Family Medicine EOR (Neurologic): New for 2026 Topic List (Smarty PANCE)

What is Ischemic Stroke?

An acute neurologic deficit caused by occlusion of a cerebral artery (thrombotic or embolic) resulting in focal brain ischemia and infarction.

What is the time window for IV tPA (alteplase) in acute ischemic stroke?

Within 3 hours of symptom onset (extended to 4.5 hours in select patients without contraindications such as age >80, anticoagulant use, severe stroke, or history of diabetes + prior stroke).

What is the time window for mechanical thrombectomy in large vessel occlusion stroke?

Up to 24 hours from last known well in select patients with favorable imaging (DAWN/DEFUSE-3 criteria).

What is the first-line imaging study for suspected acute stroke?

Non-contrast CT head — primarily to rule OUT hemorrhage before thrombolytics; MRI with DWI is more sensitive for early ischemia.

What are the absolute contraindications to IV tPA?

Active intracranial hemorrhage, recent stroke or head trauma (<3 months), recent intracranial/spinal surgery, BP >185/110 not controlled, platelets <100,000, INR >1.7, glucose <50.

What is the blood pressure goal after ischemic stroke if NOT receiving tPA?

Permissive hypertension up to 220/120 mmHg (allow autoregulation); treat only if >220/120 or end-organ damage.

What is the blood pressure goal if receiving tPA?

<185/110 before tPA and <180/105 for 24 hours after administration.

What is the most common cause of cardioembolic stroke?

Atrial fibrillation (responsible for ~20% of all ischemic strokes); anticoagulation prevents recurrence.

What artery is involved when patient presents with contralateral leg weakness > arm weakness?

Anterior cerebral artery (ACA) — homunculus places leg medially near falx.

What artery is involved when patient presents with contralateral face/arm weakness > leg, aphasia (dominant) or neglect (non-dominant)?

Middle cerebral artery (MCA) — most common stroke territory.

What is Hemorrhagic Stroke?

Acute neurologic deficit caused by bleeding into the brain parenchyma (intracerebral) or subarachnoid space, typically from hypertension or aneurysm rupture.

What is the most common cause of spontaneous intracerebral hemorrhage (ICH)?

Chronic hypertension — typically affects basal ganglia (putamen most common), thalamus, pons, cerebellum.

What is the immediate management of acute ICH?

Reverse anticoagulation, lower SBP to 140 mmHg, neurosurgery consult, elevate head of bed 30°, manage ICP, prevent seizures.

What imaging finding distinguishes ICH from ischemic stroke?

Hyperdense (bright white) blood on non-contrast CT in hemorrhage vs. hypodense (dark) area in ischemia.

What is cerebral amyloid angiopathy and where does it bleed?

Amyloid deposition in cortical vessels; causes lobar hemorrhages in elderly patients (not deep structures like hypertensive bleeds).

What is a Transient Ischemic Attack (TIA)?

Transient episode of neurologic dysfunction caused by focal brain/spinal/retinal ischemia WITHOUT acute infarction on imaging; typically resolves within 1 hour.

What is the ABCD2 score used for?

Stratifies short-term stroke risk after TIA: Age ≥60, BP ≥140/90, Clinical features (unilateral weakness/speech), Duration, Diabetes; score ≥4 = high risk requiring urgent workup.

What is the workup for TIA?

Brain MRI with DWI, carotid imaging (US/CTA/MRA), ECG, echocardiogram, fasting lipids/glucose, A1c — identify and treat underlying cause.

What is the secondary prevention for TIA/non-cardioembolic stroke?

Antiplatelet (aspirin or clopidogrel; aspirin + clopidogrel x 21-90 days for high-risk TIA), statin, BP control, lifestyle modification.

What carotid stenosis warrants endarterectomy (CEA)?

Symptomatic stenosis 70-99% (clear benefit); 50-69% (modest benefit); should be performed within 2 weeks of symptoms.

