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The ultimate consequence of cytotoxic edema is the oncotic death of neurons. [1] The swelling of the individual cells of the brain is the main distinguishing characteristic of cytotoxic edema, as opposed to vasogenic edema, wherein the influx of fluid is typically seen in the interstitial space rather than within the cells themselves. [20]
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 ...
While there is strong evidence that vasogenic edema plays a major role in HACE, cytotoxic edema, cellular retention of fluids, may contribute as well. [13] [18] Cytotoxic edema may be caused by the failure of cellular ion pumps, which results from hypoxia. Then intracellular sodium and osmolarity increase, and there is an influx of water that ...
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 ...
The "cytotoxic" theory suggests that it is direct cell damage by toxins (usually medications) that precipitates the edema. The "immunogenic" theory suggests a role for the immune system (specifically T cells). [1] [5] Some consider the cytotoxic and immunogenic theories together as a single "toxic" theory. [4]
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 behind the increase in intracranial pressure due to decreased resorption of cerebrospinal fluid (CSF).
Although it is well known that gradient echo imaging can detect hemorrhage, it is best detected with SWI. In the example shown here, the gradient echo image shows the region of likely cytotoxic edema whereas the SW image shows the likely localization of the stroke and the vascular territory affected (data acquired at 1.5 T).