Built from all 13 lectures, the case sets, and your textbook chapters. Click any topic below or use the tabs above. Look for ⭐ high-yield boxes, 🧠 mnemonics, flip-cards, and interactive quiz questions throughout.
🔎
Exam & Imaging
Localization, neuro exam, CT vs MRI, CSF
🧠
Stroke / CVA
TIA, ischemic, hemorrhagic, AVM, aneurysm
🤕
Head Trauma
Concussion, hematomas, ICP
💥
Headache
Tension, migraine, cluster, red flags
⚡
Seizures
Focal vs generalized, status, AEDs
🧩
Dementia
Alzheimer, FTD, Lewy body, vascular, NPH
🤝
Movement
Parkinson, ET, Huntington, RLS, Tourette
💪
MS & Neuromuscular
MS, myasthenia, ALS, GBS, CP
🔌
Neuropathy
Mono/poly neuropathies, Bell's, CRPS
🦴
Spinal Cord
Cord syndromes, cauda equina, abscess
🦠
CNS Infection
Meningitis, encephalitis, encephalopathy
🎯
Brain Tumors
Gliomas, mets, meningioma, presentation
😵
Syncope
Reflex, cardiac, orthostatic vs seizure
📝
Cases & Test Qs
Board-style vignettes with answers
🧠
Mnemonics
Every memory aid in one place + flip-cards
⭐ The one rule of neuroDifferential diagnosis = Localization × Time course. Always answer two questions: WHERE is the lesion? (cortex, white matter, cord, root, nerve, NMJ, muscle) and WHAT is the cause? (vascular, infectious, inflammatory, neoplastic, degenerative, toxic-metabolic). The tempo of onset narrows the "what": seconds–minutes = vascular/seizure; hours–days = infectious/inflammatory; weeks–months = neoplastic/degenerative.
🔎 Neuro Exam, Localization & Imaging
Intro to Neurology (Neuro #1) + Neuroimaging & CSF (Ch 2). The foundation for every other topic.
⭐ Master conceptDifferential = Localization × Time course. Two questions on every neuro patient: (1) Where is the lesion? and (2) What caused it? Onset tempo points to the cause — sudden (seconds) = vascular/seizure; subacute (days–weeks) = inflammatory/infectious; chronic (months) = neoplastic/degenerative.
Always screen mental status against the patient's baseline. In peds, loss of function is always concerning; in elderly, loss can be subtle/unnoticed — enlist family for history.
Sensory — light touch, pinprick/temp, vibration & proprioception in feet, extinction to double simultaneous stimulation
Extinction / DSS: two stimuli given at once; if one isn't sensed → extinction = sign of cortical (parietal) neglect. Frontal release signs (grasp reflex) and poor clock-drawing also localize to cortex.
⭐ Blood ages on CTAcute = hyperdense (white) → ~1–2 wks isodense → ~3–4 wks hypodense (dark). Noncontrast CT is the first test in acute stroke/trauma to rule out bleed.
MRI — superior soft tissue
Sequence
Bright =
Use
T1
Fat (white matter); CSF dark
Anatomy
T2
Water; CSF bright; most pathology bright
Pathology
FLAIR
T2 with CSF suppressed
Periventricular lesions (MS!)
DWI/ADC
Restricted diffusion
Acute ischemic stroke, abscess, CJD
Contrast: CT = iodine, MRI = gadolinium → tumor, infection, inflammation, subacute infarct. Spine: CT for bone, MRI for cord/roots.
🧠 MRI signal — "WW2 / H2O"
T2
"H₂O is white on T-2" — water/CSF bright on T2. Most pathology (edema) is bright on T2/FLAIR.
DWI
"Bright on DWI = Dead/Dying brain" — restricted diffusion lights up within minutes of ischemic stroke (before CT changes).
CSF Analysis (LP)
Condition
Opening P
WBC
Protein
Glucose
Normal
<20 cm H₂O
0–5 lymphs
15–45
~⅔ serum (50–80)
Bacterial meningitis
↑↑
↑↑ neutrophils (1000s)
↑↑
↓↓ low
Viral meningitis
nl/↑
↑ lymphocytes
↑
normal
SAH
↑
RBCs, xanthochromia
↑
normal
Guillain-Barré
nl
normal
↑↑
normal
MS
nl
nl/mild↑
nl/↑ (oligoclonal bands)
normal
🧠 Memory aids
GBS
Albuminocytologic dissociation — ↑protein with normal cell count.
SAH
Xanthochromia (yellow CSF from broken-down RBCs) confirms SAH when CT is negative.
Before LP: get CT first if ↑ICP signs (papilledema, focal deficit, altered consciousness) to avoid herniation. Any suspicion of ↑ICP → refer neurosurgery; never delay antibiotics for LP in suspected bacterial meningitis.
Quick check
A 68-y/o has sudden left arm weakness 45 minutes ago. Which imaging is the immediate first step, and what is it primarily looking for?
B. Non-contrast CT is fast and the first test in acute stroke — it can't show early infarct but reliably detects hemorrhage, which must be excluded before thrombolytics. DWI-MRI is most sensitive for early ischemia but isn't the immediate step.
Stroke & TIA are ALWAYS an emergency. Goal: rapidly decide if the patient qualifies for reperfusion. First step is always non-contrast head CT to rule out hemorrhage (antithrombotics are contraindicated if there's blood).
🧠 BE-FAST — recognize stroke fast
B
Balance — sudden loss of balance/coordination
E
Eyes — sudden visual loss/double vision
F
Face droop
A
Arm drift
S
Speech difficulty
T
Time — note "last known well"; call 911
Ischemic vs Hemorrhagic
Ischemic (62%)
Too little blood → not enough O₂/nutrients. Causes:
Too much blood in the closed cranial cavity. Intracerebral hemorrhage (28%) + subarachnoid (10%).
