Transient Ischemic Attack

complete reference · tissue definition · ABCD2 · DAPT ×21d · carotid + AF workup · admit-vs-discharge logic · Full Card

Symptoms / Associated Sx

• Transient focal neurologic deficit caused by ischemia without acute infarction on imaging (tissue-based definition — the old "<24h" time definition is obsolete; most true TIAs last <1h). Common: unilateral weakness/numbness, dysarthria/aphasia, amaurosis fugax (transient monocular vision loss — "a shade coming down"), homonymous field loss, gait/balance disturbance.

• By the time you see them, the exam is usually normal — diagnosis hinges on history + imaging. A persistent deficit means it is a stroke, not a TIA.

• A TIA is a medical emergency and a warning: risk of stroke is highest in the first 48 hours and first week.

Neg

• Pt denies positive, spreading visual phenomena (scintillations, fortification spectra) followed by headache — argues against migraine aura (TIA produces negative/loss symptoms; aura marches over minutes with positive symptoms, typically younger, recurrent stereotyped episodes)

• No loss of consciousness, tongue-biting, or post-event confusion — argues against seizure with Todd paralysis (focal seizures can mimic TIA but usually have positive motor activity and a post-ictal state)

• No isolated spinning vertigo with tinnitus/hearing change and direction-fixed nystagmus — argues against peripheral vestibulopathy (central causes need posterior-circulation TIA/stroke workup; HINTS exam helps)

• No global gray-out, lightheadedness, or orthostatic trigger — argues against pre-syncope/syncope (those are global hypoperfusion, not focal)

• No persistent deficit on exam and no DWI lesion on MRI — confirms TIA rather than completed stroke (if DWI is positive, reclassify and manage as ischemic stroke)

Social History (SHx)

• Tobacco, alcohol, stimulant/cocaine use (dissection, vasospasm).

• Antiplatelet/anticoagulant adherence; whether the event occurred on therapy ("breakthrough" changes the plan).

• Prior TIA/stroke, known carotid disease, AF; baseline function and fall risk.

Main Etiology

• Large-artery atherosclerosis — carotid stenosis is the key surgically-treatable cause; intracranial atherosclerosis. Cardioembolic — AF, LV thrombus, valvular disease. Small-vessel disease. Less common: arterial dissection (young, neck pain, trauma), hypercoagulable states, hyperviscosity, vasculitis, paradoxical embolism via PFO.

RF

• Modifiable: HTN, AF, diabetes, smoking, hyperlipidemia, carotid stenosis, OSA.

• Non-modifiable: age, prior TIA/stroke, family history.

• Emerging: PFO in younger cryptogenic patients; chronic inflammatory states.

Data

• Non-contrast head CT (excludes hemorrhage/mass mimicking TIA), then MRI with DWI (detects small infarcts — positive in ~30–50%, which reclassifies as stroke and raises recurrence risk; localizes territory)

• Vascular imaging — CTA head/neck or carotid duplex + transcranial Doppler (symptomatic carotid stenosis 50–99% → urgent CEA evaluation)

• ECG + telemetry ≥24h, extended monitoring (Holter/event/loop) if cryptogenic (paroxysmal AF — changes therapy from antiplatelet to anticoagulation)

• TTE ± bubble study (cardioembolic source, PFO/ASD)

• Glucose, CBC, INR/PTT, BMP, fasting lipids, A1c (rule out hypoglycemia mimic; baseline for secondary prevention; coagulopathy)

• ABCD2 score (stratifies 2-day stroke risk — guides admit vs expedited outpatient workup):

  Age ≥601 BP ≥140/901 Clinical: unilateral weakness2    speech disturbance w/o weakness1 Duration ≥60 min2    10–59 min1 Diabetes1

  0–3 low (~1% 2-day) · 4–5 moderate (~4%) · 6–7 high (~8%). ≥4 generally favors admission/observation; any score with crescendo TIAs, carotid stenosis, or AF should be admitted regardless.

DDx

Completed ischemic stroke (persistent deficit or DWI lesion — the central distinction) · migraine with aura (positive, marching symptoms, headache, young) · focal seizure / Todd paralysis (LOC, post-ictal state, positive motor activity) · hypoglycemia (glucose; reverses) · syncope/pre-syncope (global hypoperfusion, not focal) · peripheral vertigo (isolated, nystagmus, normal HINTS-central) · transient global amnesia (isolated anterograde amnesia, repetitive questioning, no other deficit)

Home Meds

• Continue and intensify statin to high-intensity.

• Start/continue antiplatelet (or escalate to DAPT if high-risk and not already anticoagulated).

• Do not abruptly lower BP in the first 24–48h; reconcile any existing anticoagulant and assess whether the event was a breakthrough on therapy.

