Nervous System & Special Senses

Transient ischemic attack: workup and ABCD2 risk stratification

Clinical Overview and When to Suspect TIA

— Old time-based definition (<24 h) is obsolete; up to 30–50% of "clinical TIAs" show DWI lesions on MRI and are reclassified as minor strokes

— Median symptom duration is actually <1 hour; lasting >1 hour with imaging lesion = ischemic stroke

— TIA is a medical emergency, not a "near miss" — 90-day stroke risk is 3–10%, with half occurring within 48 hours

— Aggressive workup + secondary prevention can reduce that risk by ~80% (EXPRESS, SOS-TIA data)

— Sudden, focal, negative neurologic symptoms (loss of function) lasting minutes

— Classic syndromes: unilateral weakness/numbness, aphasia, dysarthria, monocular vision loss (amaurosis fugax), homonymous hemianopia, ataxia, vertigo with brainstem signs, diplopia

— Symptoms reach maximum at onset (vs. migraine march or seizure spread)

— Age >60, HTN, DM, AF, prior stroke/TIA, carotid disease, smoking, hyperlipidemia, OSA, CKD

Board pearl: "Crescendo TIAs" (≥2 TIAs in 7 days, or symptoms while on antiplatelet therapy) = admit, treat as impending stroke, expedite vascular imaging.

Step 3 management: A patient calling the clinic with resolved focal weakness 3 hours ago should be sent to the ED, not scheduled for outpatient MRI next week — the <48 h window is where stroke prevention happens. Telephone triage that defers imaging is a tested patient-safety failure.

Key distinction: TIA vs. stroke is no longer about the clock — it's about whether DWI shows infarct. Both warrant identical urgency in acute workup.

Definition (tissue-based, AHA/ASA 2009): transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction on imaging

Why it matters on Step 3:

When to suspect TIA in clinic or ED:

Vascular risk substrate raises pretest probability:

Presentation Patterns and Key History

— Hemiparesis or hemisensory loss contralateral to lesion

— Aphasia (dominant hemisphere, usually left MCA)

— Hemineglect, dysgraphia, constructional apraxia (non-dominant parietal)

— Amaurosis fugax — painless monocular "curtain" or "shade" descending; ipsilateral internal carotid stenosis until proven otherwise

— Gaze preference toward the lesion

— Vertigo, diplopia, dysarthria, dysphagia, ataxia, crossed sensorimotor findings, bilateral visual symptoms, drop attacks

— Isolated vertigo is rarely TIA unless accompanied by other brainstem/cerebellar signs (HINTS exam helps)

— Time of onset and duration (was it truly resolved by arrival?)

— Exact deficits — have patient/witness mimic them

— Prior similar episodes (crescendo pattern?)

— Triggers: neck manipulation (dissection), standing (orthostatic mimic), exertion, recent MI/cardioversion (cardioembolic)

— Headache, jaw claudication, scalp tenderness in age >50 → GCA mimic

— Recent trauma, anticoagulants → consider hemorrhage mimic

— Medications, illicit drugs (cocaine, amphetamines)

— AF, valve disease, recent MI, PFO, endocarditis risk

— Pregnancy/postpartum (RCVS, eclampsia, CVST mimics)

Key distinction: Positive symptoms (tingling march, scintillating scotoma, jerking) favor migraine aura or seizure; negative symptoms (numbness, weakness, vision loss) favor ischemia. Migraine spreads over minutes; TIA is maximal at onset.

Board pearl: Amaurosis fugax = carotid Doppler same day. Ipsilateral carotid endarterectomy if 70–99% stenosis and symptoms within 6 months drops 5-year stroke risk dramatically (NASCET).

Step 3 management: Document last known well time even though the event resolved — it anchors the workup tempo and triggers the 48-hour rule.

Anterior circulation (carotid territory, ~80%):

Posterior circulation (vertebrobasilar, ~20%):

History must capture (the "TIA checklist"):

Physical Exam Findings (and Hemodynamic Assessment)

— Mental status, language (name objects, repeat phrases, comprehension)

— Cranial nerves: visual fields by confrontation, EOM, facial symmetry, palate elevation, tongue protrusion

— Motor: pronator drift (most sensitive subtle finding), finger taps, gait

— Sensory: pinprick, proprioception

— Cerebellar: finger-nose, heel-shin, tandem gait

— Fundoscopy: Hollenhorst plaque (cholesterol embolus) = carotid source

— Bilateral BP and pulses — >20 mmHg asymmetry suggests subclavian stenosis/aortic dissection

— Irregularly irregular pulse → AF

— Carotid bruit — sensitive but not specific; absence does not exclude tight stenosis (preocclusive lesions may be silent)

— Cardiac murmurs — MR, AS, mechanical valve clicks, S3

— Signs of endocarditis — splinter hemorrhages, Janeway lesions, Osler nodes, Roth spots

— Peripheral pulses, AAA palpation

— Orthostatic vitals if syncope/presyncope in DDx

— Volume status — dehydration can unmask low-flow TIA in tight stenosis

— Document target BP: in suspected TIA without thrombolysis, permissive HTN up to ~220/120 initially; aggressive lowering can extend ischemia

CCS pearl: Order bedside glucose first on any focal neuro complaint — hypoglycemia is the most common stroke mimic and is reversible in seconds. Forgetting this is a classic CCS deduction.

