Hemorrhagic Stroke ll: Pathophysiology

When a cerebral blood vessel ruptures, blood escapes into brain tissue as intracerebral hemorrhage (ICH) or into the subarachnoid space as subarachnoid hemorrhage (SAH). The accumulated blood forms a hematoma that rapidly increases intracranial pressure and compresses adjacent neural structures, causing immediate tissue injury and impaired cerebral perfusion.

The hematoma expands over minutes to hours, mechanically damaging neurons and glia while distorting white matter tracts. Increased intracranial pressure compresses blood vessels, worsening ischemia and reducing local blood flow. Tissue distortion disrupts normal neural signaling, producing acute neurological deficits.

Secondary injury develops as blood components break down within brain tissue. Hemoglobin degradation releases iron, generating reactive oxygen species that damage membranes, mitochondria, and DNA. Activated microglia release inflammatory cytokines and reactive oxygen species, intensifying injury and disrupting the blood-brain barrier, allowing fluid leakage and promoting vasogenic edema.

Vasospasm is a transient narrowing of cerebral arteries that typically occurs several days after subarachnoid hemorrhage. Free blood within the subarachnoid space irritates blood vessels, precipitating vasospasm and reducing cerebral blood flow. This delayed response can result in delayed cerebral ischemia and additional neurological damage.

In subarachnoid hemorrhage, blood entering the cerebrospinal fluid can obstruct arachnoid granulations or ventricular pathways, impairing cerebrospinal fluid drainage and circulation. This obstruction prevents normal fluid flow, leading to hydrocephalus, which further increases intracranial pressure and contributes to significant neurological injury.

Reactive oxygen species and inflammatory cytokines released by activated microglia damage the blood-brain barrier's structural integrity. This breakdown allows fluid and proteins to leak from blood vessels into surrounding brain tissue, promoting vasogenic edema and worsening the overall injury cascade.

Mass effect from the hematoma causes immediate mechanical compression and ischemia, while secondary injury from blood breakdown products develops over hours to days. Together, these interconnected mechanisms—including oxidative stress, inflammation, vasogenic edema, vasospasm, and impaired cerebrospinal fluid circulation—collectively produce substantial morbidity and long-term neurological deficits.