To the first, both Piccolino and Spaide et al. suggest Nutlin-3a side effects that increased choriocapillary vascular pressure, whether due to circulating catecholemines or hypoperfusion downstream, lead to increased hydrostatic pressure below the RPE, thus favoring extraversion of fluid into the sub-RPE and, potentially, subretinal spaces.8,9 Others continue to explain that in order for fluid to accumulate there must also be either a break in the continuity of the RPE,1,8�C10 diffuse RPE pumping dysfunction,11 or both.8,10 Histopathologic changes seen in RP may contribute to these processes and in turn lead to the development of CSR. Migration of RPE cells from Bruch��s membrane to the inner retinal layers and perivascular areas in RP may lead to weakening of the retinal pigment epithelium and the formation of breaks in the RPE.

12 This may cause leakage into the sub-retinal space or interfere with the ability of the RPE to maintain negative pressure in this potential space. Additionally, reduced choriocapillary permeability found in RP could lead to increased upstream choriocapillary arterial pressure that may be a critical process in the development of CSR.9,10 The nature of any physiologic relationship between CSR and RP is speculative at this point and would require greater understanding of pathologic mechanisms that has thus far eluded researchers. Nevertheless, plausible pathophysiologic relationships between these disorders exist. It would be prudent to consider CSR as a possible etiology in a patient with RP and acute visual loss, and vice versa.

An examination of the retinal periphery in patients with CSR may reveal early changes of RP, a finding that may have treatment implications. Literature Search We searched MEDLINE (January 1948 to September 2012) combining the following terms: retinitis pimentosa AND central serous chorioretinopathy OR central serous retinopathy OR choroid diseases. Survey of the results revealed three related references. Citation lists from each of these were then cross-referenced for appropriate reports. Finally, the ISI Web of Science database system was used to identify all articles citing the reports of interest; these results were surveyed for any applicable additions.
Age-related macular degeneration (AMD) is the leading cause of blindness and visual disability in patients aged 60 years and older in Europe and North America.

Worldwide, after cataract and glaucoma, AMD is the third leading cause of blindness, contributing to causing 8.7% of all legal blindness.1 Although the majority of patients with AMD have the non-neovascular form, characterized by drusen and atrophic changes in the retinal pigment epithelium, up to 90% of severe vision loss caused by AMD is attributable to the neovascular (exudative) form of the condition, which is characterized Brefeldin_A by choroidal neovascularization (CNV).