Objective To investigate the neuropathogenesis of Adie prime;s pupil. Methods The neuroelectrophysiological and neuroimaging data of 42 patients with Adie's pupil (lightnear 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 sensorymotor 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.
Citation： 池元伟,高玉红,彭静婷,赵毅. Neuroelectrophysiology and neuroimaging study of Adie's pupil. Chinese Journal of Ocular Fundus Diseases, 2009, 25(6): 451-453. doi: Copy