Department of Neurology, Third Faculty of Medicine, Charles University and Faculty Hospital Kralovske Vinohrady, Prague, Czech Republic.
Department of Orthopedics and Traumatology, Third Faculty of Medicine, Charles University and Faculty Hospital Kralovske Vinohrady, Prague, Czech Republic.
J Spinal Cord Med. 2022 Mar;45(2):186-193. doi: 10.1080/10790268.2020.1739893. Epub 2020 Mar 23.
The pathogenesis of adolescent idiopathic scoliosis (AIS), including the role of brain and spinal inhibitory circuits, is still poorly elucidated. The aim of this study was to identify which central inhibitory mechanisms are involved in the pathogenesis of AIS. A prospective neurophysiological study, using a battery of neurophysiological tests, such as cutaneous (CuSP) and cortical (CoSP) silent periods, motor evoked potentials (MEP) and paired-pulse transcranial magnetic stimulation (ppTMS). Neurophysiological laboratory. Sixteen patients with AIS (14 females, median age 14.4) and healthy controls. MEPs were obtained after transcranial magnetic stimulation (TMS) and recorded from the abductor pollicis muscle (APB). ppTMS was obtained at interval ratios (ISI) of 1, 2, 3, 6, 10, 15 and 20 ms. The cortical silent period (CoSP) was recorded from the APB. The cutaneous silent period (CuSP) was measured after painful stimuli delivered to the thumb while the subjects maintained voluntary contraction of the intrinsic hand muscles. The data were analyzed and compared with those from healthy subjects. The CoSP duration was significantly prolonged in AIS patients. A significantly higher amplitude of ppTMS for ISI was found in all AIS patients, without remarkable left-right side differences. No significant difference in MEP latency or amplitude nor in the CuSP duration was obtained. Our observation demonstrates evidence of central nervous system involvement in adolescent idiopathic scoliosis (AIS). Lower intracortical inhibition, higher motor cortex excitability, and preserved spinal inhibitory circuits are the main findings of this study. A possible explanation of these changes could be attributed to impaired sensorimotor integration predominantly at the cortical level.
青少年特发性脊柱侧凸(AIS)的发病机制,包括大脑和脊髓抑制回路的作用,仍未得到充分阐明。本研究旨在确定哪些中枢抑制机制参与 AIS 的发病机制。这是一项前瞻性神经生理学研究,使用一系列神经生理学测试,如皮肤(CuSP)和皮质(CoSP)静息期、运动诱发电位(MEP)和成对脉冲经颅磁刺激(ppTMS)。神经生理学实验室。16 名 AIS 患者(14 名女性,中位年龄 14.4 岁)和健康对照组。MEPs 是通过经颅磁刺激(TMS)获得的,并从拇指外展肌(APB)记录。ppTMS 在间隔比(ISI)为 1、2、3、6、10、15 和 20 ms 时获得。皮质静息期(CoSP)从 APB 记录。在拇指接受疼痛刺激的同时,受试者保持手部内在肌肉的自主收缩,测量皮肤静息期(CuSP)。对数据进行分析并与健康受试者进行比较。AIS 患者的 CoSP 持续时间明显延长。在所有 AIS 患者中,ppTMS 的振幅显著升高,ISI 为 1,且左右侧无明显差异。MEP 潜伏期或振幅以及 CuSP 持续时间无显著差异。我们的观察结果表明,中枢神经系统参与了青少年特发性脊柱侧凸(AIS)。本研究的主要发现是皮质内抑制降低、运动皮层兴奋性升高和脊髓抑制回路保留。这些变化的可能解释可以归因于主要在皮质水平上感觉运动整合受损。