Hypertensive Encephalopathy

The MRI features of the syndrome are characterized by vasogenic edema, which corresponds to bright signal on diffusion-weighted imaging (DWI) sequences as well as on apparent diffusion coefficient (ADC) maps, the latter differentiating vasogenic edema from infarction, because the latter is expected to show decreased signal to accompany the bright signal on DWI. These features are generally reversible, the same as the clinical manifestations, including cortical blindness. The features of the posterior reversible leukoencephalopathy syndrome demonstrate substantial variability, because the MRI changes can also have an anterior location, with gray, as well as white matter involvement, and there may be only partial reversibility.

An important aspect of this disorder that needs to be emphasized is that hypertensive encephalopathy is not a function of the absolute levels of systemic blood pressure elevation but rather of the percentage increase in blood pressure based on the individual patient’s baseline blood pressure. Thus a normotensive person can present with hypertensive encephalopathy after a modest blood pressure elevation, whereas a chronic hypertensive patient may require a severe blood pressure elevation in order to develop the syndrome. Although the majority of patients experience clinical recovery with concomitant resolution of the imaging changes after blood pressure control, there is the potential for persistent deficits to occur as a result of concomitant intracerebral bleeding into the areas of the brain affected by the encephalopathy.

There are a number of clinical as well as imaging variations in patients presenting with hypertensive encephalopathy. One that is occasionally seen is a syndrome predominantly affecting the brainstem and cerebellum, with presentation with headache, nausea, and vomiting, as well as mild and nonspecific brainstem signs, such as gait disturbance, in the setting of florid vasogenic edema, at times involving the whole extent of the brainstem. In some instances, the patient may actually not have any clinical signs of brainstem involvement while having florid vasogenic edema in that area; this highlights the fact that the imaging changes reflect edema, not infarction.

The pathogenesis of the clinical-radiologic syndrome of hypertensive encephalopathy is thought to reflect the effects of an acute increase in blood pressure, leading to fibrinoid necrosis of the arterial wall with increase in the permeability of the blood-brain barrier and loss of cerebral autoregulation, with the end result of formation of vasogenic edema. It is still unclear why most instances predominantly involve the posterior aspects of the cerebral hemispheres. The prevailing theory is that the posterior cerebral circulation has less sympathetic innervation than the anterior circulation, thus making it more prone to vasodilation with development of cerebral edema in the event of a sudden increase in systemic arterial pressure.

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