ICH risk: age, HTN, antithrombotics. SAH: aneurysm (80–90% of SAH), AVM, tumor, trauma.
SAH = "worst headache of my life" (thunderclap), brief LOC, vomiting, neck stiffness. Maximal at onset.
AVM
Tangle of vessels where arterial blood bypasses capillaries straight to veins (arteries + veins + glial tissue, no capillaries). High flow → aneurysm in 20–25%; vascular steal robs nearby tissue. Linked to HHT (Osler-Weber-Rendu). 1–2% of strokes (3% in young adults). Best imaging: MRI/MRA.
Aneurysm
Saccular (berry) aneurysms at circle of Willis branch points cause most spontaneous SAH. Risk: smoking, HTN, estrogen deficiency, genetics (PKD, Ehlers-Danlos, family hx). ≥1 cm tend to grow/rupture. Best imaging: CTA or angiogram. Treat: clip or coil.
Stroke Syndromes — localize by territory
Vessel
Hallmark findings
ACA
Contralateral leg > arm weakness/sensory loss; gait apraxia; abulia/personality change; urinary incontinence
MCA (most common)
Contralateral face/arm > leg weakness/sensory loss; aphasia (dominant/left); neglect (non-dominant); gaze deviates toward the lesion; homonymous hemianopsia
PCA
Homonymous hemianopsia with macular sparing; cortical blindness; alexia without agraphia; memory loss; thalamic signs
Brainstem / vertebrobasilar
"The V's": Vomiting, Visual changes, Vertigo; drop attacks, ataxia, coma; crossed signs (ipsilateral CN + contralateral body)
Lacunar
Pure motor (post. limb internal capsule/pons); pure sensory (thalamus); ataxic hemiparesis; dysarthria–clumsy hand
⭐ Eyes & aphasia tricksCortical lesion → eyes look toward the side of the lesion (away from weak side). Left MCA = aphasia (language is left-dominant in ~95%). Right MCA = neglect. "VANDD" brainstem: Vomiting, Ataxia, Nausea, Dizziness, Diplopia.
Acute Management
Reperfusion windows
IV thrombolytics (tPA/alteplase): within 3 hrs (off-label up to 4.5 hrs) of onset. Goal door-to-needle ≤60 min.
Mechanical thrombectomy: large-vessel occlusion, within 6 hrs (selected up to 24 h). Best outcomes = combined medical + surgical.
Blood pressure goals
If giving tPA: pre-treat to ≤185/110; keep ≤180/105 ×24 h (IV labetalol/nicardipine).
If NOT giving tPA: permissive HTN — only treat if SBP ≥220 or DBP ≥120; lower ~15% in 24 h.
Aspirin within 48 h (after repeat imaging shows no bleed). Minor stroke/TIA → ASA + clopidogrel ×21 days.
Hemorrhagic stroke: reverse anticoagulation (vitamin K, protamine, PCC), neurosurgery referral, control BP/ICP. Do NOT give antithrombotics. Don't rush to prognosticate — early severe deficits can reverse.
TIA
Transient focal neuro dysfunction from ischemia without infarction (tissue-based definition; old definition was <24 h). Symptoms usually resolve <5 min. High stroke risk afterward → urgent workup. ABCD² score (Age, BP, Clinical features, Duration, Diabetes) historically risk-stratifies, but the major modern risk = extracranial ICA stenosis. Carotid endarterectomy if >70% symptomatic stenosis.
🧠 Secondary prevention — "A,B,C,D,E"
A
Antiplatelets (clopidogrel/ASA); Anticoagulate if cardioembolic/AFib (warfarin or DOAC)
B
BP control (goal <130/80 after 48–72 h)
C
Cholesterol — statin to LDL <100; Carotid intervention if >70%
D
Diet (Mediterranean/DASH), Diabetes control
E
Exercise 150 min/wk, no tobacco, treat OSA
Board-style Q
A 72-y/o woman has acute right face and arm weakness and difficulty speaking. Eyes deviate to the left. Symptoms began 2 hours ago. Non-contrast CT shows no hemorrhage; glucose normal. Best next step?
A. Left MCA syndrome (right face/arm weakness, aphasia, gaze toward lesion), within the 3–4.5 h window, no hemorrhage on CT → IV thrombolytics. Don't aggressively lower BP unless >185/110 before tPA. Warfarin/LP are not acute steps.
TBI = alteration in brain function from an external force. Head struck / strikes object / acceleration-deceleration / blast / penetration. Peak age 15–25, M:F 3:1. Causes: MVA, falls (elderly), sports, assault. 75–95% are mild.
Traumatic Hemorrhages — KNOW these cold
Type
Vessel
CT shape
Classic clues
Epidural
Middle meningeal artery
Lens / biconvex (won't cross sutures)
Lucid interval then rapid decline; younger patients; temporal bone fx
Trauma-induced alteration in mental status, ± LOC. Hallmark = confusion + amnesia. Diagnosis of mild TBI: head injury, ±LOC, neuro symptoms, GCS ≥13 at 30 min.
Diffuse axonal injury: coma >6 h. LOC up to 6 h can still = concussion; 6–24 h = mild DAI; >24 h = moderate–severe DAI. Reticular activating system damage → LOC.
Decorticate (flexion, arms to "core") = cerebral hemisphere damage, motor GCS 3.
Decerebrate (extension) = brainstem damage, motor GCS 2 — worse.
🧠 "deCORticate = toward the CORE"
Flexion toward the core is the less-bad one. Decerebrate extension = closer to death (brainstem).
