A review of the available information indicates that the polymorphous light eruptions are characterized by a number of clinical and histologic features. The clinical patterns range from multiple small papules and papulovesicles, which become confluent, to large plaques. The former usually involve all of the sun-exposed areas and the latter frequently are localized to the face. Histologically, the epidermal changes vary with the clinical presentation. However, a perivascular round cell infiltrate in the dermis is present in all of the lesions. The disease has a worldwide distribution, though there is a high incidence in certain populations such as North and Latin American Indians and Finnish people. The disease usually begins in young adult life except in the American Indian population, where it tends to start in childhood. Though in several series there was a preponderance of females, males do develop the problem in significant numbers. The action spectrum falls primarily in the ultraviolet B (UVB) range. Some patients do react to ultraviolet A (UVA) rays as well. However, there is evidence that the process is not confined to any narrow band of radiation, but can be produced by any wavelength or energy source as long as one uses sufficient exposure dose to produce a delayed phototoxic erythema. Pathogenetically, it is likely that polymorphous light eruption (PMLE) actually includes more than one disease entity. Whether photoallergy plays a role in any of these responses remains to be seen. In addition, the relationship to the persistent light reactor, photosensitive eczema, and actinic reticuloid has not been clarified at this time.