Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain.
Eur Spine J. 2010 Feb;19(2):223-30. doi: 10.1007/s00586-009-1243-y. Epub 2009 Dec 24.
The aetiology of idiopathic scoliosis (IS) remains unknown; however, there is a growing body of evidence suggesting that the spine deformity could be the expression of a subclinical nervous system disorder. A defective sensory input or an anomalous sensorimotor integration may lead to an abnormal postural tone and therefore the development of a spine deformity. Inhibition of the motor cortico-cortical excitability is abnormal in dystonia. Therefore, the study of cortico-cortical inhibition may shed some insight into the dystonia hypothesis regarding the pathophysiology of IS. Paired pulse transcranial magnetic stimulation was used to study cortico-cortical inhibition and facilitation in nine adolescents with IS, five teenagers with congenital scoliosis (CS) and eight healthy age-matched controls. The effect of a previous conditioning stimulus (80% intensity of resting motor threshold) on the amplitude of the motor-evoked potential induced by the test stimulus (120% of resting motor threshold) was examined at various interstimulus intervals (ISIs) in both abductor pollicis brevis muscles. The results of healthy adolescents and those with CS showed a marked inhibitory effect of the conditioning stimulus on the response to the test stimulus at interstimulus intervals shorter than 6 ms. These findings do not differ from those reported for normal adults. However, children with IS revealed an abnormally reduced cortico-cortical inhibition at the short ISIs. Cortico-cortical inhibition was practically normal on the side of the scoliotic convexity while it was significantly reduced on the side of the scoliotic concavity. In conclusion, these findings support the hypothesis that a dystonic dysfunction underlies in IS. Asymmetrical cortical hyperexcitability may play an important role in the pathogenesis of IS and represents an objective neurophysiological finding that could be used clinically.
特发性脊柱侧凸(IS)的病因仍然未知;然而,越来越多的证据表明,脊柱畸形可能是一种亚临床神经系统紊乱的表现。感觉输入缺陷或异常的感觉运动整合可能导致异常姿势张力,从而导致脊柱畸形的发展。在肌张力障碍中,运动皮质-皮质兴奋性抑制是异常的。因此,皮质-皮质抑制的研究可能为 IS 的病理生理学提供一些关于肌张力障碍假说的见解。使用成对脉冲经颅磁刺激研究了 9 名青少年特发性脊柱侧凸、5 名先天性脊柱侧凸青少年和 8 名年龄匹配的健康对照组的皮质-皮质抑制和易化作用。在两个拇短展肌中,在不同的刺激间间隔(ISIs)下,以前的条件刺激(休息运动阈值的 80%强度)对测试刺激(休息运动阈值的 120%)引起的运动诱发电位幅度的影响进行了检查。健康青少年和先天性脊柱侧凸青少年的结果显示,在刺激间间隔小于 6 毫秒时,条件刺激对测试刺激的反应具有明显的抑制作用。这些发现与正常成年人报告的结果没有区别。然而,特发性脊柱侧凸儿童在短刺激间间隔下显示出皮质-皮质抑制异常降低。凸侧的皮质-皮质抑制实际上是正常的,而凹侧的皮质-皮质抑制显著降低。总之,这些发现支持了这样一种假说,即张力障碍功能障碍是 IS 的基础。皮质兴奋性的不对称增加可能在 IS 的发病机制中起重要作用,并且代表了一种可以在临床上使用的客观神经生理学发现。