Board pearl: A carotid bruit + amaurosis fugax + Hollenhorst plaque = ipsilateral high-grade ICA stenosis until proven otherwise; get CTA or carotid duplex urgently.

Key distinction: Tongue deviation toward the weak side and uvula deviation away suggest cortical lesion; brainstem lesions give crossed findings (ipsilateral CN + contralateral body).

By presentation, the deficit may be gone — so the exam targets etiology and residual subtle findings rather than the event itself.

Neurologic exam (NIHSS-style screen even if "normal"):

Cardiovascular exam — the embolic source hunt:

Hemodynamic assessment:

Diagnostic Workup — Initial Labs, Imaging, ECG

— Is this really ischemia (vs. mimic)?

— Is there infarct on imaging (TIA vs. minor stroke)?

— What's the mechanism (large artery, cardioembolic, small vessel, other)?

— What's the short-term stroke risk (ABCD2, imaging, vessel findings)?

— Fingerstick glucose — rule out hypoglycemia

— CBC, BMP, coags (PT/INR, PTT), troponin

— Lipid panel, HbA1c — for risk stratification and statin decision

— Pregnancy test if applicable

— Consider TSH, ESR/CRP (GCA in elderly), toxicology

— 12-lead in every patient — look for AF, flutter, MI, LVH, prior infarct, prolonged QT

— Telemetry/continuous monitoring ≥24 hours inpatient; if negative and embolic stroke suspected, outpatient ambulatory monitoring 14–30 days or implantable loop recorder (CRYSTAL-AF: ILR triples AF detection)

— MRI-DWI is gold standard — detects acute infarct, reclassifies up to half of clinical TIAs

— Noncontrast CT head if MRI unavailable or to exclude hemorrhage acutely (especially before antiplatelets in atypical cases); CT misses most small acute infarcts

— CTA or MRA of head and neck, or carotid duplex + transcranial Doppler

— Identifies carotid stenosis, intracranial stenosis, dissection, occlusion

— Time-sensitive: symptomatic ≥70% carotid stenosis → CEA within 2 weeks

Step 3 management: A TIA patient in the ED gets MRI-DWI + CTA head/neck + ECG + telemetry + labs before disposition. If unavailable in <24 h locally, admit or transfer rather than discharge with outpatient plan.

Board pearl: DWI-positive "TIA" = ischemic stroke, regardless of symptom duration — code, document, and bill accordingly; secondary prevention is identical but reclassification affects rehab and outcomes data.

Goal: within hours of presentation, answer four questions —

Stat labs (every TIA):

ECG:

Brain imaging — preferably MRI with DWI within 24 hours:

Vessel imaging (do not delay):

Diagnostic Workup — Advanced or Confirmatory Studies

— TTE is reasonable in all TIA patients to evaluate LV function, valvular disease, intracardiac thrombus

— TEE preferred when looking for PFO, atrial septal aneurysm, LA appendage thrombus, aortic arch atheroma, endocarditis vegetation — especially in cryptogenic TIA in patients <60

— Bubble study (agitated saline) for PFO; consider in young patients with cryptogenic event

— 30-day event monitor or implantable loop recorder if cryptogenic and embolic-appearing pattern

— EMBRACE and CRYSTAL-AF: extended monitoring detects paroxysmal AF in 9–30%

— Detection changes management → switch from antiplatelet to anticoagulant

— Reserve for: age <50, cryptogenic event, recurrent thrombosis, family history, livedo, miscarriages

— Antiphospholipid antibodies (lupus anticoagulant, anti-β2GPI, anticardiolipin) — most clinically actionable in stroke

— Protein C/S, antithrombin, factor V Leiden, prothrombin G20210A — limited yield in arterial events

— Draw before anticoagulation when possible (heparin/warfarin/DOAC alter assays)

— CTA arch + neck for dissection if neck pain, trauma, young patient

— Vasculitis workup (ANCA, ANA, ESR) if systemic features

— HIV, RPR in young/unusual cases

— Sickle cell screen in appropriate demographics

— MRI vessel wall imaging for intracranial vasculopathy

Key distinction: PFO closure is indicated in patients <60 with cryptogenic stroke/TIA and high-risk PFO features (large shunt, atrial septal aneurysm) — RESPECT, CLOSE, REDUCE trials. Not for older patients with competing vascular risk.

Board pearl: Cryptogenic TIA in a 35-year-old + migraine with aura → bubble study for PFO.

Step 3 management: Do not order thrombophilia panel reflexively in elderly TIA patients with classic atherosclerotic risk factors — low yield, false positives waste resources and may inappropriately trigger lifelong anticoagulation.

