Hemorrhagic stroke accounts for approximately 13% of all strokes but causes 30-50% of stroke-related mortality, making it disproportionately lethal. The two major types — intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH) — have distinct pathophysiological mechanisms, clinical presentations, and management approaches. Intracerebral Hemorrhage (ICH): ICH results from rupture of small penetrating arteries within the brain parenchyma, most commonly due to chronic hypertension. Sustained hypertension causes lipohyalinosis (fibrinoid necrosis of arteriolar walls) and formation of Charcot-Bouchard microaneurysms in small perforating arteries of the basal ganglia, thalamus, pons, and cerebellum. When these weakened vessels rupture, blood dissects into the brain parenchyma, forming an expanding hematoma. The hematoma causes injury through two mechanisms: (1) Primary injury: direct mechanical destruction of brain tissue by the expanding blood mass. (2) Secondary injury: the hematoma compresses surrounding tissue (mass effect), increases intracranial pressure (ICP), disrupts the blood-brain barrier, and triggers an inflammatory cascade. Iron and thrombin released from the clot are directly neurotoxic, causing edema that peaks at 3-5 days and extends the zone of injury beyond the original hematoma. Mass effect and herniation: As the...