edema

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Related to cytotoxic edema: Vasogenic edema
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Cytotoxic edema is the accumulation of fluid within glia, neurons, and endothelial cells most commonly due to hypoxia and usually starts within minutes of injury.
MSUD phenotypes with alterations in different anatomic brain regions Phenotype Total patients Supratentorial area Basal ganglia Classic 6 5 6 Intermittent 3 2 0 Thiamine-responsive 1 1 1 Phenotype Thalamus Pons Mesencephalon Cerebellum Classic 4 5 5 5 Intermittent 0 2 0 2 Thiamine-responsive 0 0 0 0 Involved brain regions show intramyelinic edema or cytotoxic edema; intermittent form and thiamine-responsive form present with increased signal at T2-FLAIR in the affected areas.
Evidence for cytotoxic edema in the pathogenesis of cerebral venous infarction.
MK decreased in the frontal lobe and thalamus at 30 min, which suggests a reduction in overall diffusional heterogeneity and is likely due to the following three factors: (1) ethanol can cause local cerebral ischemic and hypoxic injury in the early stage, decreasing the activity of [Na.sup.+], [K.sup.+] ATPase [9]; at the same time, ethanol disturbs intracellular energy metabolism, increasing the influx of [Ca.sup.2+] [28, 29], which jointly leads to cytotoxic edema; (2) it produces massive oxygen radical, has lipid peroxidation, and damages cell membrane [28]; (3) immunoreaction of the organization exists.
It has been reported that cytotoxic edema is decreased by the suppression of AQP4 but, on the contrary, the vasogenic type is worsened [40], suggesting that water clearance from the extracellular space is channeled through this protein.
Two main mechanisms in the pathophysiology of posterior reversible encephalopathy syndrome include vasospasm and cytotoxic edema, accompanied by increased blood pressure and disruption in cerebral autoregulation, and development of vasogenic edema (2).
The treatment of first choice for patients developing vasogenic edema includes the reduction of blood pressure and supportive measures, whereas the treatment of patients suffering from acute stroke who developed cytotoxic edema and infarction requires a more aggressive therapy, applying the treatment protocols for other etiologies, for instance, subarachnoid hemorrhage with vasospasm [14].
Eventually, the continued rise in venous pressure overcomes the arterial inflow pressure, ultimately leading to cytotoxic edema. (3) Cerebral edema can exacerbate the degree of venous obstruction leading to a cyclical cascade of edema and further cerebral venous obstruction.
Post traumatic brain edema is one of the pathophysiologic events occurring late as a secondary injury mechanism, and is thought to be generated in part by vasogenic edema due to blood brain barrier (BBB) breakdown and in part by cytotoxic edema (Koshinaga, 2000; Esen et al., 2003).
Concurrently, increased apparent diffusion coefficient (ADC) values were demonstrated in the periphery compared with normal brain tissue (Figure 1(e)), indicating vasogenic edema rather than cytotoxic edema. Follow-up MRI of brain was performed 3 weeks later, which showed lesions worsened and extended in both T1WI (Figure 2(a)) and T2WI (Figure 2(b)).
(19) In acute stage there is cytotoxic edema, leading to restricted diffusion and Low ADC value (Apparent diffusion coefficient).
An increased DWI signal combined with a decreased ADC and a decreased or normal FLAIR, indicates the presence of cytotoxic edema, which used to be seen in much lower percent of eclampsia cases [26].
(16) At the earlier time points (vasogenic edema), AQP4 has a positive effect in preventing edema formation by inhibiting water channels, but later in the course of the disease (cytotoxic edema), it has a key role in water clearance from the brain into blood vessels.
These lesions may be complicated by cytotoxic edema (lowering or pseudonormalizing ADC values) and/or hemorrhage.
(2008) to evaluate whether interstitial or cytotoxic edema is responsible for the development of DDS.
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