Echocardiography:

Prolonged cardiac monitoring for AF:

Hypercoagulable workup — selective, NOT routine:

Other targeted studies:

Risk Stratification — ABCD2 and Beyond

— A — Age ≥60 → 1 pt

— B — BP ≥140/90 at presentation → 1 pt

— C — Clinical features: unilateral weakness 2 pts, speech disturbance without weakness 1 pt, other 0

— D — Duration: ≥60 min 2 pts, 10–59 min 1 pt, <10 min 0

— D — Diabetes → 1 pt

— 0–3 (low): ~1%

— 4–5 (moderate): ~4%

— 6–7 (high): ~8%

— ABCD2 ≥4 → admit for expedited workup and monitoring

— ABCD2 <4 → may be managed in a rapid-access TIA clinic if MRI, vessel imaging, echo, and specialist follow-up within 24 h are achievable; otherwise admit

— Crescendo TIAs, AF, ≥50% symptomatic carotid stenosis, hypercoagulable state → admit regardless of score

— Modest discrimination; may miss high-risk patients with vascular lesions

— Imaging + vessel data trump ABCD2: DWI lesion or symptomatic large-artery stenosis = high risk independent of score

— Updated approaches (ABCD3-I) add dual TIA within 7 days, carotid stenosis, and DWI positivity

— Same-day evaluation with imaging, antiplatelet, statin, BP control → reduces 90-day stroke ~80%

— Reflects current Step 3 outpatient/value-based emphasis

Board pearl: ABCD2 is a triage tool, not a treatment guide — every TIA gets antiplatelet + statin + BP/glucose control + vascular imaging, regardless of score.

Step 3 management: A 62-year-old with HTN, DM, 90-min hemiparesis, BP 160/95 → ABCD2 = 7 → admit, MRI/CTA, telemetry, dual antiplatelet, statin, neurology consult.

Key distinction: A "low" ABCD2 with a symptomatic 80% carotid stenosis is a high-risk patient. Believe the vessels, not the score.

ABCD2 score estimates 2-, 7-, and 90-day stroke risk after TIA:

Score interpretation (2-day stroke risk):

Disposition guidance (general, not absolute):

Limitations of ABCD2 (Step 3 favorite):

EXPRESS-style "TIA clinic" model:

Pharmacotherapy — First-Line Antiplatelet and Statin

— Aspirin 160–325 mg loading then 81 mg daily, started immediately after hemorrhage excluded

— Dual antiplatelet therapy (DAPT) — aspirin + clopidogrel for 21 days then aspirin monotherapy, in:

— High-risk TIA (ABCD2 ≥4) or minor stroke (NIHSS ≤3)

— Start within 24 h of symptom onset (CHANCE, POINT, THALES trials)

— Clopidogrel 300–600 mg load then 75 mg daily

— Ticagrelor + aspirin is an alternative (THALES) for 30 days in similar patients

— Avoid prolonged DAPT >21–30 days — bleeding risk rises without further benefit

— Loss-of-function alleles reduce clopidogrel activation; genotype-guided therapy increasingly used but not yet mandated for TIA on Step 3 — know it exists

— Anticoagulation, not antiplatelet is mainstay (covered in chunk 15)

— Bridge timing: for TIA (no infarct), can often start DOAC within 1–3 days; larger strokes wait longer ("1-3-6-12 rule")

— Atorvastatin 80 mg or rosuvastatin 20–40 mg daily

— SPARCL: atorvastatin 80 reduced recurrent stroke 16% — class I indication regardless of baseline LDL

— Target LDL <70 mg/dL (some guidelines <55 in very high risk)

— Add ezetimibe, then PCSK9 inhibitor if not at goal

— Do not aggressively lower in first 24 h unless >220/120 or end-organ damage

— Long-term target <130/80; thiazide + ACEi combo (PROGRESS trial) particularly effective

Board pearl: Aspirin + clopidogrel for 21 days, then aspirin alone — memorize this regimen for high-risk TIA. Continuing DAPT indefinitely is a wrong-answer trap.

Step 3 management: Start the statin in the ED, not at follow-up — early initiation improves adherence and outcomes.

Acute antiplatelet therapy (non-cardioembolic TIA):

CYP2C19 considerations:

Cardioembolic source (AF, mechanical valve, LV thrombus):

High-intensity statin — start in ED:

BP control:

Procedures — Carotid Revascularization and Cardiac Interventions

— 70–99% stenosis → carotid endarterectomy (CEA) strongly indicated; NNT ~6 to prevent stroke at 2 years (NASCET)

— 50–69% stenosis → CEA reasonable, especially in men, patients >75, recent symptoms

— <50% stenosis → medical therapy only

— Timing: within 2 weeks of index event maximizes benefit; earlier is better but balance against early postop stroke risk in active infarcts

— CEA preferred in age >70 (CREST: lower periprocedural stroke with CEA in elderly)

— CAS reasonable in younger patients, surgically inaccessible lesions, prior neck radiation/surgery, high cardiac risk

— Both require operator volume; periprocedural stroke/death rate must be <6%

— Medical therapy wins over stenting (SAMMPRIS) — aggressive DAPT, statin, BP control

— Stenting reserved for refractory cases at experienced centers

— Patients <60 with cryptogenic stroke/TIA and high-risk PFO features → percutaneous closure + antiplatelet (RESPECT, CLOSE, REDUCE)

— Adds small AF risk; share decision-making

— For AF patients with contraindication to long-term anticoagulation (e.g., recurrent GI bleed)

Board pearl: Symptomatic carotid stenosis 70–99% + TIA last week → CEA within 2 weeks, not "schedule in 2 months."

