Carton, Daly & Ramani: Clinical Pathology 
'Ask the Author' Forum
Figures from the bookCarton, Daly & Ramani: Clinical Pathology
November 2006: Hypertensive encephalopathy
Q. You say that hypertensive encephalopathy occurs because of failure of autoregulation (page 75). Therefore, wouldn't the vessels DILATE (in the face of high BP), resulting in cerebral HYPERperfusion (as opposed to underperfusion)? I'm confused.
A. Under normal circumstances cerebral autoregulation operates to ensure that cerebral blood flow remains constant in the face of any changes in systemic blood pressure. This is achieved by cerebral vessels dilating in response to a fall in systemic blood pressure and constricting in response to a rise in systemic blood pressure (graphical representations of this can be found in any good physiology textbook).
In severe cases of hypertension (typically once systolic blood pressure exceeds 180 mm Hg), cerebral autoregulation fails and the cerebral blood vessels, which have been constricted as much as possible, suddenly became stretched and dilated under the influence of the hypertension. At this point there is indeed marked cerebral hyperperfusion with consequent cerebral oedema, which causes symptoms and signs of a diffuse encephalopathy. Untreated, however, the severe hypertension then causes actual destruction of small cerebral vessels (seen microscopically as fibrinoid necrosis in the vessel walls). This then causes areas of the brain to become underperfused, resulting in ischaemic injury. Clinically this may manifest with focal neurological signs in addition to the diffuse encephalopathy caused by the background cerebral oedema. So in fact hypertensive encephalopathy is associated with both hyper- and hypoperfusion of the brain; the extent of each component is likely to be a dynamic situation within and between individuals.
I hope you find these comments useful.
James Carton
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