Adie瞳孔患者的神经影像学和神经电生理检查

目的 探讨Adie瞳孔的神经发病机制.方法 回顾分析具有光-近反射分离及虹膜括约肌的节段性麻痹的Adie瞳孔特征的42例患者的神经影像学和神经电生理检查资料.其中,单侧瞳孔扩大者37例,双侧瞳孔扩大者5例.患者中,23例行头颅核磁共振成像(MRI)检查,其中1例同时行头颅CT检查.另有14、5、9、18、11、5例患者分别进行神经传导速度、四肢肌电图、双下肢肌电图、视觉诱发电位(VEP)、体感诱发电位、脑电图检查.结果 23例行MRI和CT检查的患者中,13例出现中枢神经系统中线结构解剖变异或微小病变.14例同时行肌电图和神经传导速度检查的患者中,6例表现为感觉神经传导速度减慢和多发性感觉运动性周围神经损害;18例行视觉诱发电位检查的患者中,5例P100潜伏期延长;11例行体感诱发电位检查的患者中,2例显示周围神经损害;5例检查脑电网的患者中,1例显示异常.结论 周围神经损害可能是Adie瞳孔的重要发病机制,中枢神经系统损害也参与其发病.

Neuroelectrophysiology and neuroimaging study of Adie's pupil

Objective To investigate the neuropathogenesis of Adie's pupil.Methods The neuroelectrophysiological and neuroimaging data of 42 patients with Adie's pupil (light-near dissociation and segmental palsy of iris sphincter) were retrospectively analyzed.There were 37 patients with unilateral pupil dilation and 5 patients with bilateral pupil dilation.Cranial magnetic resonance imaging (MRI,23 patients),Cranial CT scanning (1 patient),nerve conduction velocity (NCV,14 patients),limb electromyogram (EMG,5 patients),both lower extremities EMG (9 patients),visual evoked potential (VEP,18 patients),somatosensory evoked potential (SEP,11 patients) and electroencephalograms (EEG,5 patients) were performed on some of those patients.Results Central nervous system midline anatomic variations or minor lesions were found in 13/23 cases of MRI/CT imaging.Slowed sensory NCV and multiple sensory-motor peripheral nerve damages were evident in 6/14 cases of the NCV/EMG assay.5/18 patients showed prolonged latency of VEP P100.2/11 cases showed peripheral nerve damage in SEP recording.and 1/5 cases showed abnormal EEG.Conclusion Peripheral nerve damage may be an important pathogenesis of Adie's pupil,while the central nervous system damage is also involved in its pathogenesis.