Cerebral edema, cytotoxic

Cerebral ischemia causes not only reversible and then irreversible loss of brain function, but also cerebral edema (Symon et al. 1979 Hossman 1983). Ischemic edema is partly cytotoxic and partly vasogenic. Cytotoxic edema starts early, within minutes of stroke onset, and affects the gray more than the white matter, where damaged cell membranes allow intracellular water to accumulate. Vasogenic edema, which starts rather later, within hours of stroke onset, affects the white matter more, where the damaged blood-brain barrier allows plasma constituents to enter the extracellular space. Ischemic cerebral edema reaches its maximum in two to four days and then subsides over a week or two. 

Corticosteroids have been evaluated in several types of cerebral injury, including cerebral infarction. Corticosteroids reduce vasogenic edema, such as that associated with neoplasms, but not cytotoxic edema, the type associated with ischemic stroke. A large meta-analysis found no benefit to the use of corticosteroids in ischemic stroke (or intracerebral hemorrhage), and their use is not recommended, except to treat concomitant conditions that mandate it (e.g., COPD flare). 

Earliest proof of an ischemic situation on MRI can be obtained within seconds after stroke onset by perfusion imaging (PI), depicting the area of reduced cerebral blood flow (Fig. 8.2 see also Chap. 6). This is followed within minutes by a rapid delineation of the early ischemic injury (cytotoxic edema) on DWI. Focus of this chapter will be on data acquired in animal ischemia models, using PD-w, Tl-w, and T2-w MRI, and their correlation with histopathology. 

Approximately 25% of patients with TIA have cerebral infarction with transient signs in which DWI positivity corresponds to cytotoxic edema this progresses to permanent parenchymal injury and increased tissue water content visible as a lesion on T2-weighted MRI. Approximately 20% of patients have early DWI abnormality but no evidence of later T2-weighted abnormality. This suggests reversibility of the initial DWI abnormality if blood flow is restored early enough to prevent permanent parenchymal injury, as seen in patients with stroke in whom the DWI-detected lesion may regress with reperfusion. 

Cerebral tissue acidosis following ischemia or flaumatic brain injury contributes to cytotoxic brain edema formation. In vitro lactacidosis induces swelling of glial cells by intracellular Na" - and Cl accumulation by the Na" /H+-antiporter, Cr/HCOs antiporters, and the Na -K -2C1 cotransport (Staub et al., 1990 Ringel et al., 2006a). 

T cell activation and can interfere with cytoskeletal components that prevent interleukin-2 sjmthesis and release. Cytotoxic edema caused by acute cerebral ischemia is associated with reduced diffusion, reflecting the failure of membrane sodium pumps. Altered electrolyte or fluid balance can precede the onset of encephalopathy. This can be shown by fluid-attenuated inversion recovery and diffusion-weighted MRI images (36). 

BBB disruption and development of vasogenic edema. Decreased perfnsion pressnre and decreased cerebral blood flow lead to the failnre of the Na /KVATPase pump, which then leads to cytotoxic edema [74]. Parenchymal hndings on MR include cerebral swelling, venons infarctions, and gross or petechial intracranial hemorrhage, often in a nonarterial distribution. 

Increased venous pressure leads to increased intracranial pressure, decreased perfusion pressure, decreased cerebral blood flow, and cytotoxic edema... 

The pathophysiology of CVT is not completely clear. The predominant theory is that venous obstruction results in increased venous pressure, increased intracranial pressure, and increased cerebral blood volume. Increased venous pressure may result in vasogenic edema from breakdown of the blood brain barrier and extravasation of fluid into the extracellular space. Blood may also extravasate into the extracellular space. Decreased perfusion pressure and decreased cerebral blood flow may lead to the failure of the NaVKV ATPase pump and then to cytotoxic edema. Another theory is that higher pressure of thrombosed sinuses... 

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