What is Bell Palsy?

Acute idiopathic unilateral peripheral (lower motor neuron) facial nerve (CN VII) paralysis affecting both upper and lower face, often associated with HSV reactivation.

How do you differentiate Bell palsy from a central (stroke) cause of facial weakness?

Bell palsy = ENTIRE half of face affected (cannot wrinkle forehead or close eye); central lesion = forehead SPARED due to bilateral cortical innervation.

What is the first-line treatment for Bell palsy?

High-dose oral corticosteroids (prednisone 60-80 mg/day) within 72 hours of onset; consider adding antivirals (valacyclovir) in severe cases.

What is the most important eye care for Bell palsy patients?

Artificial tears during day, lubricating ointment at night, eye patch/taping eyelid closed to prevent corneal exposure and ulceration.

What is the prognosis of Bell palsy?

~70-85% of patients recover completely within 3-6 months, even without treatment; worse prognosis if complete paralysis.

What is Alzheimer Disease?

Most common cause of dementia, a progressive neurodegenerative disorder characterized by amyloid plaques and neurofibrillary (tau) tangles causing cortical atrophy.

What is the earliest cognitive symptom of Alzheimer disease?

Short-term memory loss (impaired recent recall), followed by language difficulties, visuospatial problems, and executive dysfunction.

What is the first-line medication class for mild-to-moderate Alzheimer disease?

Cholinesterase inhibitors: donepezil, rivastigmine, galantamine — modest symptomatic improvement.

What medication is added for moderate-to-severe Alzheimer disease?

Memantine (NMDA receptor antagonist) — can be used alone or with cholinesterase inhibitor.

What imaging findings are seen in Alzheimer disease?

MRI shows generalized cortical atrophy, especially of hippocampus and medial temporal lobes; PET shows decreased metabolism in temporoparietal regions.

What is Dementia?

Progressive cognitive decline involving memory plus at least one other cognitive domain (language, executive function, visuospatial, praxis) that interferes with daily function — alert sensorium.

What are the four most common types of dementia?

Alzheimer disease (most common), vascular dementia, Lewy body dementia, frontotemporal dementia.

What features distinguish Lewy Body Dementia?

Triad: visual hallucinations, fluctuating cognition, parkinsonism (rigidity, bradykinesia); REM sleep behavior disorder; severe antipsychotic sensitivity.

What characterizes Frontotemporal Dementia (Pick disease)?

Early personality/behavior changes, disinhibition, apathy, executive dysfunction; relative sparing of memory; younger onset (50-60s).

What characterizes vascular dementia?

Stepwise cognitive decline with focal neurologic deficits, history of stroke/TIA, vascular risk factors; MRI shows white matter changes and old infarcts.

What screening tools assess for dementia?

Mini-Mental State Examination (MMSE; <24 abnormal), Montreal Cognitive Assessment (MoCA; <26 abnormal), Mini-Cog (3-word recall + clock draw).

What is Delirium?

Acute, fluctuating disturbance of attention and awareness with cognitive impairment, developing over hours to days — typically reversible.

What are the key features distinguishing delirium from dementia?

Delirium: ACUTE onset, fluctuating, IMPAIRED attention/consciousness, often reversible; Dementia: gradual, progressive, alert consciousness preserved early.

What is the most common cause of delirium in hospitalized elderly?

Multifactorial — infection (UTI, pneumonia), medications (anticholinergics, benzodiazepines, opioids), metabolic derangements, dehydration, hypoxia.

What is the mnemonic for causes of delirium?

DELIRIUMS: Drugs, Electrolytes, Lack of drugs (withdrawal), Infection, Reduced sensory input, Intracranial, Urinary/fecal retention, Myocardial/pulmonary, Stroke.

What is the management of delirium?

Identify and treat underlying cause; non-pharmacologic measures first (reorientation, sleep hygiene, mobility); low-dose haloperidol for severe agitation; AVOID benzodiazepines except in alcohol/benzo withdrawal.

