INTRODUCTION

The multiple evanescent white dot syndrome (MEWDS) was first described in 1984 by Jampol and associates.^[1] Within the same year, Takeda and co-workers independently reported in the Japanese literature, the clinical findings of four patients with presentations indistinguishable from MEWDS; they proposed the term acute disseminated retinal pigment epitheliopathy.^[2] The subjective, demographic, clinical, fluorescein angiographic, and electrophysiological findings of MEWDS represent a distinct clinical entity.

SUBJECTIVE COMPLAINTS

The usual presenting symptom is the acute onset of decreased or blurred vision often accompanied by dark or black spots in the periphery. Virtually all patients also note photopsia, described as flickering or shimmering lights. The photopsia sometimes seems to originate from temporal scotomas. Commonly, patients describe a preceding 'flu-like' illness.^[3,4] Rarely, patients report headaches^[5] accompanying the visual symptoms or ocular discomfort.^[6]

DEMOGRAPHICS

Most patients are myopic^[7] females in roughly the third decade of life. The reported age range of cases is 10⁸ to 67^[9] years old. MEWDS does not appear to have a racial predilection.

CLINICAL FINDINGS

The presenting visual acuity ranges from 20/20 to 20/400. Some patients may have an afferent papillary defect. The anterior segment examination is normal except for the occasional presence of mild iritis. The most striking findings on posterior slit-lamp biomicroscopic examinations are numerous small white spots, ~100-200 ?m in size and located at the level of the retinal pigment epithelium (RPE) or deep retina. They are most prominently seen encircling the posterior pole and in the perifoveal region, but the fovea is spared (Figs 158.1 to 158.3). The spots are discrete and are not associated with overlying exudative changes. They are sometimes migratory, clearing in one area while appearing in another, over a period of several days. If spots are large in size, the center of the spot may resolve before the periphery.^[10] Usually, the lesions resolve entirely, leaving behind a characteristic foveal RPE granularity in most cases (Fig. 158.4). Other findings sometimes include a few cells in the posterior vitreous,^[11]mild blurring of the disk margin, and isolated areas of perivascular sheathing. When seen, the cellular reaction in the posterior vitreous is mild and transient in the early stages of the disease.

ATYPICAL MANIFESTATIONS

While atypical, cotton wool spots have been noted in MEWDS.^[12] Prior to the typical appearance of macular spots, MEWDS rarely may first manifest with a large peripapillary outer retinal lesion^[13] or geographic circumpapillary discoloration.^[14] MEWDS can result in midperipheral, peripapillary, and even macular chorioretinal scarring, typically in patients with recurrent or bilateral disease. One report describes a patient diagnosed with MEWDS who developed transient reddish-brown spots after resolution of the acute MEWDS lesions.^[15]

MEWDS can occasionally be seen with multiple, large lesions, up to 1000 mm in size, and granular, pigmented, placoid lesions in association with a panuveitis.^[16] Patients with recurrent MEWDS can develop choroidal neovascularization.^[17,18] This may cause some diagnostic confusion with multifocal choroiditis (MFC), especially after the acute phase of the disease has resolved.^[19]

VISUAL FIELDS

The visual field findings are variable in MEWDS, ranging from normal to a generalized depression (Fig. 158.5). Large blind spots are a frequent finding. In his original description, Jampol noted optic nerve edema clinically in some patients. Arcuate scotomas, cecocentral scotomas, and central depression have also been reported.^[20] The field loss is sometimes exaggerated when compared with the clinical findings in the retina and at the disk.

FLUORESCEIN ANGIOGRAPHY

The fluorescein angiography findings in MEWDS are characterized by early punctate hyperfluorescent spots, 50-500 mm in diameter, at the level of the RPE, often corresponding to the white dots observed clinically.^[21] Classically, these punctate spots assume a wreath-shaped pattern. The late-phase fluorescein angiogram reveals staining in the area of the spots and the optic nerve head (Figs 158.1c,d and 158.3c,d). Late capillary leakage in the perifoveal area and focal areas of vasculitis are occasionally noted. Capillary leakage of the optic nerve head can be present. The spots often resolve angiographically within 4-6 weeks and are thought to represent inflammatory lesions at the level of the photoreceptors, RPE, and choroid.

