Investigating the structure and function of the retinohypothalamic tract in multiple sclerosis by optical coherence tomography (OCT) and pupillometry
ECTRIMS Online Library. Sguigna P. 10/04/13; 34620; P1140
Disclosure(s): Teresa Frohman has received speaker and consultant fees from Biogen Idec, Novartis and Acorda
Dr. Shin Beh reports no disclosures.
Dr. Calabresi has provided consultation services to Novartis, EMD-Serono, Teva, Biogen-Idec; and has received grant support from EMD-Serono, Teva, Biogen-Idec, Genentech, Bayer, Abbott, and Vertex.
Dr. Laura Balcer has received honoraria for consulting on development of visual outcomes for MS trials from Biogen-Idec, Novartis, Acorda, Vaccinex and Bayer. She is on a clinical trial advisory board for Biogen-Idec.
Dr. Elliot Frohman has received speaking and consulting fees from Biogen Idec, TEVA Neuroscience, Acorda, Bayer, and Novartis. He has received consulting fees from Biogen Idec, TEVA Neuroscience, Acorda, Novartis, and Abbott Laboratories.
Ethan Meltzer has nothing to disclose.
Peter Sguigna has nothing to disclose.
Amy Conger has nothing to disclose
Darrel Conger has nothing to disclose.
Victoria Stokes has nothing to disclose.
Peter Sguigna
Contributions
Contributions
Abstract
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.
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.
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.
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.
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