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For example, when cytotoxic edema occurs in the endothelial cells of the blood–brain barrier, oncotic cell death contributes to loss of integrity of the blood–brain barrier and promotes the progression to vasogenic edema. [8] When brain edema types are combined, there is typically a primary form and the edema type and context of the cause ...
High-altitude cerebral edema (HACE) is a medical condition in which the brain swells with fluid because of the physiological effects of traveling to a high altitude. It generally appears in patients who have acute mountain sickness and involves disorientation, lethargy, and nausea among other symptoms.
Cerebral edema is mainly classified into cytotoxic edema, vasogenic edema and interstitial edema. Cytotoxic edema affects both the white and gray matter and results from the swelling of cellular elements such as neurons, glia and endothelial cells. Vasogenic edema affects white matter and results from blood brain barrier (BBB) breakdown ...
ARIA-E refers to cerebral edema, involving the breakdown of the tight endothelial junctions of the blood-brain barrier and subsequent accumulation of fluid. [3] In a double-blind trial of the humanised monoclonal antibody solanezumab (n = 2042), sixteen patients (11 taking the drug, 5 taking a placebo), or 0.78% developed ARIA-E.
According to the over-regulation conception, brain vessels spasm in response to acute hypertension, which results in cerebral ischemia and cytotoxic edema. [14] [15] According to the autoregulation breakthrough conception, cerebral arterioles are forced to dilate, leading to vasogenic edema. [12] Cerebral edema can be generalized or focal ...
Instead, it is most commonly associated with hemorrhage of small vessels in the cerebral cortex. [2] The strongest risk factor for intraparenchymal hemorrhage associated with cerebral amyloid angiopathy is old age, and cerebral amyloid angiopathy is most frequently seen in patients who already have, or will soon be diagnosed with, dementia. [3]
The "vasogenic" theory posits that elevated blood pressure overcomes the normal capability of blood vessels in the brain to maintain a normal cerebral blood flow. The excessive pressure damages the endothelial layer and the blood–brain barrier, leading to swelling (edema).
The thrombosis of the veins themselves causes venous infarction (damage to brain tissue due to a congested and therefore insufficient blood supply). This results in cerebral edema (both vasogenic and cytotoxic edema), and leads to small petechial haemorrhages that may merge into large haematomas. Thrombosis of the sinuses is the main mechanism ...