Circadian rhythm dysfunction in glaucoma: A hypothesis

Girardin Jean-Louis¹^,2^,3^,4 , Ferdinand Zizi¹^,2^,3^,4 , Douglas R Lazzaro¹ and Arthur H Wolintz¹

¹Department of Ophthalmology, SUNY Downstate Medical Center, New York, USA

²Sleep Disorders Center, Department of Neurology, SUNY Downstate Medical Center, New York, USA

³Brooklyn Research Foundation on Minority Health, Kingsbrook Jewish Medical Center, New York, USA

⁴Brooklyn Center for Health Disparities, SUNY Downstate Medical Center, New York, USA

author email corresponding author email

Journal of Circadian Rhythms 2008, 6:1doi:10.1186/1740-3391-6-1


Published:	10 January 2008

Abstract

The absence of circadian zeitgebers in the social environment causes circadian misalignment, which is often associated with sleep disturbances. Circadian misalignment, defined as a mismatch between the sleep-wake cycle and the timing of the circadian system, can occur either because of inadequate exposure to the light-dark cycle, the most important synchronizer of the circadian system, or reduction in light transmission resulting from ophthalmic diseases (e.g., senile miosis, cataract, diabetic retinopathy, macular degeneration, retinitis pigmentosa, and glaucoma). We propose that glaucoma may be the primary ocular disease that directly compromises photic input to the circadian time-keeping system because of inherent ganglion cell death. Glaucomatous damage to the ganglion cell layer might be particularly harmful to melanopsin. According to histologic and circadian data, a subset of intrinsically photoresponsive retinal ganglion cells, expressing melanopsin and cryptochromes, entrain the endogenous circadian system via transduction of photic input to the thalamus, projecting either to the suprachiasmatic nucleus or the lateral geniculate nucleus. Glaucoma provides a unique opportunity to explore whether in fact light transmission to the circadian system is compromised as a result of ganglion cell loss.