Cerebrovascular Disease & Hemorrhage

Stroke types and ischemic mechanisms

Definition and split. Stroke is a sudden focal neurologic deficit of vascular cause. About 87% are ischemic (thrombotic, embolic, or lacunar) and 13% hemorrhagic (intracerebral or subarachnoid). Infarcted brain undergoes liquefactive necrosis: enzymes digest the lipid-rich, collagen-poor tissue into a fluid-filled cavity. A transient ischemic attack (TIA) is a brief focal deficit without infarction and often precedes stroke.

Thrombotic stroke. Thrombus forms on atherosclerotic plaque at branch points (carotid bifurcation, MCA). Occlusion is gradual, often with a stepwise course and prior TIAs, and the infarct is pale (anemic).

Embolic stroke. An embolus, classically from atrial fibrillation or carotid plaque, lodges suddenly, so the deficit is maximal at onset. Emboli favor the MCA, may hit multiple territories, and the infarct can become hemorrhagic when the clot lyses and blood reperfuses dead tissue.

Lacunar infarcts. Small deep strokes from lipohyalinosis and microatheroma of penetrating arteries, driven by chronic hypertension and diabetes. They strike the internal capsule (pure motor), the thalamic VPL (pure sensory), the pons, and the basal ganglia.

Watershed infarcts. Border zones between the ACA–MCA and MCA–PCA territories are the last fields reached by two arterial supplies, so they die first during severe hypotension or hypoperfusion (shock, cardiac arrest). ACA–MCA border-zone infarcts weaken the proximal arms (shoulders) more than the legs, a "man-in-a-barrel" pattern; MCA–PCA border zones in visual cortex cause visual deficits.

The evolving infarct

Core and penumbra. The infarct core dies quickly, but the surrounding ischemic penumbra is reversibly injured tissue kept marginally alive by collaterals. Rapid reperfusion (tPA, thrombectomy) rescues the penumbra, the basis of "time is brain."

Selective vulnerability. Neurons are the most sensitive cells to hypoxia; the hippocampus, neocortex, cerebellar Purkinje cells, and watershed zones are injured first.

Histologic timetable. Microscopic changes follow a predictable sequence, useful for dating an infarct.

Acute ischemic stroke management

Image first. A non-contrast head CT is obtained immediately to exclude hemorrhage; early ischemia may look normal on CT, whereas diffusion-weighted MRI detects it sooner.

Reperfuse. Give IV tPA within 3 to 4.5 hours of onset if there is no contraindication. Mechanical thrombectomy for a large-vessel occlusion extends the treatment window.

tPA is contraindicated when CT shows bleeding; giving a thrombolytic into a hemorrhagic stroke is catastrophic.

Spontaneous hemorrhage: intracerebral and subarachnoid

Hypertensive intracerebral hemorrhage. The most common spontaneous ICH, from rupture of Charcot-Bouchard microaneurysms of the lenticulostriate vessels. The basal ganglia (putamen) is the classic site, followed by the thalamus, pons, and cerebellum.

Cerebral amyloid angiopathy. β-amyloid deposits in cortical vessel walls cause recurrent lobar (not deep basal ganglia) hemorrhages in normotensive elderly patients; it is a common cause of spontaneous lobar ICH.

Subarachnoid hemorrhage (SAH). Usually a ruptured saccular (berry) aneurysm, most often at the anterior communicating artery; these aneurysms arise at circle of Willis branch points where the arterial media is weak. SAH causes a sudden thunderclap "worst headache of life" with nuchal rigidity. CT shows blood in the basal cisterns; if CT is negative, lumbar puncture reveals xanthochromia. Associations are ADPKD, Ehlers-Danlos syndrome, and Marfan syndrome.

A posterior communicating artery aneurysm can compress CN III, causing a palsy with a blown pupil.

Complications of SAH.

• Early rebleeding.
• Vasospasm at days 3–10 causing delayed ischemia; nimodipine helps prevent it.
• Communicating hydrocephalus from impaired CSF resorption.

The aneurysm is secured by surgical clipping or endovascular coiling.

Traumatic hematomas and the four bleeds

Epidural hematoma. Arterial bleeding from the middle meningeal artery after a temporal bone fracture at the pterion. A lucid interval precedes rapid deterioration. CT shows a biconvex (lens-shaped) hematoma that does not cross suture lines, where the dura is tightly attached. Uncal herniation compresses CN III and blows the pupil; this is a neurosurgical emergency.

Subdural hematoma. Venous bleeding from torn bridging veins, seen in the elderly and in alcoholics (brain atrophy stretches the veins) and in shaken infants, who often also have retinal hemorrhages. CT shows a crescent-shaped collection that crosses suture lines. Onset is gradual with fluctuating consciousness.

Subdural blood crosses suture lines but not the midline (limited by the falx); epidural blood can cross the midline but not sutures.