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Pupil Constriction Latency in Optic Neuritis

視神經炎之瞳孔收縮遲滯反應

摘要


Using binocular infrared pupillometer (C-2515, Hamamatsu Photonics), 12 patients (14 eyes) of optic neuritis were examined in both acute and recovery stages. Pupil constriction latency (CL) was prolonged in acute stage as compared with normal fellow eyes (p<0.001). In recovery stage, constriction latency improved significantly (p<0.05). Constriction velocity (CV) was decreased in acute stage as compared with normal fellow eye (p<0.05), however it did not seem to improve in recovery sage (p=0.721). As for dilatation velocity (DV), in both acute and recovery stages, there were no significant differences between affected eyes and normal fellow eyes By theoretical deduction, the constriction latency prolongation can be shown to be due to afferent route rather than efferent route. The CL prolongation in acute stage can be explained by optic nerve demyelination, as generally agreed. Like other visual functions it improved during recovery to a near normal level. The CV was impaired in both acute and recovery stages, and there seemed to be no improvement. The DV was normal in both acute and recovery stage, which we consider to be the effect of a constant sympathetic stimulation. The afferent and efferent routes are differentiated by deduction-which is not possible by traditional pupil examination methods such as pupil cycle time or relative afferent pupillary defects.

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並列摘要


Using binocular infrared pupillometer (C-2515, Hamamatsu Photonics), 12 patients (14 eyes) of optic neuritis were examined in both acute and recovery stages. Pupil constriction latency (CL) was prolonged in acute stage as compared with normal fellow eyes (p<0.001). In recovery stage, constriction latency improved significantly (p<0.05). Constriction velocity (CV) was decreased in acute stage as compared with normal fellow eye (p<0.05), however it did not seem to improve in recovery sage (p=0.721). As for dilatation velocity (DV), in both acute and recovery stages, there were no significant differences between affected eyes and normal fellow eyes By theoretical deduction, the constriction latency prolongation can be shown to be due to afferent route rather than efferent route. The CL prolongation in acute stage can be explained by optic nerve demyelination, as generally agreed. Like other visual functions it improved during recovery to a near normal level. The CV was impaired in both acute and recovery stages, and there seemed to be no improvement. The DV was normal in both acute and recovery stage, which we consider to be the effect of a constant sympathetic stimulation. The afferent and efferent routes are differentiated by deduction-which is not possible by traditional pupil examination methods such as pupil cycle time or relative afferent pupillary defects.

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