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transient ischemic attack

NeurologyNervous systemCardiovascular systemEye (retina)

Summary

A transient ischemic attack (TIA) is a transient episode of focal neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia WITHOUT acute infarction (tissue-based definition; no DWI lesion). Symptoms typically resolve within minutes to <1 hour (classically defined as <24 h), and TIA is a major warning sign for stroke, with the highest risk in the first 48 hours.

Detail

**Definition** - Tissue-based definition (AHA/ASA 2009): transient neurologic dysfunction from focal ischemia of brain, spinal cord, or retina without acute infarction. The old time-based definition was <24 h. Most TIAs last <1 h. If MRI DWI shows infarct, it is a stroke even if symptoms resolved.

**Pathophysiology** - Transient interruption of blood flow with reperfusion before irreversible neuronal death. Mechanisms mirror ischemic stroke: - Large-artery atherosclerosis with artery-to-artery embolism (e.g., carotid bifurcation plaque), or hemodynamic low flow from stenosis. - Cardioembolism (atrial fibrillation, LV thrombus after MI, valvular disease/endocarditis, patent foramen ovale with paradoxical embolism). - Small-vessel (lacunar) disease from lipohyalinosis in hypertension and diabetes. - Less common: dissection, hypercoagulable states, vasculitis, sickle cell disease.

**Clinical presentation (by vascular territory)** - Carotid/anterior circulation (MCA/ACA): contralateral weakness or sensory loss, aphasia (dominant hemisphere), neglect (nondominant hemisphere), and amaurosis fugax (transient monocular vision loss, "curtain coming down" from ophthalmic artery emboli, ipsilateral to the lesion). - Vertebrobasilar/posterior circulation: vertigo, diplopia, dysarthria, ataxia, dysphagia, bilateral or crossed deficits, and homonymous hemianopia (PCA). Isolated vertigo is rarely a TIA. - Symptoms are sudden onset, negative (loss of function), and maximal at onset. This contrasts with migraine aura (positive symptoms that march) and seizure (positive, spreading motor activity, then postictal Todd paralysis).

**Diagnosis/workup (urgent, ideally within 24 h)** - Immediately: check glucose to exclude hypoglycemia (a mimic), ECG, and vitals. - Noncontrast CT head to exclude hemorrhage. MRI with DWI is preferred to detect infarct, which would reclassify the event as stroke. - Vascular imaging of head and neck: CTA, MRA, or carotid duplex ultrasound. - Cardiac evaluation: telemetry/prolonged rhythm monitoring for AF, and echocardiography (TTE, ± TEE/bubble study for PFO). - Labs: lipids, HbA1c, CBC, coagulation studies. - Risk stratification: ABCD2 score (Age ≥60, BP ≥140/90, Clinical features: unilateral weakness = 2, speech disturbance without weakness = 1, Duration ≥60 min = 2, 10–59 min = 1, Diabetes). Higher scores mean greater short-term stroke risk. Current guidelines favor prompt evaluation of all TIAs rather than relying on ABCD2 alone.

**Management** - Antiplatelet therapy: aspirin, or short-term dual antiplatelet therapy (aspirin + clopidogrel for ~21 days) for high-risk TIA (ABCD2 ≥4) or minor stroke (CHANCE/POINT trials), followed by single antiplatelet therapy. - Anticoagulation if atrial fibrillation (DOACs preferred, e.g., apixaban, over warfarin in nonvalvular AF). - Carotid revascularization: carotid endarterectomy for symptomatic stenosis of 70–99% (benefit also for 50–69% in select patients), ideally within 2 weeks of the event. Carotid stenting is an alternative in selected patients (e.g., high surgical risk). - Risk-factor control: high-intensity statin, BP control, diabetes management, smoking cessation, diet/exercise. - Thrombolysis (alteplase/tenecteplase) is NOT indicated for a fully resolved TIA. It is used for acute ischemic stroke within 4.5 h of last known well, when there are persistent disabling deficits.

**Prognosis/high-yield points** - About 5% of patients have a stroke within 2 days, and ~10–15% within 90 days, with the highest risk in the first 48 hours. - TIA is a medical emergency, and the term "mini-stroke" should be avoided. - Amaurosis fugax = retinal TIA from ipsilateral carotid disease. Hollenhorst plaques (cholesterol emboli) may be seen on funduscopy. - Carotid bruit is an unreliable sign. - Subclavian steal syndrome causes vertebrobasilar TIA symptoms with arm exercise, along with a BP differential between arms. - Mimics: hypoglycemia, migraine aura, seizure with Todd paralysis, syncope, peripheral vertigo, and demyelination (MS). - Differentiate from stroke: a TIA has no persistent deficit and no infarct on DWI.

Sources

  • First Aid for the USMLE Step 1 (Neurology: Stroke/Vascular)
  • Pathoma / Robbins & Cotran Pathologic Basis of Disease (CNS cerebrovascular disease)
  • AHA/ASA Scientific Statement: Definition and Evaluation of TIA (Easton et al., Stroke 2009)
  • AHA/ASA 2021 Guideline for Prevention of Stroke in Patients with Stroke and TIA
  • CHANCE and POINT trials (dual antiplatelet therapy after minor stroke/TIA)
  • UWorld Step 1/Step 2 CK Question Bank (Neurology)
  • Harrison's Principles of Internal Medicine (Ischemic Stroke chapter)

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