, dizziness, amnesia; loss of consciousness is NOT required.
  • Structural imaging is normal — concussion is a clinical, functional diagnosis.
  • Cognitive and physical rest initially, then a gradual return to activity as symptoms allow.
Return to Play
Graded, Symptom-Limited Stepwise Progression
  • No same-day return to play after a diagnosed concussion
  • Advance one stage per day only if asymptomatic; drop back a stage if symptoms recur
  • Full contact only after medical clearance and a return to baseline
When to Image — Non-Contrast CT
  • Obtain CT for: GCS <15 at 2 h, suspected open/depressed or basilar skull fracture, ≥2 episodes of vomiting, age ≥65, dangerous mechanism, focal deficit, seizure, or coagulopathy/anticoagulation.
  • These mirror the Canadian CT Head Rule — applied to minor head injury with witnessed LOC, amnesia, or confusion.
  • MRI is more sensitive for diffuse axonal injury but CT is first-line acutely to exclude a surgical bleed.
Post-Concussive Syndrome
  • Persistent headache, dizziness, difficulty concentrating, irritability, and sleep disturbance lasting weeks to months after a concussion.
  • Management is supportive and symptom-directed with gradual return to activity.
Classic Board Trap
Second-impact syndrome — a second head injury before a first concussion has resolved causes rapid, often fatal cerebral edema. This is why there is no same-day return to play and why clearance must precede contact.
Clinical Vignette
A 16-year-old took a helmet-to-helmet hit, was briefly dazed, and now feels 'back to normal' and wants to return to the game.
Answer: No same-day return to play after a concussion. Use a graded, symptom-limited progression and require medical clearance before contact — a second impact before recovery risks fatal cerebral edema.
Tier 2
Module 18
Additional High-Yield Disorders
CRPS · Tourette & tics · restless legs · cerebral palsy · Wernicke-Korsakoff
🩺 Opening Clinical Vignette
🟡 INTERMEDIATE
A 44-year-old chronic alcoholic is brought to the ED confused and ataxic. His wife reports he hasn't eaten in days. His glucose is 48 mg/dL. The nurse is about to give D50W.
⏸ Pause & Discuss — Before Reading Further
What must happen before the glucose is given, and why does the order matter?
✓ Answer
IV thiamine 100mg must be given BEFORE glucose. Giving glucose first in a thiamine-depleted patient precipitates Wernicke encephalopathy by consuming the remaining thiamine stores in glucose metabolism → acute Wernicke (confusion + ophthalmoplegia + ataxia). If Wernicke progresses untreated → Korsakoff syndrome (irreversible confabulation + anterograde amnesia). The mnemonic: 'Thiamine before sugar — always.'
💡 Teaching Pearl
The thiamine-before-glucose rule is one of the most reliably tested clinical pearls in neurology and emergency medicine. It appears on the PANCE as a 'what is the most appropriate next step' question — the trap being giving dextrose first because hypoglycemia is the obvious acute problem. Teaching the mechanism (thiamine is a cofactor for glucose metabolism) makes the rule unforgettable.
Complex Regional Pain Syndrome (CRPS)
  • Chronic regional pain out of proportion to the inciting injury, usually after limb trauma, surgery, or immobilization.
  • Type I (no nerve injury, formerly reflex sympathetic dystrophy) vs Type II (with a defined nerve injury, formerly causalgia).
  • Allodynia and hyperalgesia plus autonomic/trophic changes: edema, temperature and color asymmetry, altered sweating, and skin/hair/nail changes; late atrophy and contracture.
  • Clinical diagnosis (Budapest criteria); X-ray may show patchy osteopenia and a 3-phase bone scan can support it.
  • Treatment: early mobilization and physical therapy are central; add analgesics, gabapentinoids, bisphosphonates; sympathetic blocks for refractory cases.
Tourette Syndrome & Tic Disorders
  • Onset in childhood (<18 years), boys > girls; multiple motor tics + ≥1 vocal tic present for >1 year, waxing and waning.
  • Tics are briefly suppressible and preceded by a premonitory urge; strongly associated with ADHD and OCD.
  • Treatment: education and behavioral therapy (CBIT) first-line; for impairing tics, alpha-2 agonists (clonidine, guanfacine), with antipsychotics or VMAT2 inhibitors reserved for severe cases.