Step 3 management: While awaiting CEA, the patient must be on aspirin + statin + BP control; do not stop antiplatelet preoperatively. Surgeons operate through aspirin for CEA.

Key distinction: Asymptomatic carotid stenosis (incidental bruit, no TIA) is a different decision tree — usually medical management; CEA only in selected younger patients with >70% stenosis.

Symptomatic carotid stenosis (TIA or stroke in ipsilateral territory within 6 months):

CEA vs. carotid artery stenting (CAS):

Near-occlusion or full occlusion: revascularization generally not beneficial; medical management

Intracranial atherosclerosis:

PFO closure:

Left atrial appendage occlusion (Watchman):

Special Populations — Elderly and Renal/Hepatic Impairment

— Higher absolute stroke risk after TIA → benefit of prevention is greater, but bleeding risk also rises

— Do not withhold antiplatelet, statin, or anticoagulation based on age alone

— Fall risk ≠ contraindication to anticoagulation in AF — modeling shows a patient must fall ~295 times/year for falls to outweigh stroke prevention benefit

— CEA: age >75 is not a contraindication and may actually derive greater benefit (NASCET subgroup)

— Polypharmacy review — check for interactions (clopidogrel + PPIs like omeprazole/esomeprazole reduce activation; prefer pantoprazole)

— Cognitive screen — capacity to adhere to dual antiplatelet, anticoagulation

— Stroke risk increased; bleeding risk also higher

— DOAC dosing (for AF):

— Apixaban: 2.5 mg BID if 2 of 3 — age ≥80, weight ≤60 kg, Cr ≥1.5

— Dabigatran: avoid if CrCl <30

— Rivaroxaban: 15 mg daily if CrCl 15–50

— Edoxaban: avoid if CrCl >95 (paradoxically less effective) and reduce if 15–50

— Hemodialysis + AF: warfarin or apixaban; evidence evolving

— Statins: atorvastatin and fluvastatin do not require renal adjustment; rosuvastatin cap at 10 mg if CrCl <30

— Child-Pugh C: avoid all DOACs; Child-Pugh B: avoid rivaroxaban, others with caution

— Statins generally safe; avoid in active decompensated liver disease

— Warfarin difficult due to baseline coagulopathy

Board pearl: Apixaban dose reduction requires 2 of 3 criteria (age ≥80, weight ≤60, Cr ≥1.5) — a classic Step 3 trap with single-criterion patients getting under-dosed.

Step 3 management: Elderly TIA patient on warfarin with subtherapeutic INR + AF → restart anticoagulation, address adherence, consider switch to DOAC if eligible.

Elderly (≥75):

CKD:

Hepatic impairment:

Special Populations — Pregnancy, Pediatrics, Young Adults

— Stroke risk highest in third trimester and 6 weeks postpartum

— Specific mechanisms: eclampsia/preeclampsia, RCVS, cerebral venous sinus thrombosis (CVST), peripartum cardiomyopathy, paradoxical embolism via PFO, amniotic fluid embolism

— Imaging: MRI without gadolinium preferred; non-contrast CT acceptable with shielding if needed

— Aspirin 81 mg is safe throughout pregnancy and used for preeclampsia prevention

— Avoid warfarin in 1st trimester (embryopathy) and near delivery; LMWH is standard parenteral anticoagulant

— DOACs contraindicated in pregnancy and lactation

— Statins: traditionally contraindicated; FDA has softened language but generally hold during pregnancy

— Cervical artery dissection (especially with neck pain, trauma, chiropractic manipulation) — leading cause of stroke in young adults

— PFO/paradoxical embolism

— Hypercoagulable states — APLS, factor V Leiden

— Vasculitis (Takayasu, primary CNS), moyamoya

— Substance use — cocaine, methamphetamine, cannabis

— Migrainous infarction (rare, diagnosis of exclusion)

— Genetic — CADASIL, Fabry, sickle cell

— OCPs + smoking + migraine with aura = stroke risk triad

— Sickle cell disease — annual transcranial Doppler screening ages 2–16; abnormal TCD → chronic transfusion

— Congenital heart disease, moyamoya, infection (varicella vasculopathy)

Key distinction: Sudden severe headache + neck pain + Horner syndrome + focal deficit in a young patient = carotid dissection until imaging proves otherwise. Treatment: antiplatelet or anticoagulation × 3–6 months (CADISS: equivalent).

Step 3 management: Postpartum woman with TIA-like symptoms + thunderclap headache → MRV/CTV for CVST and consider RCVS; LMWH if CVST confirmed, even with small hemorrhage.

