Cerebral Hyperperfusion Syndrome and Related Conditions

Abstract

Cerebral vasoconstriction is a normal physiological response under determined conditions to preserve a normal cerebral blood flow. However, there are several syndromes, with impaired cerebral autoregulation and cerebral vasoconstriction, not related with infection or inflammation, which share the same radiological and clinical presentation. We review here the cerebral hyperperfusion syndrome and related conditions such as hypertensive encephalopathy, posterior reversible encephalopathy syndrome, and reversible cerebral vasoconstriction syndrome. These syndromes might share the same pathophysiological mechanism with endothelial damage, cerebral vasoconstriction, blood-brain barrier disturbance, cerebral edema, and, occasionally, intracerebral hemorrhage, with fatal cases described in all. Despite knowledge of these syndromes, they still remain unknown to us. Why these entities present in some patients and not in others goes further than the actual understanding of these diseases. We have to consider that a genetic susceptibility and molecular disturbances may be involved. Thus, more studies are needed in order to better characterize such syndromes.

Chemotherapy-associated hemorrhagic posterior reversible encephalopathy syndrome (PRES) with considerations for circle of Willis variants on cerebral blood flow and autoregulation: A case report

“…This hyperperfusion, in turn, can result in endothelial injury, disruption of the blood-brain barrier, and consequent vasogenic edema, especially in the posterior cerebral regions that are less protected by sympathetic innervation. [19] However, there are also cases of PRES where hypoperfusion due to vasoconstriction is suggested as the primary mechanism. Impaired or reduced CBF has been observed in some cases of PRES.…”

A Rare Case of Postoperative Encephalopathy in Twin

“…Mechanistically, the role of BBB permeability, neurovascular autoregulation, and mitochondrial metabolism in developing encephalopathy has been suggested. However, there is a paucity of research expanding on the underlying genetic component involved in those mechanisms [ 1 , 2 , 9 , 10 ]. To our knowledge, this is the first report of postoperative encephalopathy in identical twins.…”

“…There is some literature on mechanisms underlying various etiologies of encephalopathy. For example, at the molecular level, genetic factors that alter mitochondrial metabolism can increase blood-brain barrier (BBB) permeability and subsequently increase the susceptibility to septic encephalopathy in murine models [ 1 ]. On the clinical scale, variations in patient susceptibility to hypertensive encephalopathy raise the question of genetic components involved in endothelial regulation, cerebral vascular autoregulation, and BBB disturbance [ 2 ].…”

Blood Pressure Variability After Cerebrovascular Events: A Possible New Therapeutic Target

“…3,5 When blood pressure exceeds the upper limit of mechanic autoregulation, vasocontraction depends on the sympathetic nervous system. 5 Regulatory vasoconstriction is less effective than vasodilation; although cerebral vessels can increase their caliber up to 65%, vasocontraction does not exceed 10%. e5…”

“…3 It depends on the ability of small arteries, arterioles, and the capillary bed to change their caliber in response to chemical (e.g., nitric oxide, carbon dioxide, and endothelin-1) and mechanical or myogenic factors (increased or decreased transmural pressure). 3,5 When blood pressure exceeds the upper limit of mechanic autoregulation, vasocontraction depends on the sympathetic nervous system. 5 Regulatory vasoconstriction is less effective than vasodilation; although cerebral vessels can increase their caliber up to 65%, vasocontraction does not exceed 10%.…”