The coma in glaucoma: Retinal ganglion cell dysfunction and recovery

Author(s): Fry LE (1), Fahy E (2), Chrysostomou V (3), Hui F (2), Tang J (2), van Wijngaarden P (2), Petrou S (4), Crowston JG (5)

1 Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, VIC, Australia; Monash University, VIC, Australia.
2 Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, VIC, Australia; Ophthalmology, University of Melbourne, Department of Surgery, VIC, Australia.
3 Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, VIC, Australia.
4 Florey Institute of Neuroscience and Mental Health, VIC, Australia; Department of Medicine, University of Melbourne, VIC, Australia.
5 Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, VIC, Australia; Ophthalmology, University of Melbourne, Department of Surgery, VIC, Australia. Electronic address: crowston@unimelb.edu.au.

Retinal ganglion cell (RGC) degeneration causes vision loss in patients with glaucoma, and this has been generally considered to be irreversible due to RGC death. We question this assertion and summarise accumulating evidence that points to visual function improving in glaucoma patients with treatment, particularly in the early stages of disease. We propose that prior to death, RGCs enter periods of dysfunction but can recover with relief of RGC stress.

We first summarise the clinical evidence for vision improvement in glaucoma and then detail our experimental work that points to the underlying processes that underpin clinical improvement. We show that functional recovery can occur following a prolonged course of RGC dysfunction and demonstrate how the capacity for recovery can be modified. Detecting RGC dysfunction and augmenting recovery of such 'comatosed' RGCs holds clinical potential to improve early detection of glaucoma and improve visual function.

Prog Retin Eye Res. 2018 Apr 6. pii: S1350-9462(17)30102-7. doi: 10.1016/j.preteyeres.2018.04.001.

http://www.ncbi.nlm.nih.gov/pubmed/29631042

Keywords: Dendritic remodeling; Glaucoma; Intraocular pressure; Neuroplasticity; Neuroprotection; Neurorecovery; Optic nerve; Recovery of function; Retina; Retinal ganglion cell; Synaptic loss; Visual recovery

Experimental Paper of the Month manager: Andreas Boehm