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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 ...
Extracellular brain edema, or vasogenic edema, is caused by an increase in the permeability of the blood–brain barrier. [18] The blood–brain barrier consists of astrocytes and pericytes joined with adhesion proteins producing tight junctions. [1] Return of blood flow to these cells after an ischemic stroke can cause excitotoxicity and ...
If the swelling is untreated, it causes death by brain herniation. [4] The brain swelling is likely a result of vasogenic edema, the penetration of the blood–brain barrier by fluids. [16] This process has been observed in MRI studies. Hypoxia increases extracellular fluid, which passes through the vasogenic endothelium in the brain.
The blood–brain barrier is formed by the brain capillary endothelium and excludes from the brain 100% of large-molecule neurotherapeutics and more than 98% of all small-molecule drugs. [28] Overcoming the difficulty of delivering therapeutic agents to specific regions of the brain presents a major challenge to treatment of most brain disorders.
Impaired cranial venous outflow can lead to increased venous pressure, decreased cerebrospinal fluid (CSF) absorption, brain cortex hypoperfusion, brain edema, blood–brain barrier (BBB) disruption, inflammatory reactions, hemorrhagic complications, and increased intracranial pressure. [1]
The ischemic (ischaemic) cascade is a series of biochemical reactions that are initiated in the brain and other aerobic tissues after seconds to minutes of ischemia (inadequate blood supply). [1] This is typically secondary to stroke , injury, or cardiac arrest due to heart attack .
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 ...