§
System 05 · ~8% of exam

Neurology

Localize first (cortex, subcortical, brainstem, spinal cord, nerve root, peripheral nerve, NMJ, muscle), then think of etiology. Headache, focal deficit, altered mental status, seizures, and weakness drive vignettes.

Chief complaints

BUILD THE DIFFERENTIAL

Vignettes enter through one of these doors. Each complaint lays out the full differential, marks the can't-miss diagnoses, and tells you the next right action for each.

HeadacheFocal neurologic deficitAltered mental statusSeizuresWeakness
CHIEF COMPLAINT · HIGH-YIELD

Headache

Separate primary (migraine, tension, cluster) from secondary (the killers).

Red flags (SNOOP): Systemic (fever, weight loss, cancer, HIV), Neurologic (focal deficit, altered mental status, seizure), Onset (sudden thunderclap), Older (new after 50), Pattern change (worse, frequency, new character). Any red flag gets imaging.

Diagnosis Key features / clues Next step
Subarachnoid hemorrhage Thunderclap headache (worst of life, peak < 1 min), meningismus, photophobia, vomiting, LOC. Non-contrast CT head · if negative and < 6 hours, sufficient · otherwise LP (xanthochromia) · CT angio if positive
Bacterial meningitis Fever, headache, neck stiffness, altered mental status. Photophobia. Petechial rash (meningococcal). Blood cultures + empiric antibiotics + dexamethasone BEFORE LP if CT needed or delayed · LP when safe
Giant cell arteritis Age > 50, new headache, jaw claudication, vision loss or amaurosis fugax, elevated ESR/CRP, polymyalgia rheumatica association. Start high-dose steroids IMMEDIATELY · temporal artery biopsy within 2 weeks (does not affect biopsy yield)
Stroke / TIA Sudden focal neurologic deficit, may have headache. Non-contrast CT · CT angio · stroke protocol
Increased ICP / mass Headache worse in morning or with Valsalva, vomiting without nausea, papilledema, focal signs. MRI brain
Idiopathic intracranial hypertension Young obese woman, headache, papilledema, visual obscurations. Normal MRI/MRV. LP shows elevated opening pressure · acetazolamide · weight loss · VP shunt if vision threatened
Migraine Unilateral, throbbing, photophobia/phonophobia, nausea, aura in some, lasting 4–72 hr. Abort: triptans + NSAID. Prophylaxis: propranolol, topiramate, amitriptyline, CGRP inhibitors if ≥ 4/month
Tension-type Bilateral, band-like, mild to moderate, no photophobia/phonophobia. NSAIDs · stress management
Cluster Severe unilateral periorbital, lacrimation, rhinorrhea, ptosis, miosis. Attacks in clusters. Abort: 100% O2, sumatriptan SC. Prophylaxis: verapamil
= can't-miss diagnosis · rule out first
Exam-style stem
A 68-year-old woman with new-onset right-sided temporal headache for 2 weeks, with jaw pain when chewing and one episode of transient vision loss. ESR 92.
Next step?
Answer › Start high-dose prednisone (60 mg/day) IMMEDIATELY. This is GCA. Do not wait for biopsy. Temporal artery biopsy within 2 weeks, biopsy yield is preserved. Untreated GCA causes permanent blindness.
Pearl
Thunderclap = SAH until CT + LP prove otherwise. Do not accept migraine as the diagnosis in a first thunderclap.
Pearl
A CT within 6 hours of SAH onset has nearly 100% sensitivity. Past 6 hours, LP is required to rule out.
Pearl
Triptans are contraindicated with coronary artery disease, uncontrolled HTN, and recent ergot or other triptan use within 24 hours.
CHIEF COMPLAINT · HIGH-YIELD

Focal neurologic deficit

Stroke until proven otherwise. Localize, then get imaging.

Time of onset determines thrombolysis candidacy. Last known well. NIHSS. Non-contrast CT first to exclude hemorrhage. Anterior circulation vs posterior. Ischemic vs hemorrhagic vs mimics (seizure with Todd paralysis, migraine, hypoglycemia, mass, MS, conversion).

