Reversible Posterior Leukoencephalopathy Syndrome
نویسندگان
چکیده
Hinchey et al used the term „reversible posterior leukoencephalopathy syndrome“ in 1996 to describe a syndrome characterized by headache, confusion, seizures and vision disturbances, including cortical blindness, connected with reversible changes on brain magnetic resonance imaging (MRI) which pointed to the white matter eodema, predominantly in the posterior brain regions (1). Initially, this syndrome was believed to be secondary to arterial hypertension, with or without hypertensive encephalopathy, renal disease, or immunosuppressive therapy, such as cyclosporin A, tacrolimus and interferon-α. However, it has recently been identified in a wide variety of conditions, including eclampsia, hemolytic-uremic syndrome, connective tissue diseases, vasculitis, malignancies, chemotherapy, transfusions, intravenous immunoglobulin (IVIG) therapy, therapy with erythropoietin, thrombotic thrombocytopenic purpura, porphyria, etc. (2-14). The normal response of the cerebral arterioles to acute rising blood pressure is sympathetic nerve-mediated vascular constriction to prevent increasing blood flow (autoregulation). But in the case of reversible posterior leukoencephalopathy syndrome, the response does not work well when there is excess high pressure or recent onset of a modest increase in blood pressure, and excess dilatation of the arterioles following disruption of cerebral small vessel endothelial cells (i.e., the blood-brain barrier) can occur, resulting in vasogenic brain edema. Therefore, disruption of cerebral vascular endothelial cells plays a critical role in the pathogenesis of reversible posterior leukoencephalopathy syndrome In this article we describe a case of a patient with clinical signs and neuroradiological presentation typicial for reversible posterior leukoencephalopathy syndrome.
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