Basilar Skull Fracture & CSF Leak
🧠 Basilar skull fracture signs
1
Raccoon eyes (periorbital ecchymosis)
2
Battle sign (mastoid/postauricular bruising)
3
Hemotympanum
4
CSF rhinorrhea / otorrhea
5
CN palsies (e.g., facial)
Confirm CSF leak:Halo/ring test (CSF separates from blood on gauze), CSF glucose >30 (rhinitis <10), and most reliably β-2 transferrin. Depressed skull fracture = neurosurgical emergency.
When to CT the head
Common validated criteria (≥1 → image): GCS <15 at 2 h, suspected skull/basilar fracture, vomiting ≥2×, new neuro deficit, seizure, anticoagulant/bleeding diathesis, age ≥60–65, dangerous mechanism, retrograde amnesia ≥30 min, intoxication. Refer/admit: "talked and deteriorated," focal deficit, skull fx, GCS <13, mass effect/midline shift, >1 cm EDH/SDH (smaller resolve), penetrating/blast.
Signs of ↑ICP (GCS ≤8, posturing) → reduce ICP BEFORE CT (head elevation, hyperventilation, mannitol/hypertonic saline) and intubate to protect airway.
Management & Sequelae
Return to play / learn
Rest 24–48 h then graded return only if symptoms don't worsen. CDC 6-step return-to-play (start when symptom-free off meds). Return-to-learn = cognitive rest (limit screens/reading). Subsequent concussion risk highest 7–10 days after first; risk escalates with each.
Symptomatic tx: acetaminophen/NSAIDs sparingly (rebound HA), abortive for migraine, ondansetron for nausea, melatonin/sleep hygiene.
Complications
Post-concussive syndrome (~30–80%): persistent HA, fatigue, irritability, dizziness, insomnia, noise sensitivity, cognitive impairment (~2 mo; most resolve by 3 mo). Post-traumatic seizures/epilepsy (more severe injury, kids). CN I & VII most commonly injured. CTE linked to years of play (not # reported concussions); doubled suicide risk in meta-analysis.
Typical concussion course: symptoms over 1–2 days, worst at 7–10 days, mostly resolved by 1 month.
Board-style Q
A 19-y/o is hit in the temple by a baseball, briefly loses consciousness, wakes and feels fine, then 1 hour later becomes rapidly obtunded with a fixed dilated right pupil. Most likely diagnosis?
Neuro #4. "Headache is a symptom, not a diagnosis." 90% of primary HA = tension, migraine, or cluster.
⚡ Thunderclap headache = sudden, max intensity in <1 minute → subarachnoid hemorrhage until proven otherwise. Medical emergency → non-contrast CT, then LP if CT negative (xanthochromia).
⭐ Buzzword shortcutsMigraine patient wants to lie still in the dark; cluster patient can't sit still (paces). Cluster has autonomic features + circadian/seasonal clustering (attacks same time daily for weeks, then remission). Tension = the boring "band."
🧠 Migraine quick screen = "PIN"
P
Photophobia
I
Incapacity (disabling)
N
Nausea
Any HA in last 3 months with PIN → screen positive for migraine. (Also "POUND": Pulsatile, 4–72 hr (One day), Unilateral, Nausea, Disabling.)
Prevent:Verapamil (chronic, 1st-line); prednisone taper / DHE while titrating verapamil.
⭐ Must-know triggers/contraindicationsTriptans & ergots = vasoconstrictors → contraindicated in CAD, uncontrolled HTN, vascular disease; never give DHE within 24 h of a triptan. Status migrainosus (>72 h) → IV ketorolac + metoclopramide + fluids ± dexamethasone (prevents recurrence). Medication overuse headache: ≥15 HA days/mo + abortive overuse → treat by withdrawing the offending med.
Board-style Q
A 38-y/o man has 6 weeks of severe right-sided orbital headaches lasting ~1 hour, occurring nightly, with ipsilateral tearing, nasal congestion, and a droopy eyelid. He paces during attacks. Fastest abortive therapy?
B. Classic cluster headache (unilateral orbital pain, autonomic features, restlessness, circadian clustering). Best/fastest abortive = high-flow 100% O₂ (SQ/nasal triptan is 2nd). Verapamil is preventive, not abortive; amitriptyline is for tension/migraine prophylaxis.
Provoked / acute symptomatic: at/near a brain insult (within 1 wk of stroke/TBI/anoxia/surgery, active CNS infection, within 24 h of severe metabolic derangement). ~25–30% of first seizures.
Unprovoked: no identifiable cause.
Epilepsy = ≥2 unprovoked seizures >24 h apart, OR 1 unprovoked + high recurrence risk (≥60%), OR an epilepsy syndrome.
Focal vs Generalized
Focal — begins in one area; may spread. Sub-classified by awareness (retained vs impaired).
Helpful tests:serum lactate ↑ within 2 h favors a generalized convulsion over syncope. ECG to rule out cardiogenic syncope; EEG confirms/localizes (ictal + interictal); MRI for structure. TIA gives negative symptoms (loss); seizures give positive symptoms (jerking, tingling). Psychogenic nonepileptic seizures (PNES) = video-EEG.
Status Epilepticus — EMERGENCY
Status epilepticus = seizure >5 min, or serial seizures without return to baseline. Most seizures self-terminate within 2 min. Treat & evaluate simultaneously.
