Buspirone in the treatment of levodopa induced dyskinesias.

either relapsing or progressive over a period of six to 12 months by the time of presentation. Two patients have had bilateral disease.47 Some patients have responded to and stabilised on steroids and in a number, surgical biopsy has been performed to confirm the diagnosis. Dutton felt that surgical decompression of the nerve helped stabilise the condition. Optic perineuritis is best confirmed histologically, because other causes of optic nerve sheath lesions, particularly meningioma cannot always be excluded by neuroimaging alone. Most reports have described thickening of the optic nerve sheath from fibrotic changes with varying amounts of chronic lymphocytic or plasma cell infiltrate or granulomatous changes. The intracranial nerve has been found to be pale and atrophic with chronic inflammatory infiltration as in our own case and that of Zhang2 or swollen with perivasculitis.3 The most complete description ofpathological changes4 showed concentric deposition ofcollagenous fibroconnective tissue in the dural sheath with necrobiotic granulomas and a chronic inflammatory infiltrate causing a compressive optic neuropathy with ischaemic infarction. The inflammatory reaction did not extend beneath the pia mater. Electron microscopy showed exuberant fibroplasia, collagenosis and elastogenesis associated with focal extracellular collagen degeneration. The histological changes are non-specific. In suspected cases, biopsy is better taken from the intraorbital nerve rather than intracranially so that detailed examination of the optic nerve sheath can be performed. PHILIP G HYKIN DAVID J SPALTON Medical Eye Unit, St Thomas' Hospital, London SEI 7EH, UK