Restless Legs Syndrome
  • Uncomfortable urge to move the legs, worse at rest and in the evening, relieved by movement; often with periodic limb movements of sleep.
  • Check for secondary causes: iron deficiency (ferritin), pregnancy, ESRD, and peripheral neuropathy.
  • Treatment: repletion of iron if ferritin is low; alpha-2-delta ligands (gabapentin, pregabalin) or dopamine agonists — limit dopaminergics given the risk of augmentation.
Cerebral Palsy
  • Non-progressive motor disorder from injury to the developing brain (prenatal/perinatal); risk factors include prematurity, low birth weight, intrauterine infection, and hypoxic-ischemic injury.
  • Spastic type is most common (spastic diplegia classic) > dyskinetic > ataxic; findings include hypertonia, persistent primitive reflexes, delayed milestones, scissoring gait, and toe-walking.
  • Comorbidities: epilepsy, intellectual disability, strabismus, and hearing/vision and feeding difficulties — though many patients have normal intelligence.
  • Management is multidisciplinary: PT/OT, spasticity control (baclofen, botulinum toxin), and orthopedic care.
Wernicke-Korsakoff Syndrome
  • Thiamine (B1) deficiency — alcohol use disorder, malnutrition, hyperemesis, or bariatric surgery.
  • Wernicke triad: encephalopathy (confusion) + ophthalmoplegia/nystagmus + ataxia.
  • Korsakoff is the chronic stage: anterograde and retrograde amnesia with confabulation, often irreversible.
Classic Board Trap
Give IV thiamine BEFORE glucose. Administering glucose first in a thiamine-deficient patient can precipitate or worsen Wernicke encephalopathy.
Module D · Must-Know Differentials
High-Yield Neurology Diagnostic Frameworks
7 clinical decision trees — the scenarios most likely to appear on the PANCE as "what is the most likely diagnosis?"
D-1
Acute Onset Headache — The "Worst of My Life" Framework
DiagnosisKey FeatureImmediate Action
Subarachnoid HemorrhageThunderclap — maximal at onset, "worst headache of my life," meningismusCT head → LP if CT negative (xanthochromia)
Bacterial MeningitisFever + neck stiffness + photophobia + petechiae. Hours to developBlood cultures → abx + dex → LP
Hypertensive EmergencyBP >180/120 + end-organ damage. Occipital headacheIV labetalol or nicardipine, reduce MAP 25%
Cerebral Venous ThrombosisProgressive HA + papilledema + seizure. Pregnancy/OCPMRI/MRV → anticoagulation
Giant Cell ArteritisAge >50 + temporal tenderness + jaw claudication + ↑ESR/CRPHigh-dose steroids immediately, biopsy after
Migraine with auraUnilateral, pulsating, 4–72h, aura precedesTriptans, avoid triggers
Cluster HeadacheMale, periorbital, autonomic (lacrimation/rhinorrhea), 15–180 minO₂ 100% + sumatriptan SQ
D-2
Acute Focal Neurologic Deficit — Stroke vs Mimic
DiagnosisKey Distinguishing FeatureTime-Critical Action
Ischemic StrokeSudden onset, maximal at start, no headache (usually), NIHSS scoreCT (no blood) → tPA if ≤4.5h → thrombectomy if ≤24h large vessel
Hemorrhagic StrokeSevere headache + vomiting + rapid deterioration. CT: hyperdenseBP control (target <140), neurosurgery consult
TIAFocal deficits resolving <24h (usually <1h). ABCD² score for riskABCD² ≥4 → admit. Start antiplatelet immediately
Todd's ParalysisPost-seizure focal weakness lasting minutes to hours. History of seizureNo tPA — ensure seizure history is obtained
HypoglycemiaFocal deficits + glucose <50 mg/dL. Resolves with dextroseCheck glucose FIRST before activating stroke code
Complex MigraineAura with motor/sensory deficit. Gradual spread (march), headache followsDiagnosis of exclusion — rule out stroke first
MS RelapseYoung woman, prior episodes, symptoms >24h, white matter lesions on MRIIV methylprednisolone for relapse
D-3