Treatment ladder
ABCs; check glucose → give thiamine + dextrose; correct metabolic (careful with low Na⁺)
Benzodiazepine first-line: IV lorazepam (or IM midazolam); repeat in 10–15 min
IV antiseizure med: fosphenytoin 20 PE/kg (or levetiracetam/valproate)
Chronic Management
Antiseizure meds (by type)
First-line (expert opinion): levetiracetam (few interactions), lamotrigine. Absence: ethosuximide or valproate. Avoid valproate in women of childbearing age (teratogen). 60% respond to first agent. Start meds if: 2nd seizure, uncorrectable cause, epileptiform EEG, abnormal exam, or first seizure during sleep.
Age 6 mo–5 yr, temp >100.4°F, no CNS infection. Simple = generalized, <15 min, once per illness. Complex = focal, >15 min, or repeats. ≥98% do NOT develop epilepsy. LP if meningeal signs, unimmunized 6–12 mo, or on antibiotics. Usually no treatment; diazepam if >10 min; fosphenytoin if status.
Board-style Q
A 24-y/o has a generalized tonic-clonic seizure that has continued for 8 minutes in the ED. Glucose is 95. What is the first-line pharmacologic treatment?
B. This is status epilepticus (>5 min). After ABCs/glucose, first-line = IV benzodiazepine (lorazepam), then load fosphenytoin if it continues. Glucose is normal so dextrose isn't the answer here.
🧩 Dementia & Neurocognitive Disorders
Neuro #5 (part B). Alzheimer · Frontotemporal · Lewy body · Vascular · Normal pressure hydrocephalus.
Dementia
Acquired loss of cognition interfering with daily life; not due to delirium/psych. ≥1 domain (memory, language, executive, attention, visuospatial, social). Young-onset <65.
Delirium
Acute, fluctuating confusion/AMS — reversible, look for a cause (infection, meds, metabolic). Dementia is chronic & progressive.
MCI
Mild memory changes, ADLs preserved. Missed appointments, trouble following a movie — but still independent.
Workup of new dementia: cognitive testing (MMSE/MoCA), labs to find reversible causes — B12, TSH, CMP; screen depression. Neuroimaging (MRI) if acute/rapid/focal or to rule out subdural/stroke/tumor. "5 dope ants eat herbs" = med classes that impair memory (analgesics, antibiotics, anticholinergics, antiseizure, antidepressants, GI, herbal).
The 5 Dementias — compare & contrast
Type
Hallmark
Key features
Treatment
Alzheimer (60–80%)
Insidious memory loss (episodic, anterograde)
Amyloid-β plaques + tau tangles; ↓ACh; hippocampal/medial temporal atrophy on MRI; exam normal until late
Donepezil, rivastigmine, galantamine. ↑ACh → mild but stable symptomatic benefit at all stages. First-line at diagnosis.
Memantine (NMDA antagonist)
Blocks glutamate excitotoxicity. Add in moderate–severe AD. (Anti-amyloid mAbs lecanemab/donanemab = specialized centers; aducanumab off market — "untestable update.")
Board-style Q
A 64-y/o woman has vivid dreams where she acts out and falls out of bed, fluctuating attention, recurrent visual hallucinations of animals, and mild bradykinesia/rigidity without tremor. She worsened dramatically on a psychotropic. Most likely diagnosis?
B.Lewy body dementia: fluctuating cognition + visual hallucinations + parkinsonism + REM sleep behavior disorder, plus severe neuroleptic sensitivity (worsened on a psychotropic/antipsychotic). Avoid antipsychotics; use cholinesterase inhibitors.
Tremor types:Rest (Parkinson — worse at rest, "pill-rolling") · Postural (held against gravity) · Intention (worsens approaching target — cerebellar) · Action/essential (with movement). Movement disorders are hyperkinetic (too much: chorea, tics, dyskinesia) or hypokinetic (too little: Parkinson).
⭐ Essential Tremor vs Parkinson — the #1 differential
Essential Tremor
Parkinson Disease
When
Action/postural (worse with movement)
Rest (worse at rest, improves w/ movement)
Symmetry
Symmetric (bilateral)
Asymmetric
Tremor look
Fine, 4–10 Hz; head/voice
Pill-rolling, slower
Alcohol
Improves with alcohol
No change
Other signs
None (maybe subtle cerebellar)
Bradykinesia, rigidity, postural instability
Treatment
Propranolol or primidone
Carbidopa-levodopa
⭐ Two-second discriminatorET = worse with action, better with alcohol, symmetric.PD = worse at rest, asymmetric, + bradykinesia/rigidity. Wilson disease for any unexplained tremor <40 y.
Irresistible urge to move legs, evening/night (circadian), relieved by movement, not painful. ↓CNS iron, dopaminergic. Check ferritin/iron → replace if low. Tx: dopamine agonists (pramipexole, ropinirole) or gabapentinoids. Worsened by antihistamines, dopamine blockers, antidepressants.
Tourette Disorder
Childhood-onset (avg 6 y, M 3:1) motor + vocal tics >1 yr. Tics are suppressible, preceded by premonitory urge, worse with stress. Dopamine hypersensitivity. Comorbid ADHD & OCD. Tx: treat most disabling feature; α-2 agonists (clonidine, guanfacine), dopamine antagonists (can cause TD). Improves over time in ~40%.
A 68-y/o man reports a 2-year tremor in his right hand that is most noticeable when his hand rests in his lap and improves when he reaches for objects. He also has slowed movements and cogwheel rigidity. Best initial pharmacologic therapy?
B.Resting asymmetric tremor + bradykinesia + cogwheel rigidity = Parkinson disease. Most effective therapy = carbidopa-levodopa. Propranolol/primidone treat essential (action) tremor. Dopamine agonists are an option but levodopa is most effective, especially in older patients.
