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phylline or phenylephrine, but it occurs most often in patients with rapidly worsening essential hypertension In eclampsia, which may be considered a special form of hypertensive encephalopathy, and in acute renal disease, particularly in children, encephalopathic symptoms may develop at blood pressure levels considerably lower than those of hypertensive encephalopathy of essential type In eclampsia, the retinal and cerebral lesions are the same as those that complicate malignant nephrosclerosis; in both there is also failure of autoregulation of the cerebral arterioles In the pathogenesis of pre-eclampsia, inhibition of an endothelium-derived relaxing factor by hemoglobin has been postulated by Sarrel and colleagues See page 291 for a discussion of eclamptic seizures Laboratory Features Hypertensive encephalopathy is marked by characteristic changes on CT scanning and MRI The radiologic ndings are often misinterpreted as large areas of infarction or demyelination, but their tendency to normalize over several weeks is remarkable As summarized by Hauser and coworkers, the main nding is a bilateral increase in T2 signal intensity in the white matter on MRI and a corresponding reduced density (edema) on CT, usually concentrated in the posterior part of the hemispheres (Fig 34-29) This condition is one of the causes of reversible posterior leukoencephalopathy These imaging characteristics are due to an accumulation of uid, but unlike the edema in trauma, neoplasm, or stroke there is little or no mass effect and the water does not tend to course along white matter tracts such as the corpus callosum In addition, scattered cortical lesions occur in a watershed distribution and probably correspond to small infarctions These same ndings in the white matter and cortex occur in eclampsia (Fig 34-30) and have been seen in cases of diffuse vasospasm due to sympathomimetic and serotoninergic drugs, discussed further on Finally, it should be mentioned that hypertensive encephalopathy and eclampsia have at times caused subarachnoid hemorrhage Most such cases are not due to the rupture of an intracranial aneurysm and are not as overwhelming as in the latter case; indeed, the headache associated with this form of hemorrhage tends to be much milder than with aneurysmal rupture and it may even be absent Most often the bleeding is mainly a feature of the radiologic examination of the brain as described by Shah The mechanism is obscure In many but not all the cases, the CSF pressure and protein values are elevated, the latter to more than 100 mg/dL in some instances, but there is no cellular reaction Pathophysiology Neuropathologic examination reveals a rather normal-looking brain, but in some cases cerebral swelling, hemorrhages of various sizes, or both will be found In extreme cases, a cerebellar pressure cone re ects an increased volume of tissue and increased pressure in the posterior fossa; in rare instances lumbar puncture appears to have precipitated fatalities Microscopically there are widespread minute infarcts in the brain (with a predilection for the basis pontis), the result of brinoid necrosis of the walls of arterioles and capillaries and occlusion of their lumens by brin thrombi (Chester et al) This is often associated with zones of cerebral edema Similar vascular changes are found in other organs, particularly in the retinae and kidneys Volhard originally attributed the symptoms of hypertensive encephalopathy to vasospasm This notion was reinforced by Byrom, who demonstrated, in rats, a segmental constriction and dil-.

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