The precise mechanism is<unk>  is not fully understood, it is considered to be related to a problem with the blood vessels of the brain. There are several theories as to why these blood vessels may become inappropriately permeable and allow the surrounding brain tissue to become swollen. The "vasogenic" theory posits that elevated blood<unk> sure overcomes the normal capability of blood vessels in the brain to maintain a normal cerebral blood flow. The excessive<unk> sure damages the endothelial layer and the blood-brain barrier, leading to swelling (edema). The predilection toward the<unk>  brain may be explained by the reduced density of sympathetic innervation in the<unk>  circulation compared to the anterior circulation. The "vasogenic" theory seems to explain the almost 50% of cases of<unk>  where there had been severely elevated blood<unk> sure. It is also called the "breakthrough" theory, or the "hyperperfusion theory". This theory does not explain the edema in many other cases where the blood<unk> sure has been normal or even low; in fact, the edema tends to be more severe in those without abnormally elevated blood<unk> sure. In<unk>  secondary to other causes, the blood vessel damage has been attributed to other mechanisms. 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). Some consider the cytotoxic and immunogenic theories together as a single "toxic" theory. There appears to be a role of cytokines in causing endothelial dysfunction. Finally, according to the "neuropeptide/cerebral vasoconstriction" theory, some specific substances (endothelin 1, thromboxane A2) trigger spasm of the blood vessels with resultant vessel wall damage and edema. The latter hypothesis is supported by the frequent finding of diffuse blood vessel spasms (vasoconstriction) in many people with<unk> , and the evidence for decreased perfusion, although the spasm may also be a consequence of the blood vessel damage rather than the cause. Some, therefore, include the vasospasm in the "toxic" theory. It is considered likely that these multiple mechanisms all potentially play a role in the development of<unk> .
Posterior reversible encephalopathy syndrome
Viral encephalitis
Autoimmune encephalitis
Lymphocytic meningoradiculitis
Limbic encephalitis
Wernicke encephalopathy
Chronic traumatic encephalopathy
Hypertensive leukoencephalopathy