⭐ Localize the lesion firstMS = CNS (brain/cord) demyelination. GBS = peripheral nerve/root demyelination. Myasthenia = neuromuscular junction (postsynaptic AChR). ALS = motor neurons (UMN + LMN). Match the level to the signs.
Guillain-Barré Syndrome (GBS)
Pattern & cause
Immune-mediated polyneuropathy (most common = AIDP). Ascending symmetric weakness + areflexia, 1–4 wks after infection. Campylobacter jejuni (#1), also CMV, influenza, HIV, COVID. Peaks at 2–4 wks. Watch respiratory failure & dysautonomia.
Dx & treatment
LP: albuminocytologic dissociation (↑protein, normal WBC). EMG/NCS: slowed conduction/block. Treat: IVIG OR plasmapheresis (NOT steroids — ineffective in GBS!). Supportive: monitor FVC/NIF, ICU if respiratory/autonomic. 80% walk by 1 yr.
Chronic immune-mediated CNS demyelination. Lesions disseminated in TIME & SPACE (McDonald criteria). F:M 2:1, onset 28–31, ↑ with distance from equator. Leading cause of non-traumatic neuro disability in young adults. Courses: relapsing-remitting (85%) → secondary progressive; primary progressive (10%).
Myasthenic crisis = respiratory failure (out of proportion to limb weakness), often triggered by infection/surgery/meds → ICU, intubate, IVIG/PLEX. Distinguish from cholinergic crisis (too much AChE inhibitor).
ALS & the UMN/LMN game
Sign
Upper Motor Neuron
Lower Motor Neuron
Tone
Spasticity ↑
Flaccid ↓
Reflexes
Hyperreflexia, clonus, +Babinski
Hypo/areflexia
Bulk
Normal/disuse
Atrophy, fasciculations
ALS ("Lou Gehrig's") = most common adult motor neuron disease. BOTH UMN + LMN signs, NO sensory loss, asymmetric limb weakness (hand weakness, foot drop). Steady progression, no remissions. Riluzole (glutamate blocker) = only FDA drug, prolongs life ~2–3 mo. Death in 3–5 yrs. Clue: hyperreflexia + Babinski + clonus (UMN) alongside atrophy + fasciculations (LMN) with intact sensation.
Cerebral Palsy
Non-progressive disorder of tone/posture from early brain injury (≤30 days postnatal). Types: spastic (most common), dyskinetic, ataxic. Appears 4 mo–2 yr (missed/delayed milestones, persistent primitive reflexes). Does NOT involve loss of attained milestones, progression, or sensory loss (those suggest a different disease). Dx clinical; MRI abnormal 85–90%. Multidisciplinary tx; spasticity → baclofen, botulinum toxin, rhizotomy. Comorbid: intellectual disability (~50%), seizures, vision/hearing/speech.
Board-style Q
A 35-y/o woman reports drooping eyelids and double vision that are mild in the morning and worsen through the day, plus fatigable chewing. Pupils are normal. What antibody is most likely positive, and what is first-line symptomatic treatment?
Treat: the underlying cause + symptoms (gabapentin, TCAs, duloxetine). Foot/nail care in diabetics. Red flags needing fuller workup: asymmetry, motor-predominant, acute onset, autonomic involvement, sensory ataxia. (Note: a "whole one side numb" acute presentation → think brainstem/thalamic stroke, not polyneuropathy.)
Complex Regional Pain Syndrome (CRPS)
Pain in one limb disproportionate to the inciting event (fracture, crush, sprain, surgery — even CTS release), appearing 4–6 weeks later. F:M >2:1, postmenopausal. Features across categories: sensory (allodynia, hyperalgesia), vasomotor (temp/color asymmetry), sudomotor/edema (sweating, swelling), motor/trophic (↓ROM, skin/nail/hair changes). XR may show patchy decalcification. Clinical diagnosis. Tx: early mobilization (also prevention), NSAIDs, PT/OT, prednisone taper if moderate, pain-management referral.
Board-style Q
A 30-y/o pregnant woman has 3 weeks of nighttime tingling and pain in the thumb, index, and middle fingers of her right hand, relieved by shaking it out. Thenar bulk is preserved. Best initial management?
B. Classic carpal tunnel syndrome (median nerve, digits 1–3, nocturnal, pregnancy-associated). Mild–moderate without atrophy → conservative first: neutral night splint ± steroid. Surgery is for severe/progressive motor deficit or failed conservative care.
MVA, falls, violence, sports. Half are cervical. Primary injury (gray matter, <1 h, irreversible) + secondary injury (white matter, ischemia/edema/excitotoxicity over 72 h, max 3–6 d). 25% of damage happens after the event (improper transport). UMN below lesion, LMN at lesion. T1 landmark: above = UE+LE, below = LE only. Fractures: Jefferson (C1), Hangman (C2), Chance (seatbelt flexion-distraction), burst.
Eval & management
Immobilize + ABCs. C3–5 → diaphragm/respiratory effects. NEXUS criteria to clear C-spine without imaging (no midline tenderness, no focal deficit, normal alertness, no intoxication, no distracting injury); otherwise CT. Neurogenic/spinal shock: loss of sympathetic tone → bradycardia + hypotension → maintain MAP 90–100 (fluids, pressors). High-dose methylprednisolone for secondary injury (controversial). C7 triceps = independent transfers.
Spinal shock (transient, immediately post-injury): flaccid paralysis, areflexia, anesthesia, ± priapism — from K⁺ efflux blocking transmission; may fully reverse. Neurogenic shock = the hemodynamic picture (bradycardia + hypotension) of lost sympathetic tone (see Shock concepts).
