Further Characterization of the Melanopsin-Mediated Pupillary Light Reflex in Multiple Sclerosis

Optic neuritis, the hallmark of multiple sclerosis (MS), causes well-documented dysfunction of the retinogeniculocalcarine, and retinomesencephlic pathways. Recent work in our laboratory indicates that there is dysfunction of the intrinsically photosensitive melanopsin containing retinal ganglion cells (ipRGCs), which are responsible for the vast majority of the input into the retinohypothalamic tract, and to a degree the retinomesencephalic tract. It has been postulated that this dysfunction could contribute to the symptomatology of multiple sclerosis, specifically affecting sleep-wake cycles, sexual drive, glucose homeostasis, and other neuroendocrine reflex arcs. Previous studies have shown dysfunction of this ipRGCmediated retinomesencephalic tract in multiple sclerosis; however, exactly where along this tract the dysfunction lies is undefined.