Pregnancy and postpartum:

Young adults (<50) with TIA — broaden differential:

Pediatrics (uncommon TIA but tested):

Complications and Adverse Outcomes

— 3–10% 90-day stroke risk after untreated TIA

— ~50% of post-TIA strokes occur within 48 hours

— Aggressive secondary prevention reduces this by ~80%

— Heralds unstable plaque or ongoing cardioembolism

— Crescendo TIA (≥2 in 7 days) carries impending-stroke risk; admit, heparin bridge considered case-by-case, expedite revascularization

— Repeated subclinical infarcts → multi-infarct dementia

— Step-wise cognitive deterioration distinguishes from Alzheimer's

— Up to 30% within first year; screen with PHQ-9 at follow-up

— SSRIs reasonable; avoid TCAs (anticholinergic, fall risk)

— Bleeding from antiplatelets/anticoagulants — GI most common; intracranial most dangerous

— Statin myopathy (rare rhabdomyolysis), hepatotoxicity (rare)

— CEA complications: stroke (~2–3%), MI, cranial nerve injury (hypoglossal, vagal, marginal mandibular), neck hematoma with airway compromise, hyperperfusion syndrome (headache, seizures, ICH days after CEA)

— CAS complications: periprocedural stroke (higher than CEA in elderly), access site issues, contrast nephropathy

— Patients with TIA generally restricted from driving for a period (state-specific, often 1 month after event with normal exam); commercial drivers longer

Board pearl: Post-CEA severe ipsilateral headache + hypertension + seizure = cerebral hyperperfusion syndrome — aggressive BP control prevents hemorrhagic conversion.

Step 3 management: At every follow-up, screen for depression, adherence, BP, lipids, glucose, AF, and driving status — Step 3 loves the longitudinal cadence.

Key distinction: A new focal deficit in a recent TIA patient on aspirin alone may indicate need for DAPT initiation (if within window) or anticoagulation if newly detected AF.

Ischemic stroke — the dominant complication:

Recurrent TIA:

Cognitive decline and vascular dementia:

Post-stroke depression and anxiety:

Iatrogenic complications:

Aspiration, falls, deconditioning if residual deficits

Driving risk:

When to Escalate — ICU, Consult, Inpatient Triage

— ABCD2 ≥4

— Crescendo TIAs (≥2 in 7 days) or symptoms on current antiplatelet

— Symptomatic carotid stenosis ≥50% or intracranial large-artery stenosis

— AF or other cardioembolic source newly identified

— DWI-positive lesion (= minor stroke)

— Unable to complete workup within 24 h as outpatient

— Hypercoagulable state, suspected dissection, suspected endocarditis

— Fluctuating deficits suggesting impending stroke in progress

— Hemodynamically unstable AF, MI, or aortic dissection

— Post-CEA monitoring for BP lability or hyperperfusion

— Status post tPA if reclassified as stroke

— Neurology — every TIA, ideally vascular neurology

— Vascular surgery — for symptomatic carotid stenosis

— Cardiology — AF, structural heart disease, PFO

— Endocrinology — if poorly controlled DM affecting management

— PT/OT/Speech — even mild residual deficits benefit from rehab evaluation

— ABCD2 <4, no high-risk vascular lesion, no AF

— MRI, vessel imaging, echo, and specialist visit can occur within 24 hours

— Reliable patient, transportation, telephone access

CCS pearl: On a CCS case, after stabilizing and starting aspirin + statin, order MRI brain, CTA head/neck, echo, telemetry, lipid panel, HbA1c, and neurology consult — moving the clock forward without these orders is a common scoring loss.

Step 3 management: Do not discharge a TIA patient from the ED Friday evening with a Monday neurology appointment if MRI/CTA aren't done — the 48-hour stroke window is exactly when they're at risk. Admit or arrange same-/next-day workup.

Board pearl: New AF detected on TIA telemetry → start anticoagulation, stop antiplatelet (unless concurrent CAD indication).

Admit to stroke unit/inpatient for:

ICU/step-down indications (uncommon for pure TIA but possible):

Consultations to anticipate (CCS-style orders):

Outpatient TIA clinic pathway is acceptable only if:

Key Differentials — Same-Category (Vascular) Causes

— Same workup and prevention as TIA; differs only in tissue infarction

— Larger infarcts may qualify for thrombectomy if within 24 h and large vessel occlusion

— Sudden focal deficit but typically progressive headache, vomiting, depressed consciousness, marked HTN

— CT distinguishes immediately — always image before antiplatelet/anticoagulant

— Thunderclap headache, meningismus, often without focal deficit early; CT then LP if CT negative

— Headache + focal deficit + seizure; risk factors include pregnancy, OCPs, dehydration, hypercoagulability

— Diagnosis: MRV or CTV

— Treatment: anticoagulation (LMWH then warfarin) even with small hemorrhagic conversion

— Young, neck pain/trauma, Horner syndrome (carotid) or posterior circulation symptoms (vertebral)

— CTA/MRA neck with fat-sat sequences

— Antiplatelet or anticoagulation × 3–6 months

— Recurrent thunderclap headaches, postpartum or with vasoactive drugs/SSRIs

— "Sausage on a string" angiography

— Calcium channel blockers (verapamil, nimodipine)

— Multifocal deficits, headache, encephalopathy; CSF inflammatory, vessel wall MRI helpful

— Slow march, positive then negative symptoms, headache; family history common

Key distinction: TIA symptoms are maximal at onset and resolve completely. Stroke symptoms persist or progress. SAH/ICH typically have headache and altered mental status. Migraine evolves over minutes.

