[1] The predilection for the basal ganglia can be explained by the abundance of astrocytes and large metabolic demand of this area, with the classic MRI findings thought to occur as a result ofthe
gemistocyte (swollen, reactive astrocyte) accumulation, hyperviscosity, neuronal dysfunction and possible cytotoxic oedema.
Some foci had gemistocyte aggregation and a few ganglion cells that were accompanied by mild infiltration of chronic inflammatory cells throughout (figure 2, B).
(3) The tumor we describe belongs in this category, although our case is unique in view of our distinguishing findings of the absence of fibrosis and neuronal tissue and the presence of abundant gemistocytes, mild vascular proliferation, perivascular cuffing, mild cellular anaplasia, and mitoses.
Possible hypotheses for putaminal T1 hyperintensity include a protein hydration layer in the swollen
gemistocytes, putaminal petechial hemorrhage, demyelination, transient ischemic changes, and localized Wallerian degeneration (5).
Currently, hyperviscosity is suggested to be the most plausible mechanism because of the following findings [14]: elevated serum osmolarity at the time of HH, variable T2-weighted MR signal changes that reflect the difference in patterns and severity of hyperviscosity, and elevated myoinositol and choline levels seen on MR spectroscopy that are in line with a finding of abundant
gemistocytes with increased protein content [14-17].
These authors explain T1 hyperintensity from the protein hydration layer inside the cytoplasm of swollen gemistocytes appearing after an acute cerebral injury.
Other authors suggest that high T1 signal could be related to manganese accumulation on gemistocytes [9].
At the end of all this process, astrocytes are stimulated and observation of
gemistocytes which are swelled reactive astrocytes and neuronal loss and gliosis in the striatal region in acute and chornic injuries in autopsy studies is explained in this way (9,11).
Changes were characterized by white matter spongiosis with numerous digestion chambers containing phagocytosing myelinophages and scattered interstitial
gemistocytes. No inflammatory reaction was detected.
Histologically, they consist of bland spindle-shaped and polygonal fibrous astrocytes, or large cells with glassy, eosinophilic cytoplasm, similar to
gemistocytes of subependymal giant cell astrocytoma.
Gemistocytes were first described by Franz Nissl as glia (gemaestete glia) with voluminous cytoplasm.
Additional features, if present (1) Hemosiderin deposition (2) Calcification (3) Microcyst formation (4) Mitotic activity (5) Pleomorphism (6) Presence of
gemistocytes (7) Vascular proliferation (8) Necrosis d.