Traumatic optic neuropathy (TON) causes visual loss in 2% of patients with traumatic brain injury (TBI). TON includes primary disruption of optic nerve axons and secondary degeneration for example due to subsequent compression. Despite significant research into different treatments including corticosteroids and erythropoietin, no neuroprotective or axonal protective agent has proven benefit. However, where optic nerve compression exists, surgical decompression is standard.
Whist symptomatic visual loss occurs in 2% of patients after TBI, recent evidence suggests that at least 50% of patients with moderate to severe TBI have TON on clinical testing and we hypothesise that the severity of retinal ganglion cell death relates to the extent of global neuronal loss after TBI.
The optic nerve is an accessible CNS tract, formed entirely by axons of retinal ganglion cells located in the inner retina. Optical coherence tomography (OCT) allows direct, non-invasive, assessment of retinal nerve fibre and retinal ganglion cell structural integrity in patients, whilst visual function testing allows detailed characterisation of the functional consequences of any abnormality.
We plan to retrospectively and prospectively assess the effects of time to decompression on functional outcome after traumatic optic nerve decompression by examining records of past patients who have had optic nerve compression and prospectively following patients with traumatic optic nerve compression to relate retinal ganglion cell loss to rapidity of decompression. We also plan to image retinal ganglion cells using OCT as part of the Red Diamond study to relate retinal findings to TBI severity.
Lastly, we plan to add OCT and visual function assessments to the RECOS study to relate retinal findings to the development of CTE.