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Show loumal of Clilliml N,'un""I",tI",I"",logv 6(2I: /2.1-/25, /986. Abstracts , )'1Xh Ravl'n 1',,'''. :'\l'1\' York Australian Association of Neurologists' Annual Scientific Meeting-1985 Isla M. Williams, M.D. The Annual Scientific Meeting of the Australian Association of Neurologists 1985 was held in Singapore. Ten papers of interest to neuro-ophthalmologists were presented and will be reviewed briefly. t 1. Drs. B. J. Brew, R. Garrick, and M. Steiner pointed out in their paper. A Casl.' of Optic Neuritis SeCLl/Idartl to Mllcoplasllla Plleulllolliae Infect ioIl , that Mycopla~ma plle·umollial.' is a well-recognized human pathogen. The spectrum of clinical manifestations is wide. The neurological complications include encephalitis, meningitis, acute cerebellar ataxia, cranial nerve palsies, transverse myelitis, and a Guillain- Barre-like illness. They mentioned two reports of optic neuritis as complications, but none has appeared to date in the English literature. The pathogenesis of the neurological complications is conjectural and includes direct invasion, superadded infection, and autoimmune and toxic mechanisms. The paper described the clinical features of a patient with optic neuritis as the only neurological complication of Mycoplasma pnl.'lllllOllial.' infection of the lung. The results of serial visual-evoked potentials were discussed in relation to a presumed pathogenetic mechanism for the development of optic neuritis. The authors suggested that all cases of optic neuritis be checked for the evidence of recent mycoplasma infection. This information will be helpful in defining the long-term prognosis with respect to multiple sclerosis. t 2. Drs. J. W. Dunne and R. H. Edis stated that optic neuropathy in Graves' disease is an uncommon but potentially treatable cause of disabling visual loss. In their paper Optic Nerve Imlolwmellt ill Graves' Ophthalmopathy: A Case Report and Review, they stated that optic nerve damage is probably secondary to compression by swollen extraocular muscles at the apex of the orbit. The visual loss is usually bilateral and insidiously progressive, although accelerated visual loss, fluctuations in vi- /23 sion, and features mimicking orbital cellulitis may occur. Ocular congestive symptoms and proptosis have no direct relationship to the severity of visual loss. Early diagnosis is facilitated by orbital CT scanning. Oral corticosteroids and radiotherapy, alone or in combination, are the primary modalities of medical treatment. Surgical decompression of the orbit can be used where medical approaches have failed. t 3. Drs. B. J. Brew, P. Benecke, W. J. Burke, T. Playfair, and R. Penny reported A Case of VogtKoyallagi- Harada Disl.'ase Successfully Treated with Cyclosporill. Vogt-Koyanagi-Harada disease is a rare entity primarily affecting the uvea, meninges, and the skin. The authors maintained that it is currently felt to be related to a defect in immunological surveillance of melanocyte surface antigens. The disease is manifested clinically by headache, dysaCOUSiS, vertigo, impaired vision, and vitiligo. Evidence suggests that steroids decrease the risk of permanent blindness. However, there is a propensity for recurrence. This report described a typical case of VogtKoyanagi - Harada disease that failed to respond to steroids and cytotoxic agents. With the introduction of Cyclosporin, the blindness and the neurological complications of vertigo and dysacousis promptly resolved. There were no recurrences. This was said to be the second report in the literature of the use of Cyclosporin in this disease. The authors suggested that consideration be given to the use of Cyclosporin in this disabling disease. 4. Drs. P. A. Kempster, R. A. McDonald, and R. D. Rollinson reported Illtracrallial Hypertellsioll Associatl.' d with Acute Posterior Multifocal Placoid Pigment £1/itheliopathy (a choroidal vasculopathy) in a 30year- old male who presented with rapidly developing bilateral visual impairment. The fundal appearances and fluorescein angiography were typical of acute posterior multifocal placoid pigment epitheliopathy. Cerebrospinal fluid (CSF) examina- |
