The primary cause of hypertensive encephalopathy is thought to be fluid extravasation through the inter-stitium, resulting from overdistension of the distal small cerebral vessels (breakthrough of autoregulation) causing vasogenic edema . Ischemic processes can be triggered by vasospasm of the cerebral arteriole in response to a severe increase in blood pressure (overregulation). This will usually result in infarctions. Hypertensive encephalopathy is a clinical syndrome in which morphological and clinical phenomena are not correlated to each other. However, plasma proteins, including fibrin, are deposited in the walls of small arteries (hypertensive vascu-lopathy). This process leads to destruction of smooth muscle cells (fibrinoid necrosis).
The most common abnormality is seen in bilateral parieto-occipital subcortical white matter. However, these lesions can occur in the gray matter but can also involve the frontal lobes, basal ganglia,thalamus, cerebellum and brain stem. They are potentially reversible; however, if left untreated, permanent neurologic deficits or even death may occur as a result of ensuing cerebral infarction or hemorrhage. The prognosis probably depends on the extent of cytotox-ic edema, which may be seen in severe cases. DW im-
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