Spinal Epidural Abscess (SEA)
Classic triad: fever + back pain + neuro deficit (full triad in the minority — fever is most often absent). Risk: IVDU, diabetes, alcohol, HIV, trauma, spinal procedures, tattooing/acupuncture, contiguous infection. Labs often normal except ↑ESR/CRP; get blood cultures ×2. MRI WITH contrast (XR/CT inadequate). Treat: empiric vancomycin + ceftriaxone (cover MRSA, strep, gram-negatives) right after cultures, + surgical decompression/drainage for any neuro deficit or progression. Paralysis before surgery rarely resolves. Mortality 5–7%.
Other myelopathies
Transverse myelitis
Inflammation of one cross-sectional cord level (infectious or autoimmune — think MS/NMO). Bilateral motor/sensory + bladder below the level.
A 57-y/o man with 1 month of low back pain has acute worsening, new difficulty urinating, and numbness "around the anus" when wiping. Strength is mildly reduced in both legs. Most appropriate next step?
B. Saddle anesthesia + urinary retention + bilateral leg involvement = cauda equina syndrome, a surgical emergency → emergent MRI then decompression. Delay risks permanent bowel/bladder/motor loss.
Fever + nuchal rigidity + altered mental status (+ headache). Full triad in minority; GCS usually 14 — if cerebral function clearly altered, think encephalitis or complication. Signs: Kernig, Brudzinski (low sensitivity). Petechial/purpuric rash → Neisseria meningitidis (doesn't blanch).
Empiric antibiotics by age
Age
Bugs
Empiric tx
Neonate
GBS, Listeria, E. coli
Ampicillin + cefotaxime (+gent)
3 mo–50 y
S. pneumo, N. meningitidis, H. flu
Vancomycin + ceftriaxone
>50 y / immunocomp
+ Listeria, gram-negatives
Vanc + ceftriaxone + ampicillin
+ Dexamethasone ×4 days (give before/with 1st antibiotic — protects hearing, esp. S. pneumo).
CSF: bacterial vs viral
Bacterial
Viral
Opening P
↑↑ (>180)
nl/↑
WBC
↑↑ PMNs (100s–1000s)
↑ lymphocytes
Protein
↑↑ (>50)
↑ mild
Glucose
↓ (<30% serum)
normal
Lactate
↑ (>35)
normal
Sequence matters: blood cultures → start antibiotics + dexamethasone → LP. CT before LP only if ↑ICP risk (immunocompromised, CNS disease, new seizure, papilledema, focal deficit, ↓consciousness) — and never delay antibiotics for the CT. Meningococcus → prophylax close contacts (rifampin, cipro, or ceftriaxone). Vaccinate (MenACWY at 11 & 16). Mortality ~16%; sequelae: hearing loss, hemiparesis, epilepsy.
Encephalitis
Brain parenchyma inflammation + neuro dysfunction. Usually viral — HSV-1 is the classic (temporal lobe, ~1000/yr), also enterovirus, West Nile (flaccid paralysis), VZV (vesicles), mumps (parotitis), rabies (hydrophobia). Presents like meningitis plus altered brain function (focal deficits, seizures, aphasia, personality change). CSF: lymphocytic, ↑protein, normal glucose, RBCs suggest HSV-1; EEG abnormal; PCR (HSV/VZV/enterovirus). MRI: temporal lobe changes in HSV. Treat HSV empirically: IV acyclovir 10 mg/kg q8 — start early, don't wait for PCR.
⭐ Don't-missAny encephalitis picture (fever + confusion/aphasia/seizure, esp. temporal-lobe signs) → start IV acyclovir immediately for possible HSV-1; it's treatable and devastating if missed.
↑ammonia (hallmark, not required), asterixis, worse after meals. Precipitants: GI bleed, infection, lytes. Tx: lactulose + rifaximin, treat precipitant, protein moderation.
Wernicke
Thiamine (B1) deficiency — triad Confusion + Ataxia + Ophthalmoplegia/nystagmus. Give thiamine BEFORE glucose. Korsakoff = amnesia + confabulation.
PRES (hypertensive)
Severe HTN → HA, visual changes, seizures, AMS; posterior edema on MRI. Tx: labetalol/nicardipine; reversible.
🧠 "Wernicke = COAT rack" & thiamine-first
Confusion, Ophthalmoplegia, Ataxia, Thiamine. In an alcoholic/malnourished patient, thiamine before dextrose or you precipitate Wernicke.
Board-style Q (from your lecture)
A 30-y/o man has altered mental status, fever, and nuchal rigidity; you suspect bacterial meningitis. Most appropriate sequence?
B. With AMS (an indication for CT before LP), you must not delay treatment: blood cultures → steroids + antibiotics → CT → LP. Empiric therapy and dexamethasone go in before imaging when ↑ICP risk is present.
Board-style Q (from your lecture)
CSF: protein 72, glucose 50 (serum 100), 235 WBC/µL with 60% lymphocytes, Gram stain/culture pending. Most consistent with?
B. Lymphocytic predominance, mildly ↑protein, and normal glucose (CSF:serum 50:100 = normal ratio) = viral meningitis. Bacterial would show PMNs, very high protein, and low glucose.
Progressive focal neuro deficit (68%), headache (54%), focal seizures (26%), N/V, AMS, personality change. Symptoms from mass effect, invasion, and vasogenic edema.
⭐ Tumor headache red flagsWorse in early morning / nocturnal, worse with cough/lying down/Valsalva, progressively worse, wakes from sleep, new pattern, + neuro deficits, ± N/V.
