Stroke (Ischemic, Hemorrhagic & TIA)

About 87% of strokes are ischemic — an artery is occluded and the territory beyond it loses blood flow. Roughly 10–15% are hemorrhagic — a vessel ruptures and bleeds into the brain parenchyma (intracerebral hemorrhage, ICH) or into the subarachnoid space (SAH). From the bedside they can look identical: a sudden focal deficit in a vascular territory.

Yet the treatments are exact opposites. Ischemic stroke is treated by restoring flow — thrombolysis, mechanical thrombectomy, then antithrombotics. In hemorrhagic stroke thrombolysis is never given and anticoagulants exacerbate the bleeding — care is blood-pressure lowering, reversal of any anticoagulation, and surgery when indicated. The drug that saves one patient kills the other.

That is why the noncontrast head CT is the hinge of every acute stroke pathway: emergency brain imaging happens on arrival, before treating, because hemorrhage must be excluded before IV alteplase can even be considered — thrombolysing a bleed makes it worse. Everything the stroke team does in the first hour is organized around reaching that fork fast.

Ischemic occlusion comes in three flavors: thrombotic — the obstruction forms within the affected vessel itself (atherosclerosis, dissection, fibromuscular dysplasia, inflammatory disease); embolic — circulating debris formed elsewhere lodges in a cerebral vessel; and lacunar — infarcts of the small penetrating arteries in subcortical regions, which generally lack collateral circulation. Large-artery atherosclerosis is the most common substrate for thrombosis, and in atrial fibrillation a thrombus forms in the fibrillating atria and dislodges into the arterial supply — the classic cardioembolic source.

Downstream of the occlusion, two zones form. Tissue that depended on that single artery infarcts — the infarct core. Surrounding it, the ischemic penumbra still receives partial flow through collateral circulation and is salvageable; brain cells begin to die when perfusion falls below roughly 30% of normal (< 15 mL/100 g/min). The penumbra is the entire point of acute stroke care: it is brain that can still be rescued, but only while the collaterals hold.

This is what "time is brain" means — every minute counts because the penumbra is converting to core for as long as the artery stays blocked. Timely revascularization is the goal of every acute-stroke pathway, and it also explains a counterintuitive nursing rule: acute ischemic stroke impairs cerebral autoregulation, so the penumbra’s perfusion depends directly on systemic blood pressure — which is why an alarming-looking BP is often deliberately left alone (permissive hypertension, below).

Hemorrhagic injury unfolds in two phases. The primary injury is mechanical: the expanding hematoma compresses brain tissue and raises intracranial pressure. The secondary injury follows — inflammation, blood–brain-barrier disruption, edema, and free-radical overproduction continue damaging tissue after the initial bleed.

And the bleed is rarely finished at presentation. Hematoma expansion occurs within 3–12 hours — about one-third of hematomas expand within the first 3 hours, more than 70% of ICH cases show expansion within the first 24 hours, and 26% of patients show enlargement within an hour of the initial CT. This is why the first hours of hemorrhagic stroke are pure vigilance: serial neuro checks, aggressive blood-pressure control, and reversal of any anticoagulant.

Where the bleed sits tells you why it happened. Hypertension is the leading cause (over 60% of primary bleeds): chronically high pressure ruptures the small penetrating arteries (50–700 μm), producing nonlobar hemorrhage in the basal ganglia, thalamus, pons, and cerebellum. Cerebral amyloid angiopathy — amyloid-β stiffening small-to-medium cortical vessels — produces lobar ICH in older adults. Anticoagulants, arteriovenous malformations, ruptured aneurysms, and vasculitis account for the rest.

A transient ischemic attack is now defined by tissue, not the clock: a transient focal deficit without acute infarction or tissue injury. Symptoms generally last under an hour (patient materials say up to 24 hours) — the "mini-stroke" where blood supply to part of the brain is briefly blocked and the deficit resolves. But you cannot tell a TIA from a stroke at onset, so the patient goes to the hospital immediately, every time.

A TIA is the warning shot: stroke risk is highest in the first 48 hours, and while comprehensive treatment holds 90-day stroke risk to about 5%, approximately 20% of patients may experience a stroke within 3 months if appropriate evaluation and treatment are not initiated. Treatment reduces recurrence risk by at least 80% — a TIA worked up urgently is one of medicine’s best prevention opportunities. The ABCD2 score (Age > 60 · BP ≥ 140/90 · Clinical features · Duration · Diabetes) stratifies that risk, and a score of 4 or more warrants admission.

The workup is a hunt for the source: brain MRI with diffusion weighting within 24 hours, urgent vessel imaging (CTA/MRA from aortic arch to vertex), echocardiography — and ECG with prolonged rhythm monitoring, primarily to find paroxysmal atrial fibrillation. Finding afib changes everything, because it reveals the cardioembolic chain that antiplatelets alone cannot break.