Gialopsou Aikaterini, Houlgreave Mairi S, Farr Isabel, Jackson Stephen R
School of Psychology, University of Nottingham, University Park, Nottingham NG7 2RD, UK.
Sir Peter Mansfield Imaging Centre, School of Physics and Astronomy, University of Nottingham, University Park, Nottingham NG7 2RD, UK.
Brain Commun. 2025 Jun 18;7(4):fcaf247. doi: 10.1093/braincomms/fcaf247. eCollection 2025.
Tourette syndrome is a neurological disorder characterized by the occurrence of vocal and motor tics. The pathophysiology of Tourette syndrome has been linked to a substantial reduction in the number of inhibitory GABAergic interneurons found within the striatum, which may lead to increased neural 'noise' within the cortical-striatal-thalamic-cortical circuit implicated in movement production. In the current study, we used EEG to investigate increased neural noise in a group of 19 adults with Tourette syndrome compared to a matched neurotypical control group. We operationalized neural noise in this study as increased trial-by-trial variability in the magnitude and/or the timing of responses to a discrete somatosensory stimulation event. Specifically, we examined trial-by-trial variability in responses to a single pulse of median nerve electrical stimulation. Our results demonstrate that the P100 somatosensory evoked potential, which has been associated with conscious perception of tactile stimuli, was significantly increased in the Tourette syndrome group. Importantly, however, while the timing, temporal variability and spatial topography of early- and mid-latency somatosensory evoked potential components (e.g. N20, P45, N60, P100) did not differ in the Tourette syndrome group, when compared to matched controls, trial-by-trial variability was substantially increased in the Tourette syndrome group, but this was normalized in response to stimulation. These findings may indicate that the trial-by-trial recruitment of neuronal sensorimotor populations is less stable at rest in individuals with Tourette syndrome compared to controls but may normalize in response to stimulation.
抽动秽语综合征是一种神经系统疾病，其特征为出现发声和运动抽动。抽动秽语综合征的病理生理学与纹状体内抑制性γ-氨基丁酸能中间神经元数量的大幅减少有关，这可能导致参与运动产生的皮质-纹状体-丘脑-皮质回路中的神经“噪声”增加。在本研究中，我们使用脑电图来调查19名患有抽动秽语综合征的成年人与一组匹配的神经典型对照组相比神经噪声是否增加。在本研究中，我们将神经噪声定义为对离散体感刺激事件的反应幅度和/或时间上逐次试验变异性的增加。具体而言，我们检查了对正中神经电刺激单个脉冲反应的逐次试验变异性。我们的结果表明，与触觉刺激的意识感知相关的P100体感诱发电位在抽动秽语综合征组中显著增加。然而，重要的是，虽然与匹配的对照组相比，抽动秽语综合征组早期和中期潜伏期体感诱发电位成分（如N20、P45、N60、P100）的时间、时间变异性和空间地形图没有差异，但抽动秽语综合征组的逐次试验变异性大幅增加，但这种情况在刺激反应中恢复正常。这些发现可能表明，与对照组相比，抽动秽语综合征患者在静息状态下神经元感觉运动群体的逐次试验募集不太稳定，但在刺激反应中可能恢复正常。