Diagnosis Key features / clues Next step
Ischemic stroke Sudden focal deficit consistent with vascular territory, over minutes. Non-contrast CT (rule out bleed) · tPA if within 4.5 hr · thrombectomy if LVO within 24 hr
Hemorrhagic stroke Sudden deficit with headache, vomiting, altered mental status. CT shows blood. Reverse anticoagulation · BP control (140–160 systolic) · neurosurgery consult
TIA Focal deficit resolving within 24 hours (usually < 1 hr). MRI (rule out infarct), carotid imaging, echo, telemetry · DAPT 21 days then single antiplatelet · statin
Hypoglycemia Diabetic on insulin, sweating, tremor, focal deficit mimicking stroke. Fingerstick glucose BEFORE CT · D50
Seizure with Todd paralysis Witnessed seizure, postictal hemiparesis resolving over hours. Imaging + EEG
Multiple sclerosis Young woman, recurrent neurologic episodes in different locations, internuclear ophthalmoplegia, optic neuritis. MRI brain and spine with contrast · LP for oligoclonal bands
= can't-miss diagnosis · rule out first
Exam-style stem
A 72-year-old man with AFib (on warfarin, INR 1.8) presents with sudden right hemiparesis and aphasia 90 minutes ago. NIHSS 18. CT: no hemorrhage. CTA: left MCA occlusion.
Next step?
Answer › Endovascular thrombectomy. Large vessel occlusion, within window, high NIHSS. tPA is contraindicated with INR > 1.7. Thrombectomy alone is appropriate.
Pearl
tPA contraindications: recent bleed, recent surgery, intracranial mass, uncontrolled HTN > 185/110, low platelets, therapeutic anticoagulation, recent stroke or head trauma within 3 months.
Pearl
BP goals diverge: ischemic stroke allow permissive HTN (treat only if > 185/110 for tPA or > 220/120 otherwise). Hemorrhagic aim 140–160 systolic.
Pearl
MCA stroke territory: contralateral face/arm > leg weakness, aphasia (dominant), neglect (non-dominant). ACA: leg > arm weakness. PCA: visual field defects.
CHIEF COMPLAINT · HIGH-YIELD

Altered mental status

Glucose, oxygen, and basic vitals first. Then structural vs toxic-metabolic vs infectious vs psychiatric.

Acute delirium in the elderly is infection, medication, metabolic, or ictal until proven otherwise. Young patient: toxic ingestion, post-ictal, infection. Check glucose, O2, toxicology, CBC, BMP, LFTs, ammonia, TSH, B12, ABG, head CT. LP if meningitis suspected. EEG if subclinical status.

Diagnosis Key features / clues Next step
Hypoglycemia Insulin use, sulfonylureas, hepatic failure, alcohol. Fingerstick glucose → D50 if < 70
Opioid overdose Miotic pupils, respiratory depression, bradycardia. Naloxone · support ventilation
Sepsis / CNS infection Fever, infectious source, leukocytosis. Cultures + antibiotics within 1 hour · lactate · fluids · LP if suspected meningitis
Intracranial hemorrhage Headache, focal deficit, anticoagulation. Non-contrast CT · reverse anticoagulation · neurosurgery
Hepatic encephalopathy Cirrhosis, asterixis, precipitant (GI bleed, infection, constipation). Lactulose · rifaximin · identify precipitant
Wernicke encephalopathy Alcohol use, confusion + ataxia + ophthalmoplegia. IV THIAMINE before glucose · then treat as needed
Delirium Acute, fluctuating, inattention, altered LOC. Elderly, hospital, often multifactorial. Identify and treat cause · non-pharmacologic (reorient, sleep-wake) · antipsychotic (haloperidol or quetiapine) only if severe agitation
Non-convulsive status epilepticus Persistent altered mental status without obvious cause, history of seizure. EEG · benzodiazepine trial
= can't-miss diagnosis · rule out first
Exam-style stem
A 68-year-old homeless man with chronic alcohol use is confused, ataxic, and has lateral gaze palsy. Hypoglycemic.
Most appropriate initial management?
Answer › IV thiamine 500 mg BEFORE IV glucose. Wernicke encephalopathy. Glucose without thiamine in a thiamine-deficient patient can precipitate or worsen Wernicke.
Pearl
Always check glucose in altered mental status. It's cheap, fast, and lethal if missed.
Pearl
Classic Wernicke triad (confusion + ataxia + ophthalmoplegia) is complete in only 10%. Any one of these in an alcoholic or malnourished patient gets IV thiamine.
Pearl
In the elderly, UTI is commonly blamed for delirium. Be cautious, many such patients have other causes, and asymptomatic bacteriuria is common. Look past the obvious.
CHIEF COMPLAINT

