3.5
出血性卒中 II：病理生理学
当脑血管破裂时，血液会流入周围脑组织，导致脑内出血（ICH），或流入蛛网膜下腔，导致蛛网膜下腔出血（SAH），从而引发出血性脑卒中。由于颅腔是一个刚性空间，血管外血液的突然积聚会迅速增加颅内压，压迫邻近的神经结构，导致即刻的组织损伤和脑灌注受损。
质量效应与原发性损伤
外渗的血液形成血肿，数分钟至数小时…
当脑内的血管破裂时，会发生出血性卒中，导致血液流入脑组织，称为脑内出血（intracerebral hemorrhage，ICH），或流入蛛网膜下腔，称为蛛网膜下腔出血（subarachnoid hemorrhage，SAH）。
随着血液积聚，会形成血肿，导致颅内压升高并压迫邻近的脑组织。
这种受压会损伤脑细胞并扰乱正常的血流，从而导致进一步的损伤。
除了最初的出血外，当血红蛋白和铁等血液成分渗入周围组织时，会发生继发性损伤。这些成分对脑细胞具有毒性，并引发氧化应激和炎症反应。
作为反应，小胶质细胞会释放炎症性细胞因子并产生活性氧，从而加剧细胞损伤并破坏血脑屏障。
在蛛网膜下腔出血（SAH）中，可能会发生血管痉挛或血管持续性狭窄，导致延迟性脑缺血。
与此同时，进入脑脊液的血液可能阻塞引流通路，导致脑积水。
这些相互关联的过程共同导致了严重的脑损伤和长期的神经功能缺陷。
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Q1: What happens to the brain when a blood vessel ruptures during a hemorrhagic stroke?
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.
Q2: How does the hematoma cause damage to brain tissue?
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.
Q3: What are secondary injury mechanisms in hemorrhagic stroke?
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.
Q4: What is vasospasm and how does it complicate subarachnoid hemorrhage?
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.
Q5: How does blood in the cerebrospinal fluid lead to hydrocephalus?
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.
Q6: Why does the blood-brain barrier break down after hemorrhagic stroke?
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.
Q7: How do mass effect and secondary injury work together in hemorrhagic stroke?
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.