School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
School of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Mov Disord. 2020 Jul;35(7):1173-1180. doi: 10.1002/mds.28042. Epub 2020 Apr 6.
The neurophysiological disruptions underlying blepharospasm, a disabling movement disorder characterized by increased blinking and involuntary muscle spasms of the eyelid, remain poorly understood.
To investigate the neural substrates underlying reflexive blinking in blepharospasm patients compared to healthy controls using simultaneous functional MRI and surface electromyography.
Fifteen blepharospasm patients and 15 healthy controls were recruited. Randomly timed air puffs to the left eye were used to induce reflexive eye blinks during two 8-minute functional MRI scans. Continuous surface electromyography and video recordings were used to monitor blink responses. Imaging data were analyzed using an event-related design.
Fourteen blepharospasm patients (10 female; 61.6 ± 8.0 years) and 15 controls (11 female; 60.9 ± 5.5 years) were included in the final analysis. Reflexive eye blinks in controls were associated with activation of the right hippocampus and in patients with activation of the left caudate nucleus. Reflexive blinks in blepharospasm patients showed increased activation in the right postcentral gyrus and precuneus, left precentral gyrus, and left occipital cortex compared to controls. Dystonia severity negatively correlated with activity in the left occipital cortex, and disease duration negatively correlated with reflexive-blink activity in the cerebellum.
Reflexive blinking in blepharospasm is associated with increased activation in the caudate nucleus and sensorimotor cortices, suggesting a loss of inhibition within the sensorimotor corticobasal ganglia network. The association between decreasing neural response during reflexive blinking in the cerebellum with disease duration suggests an adaptive role. © 2020 International Parkinson and Movement Disorder Society.
眼睑痉挛是一种致残性运动障碍，其特征为眨眼增多和眼睑不自主肌肉痉挛，但其神经生理紊乱仍知之甚少。
通过同时进行功能磁共振成像和表面肌电图检查，研究眼睑痉挛患者反射性眨眼的神经基础与健康对照者的不同。
共纳入 15 例眼睑痉挛患者和 15 例健康对照者。在两次 8 分钟的功能磁共振成像扫描中，用随机定时的向左眼吹空气的方法诱发反射性眨眼。连续进行表面肌电图和视频记录以监测眨眼反应。使用事件相关设计分析成像数据。
最终纳入 14 例眼睑痉挛患者（10 例女性；61.6±8.0 岁）和 15 例对照者（11 例女性；60.9±5.5 岁）。在对照者中，反射性眨眼与右侧海马体的激活有关，而在患者中与左侧尾状核的激活有关。与对照者相比，眼睑痉挛患者的反射性眨眼在右侧中央后回和楔前叶、左侧中央前回和左侧枕叶显示出更高的激活。肌张力障碍严重程度与左侧枕叶的活性呈负相关，疾病持续时间与小脑的反射性眨眼活性呈负相关。
眼睑痉挛的反射性眨眼与尾状核和感觉运动皮质的活性增加有关，提示感觉运动皮质基底节网络内的抑制丧失。小脑在反射性眨眼时神经反应的减少与疾病持续时间之间的关联表明了小脑的适应性作用。 © 2020 国际帕金森病和运动障碍学会。
