Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.

Mechanisms of Transient Cerebral Ischemia

Transient cerebral ischemia may arise through several mechanisms. One mechanism involves atherosclerotic plaque within large extracranial or intracranial arteries. Plaque may significantly narrow the vessel lumen, impairing perfusion. Symptoms can emerge during episodes of systemic or relative hypotension, when blood pressure falls below the level needed to sustain adequate flow through the stenotic region. In some cases, a plaque surface becomes unstable and forms a small thrombus that temporarily occludes the artery before spontaneously fragmenting or dissolving.

A second mechanism involves embolic obstruction. Emboli may originate from the heart—commonly due to atrial fibrillation, ventricular thrombi, or valvular disease—or from ulcerated atherosclerotic plaque in major arteries, particularly at the carotid bifurcation. Once an embolus travels to the cerebral circulation and briefly lodges in an artery, it blocks local blood flow until it migrates or dissolves.

A third mechanism occurs in the setting of high-grade stenosis of the carotid or vertebral arteries. When these vessels are severely narrowed, cerebral perfusion becomes flow-dependent. Even modest reductions in systemic blood pressure can drop perfusion below the threshold required for normal neuronal function, producing transient ischemic symptoms.

Across all mechanisms, symptoms resolve once perfusion is restored. However, TIAs indicate significant underlying vascular disease and warrant urgent evaluation to prevent subsequent ischemic stroke.