Posterior scleritis is an uncommon form of scleral inflammation. While the prevailing consensus is that scleritis is an immune-mediated disease,1 its precise pathogenesis remains enigmatic.

We describe a 23-year-old man with intermittent painful right eye and vision loss since 3 years due to posterior scleritis, which resolved when taking recreationally 3,4-methylenedioxymethamphetamines (MDMA, ‘ecstasy’).

Case report

A healthy 23-year-old man was referred to our hospital with pain and severe loss of visual acuity in the right eye (20/400) since 3 months. History revealed similar episodes during the last 3 years, which resolved partially when using ecstasy on a recreational basis. Since the patient had stopped ecstasy abuse 3 months ago, symptoms worsened.

Echographic evaluation showed choroidal thickening and oedema in Tenon's space in the right eye (Figure 1a). Clinical examination revealed a swollen optic disc surrounded with chorioretinal folds (Figure 1b). Pupillary reflexes and ocular motility were normal. Goldmann visual field revealed a central scotoma (Figure 2a) and colour vision was discretely disturbed on the red–green axe. Latencies were normal, but amplitudes were smaller on pattern visual evoked potential (VEP; Figure 1c). Examination of the left eye was unremarkable.

Figure 1
figure 1

(a) B-scan echographic examination of the right eye showing choroidal thickening and oedema in Tenon's space at presentation; (b) red-free image of the right optic nerve surrounded by chorioretinal folds; and (c) pattern visual evoked potential (pVEP) showing half of the height of the amplitudes in the right eye compared to the left eye, and normal latencies.

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Figure 2
figure 2

Goldmann visual field analysis tested with object V4, I4, and I2 (a) at presentation, showing normal peripheral limits in the left eye; (b) constriction of the peripheral limits and a central scotoma in the right eye; (c) after 3 months of high-dose corticosteroid regimen, the left eye stayed within normal limits; and (d) right eye examination showed almost normalization with, however, still a central scotoma.

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Treatment with oral steroids was instituted (1 mg/kg), and tapered slowly. Visual acuity recovered to 20/25 and the central scotoma regressed over 3 months (Figure 2b and c).

Comment

The role of cellular immune dysfunction in posterior scleritis is suggested by immunopathological findings showing a predominance of T cells, mostly CD4+ lymphocytes, infiltrating the scleral fibers.1 Oral corticosteroids are the treatment option when nonsteroidal inflammatory drugs fail.

Ecstasy is a psychostimulant drug that acts on the central nervous system. Amphetamine isomers have been described to induce acute nonarteritic ischaemic optic neuropathy.2 Ecstasy also activates the hypothalamic pituitary adrenal axis, which induces a significant rise in cortisol plasma concentrations and a depression in immune function.3, 4, 5

In summary, we present here a patient with long-standing, unrecognized posterior scleritis. Reminiscent episodes following recreational use of ecstasy were most probably due to a depression in cellular immunity. It is important for physicians to recognize the atypical course of some eye diseases such as posterior scleritis because of ecstasy abuse.