Board pearl: Any focal deficit + thunderclap headache = CT/CTA → LP if CT negative to evaluate SAH/RCVS/dissection.

Step 3 management: Do not assume "TIA" without MRI + vessel imaging — vascular mimics like CVST and dissection demand different treatment.

Ischemic stroke (DWI-positive):

Intracerebral hemorrhage (ICH):

Subarachnoid hemorrhage:

Cerebral venous sinus thrombosis (CVST):

Cervical artery dissection:

Reversible cerebral vasoconstriction syndrome (RCVS):

Primary CNS vasculitis / systemic vasculitis:

Migrainous aura with deficit (hemiplegic migraine):

Key Differentials — Other-Category (Non-Vascular) Mimics

— Focal deficits possible (especially in elderly, prior strokes); resolves with glucose

— Fingerstick first on every "stroke alert"

— Postictal focal weakness lasting minutes to 36 h

— History of jerking, tongue bite, incontinence, prior seizures; EEG helpful

— Positive visual symptoms (scintillating scotoma) marching over 20–60 min, followed by headache

— Hemiplegic migraine can mimic TIA closely; first episode always warrants imaging

— Inconsistent exam, give-way weakness, Hoover sign positive, non-anatomic sensory loss; diagnosis of exclusion after imaging

— Isolated vertigo without other brainstem signs; HINTS exam (head impulse, nystagmus, test of skew) distinguishes peripheral from central

— Isolated peripheral CN VII (forehead involved) — not a TIA

— Cortical facial weakness spares forehead

— Global hypoperfusion → loss of consciousness, not focal deficit; rare exception is bilateral subclavian/vertebrobasilar disease causing drop attacks

— Diffuse rather than focal, but may unmask old deficits ("recrudescence")

— Usually progressive but can present with seizure or sudden deficit; imaging differentiates

— Subacute, age 20–40, often optic neuritis, internuclear ophthalmoplegia; MRI with demyelinating lesions

Key distinction: Forehead sparing = central (cortical) lesion; forehead involved = peripheral CN VII (Bell). Critical for Step 3 differentiation of stroke from Bell palsy.

Board pearl: Recrudescence — old stroke deficits reappear during infection, hyponatremia, or hypoglycemia. Treat the metabolic cause; symptoms resolve. Don't anticoagulate reflexively.

Step 3 management: A patient with "TIA" who has normal MRI/CTA and inconsistent exam → consider functional disorder; refer to neurology, avoid escalating empirical therapy.

Hypoglycemia:

Seizure with Todd paralysis:

Migraine with aura:

Functional/conversion disorder:

Peripheral vertigo (BPPV, vestibular neuritis):

Bell palsy:

Syncope/presyncope:

Metabolic encephalopathy, hyponatremia, hypercalcemia:

Brain tumor or subdural hematoma:

MS exacerbation:

Secondary Prevention and Discharge Plan

— Non-cardioembolic: aspirin 81 mg indefinite, OR clopidogrel 75 mg, OR aspirin+dipyridamole; DAPT only for 21 days post high-risk event

— Cardioembolic (AF): DOAC preferred (apixaban, rivaroxaban, edoxaban, dabigatran) over warfarin in non-valvular AF

— Warfarin (INR 2–3) for mechanical valve or moderate-severe mitral stenosis

— APLS-related stroke: warfarin INR 2–3 (DOACs inferior — TRAPS trial)

— High-intensity (atorvastatin 80 or rosuvastatin 20–40); target LDL <70

— Add ezetimibe → PCSK9i if not at goal

— Target <130/80

— Preferred agents: ACEi/ARB + thiazide (PROGRESS regimen — perindopril + indapamide)

— HbA1c target individualized, generally <7%

— Pioglitazone reduces recurrent stroke in insulin-resistant non-diabetics (IRIS trial) but weight gain, HF, bladder cancer concerns

— GLP-1 agonists, SGLT2 inhibitors preferred for cardiovascular risk reduction in T2DM

— Smoking cessation — single biggest modifiable factor; offer varenicline/bupropion/NRT

— Mediterranean or DASH diet; sodium <2.3 g/day

— Exercise ≥150 min/week moderate aerobic

— Alcohol ≤2 drinks/day men, ≤1 women; eliminate if recurrent events

— Weight loss if BMI elevated

— OSA screening — STOP-BANG; treat with CPAP

Board pearl: AF + prior TIA = CHA₂DS₂-VASc ≥2 automatically → anticoagulate, not antiplatelet.

Step 3 management: Discharge checklist: antithrombotic, statin, BP regimen, diabetes plan, smoking cessation, neurology follow-up within 1–2 weeks, PCP within 1 week, driving counseling, return precautions ("FAST" — face, arm, speech, time).

