Fig. 1From: Disseminated necrotizing leukoencephalopathy eight months after alemtuzumab treatment for multiple sclerosisClinical course and histopathology of DNL as well as MS lesions. The clinical course is illustrated in (a) with the expanded disability status scale (EDSS, score ranging from 0 to 10 with higher numbers indicating more severe disability), relapses (red arrows) and MS-specific treatment indicated over time. Clinical stability was achieved with natalizumab (Ntz) and alemtuzumab (Alz), but numerous relapses occurred with interferon beta-1b (IFNb1b) and fingolimod (FTY) treatment. Eight months after alemtuzumab infusions were given, DNL developed (b-h), characterized by multifocal disseminated necrotic lesions within the white matter (arrows in b and c, LFB/PAS), but not grey matter (arrowheads in b). In addition to DNL, typical MS lesions were present (arrowheads in C indicate remyelinated MS lesion). DNL lesions were characterized by acute and complete tissue destruction with a loss of myelin (d, LFB/PAS), oligodendrocytes and astrocytes (e, anti-GFAP), pronounced axonal damage (f, anti-APP, insert shows many APP-positive, brown stained damaged axons in higher magnification) and numerous macrophages (g, KiM1P) in the absence of lymphocytic infiltration (h, anti-CD3). In contrast, MS lesions showed demyelination (i, LFB/PAS) with axonal preservation (not shown), lymphocytic inflammation (j, anti-CD3) and a sparse infiltrate with macrophages (k, KiM1P). Scale bars represent 200 μm in b (valid for b and c) and d (valid for d-i and k) as well as 100 μm in j Back to article page