Objective: To characterize the retinohypothalamic tract in the setting of multiple sclerosis and a history of optic neuritis by directly interrogating the functional output of the hypothalamus via body temperature, early morning melatonin suppression, and sleep, fatigue, and depression questionnaires.
Background: Optic neuritis, the hallmark of multiple sclerosis, 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. However, there is no previously published work directly investigating retinohypothalamic dysfunction in MS patients.
Design/Methods: Normal controls and patients with MS, were enrolled in this study. Using a pupillometer with highly selective light frequencies and pupil tracking software, we preferentially stimulate the ipRGCs and measured the consensual light reflex. We also correlate these findings with OCT and other metrics.
Results: Our results indicate that there is retinohypothalamic pathway dysfunction secondary to anterior visual system disease in patients with MS and evidence of ipRGC dysfuncion and ganglion cell layer and inner plexiform layer thinning as well as RNFL thinning on OCT.
Conclusions: Retinohypothalamic dysfunction is a potential contributor to fatigue, depression, and disease burden in multiple sclerosis. Our work indicates a potential contributor to MS symptoms that is amenable to future therapeutic intervention.