Antithrombotic — match to mechanism:

Statin:

Blood pressure:

Diabetes:

Lifestyle (counsel and document):

Vaccinations: influenza, pneumococcal, COVID-19 — reduce systemic inflammation triggers

Follow-Up, Monitoring, Rehab, Counseling

— Primary care within 1 week post-discharge — medication reconciliation, BP, adherence, depression screen

— Neurology within 1–2 weeks for stroke specialist confirmation of plan

— Vascular surgery within days if CEA planned

— Cardiology for AF management, PFO closure discussion

— 3-month and 6-month check-ins for risk factor optimization

— BP — home BP logs; target <130/80

— Lipids — LDL 4–12 weeks after starting statin; reassess every 3–12 months

— HbA1c every 3 months until at goal, then every 6 months

— Renal function and electrolytes with ACEi/ARB/diuretics (1–2 weeks after initiation, then periodically)

— LFTs and CK with statin only if symptomatic

— INR weekly→monthly for warfarin; annual renal function for DOACs (more often if CKD)

— Holter/event monitor results if extended cardiac monitoring ordered

— Even "no residual deficit" patients benefit from PT/OT evaluation — subtle cognitive, balance, fine motor deficits common

— Speech therapy if any language/swallow concern

— Vocational rehab if relevant

— Cardiac rehab for coexisting CAD

— FAST warning signs and call 911 (not the clinic) for new deficits

— Driving restrictions — typically 1 month after TIA with normal exam; commercial drivers per DOT guidance; document the conversation

— Sexual activity, exercise return — generally resume gradually within days for TIA

— Travel, altitude, air travel — usually safe after stable workup

— Medication adherence — discontinuation of antithrombotic is a major cause of recurrent stroke

Step 3 management: Schedule all follow-ups before discharge — transitions-of-care failures (no PCP, no neuro, no med reconciliation) are heavily tested patient-safety items.

Board pearl: Stopping aspirin for elective procedure in post-TIA patient → discuss with neurology; many minor procedures can proceed on aspirin.

Follow-up cadence:

Monitoring parameters:

Rehabilitation:

Counseling — must-cover topics:

Ethical, Legal, and Patient Safety Considerations

— Disclose periprocedural stroke risk (~2–6%), MI, death, cranial nerve injury for CEA

— Shared decision-making essential, particularly PFO closure in cryptogenic stroke where benefit is modest

— Document discussion of medical alternatives

— Variable by state; many states mandate physician reporting of conditions causing loss of consciousness or focal neurologic events to DMV

— Commercial drivers (CDL) — DOT regulations require longer abstinence

— Document the driving conversation in every TIA discharge note — failure to counsel is medicolegally exposed

— TIA may transiently impair judgment, especially with aphasia/neglect

— Reassess capacity before consenting to procedures or against-medical-advice (AMA) departures

— Aphasic patients require augmented communication and possibly surrogate decision-makers; do not equate aphasia with incapacity

— Medication reconciliation at discharge — clarify which antithrombotic, statin dose, BP regimen

— Warm handoff to PCP and neurology; written instructions; teach-back method

— High-risk discharge times: weekends, evenings, after-hours — ensure follow-up appointments are confirmed, not just suggested

— Pillbox, family involvement for cognitively impaired or elderly

— Education on bleeding signs, fall prevention, drug interactions (NSAIDs, fluconazole, amiodarone with warfarin)

— MedicAlert bracelet

— Reversal agents availability: idarucizumab (dabigatran), andexanet alfa (factor Xa inhibitors), 4F-PCC (warfarin)

— Disparities in TIA workup completion in rural/uninsured patients

— Telestroke and TIA pathways improve access; advocate within health system

Board pearl: Aphasia ≠ incapacity — use written/picture aids and reassess; bypassing the patient to family is an ethics violation.

Step 3 management: A TIA patient who insists on driving home from the ED → counsel against, document, offer transportation alternatives; do not physically restrain but consider notifying DMV per state law if pattern persists.

Informed consent for CEA/CAS/PFO closure:

Driving and reporting laws:

Capacity assessment:

Transitions-of-care safety (Step 3 perennial):

Anticoagulation safety:

Equity and access:

High-Yield Associations and Rapid-Fire Facts

— Pure motor (posterior limb internal capsule)

— Pure sensory (thalamus)

— Ataxic hemiparesis, dysarthria-clumsy hand

Board pearl: Sudden monocular vision loss like a "descending curtain" + carotid bruit → carotid duplex same day, plan CEA.

Step 3 management: Every TIA encounter should mentally check: mechanism (LAA/cardioembolic/small vessel/other), score (ABCD2), studies (MRI/CTA/echo/ECG/labs), secondary prevention (antithrombotic, statin, BP, lifestyle), system of care (follow-up, rehab) — the "5 S's."

Amaurosis fugax → ipsilateral internal carotid stenosis; check Hollenhorst plaque on fundoscopy

Aphasia + right hemiparesis → left MCA territory

Hemineglect, dressing apraxia → right (non-dominant) parietal

Wallenberg (lateral medullary) syndrome → PICA territory: ipsilateral Horner, facial sensory loss; contralateral body sensory loss; ataxia, dysphagia, hoarseness

Locked-in syndrome → basilar artery thrombosis affecting ventral pons

Top-of-the-basilar → bilateral occipital, thalamic, midbrain symptoms — vision loss, altered consciousness

Lacunar syndromes (small vessel, HTN/DM):

Carotid dissection → young, neck pain, Horner (ipsilateral ptosis, miosis, anhidrosis spares face if postganglionic)

