Spectrum and Potential Pathogenesis of Reversible Posterior Leukoencephalopathy Syndrome

Uremic Encephalopathy: MR Imaging Findings and Clinical Correlation

“…13,14 Several pathologic studies reported cytotoxic edema in posterior reversible encephalopathy syndrome associated with fibrinoid necrosis and microinfarction 32 and suggested a causal relationship between cytotoxic edema and larger areas of vasogenic edema. 33 However, in this study, there was no significant difference in the extent of vasogenic edema between groups with cytotoxic edema and other groups with vasogenic edema in basal ganglia lesions.…”

Cytotoxic Edema in Posterior Reversible Encephalopathy Syndrome: Correlation of MRI Features with Serum Albumin Levels

“…A correlation between the presence of vasculopathy and ischemia was recently reported, suggesting a causal relationship between cytotoxic edema and larger areas of vasogenic edema. 26 The normally protective vasoconstrictive response can progress into vasospasm, leading to local hypoxia, BBB disruption, fluid extravasation, and subsequent edema. 27 Enhanced systemic endothelial activation (swelling) and leukocyte trafficking and vasoconstriction, alone or in combination, may result in brain and systemic hypoperfusion.…”

“…A larger area of edema is typically contiguous and crosses large vessel boundaries, rather than being a watershed pattern. 26 The mass effect induced by larger areas of vasogenic edema would compress or shift the vessels passing through or around the edema region, which may result in regional hypoperfusion, elevation of tissue pressure, and reduction of CBF to ischemic levels, as well as vasoconstriction. 5,28 Subsequently, the areas surrounding marked vasogenic edema may progress to cytotoxic edema.…”

Blood–retina-barrier disruption accompanying blood–brain-barrier dysfunction in posterior reversible encephalopathy syndrome

“…[1] Forced dilatation of cerebral arteries and disruption of the integrity of the blood-brain-barrier is considered as one of the mechanisms that underlie vasogenic edema observed in hypertensive PRES, which manifests as contrast enhancement within the lesions on imaging studies [2,3]. Alternatively, ischemia triggered by systemic inflammation, endothelial injury and vascular dysfunction is also suggested to contribute to vasogenic edema observed during PRES [4].…”

“…Alternatively, ischemia triggered by systemic inflammation, endothelial injury and vascular dysfunction is also suggested to contribute to vasogenic edema observed during PRES [4]. Regardless of the exact inciting pathophysiology, if we consider vasogenic edema and parenchymal hemorrhage -which not uncommonly complicates PRES -as the most downstream events during the course of blood-brain-barrier dysfunction [2,3], it is plausible to expect the presence of a large amount of cerebral tissue with more subtle impairments in blood-brain-barrier integrity during the course of sudden blood pressure elevations that have not proceeded to the phase of vasogenic edema. On the other hand it is also very well known that the blood-retina-barrier highly resembles the blood-brain-barrier both anatomically and functionally, and pathophysiologic conditions affecting the cerebral circulation might lead to similar disturbances in the retinal microcirculation, as well [5].…”