INDOCYANINE GREEN ANGIOGRAPHY

On indocyanine green (ICG) angiography, hypofluorescent spots are seen (Fig. 158.6), which may be more extensive and may persist longer than spots observed on fluorescein angiography. Peripapillary hypofluorescence on ICG may account for the enlarged blind spot and other field abnormalities observed secondary to choroidal hypoperfusion of the optic nerve and peripapillary area.^[22] In an evidence-based review of chorioretinal diseases, the use of ICG for the diagnosis and management of MEWDS was 'recommended with moderately strong supporting evidence'.^[23] ICG may be particularly useful in cases with subtle clinical findings and absent fluorescein angiographic changes. ICG can also be used to follow the clinical course.^[24]

ELECTROPHYSIOLOGY

The electrophysiologic findings were described for three of the original patients reported to have MEWDS.^[25] During the acute phase of the illness, the Ganzfield electroretinogram (ERG) a-wave and early receptor potential amplitudes were profoundly decreased. This suggests that photoreceptors are involved during active disease. These normalize with resolution of the disease.^[26] Additionally, S-cone reductions are more pronounced than in the L- or M-cone systems on Ganzfield ERG.^[27] The multifocal ERG, which reflects the cone activity of the central retina, demonstrates a supranormal response in acute disease of less than 2 weeks duration, which may become subnormal or normalize subsequently. Similar multifocal ERG findings have been observed in other deep retinal inflammatory conditions.^[28]

Electrooculography results have also been reported to be mildly abnormal, suggesting involvement of the RPE during acute disease.^[29] Abnormal foveal densitometry has been reported for a patient with MEWDS who had normal ERG findings.^[30]

CLINICAL COURSE

Most patients with MEWDS experience a relatively short course with recovery of vision within 3-10 weeks. Usually, the vision returns to 20/30 or better, with the majority of patients regaining 20/20 vision. The white spots also disappear during this time; however, the orange foveal granularity usually persists. Some patients will have visual symptoms for much longer periods following resolution of the white spots. Even though visual acuity returns, some patients are aware of visual field defects, photopsia, or dim vision for extended periods.

Bilateral involvement is uncommon^[31-33] and has been reported as late as 4 years after initial presentation in the contralateral eye.^[34] When both eyes are involved, one eye is usually involved minimally and is asymptomatic. One reported patient was symptomatic in both eyes simultaneously.^[35] This patient experienced visual loss in the right eye after 7 weeks of vision loss in the left eye. Recurrences of MEWDS are uncommon.^[36] Choroidal neovascularization is a rare but potential late sequelae.^[37,38]

PATHOPHYSIOLOGY

MEWDS is a distinct clinical syndrome. Since it has an acute onset and is sometimes preceded by a 'flu-like' illness, a viral cause seems likely. As Gass proposed for acute zonal occult outer retinopathy, the disease may manifest first at the optic nerve margin due to the lack of surrounding neuroepithelium.^[39,40]

Clinically and angiographically, the disease process involves the RPE and outer retina. ICG findings suggest that early MEWDS involves the RPE and photoreceptors, but with periphlebitis, all layers of the retina may be involved.^[41] The ERG abnormalities suggest a metabolic disturbance of the RPE-photoreceptor complex.

One case has been described with increased serum levels of total IgG and IgM during the acute phase.^[42] MEWDS has been reported in association with recent varicella infection,^[43] increased CSF protein levels,^[44] and vaccinations for hepatitis A^[45] and B.^[46] One study documented a 3.7-fold increase in association with HLA-B51.^[47] Hormonal factors play a role in pathogenesis, owing to the gender imbalance and high rate of oral contraception usage.^[48]

DIFFERENTIAL DIAGNOSIS

MEWDS must be differentiated from other inflammatory disorders of the RPE, choroid, or retina. The primary differential diagnosis includes the white dot syndromes: MFC, punctate inner choroidopathy (PIC), acute idiopathic blindspot enlargement syndrome (AIBSE), acute posterior multifocal placoid pigment epitheliopathy (APMPPE), acute retinal pigment epitheliitis (ARPE), birdshot retinochoroidopathy, toxoplasmosis, diffuse unilateral subacute neuroretinitis (DUSN), acute macular neuroretinopathy (AMN), and primary intraocular lymphoma. In most instances, the diagnosis of MEWDS can be made confidently on clinical and angiographic examination, and other disorders can be excluded.