What is Multiple Sclerosis (MS)?

Chronic autoimmune demyelinating disease of the CNS characterized by relapsing/progressive neurologic deficits separated in time and space.

What is the classic demographic for MS?

Young women (20-40 years old), more common in Caucasians, higher latitudes (vitamin D deficiency theory).

What are common presenting symptoms of MS?

Optic neuritis (painful monocular vision loss), internuclear ophthalmoplegia, Lhermitte sign (electric shock with neck flexion), Uhthoff phenomenon (worsening with heat), sensory/motor deficits, fatigue.

What are diagnostic findings of MS on MRI?

Multiple white matter lesions ("plaques") disseminated in time and space; periventricular, juxtacortical, infratentorial, spinal cord; Dawson fingers (perpendicular to ventricles).

What CSF finding supports MS diagnosis?

Oligoclonal bands and elevated IgG index in CSF (not in serum); mildly elevated protein and lymphocytes.

What is the treatment for acute MS exacerbations?

High-dose IV methylprednisolone (1 g daily x 3-5 days); plasmapheresis if steroid-refractory.

What are first-line disease-modifying therapies for relapsing-remitting MS?

Interferon beta, glatiramer acetate, oral agents (fingolimod, dimethyl fumarate, teriflunomide), monoclonal antibodies (natalizumab, ocrelizumab).

What is Parkinson Disease?

Progressive neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra, leading to motor and non-motor symptoms.

What is the classic tetrad (TRAP) of Parkinson disease?

Tremor (resting, pill-rolling), Rigidity (cogwheel), Akinesia/bradykinesia, Postural instability.

What distinguishes Parkinson tremor from essential tremor?

Parkinson: RESTING tremor, asymmetric, improves with movement, pill-rolling, 4-6 Hz; Essential: ACTION tremor, bilateral, worse with movement, faster (6-12 Hz).

What is the first-line treatment for Parkinson disease in older patients?

Carbidopa-levodopa (most effective for motor symptoms); start at lowest effective dose to delay motor fluctuations and dyskinesias.

What are first-line agents for younger Parkinson patients (<60)?

Dopamine agonists (pramipexole, ropinirole) or MAO-B inhibitors (selegiline, rasagiline) to delay levodopa-induced complications.

What are common non-motor symptoms of Parkinson disease?

Autonomic dysfunction (constipation, orthostatic hypotension), REM sleep behavior disorder, anosmia, depression, dementia (late), micrographia, masked facies.

What is Essential Tremor?

Most common movement disorder; bilateral, symmetric postural and kinetic tremor most prominent in hands, often with positive family history; improves with alcohol.

What is the first-line treatment for essential tremor?

Propranolol (non-selective beta-blocker) or primidone (anticonvulsant); both have similar efficacy.

What characterizes Tourette syndrome?

Multiple motor tics PLUS at least one vocal tic, onset before age 18, lasting >1 year; often comorbid with OCD and ADHD.

What is the first-line treatment for tics in Tourette syndrome?

Behavioral therapy (habit reversal training); pharmacotherapy with alpha-2 agonists (clonidine, guanfacine) or antipsychotics (risperidone, aripiprazole) if severe.

What is Fetal Alcohol Spectrum Disorder (FASD)?

Spectrum of physical, cognitive, and behavioral abnormalities caused by prenatal alcohol exposure; leading preventable cause of intellectual disability.

What are the classic facial features of Fetal Alcohol Syndrome?

Smooth philtrum, thin vermillion border (upper lip), short palpebral fissures; also microcephaly, growth retardation, CNS abnormalities.

What is the minimum safe amount of alcohol during pregnancy?

NONE — there is no known safe amount or safe timing of alcohol use during pregnancy; complete abstinence is recommended.

What cognitive/behavioral findings are seen in FASD?

Intellectual disability, learning disabilities, ADHD-like symptoms, poor impulse control, social/behavioral problems, executive dysfunction.

