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Major depressive disorder, bipolar disorder and schizophrenia are currently among the most common psychiatric disorders, known to constitute a serious public health issue in terms of morbidity, mortality and functional handicap. Their pathophysiology is still unclear, but there is now increasing evidence supporting the existence of abnormalities of neurotransmission. As the retina is an extension of the central nervous system, it may be an interesting site of study which might provide a better understanding of the pathophysiology of psychiatric disorders. Several studies have demonstrated retinal abnormalities, with abnormal cone and rod responses on electroretinography (ERG), suggesting a process of functional neuronal loss, structurally supported by a decrease in the retinal nerve fiber layer thickness (RNFL) on optical coherence tomography (OCT), which suggests involvement of the molecular signal pathways of neurotransmission. These tests could be useful tools for diagnosing and monitoring psychiatric disorders. This article is an overview of the literature on retinal abnormalities observed in patients with major depressive disorder, bipolar disorder or schizophrenia, and discusses how they could be pathophysiologic markers., (Copyright © 2020 Elsevier Masson SAS. All rights reserved.)

Optic neuritis is clinically suspected when painful, rapidly progressive central visual loss occurs in a young patient who has a relative afferent pupillary defect. Ophthalmoscopy is normal in the majority of cases but papillitis or optic disc palor can occur. Several other diseases can mimic optic neuritis, such as ophthalmological conditions or other diseases affecting the visual pathways. Their appropriate clinical diagnosis is of paramount importance in order to avoid unnecessary or invasive procedures or treatments., (Copyright © 2010. Published by Elsevier Masson SAS.)

Neuroprotection of photoreceptor cells in rod-cone dystrophies: from cell therapy to cell signalling. Neuroprotection of photoreceptor cells in rod-cone degenerations is primarily targeted at preventing the loss of function. Strategies for protecting rod cells should therefore aim not only at structural preservation but also must be assessed using functional parameters (e.g., electroretinogram). Given the number of mutations leading to an impaired visual response of rods, the preservation of cones is a realistic approach since (1) numerous mutations do not affect proteins expressed by cones; (2) the secondary degeneration of cones is the main event leading to profound visual impairment; (3) even a small proportion of functional cones is sufficient for major visual functions. Our group has (1) established and confirmed the existence of non cell autonomous mechanisms promoting cone cell viability; (2) shown that rod cell protection or replacement provides a mean to extend the survival of cones; (3) demonstrated that rod-cone trophic interactions are mediated by diffusible proteins; (4) identified by expression cloning a protein mediating such interactions: RdCVF (Rod-derived Cone Viability Factor). These studies provide clues for broad neuroprotective therapies of rod-cone dystrophies.

Macular dystrophies are a group of hereditary disorders of the macula occurring in children or young adults. The most frequent in France will be presented in detail: Best disease, Stargardt macular dystrophy, cone dystrophy, X-linked retinoschisis, pattern dystrophy, and malattia leventinese. Molecular biology studies have now mapped and identified the genes involved in these macular dystrophies. Analysis of the features of fundus examination will lead to further examinations such as fluorescein angiography, indocyanine green angiography, optical coherent tomography, electroretinography, or electrooculography, in order to confirm the diagnosis. We will also present the differential diagnosis of each of these macular dystrophies.