Orthopedic Surgery Department, Hospital Arnau de Vilanova, Faculty of Health Science, Cardenal Herrera-CEU University, Calle San Clemente 12, 46015 Valencia, Spain.
Spine J. 2013 Aug;13(8):938-46. doi: 10.1016/j.spinee.2013.03.002. Epub 2013 Apr 23.
Dysfunctions in sensorimotor integration, reminiscent to those described in idiopathic dystonia, have been found in idiopathic scoliosis (IS) and might be involved in its pathogenesis. Studying the effects of experimental disruption of sensory cortex may shed further insight into the etiopathology of IS.
To evaluate whether disruption of central sensorimotor integration through partial ablation of the somatosensory cortex leads to scoliosis in developing rats and to describe the effects of such an intervention on motor cortico-cortical inhibition and facilitation.
Fifty Wistar rats aged 3 weeks were used in the study. Twenty-four rats underwent craniotomy and electrocoagulation of the sensory cortex (PAR1) in the right hemisphere. A second group of 16 rats underwent a sham operation with craniotomy but no electrocoagulation. A third group of 10 rats was used as intact controls. Four weeks after surgery, motor cortical excitability was assessed with paired-pulse electrical cortical stimulation. Neurologic and behavioral examinations were completed serially, and 10 weeks after surgery, X-ray examinations were performed in anesthetized rats to assess spinal curvature. Electromyographic recordings of paravertebral muscle activity were performed in waking rats. At the end of the study, rats were sacrificed, and histologic examinations of brain tissue were performed to confirm the extent of the lesion. A grant from a Government Health Research Fund without salaries assignment financed the study.
Almost half of the animals with somatosensory cortectomy (46%) developed scoliosis, with an average Cobb angle of 23 ± 8°. None of the animals in the sham or control groups developed scoliosis. Despite cortical lesions, no motor or behavioral deficits were apparent in the experimental group, and cortectomized rats were neurologically indistinguishable from sham or control animals, except for the presence of scoliosis. Cortico-cortical inhibition was significantly reduced in the hemisphere of scoliotic concavity in the cortectomized group but was normal in the other groups.
These findings indicate that altered sensorimotor integration may cause scoliosis without noticeable motor impairment. Reduced cortico-cortical inhibition was observed in cortectomized rats. This finding is consistent with results in adolescents with IS and suggests that alteration of cortical hemispheric balance of sensorimotor integration may play an important role in the pathogenesis of IS.
在特发性脊柱侧弯（IS）中发现了类似于特发性肌张力障碍的感觉运动整合功能障碍，这可能与该病的发病机制有关。研究感觉皮层的实验性破坏对 IS 的病因学可能会有进一步的认识。
评估通过对感觉皮层的部分消融是否会导致发育中的大鼠发生脊柱侧弯，并描述这种干预对运动皮质的皮质内抑制和易化的影响。
本研究使用了 3 周龄的 Wistar 大鼠 50 只。24 只大鼠接受了右侧大脑半球的颅骨切开术和体感皮层（PAR1）的电凝术（PAR1）。第二组 16 只大鼠接受了假手术，仅进行颅骨切开术但不进行电凝术。第三组 10 只大鼠作为完整对照组。手术后 4 周，通过双脉冲电皮质刺激评估运动皮质兴奋性。连续进行神经和行为检查，术后 10 周，对麻醉大鼠进行 X 线检查以评估脊柱弯曲度。在清醒大鼠中进行椎旁肌肉活动的肌电图记录。研究结束时，处死大鼠并进行脑组织的组织学检查以确认病变范围。政府健康研究基金拨款资助了这项研究，但没有分配工资。
接受体感皮层切除术的动物中近一半（46%）发生了脊柱侧弯，平均 Cobb 角为 23°±8°。假手术组和对照组无一例发生脊柱侧弯。尽管存在皮质损伤，但实验组的运动或行为缺陷并不明显，皮质切除大鼠在神经学上与假手术或对照组动物没有区别，除了存在脊柱侧弯外。在皮质切除组，脊柱侧弯凹侧的半球皮质内抑制明显降低，但在其他组正常。
这些发现表明，感觉运动整合的改变可能导致脊柱侧弯而没有明显的运动障碍。在皮质切除大鼠中观察到皮质内抑制减少。这一发现与青少年特发性脊柱侧弯的结果一致，提示皮质感觉运动整合的半球平衡改变可能在特发性脊柱侧弯的发病机制中起重要作用。
