Histopathologically AS shows degenerative features like hemorrhage,
hemosiderin pigmentation, cellular atypia, areas of myxoid degeneration.7 In present case also all the histological features were noted accompanied by Antoni A and B cellular configuration with verocay bodies.
Histological examination of the excision piece described characteristics compatible with PVNS, with areas of extensive necrosis and the presence of
hemosiderin deposits.
Microscopic features of IPM, as fascicles of spindle cells with nuclear palisading, amianthoid fibers,
hemosiderin pigment, and extravasated erythrocytes, were observed in our case.
Hemosiderin was not detected in the areas of necrosis.
Although a nonrecognizable cerebellar hemisphere in the posterior fossa mimicked primary cerebellar agenesis [4], T2 star-weighted angiography (SWAN) successfully detected
hemosiderin deposits enveloping the cystic lesion, which led to the diagnosis of an acquired form of DWM and selection of a surgical intervention approach.
This showed acute tubular necrosis and significant deposition of
hemosiderin, as shown by positive Perls staining.
The inflammatory cells included lymphocytes, plasma cells,
hemosiderin eaden macrophages and numerous eosinophils.
Multiple punctate foci of bloom artifact projecting predominantly in the cortex in the right hemisphere as noted on GRE sequences represent
hemosiderin deposition in areas of cerebral microhemorrhage (Figure 4).
Hemosiderin is often observed secondary to rupture of the vessels.
Lymphoplasmacytic infiltrates, xanthoma cells,
hemosiderin, and calcification were observed.
Some dotted low signals were noted in the bilateral basal ganglia lesions regions, which indicated old microbleeds and
hemosiderin deposition instead of calcifications.