The intermittent appearance and subsequent vanishing of subtle white dots observed in otherwise healthy young women was described as a specific clinical entity and given the name multiple evanescent white dot syndrome (MEWDS). Although originally reported as a relatively benign phenomenon without sequelae,'choroidal neovas-cularisation and affection of the visual acuity were later described. 23 Because the white dots in MEWDS were clinically believed to be observed mostly at the level of the pigment epithelium, it was suggested that the pathogenesis of this condition is an underlying dysfunction of the pigment epithelium and/or pigment epithelium-photo-receptor complex. 4 5 White dots of variable sizes and configurations are frequently observed in many uveitic entities where the choroid is involved in the inflammatory process. Moreover, on careful follow up, evanescence of these white dots is observed in most (if not all) of these cases6 (see Fig le and f). Thus, the fact that'multiple evanescent white dots' occur in many conditions suggests that the white dot may be an expression of a general phenomenon. The pathological sequelae and clinical outcome of white dots, however, are variable. These most probably depend, on the one hand, on the specific triggering factors and, on the other hand, on individual host response and local conditions intrinsic to the affected eye (s). Because of the scarcity of pathological specimens and the lack of reliable laboratory tests in most of these clinical entities, our assumptions regarding the process of'white dot'formation are mostly based on clinical observations. White dots can be observed as an early disease phen-omenon in the following clinical entities: discrete multifocal choroiditis (DMC), punctate inner choroidopathy (PIC), multiple evanescent white dot syndrome (MEWDS), acute blind spot enlargement (ABSE), and the big blind spot syndrome (BBSS). Typically, the white dots in these cases are confined to the posteriorpole, are small (25 to 100, um), discrete, and do not tend to coalesce (Fig 1 a). Involvement ofthe neuro-retina and its vessels and/or the presence of inflammatory cells within the vitreous is not a major feature of these entities. On the other hand, white dots are observed as a later phenomenon of the disease course in the following clinical entities: birdshot choroidopathy, serpiginous choroiditis, acute posterior multifocal placoid pigment epitheliopathy(APMPPE), Vogt-Koyanagi-Harada disease (VKH), and sympathetic ophthalmia. The white dots in these latter diseases, although mostly situated in the posterior pole, can be observed throughout the entire fundus. They are generally of larger and of variable size (50-500, um), do not have well delineated borders initially, and tend to coalesce (Fig lb). Similar manifestations are also observed in cases of infectious uveitides and especially in those associated with parasitic infections such as diffuse unilateral subacute neuroretinitis (DUSN). In these latter groups of diseases, involvement of the retina and its vessels may be a prominent feature. Furthermore, the presence of inflammatory cells within the vitreous is an early and important finding in all cases. White dots also occur in uveoretinal inflammatory disease such as sarcoid retinal vasculitis, idiopathic central retinal vasculitis, peripheral retinal vasculitis, presumed ocular histoplasmosis, and occasionally in intermediate uveitis/pars planitis in the peripheral choroid (Fig 1 c, d). In some of these conditions the white dots are evanescent (Fig 1 e, f) while in others they leave a permanent scar (seen as a window defect on fluorescein angiography). In such cases the active lesion is ill defined and …