Burwell R G, Cole A A, Cook T A, Grivas T B, Kiel A W, Moulton A, Thirlwall A S, Upadhyay S S, Webb J K, Wemyss-Holden S A
Department of Human Morphology, University of Nottingham Medical School, Queen's Medical Centre, U.K.
Acta Orthop Belg. 1992;58 Suppl 1:33-58.
There is no generally accepted scientific theory for the etiology of idiopathic scoliosis. Hence, current treatment is pragmatic and not based on knowledge of causation of the deformity. In Nottingham, we have evaluated data from studies of the hips, pelvis, spine, rib cage and trunk muscles in scoliotic (pre- and post operative) and control patients, cadavers and a mechanical model to formulate a new theory of etiology for idiopathic scoliosis (figs. 18 & 19 of ref. 15). Evidence is summarized for the view that idiopathic scoliosis results, in part, from a developmental abnormality in the central nervous system creating rib-vertebra angle asymmetry which leads to a cyclical failure of mechanisms of rotation control in the trunk; these involve rotation-inducing (pelvic) and rotation-defending (discal, ligamentous and costal) mechanisms acting mainly in gait. The mechanical breakdown of rotation occurs in association with a lateral spinal curvature and a lordotic segment to create the initial deformity of idiopathic scoliosis. Then, growth, both abnormal (secondary to vertebral hyper-pressures) and normal (linear spinal growth) with gravity adds to the initiating and continuing neuromuscular mechanisms to augment curve progression. This theory views the spine in the wider perspective of function in the trunk, evolution and development, all in relation to bipedalism. The goal of etiological research is ultimately to base a treatment on some knowledge of causation of the deformity.
对于特发性脊柱侧凸的病因,目前尚无被广泛接受的科学理论。因此,当前的治疗方法较为务实,并非基于对畸形成因的了解。在诺丁汉,我们评估了脊柱侧凸患者(术前和术后)、对照患者、尸体以及一个力学模型的髋部、骨盆、脊柱、胸廓和躯干肌肉的研究数据,以形成一种特发性脊柱侧凸病因的新理论(参考文献15的图18和19)。有证据支持这样一种观点,即特发性脊柱侧凸部分源于中枢神经系统的发育异常,导致肋骨 - 椎骨角度不对称,进而引发躯干旋转控制机制的周期性失效;这些机制包括主要在步态中起作用的旋转诱导(骨盆)和旋转防御(椎间盘、韧带和肋骨)机制。旋转的力学破坏与脊柱侧凸和前凸节段相关联,从而产生特发性脊柱侧凸的初始畸形。然后,异常生长(继发于椎体高压)和正常生长(脊柱线性生长)加上重力作用,增强了起始和持续的神经肌肉机制,促进了侧弯的进展。该理论从躯干功能、进化和发育的更广泛角度看待脊柱,所有这些都与双足行走有关。病因学研究的最终目标是基于对畸形成因的某种了解来进行治疗。