# Comparison of acute non-visual bright light responses in patients with optic nerve disease, glaucoma and healthy controls

**Authors:** M. Münch, L. Léon, S. Collomb, A. Kawasaki

PMC · DOI: 10.1038/srep15185 · 2015-10-19

## TL;DR

This study found that glaucoma patients, but not those with hereditary optic neuropathy, show reduced acute light responses, particularly in pupil function.

## Contribution

The study identifies distinct non-visual light response differences between glaucoma and hereditary optic neuropathy patients.

## Key findings

- Glaucoma patients showed reduced pupil response to light compared to controls.
- Hereditary optic neuropathy patients had similar melatonin suppression as controls.
- Glaucoma patients experienced increased sleepiness and slower reaction times during light exposure.

## Abstract

This study examined the effect of optic nerve disease, hence retinal ganglion cell loss, on non-visual functions related to melanopsin signalling. Test subjects were patients with bilateral visual loss and optic atrophy from either hereditary optic neuropathy (n = 11) or glaucoma (n = 11). We measured melatonin suppression, subjective sleepiness and cognitive functions in response to bright light exposure in the evening. We also quantified the post-illumination pupil response to a blue light stimulus. All results were compared to age-matched controls (n = 22). Both groups of patients showed similar melatonin suppression when compared to their controls. Greater melatonin suppression was intra-individually correlated to larger post-illumination pupil response in patients and controls. Only the glaucoma patients demonstrated a relative attenuation of their pupil response. In addition, they were sleepier with slower reaction times during nocturnal light exposure. In conclusion, glaucomatous, but not hereditary, optic neuropathy is associated with reduced acute light effects. At mild to moderate stages of disease, this is detected only in the pupil function and not in responses conveyed via the retinohypothalamic tract such as melatonin suppression.

## Linked entities

- **Diseases:** glaucoma (MONDO:0005041), hereditary optic neuropathy (MONDO:0020249)

## Full-text entities

- **Genes:** OPN4 (opsin 4) [NCBI Gene 94233] {aka MOP}, Opn4 (opsin 4 (melanopsin)) [NCBI Gene 30044] {aka 1110007J02Rik, Gm533}
- **Diseases:** ganglion cell injury (MESH:D045888), neuroretinal disease (MESH:D012173), MPS (MESH:D011681), ARS (MESH:D000084063), GL (MESH:D005901), LE (MESH:D020795), HON (MESH:D015418), visual loss (MESH:D014786), optic atrophy (MESH:D009896), glaucomatous optic neuropathy (MESH:D009901), pupil constriction (MESH:D015877), mitochondrial dysfunction (MESH:D028361), SPS (MESH:D016750), disturbances in sleep quality (MESH:D012893), optic nerve injury (MESH:D020221), Depression (MESH:D003866), contraction (MESH:C536214), ocular disease (MESH:D005128), sleepiness (MESH:D000077260)
- **Chemicals:** Melatonin (MESH:D008550), water (MESH:D014867), HON (-), caffeine (MESH:D002110),  (MESH:C110257),  (MESH:D017299)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC4609937/full.md

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Source: https://tomesphere.com/paper/PMC4609937