Mechanisms of axon-glial injury of the optic nerve

Abstract

The central concept underlying ideas on the pathogenesis of multiple sclerosis is that inflammatory events cause acute injury of axons and myclin. The phases of symptom onset, recovery, persistence, and progression in multiple sclerosis can be summarized as functional impairment with intact structure due to direct effects of inflammatory mediators; demyelination and axonal injury with recovery through plasticity and remyelination; and chronic axonal loss due to failure of enduring remyelination from loss of trophic support for axons normally provided by cells of the oligodendrocyte lineage. Cell death may occur in response to a state of injury from which protection would be anticipated under more favourable neurobiological conditions. Conversely, optimal growth factor environment may save cells from otherwise lethal events occurring at the cell membrane. Hence, in the context of brain inflammation, there is an inseparable interplay between immunological and neurobiological contributions to tissue injury.

Retinal nerve fiber layer thickness is associated with brain MRI outcomes in multiple sclerosis

“…In the initial stages, remyelination is observed and function is preserved until a threshold of irreversible axonal damage is reached. However, in the later stages, optic nerve atrophy and clinical visual decline is observed [26]. Our statistical analyses indicated particularly strong associations between RNFLT and NBV.…”

“…Future larger, prospective studies are needed to further explore the correlations with MRI measures, including T2-LV and other inflammatory MRI measures. The pathological spectrum of inflammatory optic neuropathy can provide a window into the etiology and pathogenesis of MS [26]. In optic neuropathy, the disease process is initiated by inflammation and is associated with demyelination.…”

Visual field defects in acute optic neuritis - distribution of different types of defect pattern, assessed with threshold-related supraliminal perimetry, ensuring high spatial resolution

“…There are many recent publications concerning the mechanism of axonal injury and optic nerve atrophy following ON [5,9,21]. The question has also been raised as to whether ON has a predilection for certain axonal areas, thus causing the typical VF pattern [6].…”

Afferent visual pathways in multiple sclerosis: a review

“…Various mechanisms of this damage have been proposed (see for review), including the effect of different substances produced by activated immune and glial cells and ischemic‐mediated axonal damage . Axons transected during acute inflammation continue to degenerate for some months (both retrograde and anterograde) and it takes a considerable time for axonal atrophy to be fully manifested …”