Gliosis
Updates to Article Attributes
Gliosis is the focal proliferation of glial cells in the CNS in response to insult. By strict definition, gliosis
Terminology
Gliosis is not synonymous with encephalomalacia which is the end result of liquefactive necrosis of brain parenchyma following an insult. Radiologically they share similarsome features and the distinction is often only of academic interest. Gliosis and encephalomalaciathey often coexist during the early and intermediate responses to injury, with gliosis waning with time 1.
Clinical presentation
- asymptomatic
- serve as a focus of seizure
Pathology
Glial cells constitute the non-neuronal component of the CNS, outnumbering the neurones 10:1, and are divided into two main groups: microglia and macroglia 1:
- microglia
- macroglia
Astrocytes and the microglia are the glial cells predominantly responsible for tissue response to injury. Astrocytosis involves the proliferation and hypertrophy of astrocytes, through complex molecular and cellular pathways. 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.
Radiographic features
MRI
Gliosis appears bright on T2 as well as FLAIR unlike encephalomalacia which follows CSF signal on all sequences.
See also
-<p><strong>Gliosis </strong>is the focal proliferation of glial cells in the CNS in response to insult. By strict definition, gliosis is not synonymous with <a href="/articles/encephalomalacia">encephalomalacia</a> which is the end result of liquefactive necrosis of brain parenchyma following an insult. Radiologically they share similar features and the distinction is often only of academic interest. Gliosis and encephalomalacia often coexist during the early and intermediate responses to injury, with gliosis waning with time <sup>1</sup>.</p><h4>Clinical presentation</h4><ul>- +<p><strong>Gliosis </strong>is the focal proliferation of glial cells in the CNS in response to insult.</p><h4>Terminology</h4><p>Gliosis is not synonymous with <a href="/articles/encephalomalacia">encephalomalacia</a> which is the end result of liquefactive necrosis of brain parenchyma following an insult. Radiologically they share some features and they often coexist during the early and intermediate responses to injury, with gliosis waning with time <sup>1</sup>. </p><h4>Clinical presentation</h4><ul>
-</ul><p><a href="/articles/astrocytes">Astrocytes</a> and the <a href="/articles/microglia">microglia</a> are the glial cells predominantly responsible for tissue response to injury. Astrocytosis involves the proliferation and hypertrophy of astrocytes, through complex molecular and cellular pathways. 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 <sup>1</sup>. </p><h4>Radiographic features</h4><h5>MRI</h5><p>Gliosis appears bright on T2 as well as FLAIR unlike encephalomalacia which follows <a title="CSF" href="/articles/cerebrospinal-fluid-1">CSF</a> signal on all sequences.</p><h4>See also</h4><ul>- +</ul><p><a href="/articles/astrocytes">Astrocytes</a> and the <a href="/articles/microglia">microglia</a> are the glial cells predominantly responsible for tissue response to injury. Astrocytosis involves the proliferation and hypertrophy of astrocytes, through complex molecular and cellular pathways. 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 <sup>1</sup>. </p><h4>Radiographic features</h4><h5>MRI</h5><p>Gliosis appears bright on T2 as well as FLAIR unlike encephalomalacia which follows <a href="/articles/cerebrospinal-fluid-1">CSF</a> signal on all sequences.</p><h4>See also</h4><ul>
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