Temporal: seizures with olfactory/gustatory hallucinations, lip-smacking
Occipital: homonymous hemianopia, visual agnosia
Pituitary: bitemporal hemianopia, endocrine
Brainstem/cerebellar: CN palsy, ataxia, nystagmus
↑ICP — two triads: Early = headache + vomiting + papilledema. Late = Cushing's triad: hypertension (widened pulse pressure) + bradycardia + irregular respirations → impending herniation.
Evaluation & Management
Workup
MRI with/without contrast (CT if MRI contraindicated). Diagnosis requires biopsy, but imaging gives clues (dural tail = meningioma; ring-enhancing differential includes abscess/mets/GBM). LP usually not useful (and risky with mass/↑ICP). Look for a non-CNS primary (CT chest highest yield).
A 60-y/o reports 6 weeks of worsening headaches that are worst on waking and with coughing, plus new morning vomiting and a focal seizure. Best initial imaging and a key clue that a mass is meningioma?
B. Progressive morning/Valsalva headache + vomiting + focal seizure = ↑ICP from a mass → MRI with contrast. A dural tail is the classic (near-pathognomonic) sign of a meningioma. LP is risky with a mass; the MCA sign is for stroke.
😵 Syncope
Neuro #2 (part 2) + Ch 23. Transient LOC from global cerebral hypoperfusion.
Syncope = transient, self-limited loss of consciousness from acute global cerebral hypoperfusion — rapid onset, brief, spontaneous complete recovery. It's a symptom, not a diagnosis. Lifetime incidence ~40%, rises after age 70. The job: was it syncope vs seizure vs cardiac? and rule out cardiac (deadly) causes.
Three mechanisms
Type
Mechanism
Clues
Reflex / neurally-mediated (vasovagal) — most common
Failure of BP control on standing (volume depletion, autonomic, meds)
SBP↓≥20 / DBP↓≥10 within 3 min standing
Cardiac — most dangerous
Arrhythmia or ↓cardiac output (structural)
Exertional, no prodrome, palpitations, family hx sudden death, abnormal ECG
⭐ PathophysiologyStanding → venous pooling → ↓venous return → ↓ventricular filling → if the baroreflex lags → hypotension → cerebral hypoperfusion → faint. Convulsive movements (myoclonus, eyes up, brief jerks, even incontinence) can occur in syncope ("convulsive syncope") and don't automatically mean seizure.
⭐ Syncope vs Seizure
Feature
Syncope
Seizure
Trigger
Position, pain, heat, emotion
None (or sleep deprivation)
Prodrome
Lightheaded, pallor, nausea
Aura (déjà vu, smell)
Movements
Few brief jerks (after LOC)
Sustained tonic-clonic
Duration
Seconds
½–2 min
Tongue bite
Tip (rare)
Lateral
Recovery
Rapid
Postictal confusion
Evaluation
History (incl. eyewitnesses) + physical/neuro exam + orthostatic vitals (supine, then standing at 3 min) + ECG. If clearly neurally-mediated with normal ECG → no further testing. Rule out cardiac red flags: exertional syncope, no prodrome, palpitations, structural heart disease, family history of sudden death, abnormal ECG → cardiac workup (echo, monitoring, etc.).
Treatment (reflex/vasovagal): reassurance, rest, avoid triggers, plasma volume expansion (fluids/salt), isometric counter-pressure maneuvers (leg crossing, hand grip) at prodrome. Refractory → fludrocortisone, midodrine, or beta-blockers. (Tilt-table test confirms when atypical.)
Board-style Q
A 19-y/o college student faints after standing in a hot lecture hall; she felt warm, nauseated, and lightheaded beforehand, recovered fully in 30 seconds, and has a normal exam and ECG. Most appropriate next step?
A. Classic vasovagal syncope — clear trigger, autonomic prodrome, fast recovery, normal ECG → no further workup needed. Manage with reassurance, hydration/salt, and counter-pressure maneuvers. Imaging/monitoring/meds aren't indicated without red flags.
📝 Cases & Test Questions
Board-style vignettes drawn from Neuro #10 & #12 case sets. Pick an answer, then check it.
Each topic tab also has its own quiz question. This is your mixed practice exam — great for the day before a test.
Q1 — Weakness & vision
A 28-y/o man has 1 day of double vision and left leg weakness/numbness. One year ago he had transient blurry/double vision that resolved. Exam: right eye can't abduct (lateral gaze problem), left leg weakness with hyperreflexia and +Babinski. LP is done — what is most likely on CSF?
B. Two CNS events separated in time & space (prior optic/eye symptoms, now INO + UMN leg signs) = multiple sclerosis → oligoclonal bands. Albuminocytologic dissociation = GBS; xanthochromia = SAH.
Q2 — MS relapse
A 38-y/o man with MS on glatiramer acetate has 12 hours of worsening right arm/leg weakness and numbness. Best treatment now?
A. Acute MS relapse → high-dose IV corticosteroids (methylprednisolone) to speed recovery (after ruling out infection). PLEX is for steroid-refractory relapses; DMTs prevent future attacks but aren't the acute relapse treatment.
Q3 — Neonatal meningitis
A 5-day-old presents with fever, poor feeding, and a seizure. LP shows many WBCs and high protein. Most likely organism?
B. Neonates (<1 mo): Group B Strep, Listeria, E. coli. Empiric therapy = ampicillin + cefotaxime (ampicillin covers Listeria).
Q4 — Parkinson red flag
A 55-y/o woman has 4 years of cognitive decline + gait problems/falls; family suspects Parkinson. Which finding is a RED FLAG suggesting an alternative (atypical parkinsonism) diagnosis?
B. Vertical gaze palsy (can't look down) + early falls = progressive supranuclear palsy (PSP), an atypical parkinsonism. A, C, D are all typical of idiopathic PD.
