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Gliosis is a reactive process occurring after some time following most types of central nervous system injuries and is the result of focal proliferation of glial cells, particularly astrocytes.
Although the terms astrocytic gliosis or astrocytosis are often used interchangeably with gliosis, other glial cells, particularly microglia as well as oligodendrocytes and ependymocytes, can also undergo activation in response to injury (see below) and thus the terms are considered synonymous by some authors.
Importantly, gliosis is not synonymous with encephalomalacia, which is the end result of liquefactive necrosis of brain parenchyma following an insult, although radiologically they share some features and they often coexist during the early and intermediate responses to injury, with gliosis waning with time, leaving behind a gliotic scar 1,2. Generally, encephalomalacia should be used to refer to areas of the brain that are missing, whereas gliosis should be used when parenchyma is atrophic and of high T2 signal.
Small areas of gliosis are likely to be asymptomatic, but this depends largely on the area affected. They can, however, serve as a seizure focus.
Astrocytosis involves the proliferation and hypertrophy of astrocytes, through complex molecular and cellular pathways, although, despite this increase in cell number, mitotic figures and markers of mitosis (e.g. Ki 67 or Mib-1 stains) do not demonstrate high proliferation 1,3. Their nuclei enlarge with prominent nucleoli. The cytoplasm becomes more prominently eosinophilic around the nuclei and there is also an increase in the intermediate filaments GFAP, nestin, and vimentin which can be identified immunohistochemically 2,3.
This appearance can mimic a low-grade astrocytoma which may have reactive astrocytes at its margin. Helpful features favoring gliosis over glioma include less marked increase of nuclear to cytoplasmic ratio and more regular spacing of reactive astrocytes throughout the tissue 2.
Microgliosis primarily occurs when the insult is infectious (particularly viral), as the microglial cells, which are not of neuroepithelial origin but are likely derived from monocyte or macrophage precursors, function in antigen presentation 1.
Small or subtle areas may not be visible on CT. If more pronounced it will be seen as an area of white matter hypoattenuation.
Gliosis appears as an area with increased T2/FLAIR signal, somewhat reduced T1 signal and somewhat facilitated diffusion on ADC.