3.5
AVC hémorragique II : physiopathologie
Un AVC hémorragique se développe lorsqu’un vaisseau cérébral se rompt, permettant au sang de s’échapper dans le tissu cérébral environnant, comme lors…
Un AVC hémorragique survient lorsqu’un vaisseau sanguin du cerveau se rompt, entraînant une hémorragie dans le tissu cérébral appelée hémorragie intracérébrale, ou CHI, ou dans l’espace sous-arachnoïdien, appelée hémorragie sous-arachnoïdienne, ou SAH.
À mesure que le sang s’accumule, il forme un hématome, qui augmente la pression intracrânienne et comprime le tissu cérébral proche.
Cette compression endommage les cellules cérébrales et perturbe la circulation sanguine normale, entraînant d’autres lésions.
Au-delà du saignement initial, une lésion secondaire survient lorsque des composants sanguins tels que l’hémoglobine et le fer fuient dans les tissus environnants. Ces composants sont toxiques pour les cellules cérébrales et déclenchent un stress oxydatif et une inflammation.
En réponse, la microglie libère des cytokines inflammatoires et génère des espèces réactives de l’oxygène, aggravant les dommages cellulaires et compromettant la barrière hémato-encéphalique.
Dans la SAH, un vasospasme ou un rétrécissement prolongé des vaisseaux sanguins peut survenir, provoquant une ischémie cérébrale retardée.
Par contre, le sang entrant dans le liquide céphalorachidien peut bloquer les voies de drainage, conduisant à l’hydrocéphalie.
Ensemble, ces processus interconnectés entraînent des lésions cérébrales importantes et des déficits neurologiques à long terme.
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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.