Q5 — PD pharmacology
Which medication would NOT be recommended to treat the motor symptoms of Parkinson disease?
D. Haloperidol is a dopamine antagonist — it worsens parkinsonism (and causes drug-induced parkinsonism/tardive dyskinesia). PD treatment increases dopamine (levodopa, agonists, amantadine).
Q6 — Drug-induced parkinsonism
A 35-y/o has resting tremor, rigidity, and balance difficulty; you suspect drug-induced parkinsonism. Which med is most likely responsible?
A.Metoclopramide is a dopamine-receptor blocker → drug-induced parkinsonism and tardive dyskinesia. (Same reason it can worsen RLS.)
Q7 — Tremor work-up
A 42-y/o woman has a coarse right-arm tremor present at rest AND with movement, new clumsiness, gait ataxia, and dysarthria. Which test evaluates the condition that must be ruled out?
B. Young patient + mixed tremor + ataxia/dysarthria → rule out Wilson disease (copper accumulation) with serum copper/ceruloplasmin (and slit-lamp for Kayser-Fleischer rings). Always consider Wilson in unexplained tremor <40.
Q8 — Sudden weakness
A 65-y/o abruptly drops his coffee cup and can't speak. Exam: right facial droop, dysarthria, 2/5 right arm/leg strength, increased right-sided reflexes, +right Babinski, intact sensation, no fatigability. Most likely diagnosis?
B. Sudden onset + unilateral UMN signs (face/arm/leg, hyperreflexia, Babinski) = acute stroke. GBS is ascending & areflexic; MG is fatigable without UMN signs; ALS is gradual with mixed UMN/LMN.
Q9 — Painful eye + pupil
A 52-y/o has several days of ptosis and a left eye that is "down and out" with a pupil that does NOT react to light. Most important next step?
C. A "down-and-out" eye with a fixed dilated pupil = CN III palsy with pupil involvement → compressive lesion (posterior communicating artery aneurysm) until proven otherwise → urgent MRA/CTA. (MG spares the pupil, so AChR antibodies are wrong here.)
Q10 — Orobuccolingual movements
A 65-y/o on metoclopramide and other meds for 3 years develops progressive involuntary tongue/jaw movements (lip-smacking) and arching neck spasms. Most likely diagnosis?
B. Chronic metoclopramide (dopamine blocker) + orobuccolingual dyskinesia = tardive dyskinesia. Stop the offending drug; consider a VMAT2 inhibitor.
Q11 — Exertional syncope
A 17-y/o football player passes out during warm-up sprints; he reports 3 months of declining exercise capacity with exertional dyspnea and lightheadedness. Most likely etiology?
B.Exertional syncope in a young athlete = structural cardiac (outflow obstruction, e.g. hypertrophic cardiomyopathy) until proven otherwise — a can't-miss cause of sudden cardiac death. Exertional + no prodrome are the danger signs.
Q12 — Post-GI-illness ascending weakness
A 25-y/o develops ascending leg weakness and dyspnea after a diarrheal illness 3 weeks ago; reflexes are absent, with mild distal sensory loss, HR 50, BP 90/60. Best next diagnostic/monitoring priority?
A. Post-Campylobacter Guillain-Barré with areflexia + autonomic signs (bradycardia/hypotension) + dyspnea → admit and monitor respiratory status (FVC/NIF) for impending failure; treat with IVIG or plasmapheresis (NOT steroids).
Open vignettes (think, then reveal)
55-y/o man: 2-yr right-hand resting tremor, micrographia, gait hesitation, ↓arm swing, cogwheel rigidity, masked face; wife reports he "acts out his dreams"/kicks while sleeping; ↓smell and constipation for years. Diagnosis + clue?
Parkinson disease. Asymmetric resting tremor + bradykinesia + cogwheel rigidity + micrographia. The premotor clues — REM sleep behavior disorder, hyposmia, constipation — often precede motor symptoms by years. Treat with carbidopa-levodopa.
64-y/o man: 11 months of progressive asymmetric weakness starting in the right hand, now with tripping and dysphagia. Exam: atrophy + fasciculations in the right hand/arm, but hyperreflexia in legs and left arm; sensory and cognition normal. Diagnosis?
ALS. Combined UMN (hyperreflexia) + LMN (atrophy, fasciculations) signs, asymmetric, progressive, with no sensory loss and intact cognition. Confirm with EMG. Only disease-modifying drug = riluzole.
64-y/o woman: 1 year of fluctuating cognition, recurrent visual hallucinations (animals/people), REM sleep behavior disorder (acting out dreams), mild bradykinesia/rigidity, and dramatic worsening on a psychotropic. Diagnosis + management caution?
Dementia with Lewy bodies. Fluctuating cognition + visual hallucinations + parkinsonism + REM sleep behavior disorder. Severe neuroleptic sensitivity — avoid antipsychotics (esp. typical like haloperidol); use cholinesterase inhibitors.
🧠 Mnemonics & Memory Aids Hub
Every memory aid in one place + flip-cards. Click a card to flip it.
⭐ The master ruleDifferential = Localization × Time course. Always ask WHERE (cortex → cord → root → nerve → NMJ → muscle) and WHAT (vascular, infectious, inflammatory, neoplastic, degenerative, toxic-metabolic).
Flip-cards — test yourself
BE-FAST
Stroke screen: Balance, Eyes, Face, Arm, Speech, Time
tPA window
IV thrombolytics ≤3 h (up to 4.5 h); thrombectomy ≤6 h (LVO). CT first to exclude bleed.
Bright (hyperdense): acute blood, calcium, contrast. Dark (hypodense): edema, infarct. Acute blood = white → fades to dark over weeks. First test in acute stroke/trauma.