MFC AND PIC

Several papers have described a group of patients that can probably best be lumped together as cases of MFC. They include the following: PIC,^[49] MFC and panuveitis,^[50] MFC associated with subretinal fibrosis,^[51] and recurrent MFC. The patients described in these papers are similar. As in MEWDS, they are usually young females who present with acute visual loss in one eye and spots in the fundus. Gass and Callanan posited that MEWDS, MFC, PIC, and AIBES are, in fact, manifestations of a single disease spectrum.^[52]

PIC was described by Watzke and associates in 1984. Ten moderately myopic women (aged 21-37 years) presented with blurred vision, paracentral scotomas, or light flashes. The characteristic fundus lesions are small gray-yellow spots ~100-200 ?m in diameter at the level of the RPE and inner choroids scattered throughout the posterior pole. Many lesions had an overlying serous detachment. Neither vitreous nor anterior chamber inflammation is present. The fluorescein angiogram reveals early hyperfluorescence and late staining or leakage into an overlying sensory retinal detachment. Eight of 10 patients had bilateral involvement, although symptoms were usually unilateral. The lesions developed into atrophic scars. Some scars became pigmented over time. Four of 10 patients eventually experienced subretinal neovascularization in association with perifoveal scars. Dreyer and Gass described 28 patients with MFC and panuveitis.^[53] Besides the characteristic RPE lesions resembling those seen in the presumed ocular histoplasmosis syndrome, these patients also had vitreous cells and anterior segment inflammation. Many of these patients experienced peripapillary or subfoveal subretinal neovascularization. Cantrill and Folk reported five female patients in whom progressive subretinal fibrosis developed in association with MFC.^[54] Doran and Hamilton^[55] and Palestine and co-workers^[56] had previously reported similar cases. Morgan and Shatz described a similar group of female patients with MFC who had multiple recurrences.^[57]

All these papers describe a MFC that is generally seen in young myopic females. The disorder can be chronic and recurrent. Although often presenting with unilateral symptoms, findings are usually bilateral. The RPE and inner choroidal spots vary in size but are generally larger than those seen in MEWDS. Papillitis, retinal phlebitis, vitritis, anterior uveitis, cystoid macular edema, and subretinal neovascularization can all be part of the disease process. One or more of these manifestations may predominate in a given patient. Following resolution of the spots in the acute stage, there is some degree of permanent RPE and choroidal damage, which can be atrophic, pigmentary, or cicatricial in nature. Since many disorders may mimic this idiopathic condition, a full medical work-up is needed, especially to rule out treatable infectious or inflammatory conditions such as syphilis or sarcoidosis.

A common host susceptibility factor or even a common pathogenesis may exist between MEWDS and the MFC spectrum of disease. Several cases have been observed of patients with MEWDS who subsequently develop MFC,^[58-60] and several cases are described of patients with a previous diagnosis of MFC who develop MEWDS. Both MEWDS and MFC typically affect young myopic women. However, unlike MEWDS, MFC is usually associated with bilateral involvement, deep choroidal inflammatory (rather than deep retinal/RPE) lesions, prominent vitritis and anterior chamber reaction, and early hypofluorescent spots which stain late on fluorescein angiography.^[61]

ACUTE IDIOPATHIC BLIND SPOT ENLARGEMENT

Fletcher and colleagues described a syndrome occurring primarily in young females consisting of blind spot enlargement without optic disk edema.^[62] The acute idiopathic blind spot enlargement (AIBSE) syndrome has features suggesting retinal dysfunction as its cause, including the presence of the scotoma, steep borders of the scotoma, and prolonged recovery time with photostress testing. Hamed and colleagues suggested that patients with AIBSE represent a subset of those with MEWDS, presenting for examination after the retinal spots have faded.^[63] More recently, Singh and associates suggested that MEWDS is one of several conditions that may be characterized by blind spot enlargement.^[64] Some cases of AIBSE, but not all, may be due to MEWDS. Volpe and colleagues reviewed 27 cases of AIBSE and suggest that the primary factor that distinguishes AIBSE from MEWDS is that the visual field abnormalities do not resolve in AIBSE.^[65] Patients with AIBSE can present with photopsia; visual field defects; and have abnormal funduscopic, angiographic, and electroretinographic findings.

ACUTE POSTERIOR MULTIFOCAL PLACOID PIGMENT EPITHELIOPATHY

APMPPE can also present with rapid loss of vision in a young patient.^[66] However, this condition is usually bilateral and the fundus lesions are characteristic. Multiple, flat gray-white lesions are present at the level of the RPE. These lesions are much larger than the spots of MEWDS. The lesions are hypofluorescent in the early-stage fluorescein angiogram and stain late. Extensive RPE alterations develop as lesions resolve.

