Spatial and temporal activation of spinal glial cells: role of gliopathy
in central neuropathic pain following spinal cord injury in rats.
Furthermore, chemokines seem to contribute to a reciprocal interaction between neurons, glia, and microglia in a so-called "gliopathy," that is, activation of glial cells and neuroglial interactions as a basis for chronic pain [6-8].
Going back to the proposed hypothesis regarding the role of chemokines in a chronic pain related gliopathy, future research may be directed at cross-correlating alterations in chemokine levels (such as found in the current study) with advanced functional imaging techniques which may become available in order to study such a gliopathy .
Nedergaard, "Glia and pain: is chronic pain a gliopathy?," Pain, vol.
Based on the hypothesis, retinal gliopathy
could be used as a marker of HE.
Therefore, dysregulation of glial functions of activated glial cells can be termed a "gliopathy"  characterized by increased release of gliotransmitters, increased secretion of proinflammatory cytokines, upregulation of membrane-bound receptors/ion channels, and upregulation of transporters.
In particular, persistent activation of astrocytes and microglia after SCI leads to morphologically and functionally altered glial cells in a "gliopathy." Recent clinical studies have found that people with SCI show synaptic reorganization in the cortex, thalamus, and spinal cord following SCI; they also experience below-level neuropathic pain .
Nedergaard, "Gliaandpain: ischronic pain a gliopathy
?" Pain, 2013.