Since macular edema is a major cause of visual disability in many different ocular diseases, we have approached this complication in three major areas in this text – Part 1, Pathophysiology and Diagnosis of cystoid macular edema (CME); Part II, Medical Management of CME; and Part III, Surgical Management of CME. It is clear that understanding the pathophysiology of this disease with its many different causes will result in the future development of therapeutic options that do not exist today.

As Behar-Cohen and colleagues described in Chap. 2, the mechanisms leading to macular edema are difficult to discriminate in the various clinical presentations. Nevertheless, the use of multimodal imaging (i.e., fluorescein angiography (FA), indocyanine green angiography, and spectral domain optical coherence tomography (OCT) allows a better understanding of the exact alterations of retinal structures that result in macular edema. Such an understanding will provide more appropriate and targeted treatments. However, molecular mechanisms responsible for this complication of ocular disease are most difficult to determine since the experimental models in rodents provide limited insight since they do not have a macula. Thus, the molecular mechanisms involved in the vasogenic and cytotoxic causes of macular edema still remain to be resolved. However, our current understanding is very nicely presented in this chapter.

Multimodal imaging became of primary importance in recent years to appreciate, diagnose, and follow the development and the resolution of CME in response to treatment. In Chap. 3, Grewal and Jaffe nicely outline how fluorescein angiography (FA) and fundus autofluorescence are used to evaluate CME, while spectral domain OCT allows evaluation of the location, extension, pattern, and microstructural anatomical features of CME. FA, although a technique used for decades, still is the only technique that allows identification of areas of leakage, thus providing complimentary yet distinct information for diagnosis of CME and monitoring its response to treatment. Future advances in imaging technology with higher acquisition speed and hardware motion tracking along with improved automated image segmentation analysis protocols will allow us to better characterize CME. Development of novel anatomical biomarkers can offer prognostic implications and monitor response to treatment. Newer imaging technologies including noninvasive OCT angiography hold promise to help better elucidate the pathology of CME.