Vertebral dissection → posterior neck pain, posterior circulation symptoms

CADASIL → autosomal dominant NOTCH3 mutation; recurrent subcortical strokes, migraine, dementia, young adult

Fabry disease → X-linked, α-galactosidase A deficiency; stroke, angiokeratomas, renal disease

Moyamoya → "puff of smoke" collaterals, Asian descent, young

CHANCE/POINT trial → DAPT 21 days for high-risk TIA/minor stroke

NASCET → CEA for symptomatic 70–99% carotid stenosis

CRYSTAL-AF/EMBRACE → extended monitoring detects occult AF

SPARCL → atorvastatin 80 reduces recurrent stroke

PROGRESS → perindopril + indapamide reduces recurrent stroke

IRIS → pioglitazone reduces stroke in insulin-resistant non-diabetics

NIHSS items: LOC, gaze, vision, facial palsy, motor, ataxia, sensory, language, dysarthria, neglect

Board Question Stem Patterns

— 68-year-old with 45 min of right arm weakness and aphasia, now resolved. BP 162/94. HbA1c 7.8. ABCD2 = 6.

— Answer: Admit, MRI-DWI, CTA head/neck, ECG/telemetry, echo, aspirin 325 → 81 + clopidogrel 21 days, atorvastatin 80, BP/glucose management, neurology consult.

— Same patient, CTA shows 80% left ICA stenosis ipsilateral to symptoms.

— Answer: Carotid endarterectomy within 2 weeks + continued aspirin + statin.

— TIA patient on 24-hour telemetry shows 2 minutes of AF.

— Answer: Start DOAC (e.g., apixaban 5 mg BID); stop antiplatelet unless concurrent CAD requires it.

— 35-year-old with migraine, transient right-sided weakness, MRI shows small DWI lesion, CTA normal, ECG normal.

— Answer: TTE with bubble study → PFO with right-to-left shunt → consider PFO closure + antiplatelet.

— 42-year-old with vertigo, ataxia, left Horner after neck manipulation.

— Answer: CTA neck for vertebral/carotid dissection; antiplatelet or anticoagulation × 3–6 months.

— Low ABCD2 but no MRI available locally same/next day.

— Answer: Admit or transfer; do not discharge without imaging in 48-h window.

— Focal weakness with fingerstick glucose 38.

— Answer: D50, recheck; not a TIA.

— Three TIA episodes in 5 days while on aspirin.

— Answer: Admit, escalate to DAPT, urgent vessel imaging, consider heparin bridge per neurology.

Board pearl: The "right answer" usually starts with MRI-DWI + CTA + admit + aspirin + statin — anything skipping urgent vessel imaging is almost always wrong.

Step 3 management: Read the stem for time, vessels, rhythm, score, comorbidities, and pick the option matching evidence-based prevention plus the right disposition.

Pattern 1 — "Resolved deficit, now what?"

Pattern 2 — "Carotid lesion identified"

Pattern 3 — "AF detected"

Pattern 4 — "Young patient, cryptogenic"

Pattern 5 — "Neck pain after chiropractor"

Pattern 6 — "ED disposition"

Pattern 7 — "Mimic"

Pattern 8 — "Crescendo"

One-Line Recap

TIA is a tissue-based ischemic syndrome and a stroke-prevention emergency: stratify with ABCD2 and imaging, complete MRI-DWI + CTA head/neck + ECG/telemetry + echo within 24 hours, and start aspirin (DAPT × 21 days if high risk) + high-intensity statin + BP/glucose control while pursuing mechanism-specific therapy (CEA for symptomatic 70–99% carotid stenosis within 2 weeks, anticoagulation for AF, PFO closure in selected young cryptogenic patients).

Board pearl: "TIA" without MRI-DWI is an unfinished diagnosis — half become minor strokes on imaging, and management is identical: act in the 48-hour window to prevent the next event.

Step 3 management: Close the loop — PCP in 1 week, neurology in 1–2 weeks, vascular surgery promptly if indicated, BP/lipid/A1c targets monitored longitudinally, adherence reinforced; transitions of care are where prevention is won or lost.

Workup core: MRI-DWI, CTA head/neck, ECG + ≥24 h telemetry (extend monitoring if cryptogenic), TTE (TEE/bubble in young), labs including glucose first; selective hypercoagulable workup only in young/cryptogenic.

ABCD2 in 10 seconds: Age ≥60 (1), BP ≥140/90 (1), Clinical (weakness 2 / speech 1), Duration (≥60 min 2 / 10–59 min 1), Diabetes (1); ≥4 = admit, but imaging and vessel findings override the score.

Pharmacology in 10 seconds: aspirin 81 mg lifelong (or clopidogrel); add clopidogrel for 21 days if high-risk TIA/minor stroke; atorvastatin 80 mg (LDL <70); ACEi + thiazide for BP <130/80; DOAC if AF (warfarin if mechanical valve or APLS).

Don't-miss buckets: symptomatic carotid stenosis → CEA in 2 weeks; AF → anticoagulate; dissection in the young; CVST/RCVS postpartum; hypoglycemia and Todd paralysis as mimics; document driving counseling and follow-up at discharge.