Central serous chorioretinopathy and bright light.

Abstract

Editor, W e read with great interest the article by Yang et al. (2013), reporting that central serous chorioretinopathy (CSCR) is significantly associated with the increased subfoveal choroidal thickness and the choroidal vascular dilation. In that article, the possible causes of choroidal vascular dilation, such as choroidal vascular innervation or endothelin-1 or inflammatory cytokines, have been discussed. As it was pointed out, however, the cause of choroidal vascular dilation has remained unclear. Some data in the literature may be helpful to clarify the cause of choroidal vascular dilation. It was shown that choroidal vessel diameter is mainly influenced by the temperature of the chorioretinal complex (Parver 1991); an increase in the temperature of the chorioretinal complex induces choroidal vascular dilation in both a passive (Parver et al. 1980) and a reflexive manner (Parver et al. 1983; Shih et al. 1999). The chorioretinal complex may be heated up by the light absorption in the melanosomes of the retinal pigment epithelium (RPE) and the choroid (Parver 1991). Therefore, an increase in the environmental light intensity increases the temperature of the macula which is at the focal point of the irradiating lights into the eye. If the focal heat is high enough to induce severe choroidal vasodilation but not to burn the tissue, and if the rate of the heat accumulation is higher than the rate of adaptation of choroidal circulation to bright lights, it may result in a focal serous leakage from the dilated choroidal vessels. In conclusion, CSCR may result from a response of choroidal vessels to an acute increase in the environmental light intensity. The increase in the light intensity may increase the choroidal temperature at the focal point of the irradiating lights into the eye. The resultant focal heat may induce local changes in the choroidal vessels leading to a focal leakage from the choroidal vessels and CSCR. However, this hypothesis should be experimentally tested. Future clinical researches should consider the history of acute increase in the intensity of lights to which patients with CSCR are exposed. Assessment of the relationship of increases in total time spent outdoors with prevalence of CSCR may be helpful. If the hypothesis is proved to be correct, it may be helpful to design more efficient strategies to prevent and manage CSCR.