Clinical meaning
Posterior reversible encephalopathy syndrome (PRES) is a clinico-radiological entity in which acute failure of cerebral autoregulation leads to vasogenic edema predominantly in the posterior parieto-occipital white matter. Cerebral autoregulation normally maintains constant cerebral blood flow across a mean arterial pressure (MAP) range of approximately 60-150 mmHg through myogenic arteriolar constriction and dilation. When MAP exceeds the upper autoregulatory limit — typically >150-160 mmHg in normotensive individuals, though shifted rightward in chronic hypertension — arterioles are forced open, hydrostatic pressure overwhelms the blood-brain barrier (BBB), and plasma proteins and fluid extravasate into the brain parenchyma, producing vasogenic edema. The posterior circulation (vertebrobasilar territory) is preferentially affected because it has significantly less sympathetic adrenergic innervation than the anterior (carotid) circulation; sympathetic tone is a critical component of autoregulatory vasoconstriction, so regions with less innervation have lower autoregulatory reserve. Beyond hypertensive breakthrough, PRES can result from direct endothelial toxicity — calcineurin inhibitors (cyclosporine, tacrolimus) damage the vascular endothelium by increasing endothelin-1 production, decreasing nitric oxide and prostacyclin synthesis, and disrupting tight junction proteins (claudins, occludin) of the BBB, causing vasogenic edema at normal or mildly elevated blood pressures. Similarly, cytotoxic chemotherapy agents (bevacizumab, an anti-VEGF antibody, disrupts VEGF-mediated endothelial survival signaling) and autoimmune endothelial injury (TTP, HUS, eclampsia) can trigger PRES through BBB disruption. On MRI, FLAIR sequences show hyperintense signal in bilateral parieto-occipital white matter. The critical imaging distinction is between vasogenic edema (elevated apparent diffusion coefficient [ADC] on diffusion-weighted imaging, indicating reversible interstitial edema) and cytotoxic edema (restricted diffusion with low ADC, indicating irreversible cellular injury and ischemic infarction). This transition from vasogenic to cytotoxic edema represents the point at which PRES becomes irreversible, explaining why prompt diagnosis and treatment are essential. The NP must recognize the differential diagnosis includes acute ischemic stroke (restricted diffusion in a vascular territory), cerebral venous sinus thrombosis (look for the 'empty delta' sign), and CNS vasculitis, and must integrate imaging findings with clinical context to guide urgent management.