التفاصيل البيبلوغرافية
| العنوان: |
Visual field defects of optic neuritis in neuromyelitis optica compared with multiple sclerosis. |
| المؤلفون: |
Nakajima, Hideto, Hosokawa, Takafumi, Sugino, Masakazu, Kimura, Fumiharu, Sugasawa, Jun, Hanafusa, Toshiaki, Takahashi, Toshiyuki |
| المصدر: |
BMC Neurology; 2010, Vol. 10, p45-50, 6p |
| مصطلحات موضوعية: |
MULTIPLE sclerosis, OPTIC neuritis, OPTIC nerve diseases, SUBACUTE myelooptic neuropathy, SCOTOMA, PATIENTS |
| مستخلص: |
Background: Neuromyelitis optica (NMO) is an inflammatory demyelinating disease that predominantly affects the optic nerves and the spinal cord, and is possibly mediated by an immune mechanism distinct from that of multiple sclerosis (MS). Central scotoma is recognized as a characteristic visual field defect pattern of optic neuritis (ON), however, the differing pathogenic mechanisms of NMO and MS may result in different patterns of visual field defects for ON. Methods: Medical records of 15 patients with NMO and 20 patients with MS having ON were retrospectively analyzed. A thorough systemic and neurological examination was performed for evaluating ON. The total number of relapses of ON and visual fields was investigated. Visual fields were obtained by Goldmann perimeter with each ON relapse. Results: All MS patients experienced central scotoma, with 90% of them showing central scotoma with every ON relapse. However, 53% of NMO patients showed central scotoma with every ON relapse (p = 0.022), and the remaining 47% of patients experienced non-central scotoma (altitudinal, quadrant, three quadrant, hemianopia, and bitemporal hemianopia). Thirteen percent of NMO patients did not experience central scotoma during their disease course. Altitudinal hemianopia was the most frequent non-central scotoma pattern in NMO. Conclusions: NMO patients showed higher incidence of non-central scotoma than MS, and altitudinal hemianopia may be characteristic of ON occurring in NMO. As altitudinal hemianopia is highly characteristic of ischemic optic neuropathy, we suggest that an ischemic mechanism mediated by anti-aquaporin-4 antibody may play a role in ON in NMO patients. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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