What is Gait Dysfunction?

Abnormal pattern of walking caused by neurologic, musculoskeletal, or systemic conditions affecting balance, coordination, strength, or sensation.

What gait is seen in Parkinson disease?

Shuffling gait with short steps, decreased arm swing, stooped posture, festination (involuntary acceleration), difficulty initiating and turning (en bloc).

What gait is seen in cerebellar dysfunction?

Ataxic gait — wide-based, unsteady, irregular steps, inability to perform tandem gait; falls toward side of lesion.

What gait is seen in normal pressure hydrocephalus (NPH)?

"Magnetic gait" — feet appear stuck to floor, short shuffling steps; triad: gait disturbance, urinary incontinence, dementia ("wet, wobbly, wacky").

What gait results from a foot drop?

Steppage gait — exaggerated hip flexion to clear toes; caused by common peroneal nerve injury or L5 radiculopathy.

What is the difference between migraine, tension, and cluster headaches?

Migraine: unilateral, pulsating, 4-72h, photophobia/phonophobia, nausea, ± aura; Tension: bilateral, band-like, pressing, no associated features; Cluster: unilateral, periorbital, stabbing, 15-180 min, autonomic features.

What is a Migraine?

Recurrent primary headache disorder featuring unilateral pulsating pain lasting 4-72 hours with associated nausea/vomiting and/or photophobia/phonophobia, sometimes preceded by aura.

What is the acute treatment for migraine?

NSAIDs/acetaminophen for mild; triptans (sumatriptan) first-line for moderate-severe; CGRP receptor antagonists (ubrogepant, rimegepant); antiemetics (metoclopramide); avoid opioids.

What are contraindications to triptans?

Coronary artery disease, uncontrolled hypertension, history of stroke, hemiplegic/basilar migraine, pregnancy, recent use of ergots/MAOIs.

What are the first-line preventive medications for migraine?

Beta-blockers (propranolol, metoprolol), topiramate, amitriptyline, valproate; CGRP monoclonal antibodies (erenumab) for refractory cases; consider when ≥4 headaches/month.

What is a Cluster Headache?

Severe, unilateral, periorbital "ice-pick" headache lasting 15-180 minutes, occurring in clusters (multiple times daily for weeks), with ipsilateral autonomic features (lacrimation, rhinorrhea, ptosis, miosis).

What is the acute treatment for cluster headache?

High-flow 100% oxygen (12-15 L/min via non-rebreather) for 15 minutes AND subcutaneous sumatriptan; verapamil for prevention.

What is Increased Intracranial Pressure (ICP)?

Elevated pressure within the cranial vault (>20 mmHg sustained) caused by mass effect, edema, hemorrhage, or impaired CSF drainage; can lead to herniation and death.

What is Cushing's triad and what does it indicate?

Hypertension (widening pulse pressure), bradycardia, irregular respirations — late sign of severely elevated ICP and impending brainstem herniation.

What are the classic symptoms of increased ICP?

Headache (worse in morning/with Valsalva), nausea/vomiting, papilledema, vision changes, altered mental status, focal neurologic deficits.

What is the emergent management of increased ICP?

Elevate head of bed 30°, hyperventilation to PaCO2 30-35 (short-term), mannitol or hypertonic saline (osmotic therapy), neurosurgery consult; treat underlying cause.

What is idiopathic intracranial hypertension (pseudotumor cerebri)?

Increased ICP without mass lesion, typically in young obese women; presents with headache, papilledema, visual changes, pulsatile tinnitus; treat with acetazolamide, weight loss.

What are Brain Tumors?

Abnormal growths of cells within the brain; can be primary (originate in CNS) or metastatic (most common in adults); present with focal deficits, headache, seizures, or increased ICP.

What is the most common primary malignant brain tumor in adults?

Glioblastoma multiforme (GBM, WHO grade IV astrocytoma) — aggressive, poor prognosis (~15 month median survival).

