Morishita Takashi, Higuchi Masa-Aki, Tsuboi Yoshio, Samura Kazuhiro, Inoue Tooru
Department of Neurosurgery, Fukuoka University, Faculty of Medicine, Fukuoka, Japan.
Department of Neurology, Fukuoka University, Faculty of Medicine, Fukuoka, Japan.
NMC Case Rep J. 2016 Nov 29;4(1):1-3. doi: 10.2176/nmccrj.cr.2016-0012. eCollection 2017 Jan.
Eye opening apraxia (EOA) has been described in literature as a complication of deep brain stimulation (DBS), especially after electrode implantation in the subthalamic nucleus (STN). EOA can be either worsened or alleviated by DBS depending on the etiology. Herein, we report a rare case where the progression of brain atrophy may have contributed to the delayed onset of EOA. The patient, a 73-year-old woman, had previously undergone bilateral STN-DBS for advanced Parkinson's disease (PD), which was performed by another DBS team, at the age of 68 years. She initially experienced a dramatic improvement in her motor symptoms, with no adverse events. However, she had difficulty in opening her right eye 3 years after the DBS surgery. Imaging studies showed that the brain atrophy had progressed over the past 5 years, and that the DBS electrodes were implanted through the far anterior entry points. We considered that the relative movement of the DBS might have been caused by the progression of the brain atrophy to the posterior limb of the internal capsule (IC) where the corticobulbar tract exists, and this was enhanced by the lower implantation angle. The present case illustrates the importance of the DBS insertion angle considering the a+ trophic effect and the follow-up imaging studies after DBS.