Seizures

First seizure vs status. Provoked vs unprovoked. Generalized vs focal.

First unprovoked seizure: workup (EEG, MRI, labs) to look for structural or metabolic cause. Recurrent unprovoked seizures = epilepsy. Status epilepticus = > 5 minutes of continuous seizure or 2+ without recovery.

Diagnosis Key features / clues Next step
Status epilepticus Continuous seizure > 5 minutes or recurrent without recovery. ABCs → IV benzodiazepine (lorazepam 4 mg) → 2nd agent (levetiracetam, fosphenytoin, valproate) → intubate and continuous EEG if refractory
Provoked seizure Identifiable trigger: hypoglycemia, hyponatremia, alcohol withdrawal, drug intoxication, fever (kids), head trauma. Treat underlying cause · usually no chronic antiepileptic needed
Epilepsy Two or more unprovoked seizures. EEG + MRI · antiepileptic drug based on seizure type
Syncope mimicking seizure Brief, no postictal confusion, possible tonic-clonic jerks (convulsive syncope). Cardiac workup
Psychogenic non-epileptic events Variable features, eye closure, pelvic thrusting, asynchronous movements. No postictal confusion, no elevated prolactin. Video EEG · psychiatric support
= can't-miss diagnosis · rule out first
Pearl
Status epilepticus > 30 minutes causes neuronal injury. Start IV benzos early. If refractory to two doses, escalate, do not keep redosing.
Pearl
Alcohol withdrawal seizures peak at 24–48 hours after last drink. Give benzos, not antiepileptics, as treatment and prophylaxis.
Pearl
Post-ictal elevated prolactin (within 10–20 min) suggests real seizure. Normal prolactin in PNES.
CHIEF COMPLAINT

Weakness

Localize: cortex → cord → root → plexus → nerve → NMJ → muscle. UMN vs LMN signs.

UMN: cortex, subcortical, cord. Spasticity, hyperreflexia, upgoing toes. LMN: anterior horn, root, nerve. Flaccidity, atrophy, fasciculations, hyporeflexia. Fatigable = NMJ (MG). Proximal symmetric = myopathy.

Diagnosis Key features / clues Next step
Guillain-Barré Ascending symmetric weakness, areflexia, recent infection (Campylobacter). LP (albuminocytologic dissociation) · pulmonary function (FVC, NIF) · IVIG or plasmapheresis
Myasthenia gravis Fatigable weakness, ptosis, diplopia, dysphagia, worse at end of day. Acetylcholine receptor antibodies (MuSK if AChR negative) · EMG with repetitive stimulation · pyridostigmine · immunosuppression · thymectomy
Stroke / cord compression Sudden onset with focal signs, cord compression causes bilateral leg weakness, sensory level, bowel/bladder. Emergent MRI spine · steroids · neurosurgery or oncology consult
ALS Progressive painless weakness with UMN AND LMN signs in multiple regions. EMG · riluzole · supportive care
Multiple sclerosis Relapsing-remitting neurologic deficits in young adult, optic neuritis, internuclear ophthalmoplegia. MRI brain and spine · LP (oligoclonal bands) · disease-modifying therapy
Myopathy Proximal symmetric weakness, elevated CK, statins, endocrinopathies, inflammatory. CK, ESR, TSH · EMG · muscle biopsy if inflammatory suspected
= can't-miss diagnosis · rule out first
Pearl
Bulbar symptoms (dysphagia, dysarthria) or diaphragmatic weakness (FVC < 20 mL/kg or NIF > -30) in GBS or MG means ICU admission.
Pearl
Cord compression is a time-sensitive emergency. Any back pain with new weakness, bladder/bowel changes, or saddle anesthesia gets emergent MRI.
Pearl
Internuclear ophthalmoplegia (impaired adduction with contralateral nystagmus) is MS until proven otherwise in a young patient.