What is the most common brain tumor overall in adults?

Brain METASTASES (more common than primary tumors); sources: lung > breast > melanoma > renal > colon.

What is the most common primary brain tumor in children?

Pilocytic astrocytoma (most common overall in pediatrics) and medulloblastoma (most common malignant); typically infratentorial.

What is the classic presentation of a brain tumor headache?

Worse in the morning, worse with Valsalva/coughing/bending, progressively worsening, associated with nausea/vomiting and focal neurologic deficits.

What is Peripheral Neuropathy?

Damage to peripheral nerves causing sensory, motor, or autonomic dysfunction; can be mononeuropathy (single nerve) or polyneuropathy (multiple nerves, often distal symmetric).

What is the most common cause of peripheral polyneuropathy?

Diabetes mellitus — distal symmetric sensorimotor polyneuropathy ("stocking-glove" distribution), most common in long-standing or poorly controlled disease.

What is Guillain-Barré syndrome?

Acute inflammatory demyelinating polyneuropathy causing ascending symmetric weakness, areflexia, often after GI/respiratory infection (Campylobacter jejuni classic); CSF: high protein, normal WBC (albuminocytologic dissociation).

What is the treatment for Guillain-Barré syndrome?

IVIG or plasmapheresis (equally effective); monitor respiratory status (FVC, NIF) closely; AVOID steroids (not effective).

What is trigeminal neuralgia and how is it treated?

Recurrent, brief, lancinating facial pain in trigeminal distribution triggered by light touch/chewing/wind; first-line treatment: carbamazepine; alternatives: oxcarbazepine, gabapentin, baclofen.

What is a Seizure Disorder?

Recurrent unprovoked seizures (epilepsy) caused by abnormal, excessive, synchronous neuronal activity in the brain.

What distinguishes focal (partial) from generalized seizures?

Focal: originates in one hemisphere, can be aware or impaired awareness, may secondarily generalize; Generalized: involves both hemispheres from onset (absence, tonic-clonic, myoclonic, atonic).

What is status epilepticus and how is it managed?

Continuous seizure >5 minutes or recurrent without recovery; ABCs, IV benzodiazepine FIRST (lorazepam 4 mg IV or diazepam), then load with fosphenytoin/levetiracetam/valproate; intubate and propofol/midazolam if refractory.

What is the first-line antiepileptic for focal seizures?

Levetiracetam, lamotrigine, or carbamazepine (all effective); levetiracetam preferred for fewer interactions and side effects.

What is the first-line antiepileptic for generalized tonic-clonic seizures?

Valproate (most effective but teratogenic — avoid in women of childbearing age), lamotrigine, or levetiracetam.

What is the EEG finding in absence seizures?

Generalized 3-Hz spike-and-wave discharges; first-line treatment: ethosuximide (or valproate if also having tonic-clonic seizures).

What is Subarachnoid Hemorrhage (SAH)?

Bleeding into the subarachnoid space, most commonly from rupture of a saccular (berry) aneurysm in the Circle of Willis.

What is the classic presentation of SAH?

"Thunderclap headache" — sudden, severe, "worst headache of life," peak intensity within seconds; may have nuchal rigidity, photophobia, vomiting, altered mental status, sentinel headache preceding rupture.

What is the workup for suspected SAH?

Non-contrast CT head FIRST (sensitivity ~95% within 6 hours); if negative and clinical suspicion remains, perform LUMBAR PUNCTURE looking for xanthochromia (yellow CSF) or persistent RBCs.

What is the most common location of cerebral aneurysms?

Anterior communicating artery (most common), posterior communicating artery, middle cerebral artery — all at branch points in the Circle of Willis.

What are major complications of SAH?

Rebleeding (highest risk first 24h), vasospasm (peaks days 4-14, treated with nimodipine), hydrocephalus, hyponatremia (SIADH or cerebral salt wasting), seizures.