Plan

Antithrombotic

• High-risk (ABCD2 ≥4) or confirmed TIA → DAPT: aspirin (Bayer) 325 mg load → 81 mg daily PLUS clopidogrel (Plavix) 300–600 mg load → 75 mg daily, continue dual therapy ×21 days only, then single agent (CHANCE and POINT trials reduced recurrent stroke; bleeding risk rises with longer duration).

• Low-risk: aspirin (Bayer) 81 mg daily monotherapy (or clopidogrel 75 mg if aspirin-intolerant).

• If AF identified: anticoagulate — apixaban (Eliquis) 5 mg BID (dose-reduce per age/weight/Cr); since there is no infarct, start promptly. Discontinue antiplatelet unless a separate vascular indication exists.

Risk-factor control

• Atorvastatin (Lipitor) 80 mg PO daily (SPARCL).

• BP: resume/optimize home regimen (e.g. lisinopril, amlodipine, chlorthalidone); long-term goal <130/80 — but avoid aggressive acute lowering.

• Diabetes optimization (A1c-guided); smoking cessation counseling + pharmacotherapy; OSA evaluation.

Source-directed

• Symptomatic carotid stenosis 50–99%: CEA evaluation, ideally within 2 weeks of the event (NASCET — benefit greatest at 70–99%; carotid stenting alternative in select patients).

• Cryptogenic/ESUS: extended cardiac monitoring for occult AF; PFO closure consideration in younger patients with a high-risk shunt.

Always

• PT / OT eval if any residual functional limitation, gait instability, or fall risk; most pure TIAs need no rehab.

• Trend: serial neuro exams (recurrent or persistent deficit = now a stroke → restart the stroke pathway); telemetry; glucose; document ABCD2 and disposition rationale.

• Escalation / disposition triggers: ABCD2 ≥4, crescendo TIAs (≥2 in 24–48h), symptomatic carotid stenosis, or newly-found AF → admit/observe for inpatient completion of workup, do NOT discharge. Deficit recurs and persists → manage as acute ischemic stroke (see stroke card; ICU only if it meets stroke ICU criteria — hemorrhagic conversion post-lysis, malignant edema, airway compromise).

• Discharge checklist: aspirin (Bayer) 81 mg ± clopidogrel (Plavix) 75 mg ×21 days (or apixaban/Eliquis if AF) · atorvastatin (Lipitor) 80 mg daily · BP regimen · diabetes/smoking plan · carotid surgery follow-up if indicated · neurology follow-up within 1–2 weeks · driving counseling · patient education: any recurrent or persistent deficit → call 911 (do not "wait and see").

Red Flags

• Crescendo TIAs (multiple events in escalating frequency) — impending stroke; admit, image vessels urgently, treat aggressively.
• Symptomatic high-grade carotid stenosis — needs CEA within ~2 weeks; do not send to slow outpatient route.
• Persistent deficit on re-exam or DWI lesion — this is a stroke; restart the stroke pathway.
• Newly-diagnosed AF — anticoagulation, not just antiplatelet.
• ABCD2 ≥6 / posterior-circulation symptoms — high short-term stroke risk; low threshold for admission and vascular imaging.

Senior IM Resident Pearls

• "Transient" is reassuring to the patient and alarming to you. The greatest stroke risk is in the next 48 hours — a TIA is the best warning you'll ever get to prevent a stroke. Act on it now.
• The definition is tissue-based, not time-based. Get the MRI-DWI: ~1 in 3 "TIAs" have a lesion and are actually strokes, which changes prognosis and the anticoagulation-timing rules.
• ABCD2 (Age, BP, Clinical, Duration, Diabetes) stratifies 2-day stroke risk: 0–3 low, 4–5 moderate, 6–7 high. Use it to decide tempo of workup — but override it upward for crescendo TIAs, carotid stenosis, or AF.
• DAPT is short and finite: aspirin + clopidogrel for exactly 21 days (CHANCE/POINT), then single agent. Sending a TIA patient home on indefinite dual antiplatelet is a bleeding liability.
• Find the carotid fast. A symptomatic 70–99% stenosis carries a high re-stroke rate that CEA within 2 weeks dramatically reduces — the benefit evaporates if you wait. Image the neck vessels early.
• AF rewrites the prescription — antiplatelet → anticoagulant. Don't anchor on aspirin; monitor telemetry and chase paroxysmal AF in cryptogenic cases.
• Common mistake: discharging a high-risk TIA home with an outpatient MRI "next week." If ABCD2 ≥4, crescendo, carotid disease, or AF — that workup happens inpatient. The stroke you prevent is the cheapest one.
• Common mistake: calling a positive-symptom, marching, headache-associated spell a "TIA." That's an aura. TIAs are negative (loss-of-function) events.