Hypertensive crisis Reversible edema in leukoencephalopathy, retinopathy, now myelopathy?

The definition of the clinicoradiologic syndrome posterior reversible leukoencephalopathy syndrome (PRES) has been stretched over the last decade.(1) Many regard PRES as a final common denominator for various cerebral insults, without a single etiopathogenic trigger.(1,2) The hallmark of classic PRES is hydrostatic pressure breakthrough causing cerebral vasogenic edema, commonly coupled with a history of refractory hypertension, ictal surge in blood pressure (BP), and a concomitant systemic inflammatory or uremic process.(1) High BP may be absent in PRES if there is renal failure; infection or any systemic inflammatory response syndrome; or immunomodulation as seen in eclampsia, autoimmune disorders, or chemotherapy.(1-3) PRES may thus be better defined as a neurotoxic syndrome(2) with blood-brain barrier opening or with disruption of cerebral autoregulation leading to dysperfusion with either vasogenic or cytotoxic edema.(2,3) The phenotypic umbrella of PRES now includes transient, isolated splenial edematous lesions(4) and extensive spinal cord edema. A mounting number of cases of longitudinally extensive central cord edema in the absence of infectious, demyelinating, or ischemic causes or venous engorgement from an arteriovenous fistula now warrant codifying this entity as a discrete clinical syndrome and perusal for specific risk factors