Disease deep dives

DEFINITIVE DX

Once you've identified the likely diagnosis from the chief complaint, these pages give you the presentation, workup, management, and exam pearls in depth.

DISEASE DEEP DIVE

Ischemic Stroke

Time is brain. tPA under 4.5 hours. Thrombectomy under 24 hours with LVO.

Sudden focal deficit: hemiparesis, aphasia, dysarthria, hemianopia, ataxia. Deficit matches vascular territory.

  1. Non-contrast CT. Rules out hemorrhage. Ischemic stroke is often normal early; subtle hypoattenuation, loss of gray-white differentiation.
  2. CT angiography. Identifies large vessel occlusion for thrombectomy candidacy.
  3. MRI with DWI. Most sensitive for acute ischemia. Shows infarct within minutes.
  4. Stroke workup. Carotid duplex, echo, telemetry, lipids, A1c, hypercoagulable if young.
  1. tPA. Within 4.5 hours of onset, no contraindications. BP < 185/110.
  2. Thrombectomy. Large vessel occlusion (MCA M1, ICA), NIHSS ≥ 6, within 24 hours for selected patients with favorable perfusion imaging.
  3. Permissive HTN. Do not treat BP < 220/120 unless tPA is being considered. Maintains perfusion to penumbra.
  4. DAPT for 21 days. Minor stroke or high-risk TIA. Then single antiplatelet long-term.
  5. Long-term prevention. Antiplatelet (aspirin, clopidogrel, or DAPT briefly), high-intensity statin, BP control, glycemic control, smoking cessation, AFib anticoagulation.
  6. AFib-related stroke. DOAC. Start 2 weeks after large stroke, 1 week after moderate, 1–3 days after TIA/small (depending on size).
Pearl
Wake-up strokes used to be excluded from thrombolysis. Current practice: if MRI DWI-FLAIR mismatch, tPA is reasonable, the lesion is likely < 4.5 hours old.
Pearl
Cerebellar stroke can present as isolated vertigo, vomiting, ataxia. Do not dismiss as peripheral vertigo in the elderly with vascular risk factors.
Pearl
Patent foramen ovale in cryptogenic stroke in young patients: closure is reasonable in select cases.
Exam-style stem
A 70-year-old woman with HTN had sudden right hemiparesis 3 hours ago. NIHSS 12. CT: no hemorrhage, no LVO.
Answer › IV tPA. Within window, NIHSS qualifies, no contraindications. BP needs to be < 185/110 before infusion.
DISEASE DEEP DIVE

Meningitis

Bacterial is the emergency. Fever, headache, neck stiffness, altered mental status.

Fever, headache, neck stiffness, photophobia, altered mental status. Petechial rash (meningococcemia). Infants: irritability, poor feeding, bulging fontanelle.

  1. LP. Bacterial: high WBC with PMN predominance, low glucose (< 40), high protein. Viral: lymphocytic, normal glucose, mildly elevated protein. Fungal/TB: lymphocytic, low glucose, very high protein.
  2. Head CT before LP. If focal deficit, altered mental status, papilledema, seizure, or immunocompromised.
  3. Blood cultures. Positive in most bacterial meningitis.
  1. Empiric antibiotics. Do NOT delay for LP. Ceftriaxone + vancomycin for all adults. Add ampicillin if > 50 or immunocompromised (Listeria). Add acyclovir if HSV encephalitis suspected.
  2. Dexamethasone. Before or with first antibiotic dose. Reduces mortality in S. pneumoniae meningitis.
  3. Pathogen-specific. S. pneumoniae: ceftriaxone + vanc. N. meningitidis: ceftriaxone. Listeria: ampicillin + gentamicin. HSV: acyclovir.
  4. Prophylaxis for contacts. Meningococcal: close contacts get ciprofloxacin or rifampin. H. flu: rifampin for household contacts.
  5. Vaccination. Asplenia, complement deficiency, travel to meningitis belt → meningococcal vaccines.
Pearl
In adults, empiric treatment is ceftriaxone + vanc + dex. Ampicillin added for > 50, pregnant, immunocompromised, alcoholics (Listeria coverage).
Pearl
Temporal lobe hemorrhagic lesions on MRI with meningitis picture suggest HSV encephalitis. Start acyclovir empirically.
Pearl
Neisseria meningococcal meningitis has the classic petechial or purpuric rash and waterhouse-friderichsen in fulminant cases (adrenal hemorrhage).
Exam-style stem
A 22-year-old college student has fever, headache, neck stiffness, and a petechial rash. BP 92/60, HR 120.
Answer › Meningococcal meningitis with sepsis. Blood cultures, empiric ceftriaxone + vancomycin + dexamethasone, then LP when stable. Droplet isolation. Notify public health. Prophylaxis for close contacts.
DISEASE DEEP DIVE