ACUTE RETINAL PIGMENT EPITHELIITIS

ARPE was described by Krill and Deutman in 1972.^[67] Chittum and Kalina more recently reported the findings of eight patients with ARPE.^[68] This condition is also characterized by acute loss of vision in a young patient. The ages of the first nine reported patients ranged from 18 to 45 years.^[69] Three of the nine patients had bilateral involvement. The acute findings have been described as discrete clusters of dark spots surrounded by hypopigmented halos. These spots are localized to the perifoveal region. Fluorescein angiography can reveal blockage of choroidal fluorescence from the pigmented center with a surrounding zone of hyperfluorescence corresponding to the hypopigmented halo. Gradual resolution of the fundus findings with complete recovery of vision within 7-10 weeks is typical. Subtle RPE alterations may remain.

BIRDSHOT RETINOCHOROIDOPATHY

Birdshot retinochoroidopathy or vitiliginous chorioretinitis is characterized by white or depigmented spots at the level of the RPE scattered throughout the fundus.^[70,71] The older age at presentation, chronic course, bilateral involvement, and significant vitreous involvement all help to easily distinguish this syndrome from MEWDS.

TOXOPLASMOSIS

Another cause of retinochoroiditis that must be differentiated from MEWDS is toxoplasmosis. Ocular toxoplasmosis can present with multifocal gray-white lesions at the level of the deep retina and RPE, with little or no overlying vitreous reaction.^[72] These lesions typically resolve slowly and can recur. The diagnosis of punctate outer retinal toxoplasmosis is difficult to confirm. The presence of satellite lesions and positive serologic findings for toxoplasmosis can help to make the diagnosis in the appropriate clinical setting.

DIFFUSE UNILATERAL SUBACUTE NEURORETINITIS

The early stage of DUSN can be characterized by recurrent crops of evanescent gray-white lesions at the level of the outer retina and RPE.^[73] The chronic course of DUSN with eventual development of visual loss, optic atrophy, diffuse RPE degeneration, and retinal vessel narrowing easily differentiates this disorder from MEWDS. DUSN is caused by a nematode that can sometimes be visualized in the subretinal space.^[74]

ACUTE MACULAR NEURORETINOPATHY

AMN is another cause of loss of vision and paracentral scotomas in young patients.^[75,76] This disorder can be bilateral and is characterized by cloverleaf, wedge-shaped, grayish lesions in the macular area, probably in the outer retinal layers. Interestingly, patients have been reported with AMN and MEWDS in the same eye, suggesting some similarity in their origins.^[77]

PRIMARY INTRAOCULAR LYMPHOMA

Primary intraocular lymphoma is well known to masquerade as numerous other ocular inflammatory syndromes, and MEWDS is no exception. Several cases have been reported of patients who initially presented with transient lesions of the posterior pole, simulating MEWDS. Eventually, these patients were diagnosed with primary intraocular lymphoma due to the persistence or expansion of retinal lesions or of vitreous cellular infiltration.^[78,79]

CONCLUSIONS

In summary, MEWDS is a unilateral, idiopathic, and inflammatory disease with a constellation of well-described subjective, clinical, fluorescein angiographic, and electrophysiologic features. It occurs most often as a unilateral phenomenon, predominantly in young, myopic females. The most characteristic manifestation is that of outer retinal or superficial pigment epithelial white spots, often 100-200 ?m in size, and usually confined to the posterior pole or midretinal areas. These fleeting disturbances are migratory in nature and evident on fluorescein angiography with a wreath-like distribution of early punctate hyperfluorescent spots which stain late. A persistent orange foveal granularity and mild papillitis are hallmarks of the disorder. Similarly, there are characteristic electroretinographic findings and visual field loss. The field changes exceed what might be expected on the bases of the clinical findings in the retina and at the optic nerve. The natural course is generally benign with spontaneous disappearance of the lesions and improvement of the visual function. MEWDS is often clinically differentiated from other categorized intraocular inflammatory diseases. Although there is considerable information available on the subjective, demographic, clinical, angiographic, and electrophysiologic features of this disease, a causative agent is still unknown. Further clinical research is needed to identify the precise pathogenesis.

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