First-Time Seizure — Provoked vs Unprovoked vs Epilepsy
ScenarioKey FeaturesManagement Decision
Status EpilepticusSeizure >5 min OR ≥2 without recovery. Life-threateningBenzo → fosphenytoin/levetiracetam → phenobarbital → anesthesia
Provoked SeizureIdentifiable cause: hypoglycemia, hyponatremia, alcohol withdrawal, drugsTreat cause. No ASM needed if cause corrected
Febrile Seizure (peds)Age 6mo–5yr, fever, simple = <15min, generalized, once in 24hSimple: reassure. Complex or recurrent: workup + neurology
First Unprovoked SeizureNo identifiable cause. MRI + EEG. Risk of recurrence ~40% at 2 yearsStart ASM if: brain lesion, abnormal EEG, MRI abnormality, nocturnal
Absence SeizureChild, staring spell 5–10s, no post-ictal, 3Hz spike-wave on EEGEthosuximide (first-line for absence only)
Psychogenic Non-EpilepticEvents during stress, eyes closed, prolonged, normal EEG during eventVideo-EEG monitoring diagnostic. Psychiatry referral
D-4
Altered Mental Status — Delirium vs Dementia vs Psychiatric
DiagnosisKey Distinguishing FeatureKey Action
DeliriumACUTE onset, fluctuating, inattention, reversible. Has an underlying causeFind and treat cause (infection, medications, metabolic, pain)
Wernicke EncephalopathyTriad: confusion + ophthalmoplegia + ataxia. Alcoholism or malnutritionIV thiamine BEFORE glucose — or glucose precipitates Korsakoff
Alzheimer's DementiaInsidious onset, progressive memory loss, years course. Most commonDonepezil (AChE-I). Memantine for moderate-severe
Lewy Body DementiaDementia + Parkinsonism + visual hallucinations + REM sleep behaviorAvoid antipsychotics — fatal sensitivity. Rivastigmine preferred
NPHWet (incontinence) + Wobbly (gait) + Wacky (cognitive). ReversibleLP drainage test → VP shunt if responds
Vascular DementiaStepwise decline, history of strokes, focal deficits, atherosclerosisRisk factor modification (HTN, DM, cholesterol)
FTDPersonality/behavior change before memory loss. Age <65 commonBehavioral management. No FDA-approved therapy
D-5
Weakness — UMN vs LMN vs NMJ vs Myopathy
Level of LesionExam FindingsKey Diagnosis
UMN (Cortex/Cord)Spastic, hyperreflexia, + Babinski, no atrophy, clasp-knifeStroke, MS, spinal cord compression, ALS (UMN component)
LMN (Anterior Horn/Root/Nerve)Flaccid, hyporeflexia, fasciculations, atrophy, no BabinskiGBS, neuropathy, ALS (LMN component), cauda equina, polio
NMJ (Neuromuscular Junction)Fatigable weakness, reflexes normal, no atrophy, ocular/bulbar earlyMG (worse with use), Lambert-Eaton (improves with use)
MyopathyProximal > distal, symmetric, normal reflexes early, elevated CKPolymyositis, dermatomyositis, statin-induced, muscular dystrophy
FunctionalNon-anatomic pattern, give-way weakness, variable, Hoover sign positiveFunctional neurologic disorder — psychiatry + PT
D-6
Dizziness — Vertigo vs Presyncope vs Disequilibrium
TypeKey FeaturesDiagnosis + Treatment
Central Vertigo ⚑New onset, cannot walk, direction-changing nystagmus, diplopia/dysarthriaMRI immediately — posterior fossa stroke/mass
BPPVBrief (30–60s), positional, triggered by head movement, Dix-Hallpike positiveEpley maneuver — 80% success first attempt
Vestibular NeuritisSudden prolonged vertigo, spontaneous nystagmus, no hearing loss, post-viralSteroids + vestibular rehab. Avoid meclizine long-term
Ménière DiseaseEpisodic vertigo + tinnitus + fluctuating hearing loss + aural fullnessLow-salt diet + diuretics. Intratympanic steroids/gentamicin
Presyncope"Lightheadedness," near-faint, orthostatic, cardiac or vasovagal causeTilt table, Holter, echo — cardiac workup
DisequilibriumUnsteady gait, worse in dark, elderly, peripheral neuropathy, cerebellarFall prevention, PT, treat underlying cause
D-7
Back Pain with Neurologic Features — Emergency vs Non-Emergency
