engleski

Reversible Posterior Leukoencephalopathy Syndrome

Reversible posterior leukoencephalopathy syndrome was first described by Hinchey et al. in 1996, as a syndrome clinically associated with headache, altered consciousness, seizures and visual symptoms. On brain magnetic resonance imaging (MRI), T2-weighted and diffusion-weighted images, there is hyperintense region in the parietal-occipital lobe involving lesions of the white matter, basal ganglia, brain stem, cerebellum, and gray matter. This syndrome frequently occurs in patients with hypertensive encephalopathy. 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. Initially, this syndrome was believed to be secondary to arterial hypertension, renal disease, or immunosuppressive therapy. However, it has recently been identified in a wide variety of conditions, including eclampsia, hemolytic-uremic syndrome, connective tissue diseases, malignancies, etc. Authors describe a case of a 72-year-old woman with a history of arterial hypertension, who suddenly developed headache, confusion, left homonymous hemianopsia, and left hemiparesis, associated with high blood pressure. Brain MRI revealed extensive white matter lesion in the right parietal and occipital lobe, splenium corpus callosum and left occipital lobe, suggestive of expansive process. However, after extensive diagnostic work-up, diagnosis of reversible posterior leukoencephalopathy was established, connected with arterial hypertension. Following antihypertensive and antiedematous therapy her condition improved. At the moment patient is without neurological symptoms, control brain MRI revealed resolution of the white matter lesion. Early recognizing of this syndrome is of great importance, because prompt medicamentous therapy and distinction from brain tumour can postpone invasive diagnostic procedures (stereotactic brain biopsy).

leukoencephalopathy, arterial hypertension, vasogenic edema, brain tumor

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