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Necrotizing Leukoencephalopathy (necrotizing + leukoencephalopathy)
Selected AbstractsDisseminated necrotizing leukoencephalopathy following low-dose oral methotrexateEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2007S. Raghavendra Leukoencephalopathy is a recognized complication with intrathecal or intravenous methotrexate (MTX). We report a 59-year-old lady who developed MTX leukoencephalopathy with long-term low-dose oral MTX. She developed posterior leukoencephalopathy (PLE) that initially was reversible on discontinuation of oral MTX. Four months later, she developed disseminated necrotizing leukoencephalopathy (DNL), and was left with devastating neurological deficits. The sequential conventional magnetic resonance imaging (MRI), diffusion weighted imaging (DWI), MR perfusion (MRP) and MR spectroscopic (MRS) changes are highlighted in this report. MRP and MRS showed more wide spread abnormalities than DWI. Stereotactic biopsy from the lesion revealed demyelination with macrophagic infiltration, pericapillary lymphomononucear aggregation, fibrinoid changes in the capillaries and neovascularization. Of the two cases of PLE with oral MTX reported in literature, one reversed clinically and radiologically with the discontinuation of MTX. To the best of our knowledge, this is the first reported case of DNL following oral MTX in the world literature. [source] Methotrexate-related leukoencephalopathy without radiation therapy: Distribution of brain lesions and pathological heterogeneity on two autopsy casesNEUROPATHOLOGY, Issue 2 2009Jun Matsubayashi This report concerns two rare autopsy cases of methotrexate (MTX)-related leukoencephalopathy without radiation therapy. In the first case, there were widespread necrotic foci with prominent spheroids, that is, disseminated necrotizing leukoencephalopathy (DNL), mainly in the cerebral white matter. In contrast, in the second case, there were widespread demyelinated foci without significant axonal changes, which we would like to name disseminated demyelinating leukoencephalopathy (DDL), mainly in the cerebral white matter. We emphasize that the pathology of pure MTX-related leukoencephalopathy is not uniform, and may show at least two kinds of histologic change. Furthermore, both cases did not develop significant vascular changes, which are usually induced by radiation therapy. The distribution of the lesions in two cases was examined by large specimens, including hemisphere specimens. The distribution of the lesions in the brain of our cases was also different. In the first case, the DNL lesions were predominantly distributed in the frontal and temporal lobes. In the second case, the DDL lesions were prominently localized in the occipital lobe. To our knowledge, this is the first report describing not only the pathological findings of MTX-related leukoencephalopathy without irradiation but also the precise distributions of the lesions. [source] Neuropathology of septic shockNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2002F. Gray Introduction:, Septic shock is the most frequent cause of death in intensive care units. It is often complicated by an encephalopathy and there is increasing evidence that central autonomic nervous system (CANS) dysfunction plays a crucial role in the onset and persistance of the haemodynamic failure. However, only a few neuropathological studies are available; they are always retrospective and often disagree. Material and methods:, Twenty consecutive patient who died from septic shock were examined and compared with eight patients who died from nonseptic shock in the same unit and five ,normal' controls collected from the Forensic Medicine Service. Results and conclusion:, A variety of lesions, including microabscesses, multifocal necrotizing leukoencephalopathy, haemorrhages and disseminated intravascular coagulation, were found, and were most probably related to the biological disturbances associated with sepsis. These lesions may contribute to the ,septic encephalopathy'. Ischaemic changes in ,susceptible' areas were comparable in septic shock and in nonseptic shock. In contrast, ischaemic changes in the nuclei of the CANS were significantly more severe in septic shock than in nonseptic shock. Neuronal apoptosis in these nuclei was significantly more frequent and more severe in septic shock; apoptosis did not correlate exactly with neuronal ischaemia and was associated with only mild microglial activation suggesting that circulating factors may also play a role in its causation. [source] |