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Glaucoma as a neurodegenerative disease is a valid working hypothesis to understand neural injury in the visual system. This paradigm may stimulate the discovery of innovative intraocular pressure-independent strategies to help prevent loss of vision in glaucoma patients.

Diabetes mellitus (DM) is a global epidemic and affects populations in both developing and developed countries, with differing health care and resource levels. Diabetic retinopathy (DR) is a major complication of DM and a leading cause of vision loss in working middle-aged adults. Vision loss from DR can be prevented with broad-level public health strategies, but these need to be tailored to a country's and population's resource setting. Designing DR screening programs, with appropriate and timely referral to facilities with trained eye care professionals, and using cost-effective treatment for vision-threatening levels of DR can prevent vision loss. The International Council of Ophthalmology Guidelines for Diabetic Eye Care 2017 summarize and offer a comprehensive guide for DR screening, referral and follow-up schedules for DR, and appropriate management of vision-threatening DR, including diabetic macular edema (DME) and proliferative DR, for countries with high- and low- or intermediate-resource settings. The guidelines include updated evidence on screening and referral criteria, the minimum requirements for a screening vision and retinal examination, follow-up care, and management of DR and DME, including laser photocoagulation and appropriate use of intravitreal anti-vascular endothelial growth factor inhibitors and, in specific situations, intravitreal corticosteroids. Recommendations for management of DR in patients during pregnancy and with concomitant cataract also are included. The guidelines offer suggestions for monitoring outcomes and indicators of success at a population level.

Aim: To determine in vivo whether the lateral geniculate nucleus (LGN) undergoes atrophy in patients with glaucoma and vision loss compared with normal subjects. Methods: Following institutional St Michael's Hospital Research Ethics Board approval, a prospective and masked neuroimaging study was conducted on glaucoma patients with visual-field defects affecting both eyes (n = 10) and age-matched controls (n = 8). Following informed consent, all subjects underwent 1.5-Tesla MRI. Coronal proton density magnetic resonance images of both LGNs were obtained, and LGN height measurements were measured by consensus by three neuroradiologists masked to the diagnosis. Glaucoma and control groups were compared using the t test. Results: Both LGNs were identified and visualised by 1.5-Tesla MRI for every subject. Compared with controls, the mean LGN heights in glaucoma were decreased in right LGN atrophy may be a relevant biomarker of visual system injury and/or progression in some glaucoma patients.

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PURPOSE. The purpose of this study was to determine whether cerebrospinal fluid (CSF) enters the optic nerve via a glymphatic pathway and whether this entry is size-dependent.METHODS. Fluorescent dextran tracers (fluorescein isothiocyanate [FITC]) of four different sizes (10, 40, 70, and 500 kDa) and FITC-ovalbumin (45 kDa) were injected into the CSF of 15 adult mice. Tracer distribution in the orbital optic nerve at 1 hour after injection was assessed in tissue sections with confocal microscopy. Tracer distribution within the optic nerve was studied in relation to blood vessels and astrocytes identified by isolectin histochemistry and glial fibrillary acidic protein (GFAP) immunofluorescence, respectively. Aquaporin 4 (AQP4) immunostaining was performed to assess astrocytic endfeet in relation to CSF tracer. RESULTS.One hour following tracer injection into CSF, all tracer sizes (10-500 kDa) were noted in the subarachnoid space surrounding the orbital optic nerve. In all cases, 10 kDa (n ¼ 4/4) and 40 kDa (n ¼ 3/3) tracers were noted within the optic nerve, while 70-kDa tracer was occasionally noted (n ¼ 1/4). Tracer found within the nerve was specifically localized between isolectin-labeled blood vessels and GFAP-positive astrocytes or AQP4-labeled astrocytic endfeet. The 500-kDa tracer was not detected within the optic nerve.CONCLUSIONS. To our knowledge, this is the first evidence of a glymphatic pathway in the optic nerve. CSF enters the optic nerve via spaces surrounding blood vessels, bordered by astrocytic endfeet. CSF entry into paravascular spaces of the optic nerve is size-dependent, and this pathway may be highly relevant to optic nerve diseases, including glaucoma.