Multiple Sclerosis

Relapsing-remitting demyelination in young adults. Dissemination in time and space.

Optic neuritis, internuclear ophthalmoplegia, sensory disturbance, weakness, fatigue, bladder dysfunction, Lhermitte sign, Uhthoff phenomenon.

  1. MRI brain and spine with contrast. Periventricular, juxtacortical, infratentorial, spinal cord lesions. Enhancing lesions (active) vs non-enhancing (old).
  2. LP. Oligoclonal bands and elevated IgG index support diagnosis.
  3. VEP. Delayed response if prior optic neuritis (may be subclinical).
  1. Acute relapse. High-dose IV methylprednisolone × 3–5 days. PLEX if refractory.
  2. Disease-modifying therapy. Many options. High-efficacy: ocrelizumab, natalizumab, ofatumumab. Moderate: fingolimod, dimethyl fumarate. Modest: interferon-beta, glatiramer.
  3. Symptomatic. Baclofen for spasticity, oxybutynin for bladder, modafinil for fatigue, gabapentin for neuropathic pain.
Pearl
Optic neuritis presents with painful monocular vision loss, color desaturation, relative afferent pupillary defect. Predicts MS in 50% over 15 years.
Pearl
Dawson fingers on MRI (periventricular lesions perpendicular to ventricles) are highly specific for MS.
Pearl
Avoid fingolimod and natalizumab in patients with PML risk (JC virus positive). Always test JC virus before starting natalizumab.
DISEASE DEEP DIVE

Parkinson Disease

Asymmetric resting tremor, bradykinesia, rigidity, postural instability. Loss of dopaminergic neurons.

Resting pill-rolling tremor (asymmetric), cogwheel rigidity, bradykinesia (shuffling gait, decreased arm swing, masked facies, micrographia), postural instability late. REM sleep behavior disorder often precedes.

  1. Clinical diagnosis. Bradykinesia + either rest tremor or rigidity, asymmetric onset.
  2. DAT scan. If diagnosis uncertain.
  3. Response to levodopa. Robust response supports idiopathic PD.
  1. Levodopa-carbidopa. Most effective. Titrate for symptom control. Delays sometimes used in young patients to defer motor complications.
  2. Dopamine agonists. Pramipexole, ropinirole. Option in young patients. Watch impulse control disorders.
  3. MAO-B inhibitors. Selegiline, rasagiline. Mild benefit, sometimes used early.
  4. Amantadine. For dyskinesias.
  5. Deep brain stimulation. For motor fluctuations and dyskinesias in advanced PD.
  6. Non-motor. Depression (SSRIs), dementia (rivastigmine), REM behavior disorder (melatonin, clonazepam), constipation, orthostatic hypotension (midodrine, fludrocortisone).
Pearl
Red flags suggesting atypical parkinsonism (not idiopathic): early falls (PSP), autonomic failure (MSA), dementia early (DLB), poor response to levodopa.
Pearl
Dementia with Lewy bodies: fluctuating cognition, visual hallucinations, parkinsonism, REM sleep behavior disorder. Avoid antipsychotics (severe sensitivity).