Assessment of retinal damage in traumatic brain injury

When patients suffer head injuries, they lose nerve cells in the brain. Because the eye is part of the brain, the nerve connecting the two responds to injury in the same way as other nerve cell pathways in the brain.

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What does each milestone mean?

1 = Clinical need
2 = Idea
3 = Proof of concept
4 = Proof of feasibility
5 = Proof of value
6 = Initial clinical trials
7 = Validation of solution
8 = Approval and launch
9 = Clinical use
10 = Standard of care

Aim

This project aims to:

Investigate the time window for acute optic nerve decompression
Develop ophthalmic assessment as an acute and long-term biomarker for TBI severity
Develop ophthalmic assessment as a biomarker for CTE (Chronic traumatic encephalopathy)

Lay Summary

When patients suffer head injuries, they lose nerve cells in the brain. Because the eye is part of the brain, the nerve connecting the two responds to injury in the same way as other nerve cell pathways in the brain, so when patients lose brain cells after a head injury, there is some evidence that they also lose eye cells too. The more severe a head injury, the more brain cells patients lose and we, therefore, expect that patients with more severe brain injuries will also lose more eye nerve cells. We can measure how many nerve cells an eye has by taking specialised laser pictures of the eye, called OCT scans.

We will, therefore, measure how many nerve cells the eye has in patients who have had brain injuries, to see how the number of nerve cells in the eye relates to how severe the brain injury is. We will do this in patients who have had a single severe brain injury, but also in patients who have had multiple mild injuries.

Background

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.

Method

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.