In patients with APMPPE with macular edema, visual acuity was found to be normal though mean retinal contrast sensitivity measured by microperimetry was reduced. After therapy, there was an improvement in retinal contrast sensitivity, suggesting microperimetry can be a useful tool in following response to treatment in these patients [14].

Patients with VKH may demonstrate discordance between best-corrected visual acuity and mean retinal sensitivity. In a study of 14 patients with VKH, mean BCVA over 1 year of treatment improved at a significantly greater rate than retinal contrast sensitivity. BCVA underestimated macular dysfunction perceived by VKH patients. The authors suggest that basing immunosuppressive treatment off of retinal sensitivity as measured by a microperimeter may be a more reliable measure of visual function than BCVA alone [15].

Microperimetry may also have a purpose in evaluating the clinical course of birdshot chorioretinopathy. In the early stages of the disease, characteristic hypopigmented lesions may be poorly defined or absent. Furthermore, progression of such findings is not a reliable marker to evaluate activity, as diffuse pigmentary loss is noted in the natural progression of the disease [16]. A retrospective study investigating BSCR and microperimetry found there was a statistically significant difference in retinal sensitivity defined by microperimetric analysis between active and inactive disease. Active disease correlated with reduced retinal contrast sensitivity, which improved as the disease responded to treatment. Some patients had persistent with residual dysfunction, implying microperimetry could be used to evaluate disease activity or damage in such cases [17].

Serpiginous choroiditis is usually bilateral and progressive, with multiple recurrences, leading to potentially significant vision loss. Visual outcome is related to macular involvement of the primary lesion and choroidal neovascularization. In a study looking at 28 eyes with serpiginous choroiditis, atrophic lesions were directly correlated with dense scotomas, and lesion borders, thought to be unaffected areas, corresponded to relative scotomas by microperimetric analysis. The borders that appeared normal by fundus examination however were identified as active with multimodal techniques including microperimetry. Such data revealed a larger area of involvement that was otherwise underestimated by fundus autofluorescence and fundoscopy alone. Findings were supported by choroidal filling defects on indocyanine green angiography [18].

Discordance between fundus examination and microperimetry in serpiginous choroiditis is depicted in Fig. 6.2. The right eye of a 33-year-old man with serpiginous choroiditis is shown with BCVA of 20/20 on presentation. Fundus exam showed patches of chorioretinal atrophy (Fig. 6.2a). A small area of new activity temporal to the fovea corresponded to hyperautofluorescence on fundus autofluorescence (Fig. 6.2b). 18-4 MP-1 microperimetry showed a dense scotoma centered on the lesions (0 dB) and relative scotomas in the unaffected perifoveal area (12 dB) (mean sensitivity 11 dB) (Fig. 6.2c, d). After 2 months of escalated treatment, BCVA was 20/25. While fundus exam (Fig. 6.2e) and autofluorescence (Fig. 6.2f) appeared stable, 18-4 MP-1 microperimetry showed further decrease in macular sensitivity (mean sensitivity = 9 dB) (Fig. 6.2g, h). In this case, microperimetry detected precise functional changes that might not be apparent on fundus imaging.

Microperimetry can be used to quantitatively monitor serpiginous lesions involving the macula. Fundus photo of a 20-year-old woman with serpiginous choroiditis is shown (Fig. 6.3a) with characteristic peripapillary gray-white lesions. At presentation, BCVA was 20/32. The lesions corresponded with early hyperfluorescence and late staining on fluorescein angiography (Fig. 6.3b, c) and hypofluorescence through all phases on the indocyanine green angiography (Fig. 6.3d). 10-2 MP-1 microperimetry showed decreased sensitivity that correlated with the lesions (0 dB) and relative scotomas at the lesion margins (12 dB) and two points of decreased sensitivity in unaffected areas superior to the fovea (10–12 dB) (mean sensitivity = 16 dB) (Figs. 6.3e, f).

Ampiginous variants (“relentless placoid chorioretinitis”) [19] have been described as a form of APMPPE that resembles serpiginous choroiditis with a prolonged course and widespread distribution of lesions [20]. Figure 6.4 demonstrates the clinical course of this entity. Fundus exam showed multiple yellow, gray, and white placoid lesions in the posterior pole (Fig. 6.4a) with corresponding scotomata in the 10-2 MP-1 microperimetry (mean sensitivity = 13 dB) (Fig. 6.4b, c). Despite immunosuppression, placoid lesions in ampiginous choroiditis often progress (Fig. 6.4d). In this example, 10-2 MP-1 demonstrates near-complete loss of central sensitivity (mean sensitivity 1 dB) (Fig. 6.4e, f).

JIA-related uveitis is characterized by a chronic course typically involving the anterior segment. Complications such as posterior synechiae, band keratopathy, cataract, and glaucoma have been widely reported. However, there is increasing evidence macular edema is an underestimated complication of JIA-related uveitis. In a study conducted by Paroli et al. [21], 37% of patients with JIA-related uveitis had posterior complications. Microperimetry was used to assess macular function, which showed reduced sensitivity in all eyes with macular edema. Among children with juvenile idiopathic arthritis-related uveitis and macular edema, a reduction in retinal contrast sensitivity was noted in 25% of the eyes, lingering even after resolution, suggesting microperimetry could offer a supplemental assessment to visual function.

Macular edema is the leading cause of decreased vision in uveitic patients and may be responsible for permanent visual impairment in 8.5% of cases [22]. Changes in retinal thickness caused by macular edema do not necessarily correlate with the visual acuity changes in patients with uveitic macular edema. Fixation abnormalities caused by uveitic macular edema are not always associated with poor visual acuity [5]. Repeated attacks of uveitis and macular edema may cause cumulative damage that may lead to irreversible tissue damage and decreased visual function. Studies have indicated that uveitic eyes without macular edema had lower retinal sensitivity [23]. Perimetry quantification of macular sensitivity and retinal thickness offer information regarding the impact of uveitic macular edema on retinal function.