DiagnosisMust-Have FeaturesTime Urgency
Cauda Equina SyndromeSaddle anesthesia + urinary retention + bilateral leg weakness/numbnessMRI immediately → emergency surgical decompression
Epidural AbscessFever + back pain + tenderness + progressive neurologic deficit. IV drug useMRI + emergent surgical drainage + antibiotics
Spinal Cord Compression (malignant)Cancer history + back pain + upper motor neuron signs below levelDexamethasone immediately + MRI + radiation/surgery
Central Cord SyndromeHyperextension injury (elderly) → weakness arms > legs, urinary retentionImmobilize + MRI. Most recover partially
Lumbar Disc HerniationRadicular pain below knee, positive SLR, dermatomal sensory lossConservative 6 weeks. Surgery if refractory or progressive deficit
Mechanical Back PainNo red flags, improves with rest, no radiculopathy, age 20–55NSAIDs + activity. X-ray only if >6 weeks or red flags
Module E · Comprehensive Board Pearls
High-Yield Clinical Decision Points — Neurology
The clinical rules, drug traps, and pattern recognition facts most likely to appear on the PANCE
🔴 Stroke & Cerebrovascular
  • tPA contraindications: prior hemorrhagic stroke ever, ischemic stroke or head trauma in 3 months, BP >185/110 uncorrectable, INR >1.7, platelets <100K, blood glucose <50 or >400, active bleeding
  • tPA window = 4.5 hours from last known well (not symptom onset if wake-up stroke)
  • Thrombectomy window = 24 hours for large vessel occlusion with salvageable tissue on perfusion imaging
  • BP management post-tPA: keep <180/105 for 24h. Do NOT lower BP aggressively before tPA (may extend ischemia)
  • Posterior circulation stroke: vertigo + diplopia + ataxia + crossed deficits (face ipsilateral, body contralateral). Worse prognosis
  • Lacunar strokes: pure motor, pure sensory, ataxic hemiparesis, dysarthria-clumsy hand. Small vessel disease (HTN, DM)
  • SAH management: nimodipine (oral CCB) reduces vasospasm. Systolic <160. Aneurysm clipping or coiling
🟡 Seizures & Epilepsy
  • Status epilepticus treatment sequence: Benzo (lorazepam/diazepam) → Fosphenytoin/levetiracetam → Phenobarbital → Propofol/midazolam infusion
  • Absence seizures: ethosuximide (first-line). Valproate if generalized also present. Never carbamazepine (worsens absence)
  • Valproate contraindications: pregnancy (neural tube defects), liver disease, pancreatitis. Monitor LFTs + ammonia
  • Phenytoin drug interactions: induces CYP450 — reduces OCP, warfarin, many drug levels. Zero-order kinetics (small dose change = big level change)
  • Levetiracetam (Keppra): minimal drug interactions, renal dosing, safe in pregnancy relative to others. Behavioral side effects
  • Driving restrictions: seizure-free interval required before driving (varies by state, typically 3–12 months)
  • Febrile seizure: do NOT start prophylactic ASMs after simple febrile seizure — risk of epilepsy is low (<3%)
🟣 Movement Disorders
  • Parkinson drug traps: metoclopramide, haloperidol, prochlorperazine worsen Parkinson — all block dopamine. Use ondansetron for nausea instead
  • Levodopa-induced dyskinesias: peak-dose involuntary movements. Reduce levodopa or add amantadine
  • Essential tremor vs Parkinson: ET = action/postural tremor, no rigidity, improves with alcohol. PD = rest tremor, cogwheel rigidity, bradykinesia, asymmetric
  • NMS (neuroleptic malignant syndrome): antipsychotic exposure → fever + rigidity + AMS + autonomic instability + CK elevation. Stop drug, dantrolene/bromocriptine
  • Huntington: autosomal dominant, CAG repeat on chromosome 4, anticipation. Choreiform movements + dementia + psychiatric. No treatment modifies disease
