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Editor,—Depending on the site of the inflammatory process within the scleral or episcleral tissue, scleritis can be identified as anterior scleritis, posterior scleritis or episcleritis.1 2 Diagnosing of anterior scleritis and episcleritis is much easier than diagnosing posterior scleritis because lesions can be more easily observed in the first two conditions. Posterior scleritis is probably one of the most underdiagnosed conditions in ophthalmology.1 2 Recent development in magnetic resonance imaging (MRI) technology is considered useful for diagnosing posterior scleritis.
A 40-year-old woman was first seen by her ophthalmologist on 8 December 1995, when she complained of left ocular pain. At this time, her visual acuity was 20/20 with correction in each eye. By 11 December 1995, the left visual acuity, with correction, was decreased to 20/200, and chemosis and optic perineuritis in the left eye were observed. She was referred to our clinic on 21 December 1995. On admission her visual acuity was 20/20 in the right eye and 20/400 in the left eye, with correction. No chemosis was detected on the left eye at this time. Abnormalities of extraocular movements were not observed. Funduscopy showed elevated, hyperaemic disc with a splinter haemorrhage in the left eye (Fig 1) and a normal optic disc in the right eye. Visual fields were normal on the right and constricted on the left. The left pupil was dilated and fixed (Fig 1). Instillation of 0.125% pilocarpine resulted in prompt constriction of the left pupil, indicating denervation supersensitivity (Fig 1). Fundus fluorescein angiography showed persistent dye leakage from the left disc and choroidal filling defects in the upper temporal area. Blood tests showed an erythrocyte sedimentation rate of 29 mm in the first hour, a white blood cell count of 5.9×109/l, an angiotensin converting enzyme level of 6.0 IU/l (normal, 8.3 to 21.4 IU/l), a lysozyme level of 5.3 μg/ml (normal, 5.0 to 10.2 μg/ml),Treponema pallidum hemagglutination assay and fluorescent treponemal antibody negativity, antinuclear antibodies negativity, and rheumatoid factor negativity. Virus titres for mumps, varicella zoster, herpes simplex, cytomegalovirus, rubeola, and rubella were negative. Chest and sinus x ray findings were normal. Because the manifestation of optic perineuritis and internal ophthalmoplegia associated with ocular pain in this patient suggested inflammation in the posterior pole of the globe around the optic nerve, ultrasonography, computed tomography, and MRI of the left orbit using a surface coil were carried out. Ultrasonography and computed tomography were unremarkable. On the other hand, T2 weighted images of MRI showed a high signal intensity area around the posterior sclera and the adjacent optic nerve sheath (Fig 2). This area was enhanced in gadolinium-DTPA T1 weighted images using a fat suppression technique (Fig 2). The patient was given methylpredonisolone (1 g per day for 3 days) intravenously from 26 December 1995 followed by predonisone orally (30 mg per day for 14 days). Her left visual acuity rapidly improved and reached 20/20 with correction by 7 January 1996. The optic disc oedema also rapidly improved. The high signal intensity area in T2 weighted images and the enhancement effects in gadolinium-DTPA T1 weighted images disappeared by 5 February 1996. Up to about 3 months after the first examination, no changes in the internal ophthalmoplegia had been detected.
Gadolinium enhanced MRI with a fat suppression technique was helpful for diagnosing the lesion in this patient, while ultrasonography and computed tomography were unremarkable. Although the aetiology of the inflammation in this patient remains unknown, the optic disc oedema and the internal ophthalmoplegia were caused by the posterior scleritis. The ciliary ganglion and short ciliary nerves, which innervate the sphincter pupillae muscle, locate around the optic nerve and penetrate the sclera. Therefore, the ciliary ganglion or short ciliary nerves were thought to be damaged by the inflammation around the posterior sclera. The inflammation of the sclera also extended to the optic nerve sheath and was thought to produce the optic disc oedema. Results of MRI in this patient were consistent with this hypothesis. Some previous reports indicated that MRI is useful for diagnosing posterior scleritis.3 4 This report shows that inflammatory changes in the retrobulbar area can be detected by gadolinium-DTPA T1 weighted imaging using a fat suppression technique and a surface coil.