Brain ischemia is a condition in which there is insufficient bloodflow to the brain to meet metabolic demand. This leads to poor oxygen supply in the brain and may be temporary such as in transient ischemic attack or permanent in which there is death of brain tissue such as in cerebral infarction (ischemic stroke).

The symptoms of brain ischemia reflect the anatomical region undergoing blood and oxygen deprivation, and may involve impairments in vision, body movement, and speaking.

An interruption of blood flow to the brain for more than 10 seconds causes unconsciousness, and an interruption in flow for more than a few minutes generally results in irreversible brain damage. In 1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to an hour can be at least partially recovered. Accordingly, this discovery raised the possibility of intervening after brain ischemia before the damage becomes irreversible.

The clinical presentation of brain ischemia varies depending on the affected vascular territory. Ischemia in the anterior circulation, particularly branches of the internal carotid artery, may present with unilateral weakness, speech disturbances, or visual loss in one eye (amaurosis fugax).Posterior circulation ischemia, involving the vertebrobasilar arteries, often leads to symptoms such as vertigo, diplopia, dysarthria, or bilateral motor deficits.Transient symptoms may indicate a TIA, while prolonged or severe cases may progress to permanent deficits due to cerebral infarction. Sudden loss of consciousness can occur when cerebral blood flow ceases for over 10 seconds, and irreversible brain damage generally follows within minutes.

Brain ischemia results from conditions that reduce or block cerebral blood flow. Common causes of focal ischemia include arterial thrombosis due to atherosclerosis, embolism from cardiac sources such as atrial fibrillation, and small vessel disease associated with hypertension or diabetes. Global ischemia usually arises from systemic hypoperfusion following cardiac arrest or severe hypotension. Additional risk factors include smoking, hyperlipidemia, advanced age, and a history of TIA or stroke. Rare etiologies include sickle cell anemia, which promotes vascular occlusion, and Moyamoya disease, a progressive cerebrovascular disorder affecting the intracranial arteries.

When blood supply to the brain is compromised, neurons are deprived of oxygen and glucose necessary for aerobic metabolism. This leads to rapid depletion of adenosine triphosphate (ATP) within minutes. The failure of ATP-dependent ion pumps disrupts electrochemical gradients, resulting in cellular depolarization and an influx of calcium. Elevated intracellular calcium triggers glutamate release, proteolysis, and ultimately, neuronal injury. Surrounding the infarcted core is the 'ischemic penumbra,' a zone of hypoperfused tissue that retains some metabolic activity and may be salvageable with timely intervention.

Diagnosis of brain ischemia begins with prompt clinical assessment of neurological deficits, often using tools such as the NIH Stroke Scale. Immediate brain imaging is essential to confirm ischemia and exclude hemorrhage. Noncontrast computed tomography (CT) is typically the first step due to its availability and speed. Magnetic resonance imaging (MRI) with diffusion-weighted imaging offers higher sensitivity for detecting acute ischemia. Additional studies, including CT or MR angiography and carotid Doppler ultrasound, help identify vascular occlusions or stenosis. Cardiac evaluation, such as echocardiography and ECG monitoring, may be necessary in cases with suspected embolic sources.

Focal brain ischemia occurs when a blood clot has occluded a cerebral vessel. Focal brain ischemia reduces blood flow to a specific brain region, increasing the risk of cell death to that particular area. It can be either caused by thrombosis or embolism.^{[citation needed]}