Introduction: Reversible posterior leucoencephalopathy is a clinico radiological syndrome first described in the last decade. The physiopathological mechanism governing it is not very well known. The currently accepted hypotheses are the generation of a vasogenic edema caused by failure of the mechanism that allows self regulation of the cerebral blood flow, and the production of a cytotoxic edema due to ischemia. Both experimental studies carried out in rats and the use of magnetic resonance imaging (MRI) to evaluate the diffusion of cerebral water support the first hypothesis. We report the case of a patient with reversible posterior leucoencephalopathy syndrome that was complicated by areas of cerebral infarction and we review the physiopathological mechanisms involved, basing our analysis on the findings obtained with MRI.
Case report: A female patient was admitted to our hospital because of bilateral transient amaurosis, headaches, vomiting and arterial hypertension. MRI brain scans showed bilateral cortico subcortical lesions in the occipital parietal regions, frontal and right cerebellar hemisphere convexity, with hyperintense signal in T2 and diffusion weighted imaging. Some occipital parietal regions present a diminished signal on the apparent diffusion coefficient map. The patient was treated with intravenous antihypertensive drugs and full recovery was accomplished within 10 days. A month later, according to MRI scans, there were still hyperintense areas in T2 on both occipital lobes, which were compatible with cerebral infarcts.
Discussion: The mechanism that is most frequently involved in this entity is probably vasogenic edema. In our case there were, at the same time, areas of cytotoxic edema that progressed to cerebral infarcts. MRI with sequences that evaluate the diffusion of cerebral water is useful in distinguishing between the two mechanisms.