  • DBS (deep brain stimulation): for advanced Parkinson — subthalamic nucleus target. Does not cure but improves motor fluctuations
🔵 Dementia & Cognitive
  • Lewy body dementia + antipsychotics = potentially fatal: neuroleptic sensitivity — severe rigidity, worsened cognition, death. Use rivastigmine. If antipsychotic must be used: quetiapine (lowest risk)
  • NPH triad: Wet (incontinence) + Wobbly (gait apraxia — magnetic gait) + Wacky (dementia). Gait is FIRST and MOST prominent symptom
  • Alzheimer treatment: AChE inhibitors (donepezil, rivastigmine, galantamine) for mild-moderate. Memantine for moderate-severe. Emerging anti-amyloid antibody therapies (specialist-managed) for early AD — amyloid-targeted
  • CJD (Creutzfeldt-Jakob): rapidly progressive dementia + myoclonus + ataxia. 14-3-3 protein in CSF. Prion disease. Fatal within 1 year
  • Wernicke vs Korsakoff: Wernicke (acute) = confusion + ophthalmoplegia + ataxia → thiamine IV. Korsakoff (chronic) = confabulation + anterograde amnesia = irreversible. IV thiamine BEFORE glucose
🟢 MS & Demyelinating
  • MS diagnosis (McDonald 2017): dissemination in time AND space. MRI: periventricular, juxtacortical, infratentorial, spinal cord lesions. CSF: oligoclonal bands
  • Optic neuritis + young woman = MS until proven otherwise. Afferent pupillary defect (Marcus Gunn). Treat relapse with IV methylprednisolone
  • Internuclear ophthalmoplegia (INO): MLF lesion → impaired ipsilateral adduction + contralateral nystagmus. Bilateral INO in young patient = MS
  • Uhthoff phenomenon: MS symptoms worsen with heat (fever, hot bath). Pathognomonic for demyelination — not a relapse
  • NMO (Neuromyelitis Optica): anti-AQP4 antibody. Severe optic neuritis + longitudinally extensive transverse myelitis (>3 vertebral segments). NOT MS — different treatment
  • MS disease-modifying therapy: interferon-beta or glatiramer for relapsing-remitting. Natalizumab/ocrelizumab for aggressive disease. JC virus → PML risk with natalizumab
🟠 Neuromuscular & Peripheral
  • GBS (Guillain-Barré): ascending flaccid paralysis post-infection (Campylobacter most common). Albumino-cytologic dissociation (high protein, normal cells in CSF). IVIG or plasmapheresis — NOT steroids
  • MG crisis: respiratory failure from myasthenic crisis (disease worsening) vs cholinergic crisis (too much pyridostigmine). Edrophonium test distinguishes. Both need ICU
  • MG + thymoma: 10–15% of MG have thymoma. CT chest in all MG patients. Thymectomy improves MG even without thymoma if <60 years
  • Lambert-Eaton vs MG: LEMS = proximal weakness that IMPROVES with repetition (voltage-gated Ca²⁺ channel Ab) + associated with SCLC. MG = fatigable weakness that WORSENS with repetition (AChR Ab)
  • Carpal tunnel syndrome: most common mononeuropathy. Thenar wasting + Phalen/Tinel signs. Nocturnal pain classic. EMG/NCS confirms. Splinting first, surgery if refractory
  • Diabetic neuropathy: length-dependent (feet first), glove-stocking distribution, burning pain. Treat: pregabalin, duloxetine, TCAs. Tight glucose control prevents progression
⚑ Critical Drug & Imaging Traps
  • First-line imaging in neurology: Acute stroke → CT (fast, rules out hemorrhage). MS/posterior fossa/spinal cord → MRI. Skull fracture → CT. Headache workup → MRI preferred over CT (no radiation, better resolution)
  • LP contraindications: papilledema, focal neurologic deficit, immunocompromised, anticoagulated → CT first. Mass effect + LP = herniation
  • Lumbar puncture opening pressure: normal 10–20 cmH₂O. IIH >25. Cryptococcal meningitis often >30 (therapeutic LP is the intervention)
  • Avoid in Parkinson: metoclopramide, prochlorperazine, haloperidol, most antipsychotics. Use ondansetron, domperidone (not US), or quetiapine if needed
  • Carbamazepine toxicity: SIADH (hyponatremia). Monitor sodium. Also induces own metabolism (autoinduction)
  • Topiramate side effects: kidney stones (carbonic anhydrase inhibition), cognitive slowing ("dopamax"), glaucoma. Useful in migraine prophylaxis + weight loss
  • Amantadine: treats levodopa-induced dyskinesias AND has mild anti-Parkinsonian effect. Also antiviral (influenza A — largely obsolete now)
Appendix · Quick Reference
Medications & Imaging — Board Pearls
Tier 1
Quick Reference
Medications & First-Line Imaging
The reference tables to drill the night before
★★ High Yield
Medications to Know
MedicationPrimary UseCritical Pearl
Alteplase (tPA)Acute ischemic strokeHemorrhage risk; within 4.5 h
NimodipineSAH vasospasm preventionCCB; oral only
Levodopa/carbidopaParkinson diseaseDyskinesias with long-term use
CarbamazepineTrigeminal neuralgia, focal seizuresSIADH, SJS, aplastic anemia
PyridostigmineMyasthenia gravisCholinergic crisis if overdosed
RiluzoleALSModest survival benefit; hepatotoxic
DonepezilAlzheimer diseaseCholinesterase inhibitor; GI effects
SumatriptanMigraine, clusterContraindicated in CAD
ValproateGeneralized epilepsyTeratogenic; avoid in pregnancy
MannitolIncreased ICPOsmotic diuretic; monitor osmolality
DexamethasoneTumor edema, bacterial meningitisDoes NOT help cytotoxic (stroke) edema
AcyclovirHSV encephalitisStart empirically; do not delay
First-Line Imaging
ScenarioFirst-Line Imaging
Acute stroke (<6 h)Non-contrast CT head
Stroke (subacute/confirm)MRI brain with diffusion (DWI)
SAH suspectedNon-contrast CT → LP if negative
MS workupMRI brain & spine with gadolinium
Spinal cord compressionMRI spine (emergent)
Brain tumorMRI brain with contrast
Acoustic neuromaMRI with gadolinium (IAC protocol)
Cauda equinaMRI lumbar spine (emergent)
Epidural/subduralNon-contrast CT head
Temporal arteritisTemporal artery biopsy (not imaging)
Appendix · The Pattern Bank
Must-Know Associations for the PANCE
1
Worst headache of life
Subarachnoid hemorrhage
2
Ascending paralysis after GI illness
Guillain-Barré syndrome
3
Pill-rolling resting tremor
Parkinson disease
4
Fatigable ptosis and diplopia
Myasthenia gravis
5
Young woman, optic neuritis + INO
Multiple sclerosis
6
Bilateral acoustic neuromas
Neurofibromatosis type 2
7
Caudate atrophy + chorea
Huntington disease
8
'Down and out' eye + dilated pupil
CN III palsy (PComm aneurysm)
9
Lancinating facial pain on touch
Trigeminal neuralgia
10
Saddle anesthesia + urinary retention
Cauda equina syndrome
11
Lucid interval after head trauma
Epidural hematoma
12
Elderly, crescent bleed on CT
Subdural hematoma
13
Wet, wobbly, wacky
Normal pressure hydrocephalus
14
Bitemporal hemianopia
Pituitary adenoma (chiasm)
15
Ring-enhancing lesion in HIV
Toxoplasmosis
16
Ipsilateral face + contralateral body pain/temp loss
Wallenberg (lateral medullary)
17
3 Hz spike-and-wave on EEG
Absence seizures
18
Lead-pipe rigidity + fever after antipsychotic
Neuroleptic malignant syndrome
19
Foot drop
Peroneal nerve palsy
20
Wrist drop after humeral fracture
Radial nerve palsy
21
Vertical nystagmus
Central vertigo — image now
22
Visual hallucinations + parkinsonism
Lewy body dementia
23
Cortical ribboning + myoclonus
Creutzfeldt-Jakob disease
24
Improves with repeated use + SCLC
Lambert-Eaton syndrome
25
UMN + LMN signs, normal sensation
ALS
⬡ Closing Statement
"Neurology rewards the clinician who localizes before naming. The forehead that is spared. The pupil that is blown. The reflexes that are gone in an ascending paralysis and the ones that are too brisk in a wasting limb. Find the lesion first, and the diagnosis follows."
— Rajiv Choudhary, MD, MPH
PA Neurology Bootcamp Syllabus
Rajiv Choudhary, MD, MPH