Millner P A, Dickson R A
Division of Orthopaedic Surgery, St. James's University Hospital, Leeds, UK.
Eur Spine J. 1996;5(6):362-73. doi: 10.1007/BF00301963.
For whatever reason, right-left asymmetry has attracted an illogical proportion of research effort. Non-structural scoliosis, for example secondary to a leg length inequality, is indeed a problem of right-left asymmetry, but structural scoliosis is a complex three-dimensional deformity involving all planes. Biomechanical, biological and clinical evidence indicates clearly that the problem is one of front-back asymmetry and not right-left. The importance of biological factors lies in their ability to bring the spinal column to and beyond its buckling threshold. Thus a taller and more slender spine is more liable to bend and, being stiffer in the sagittal plane, favours movement into other planes. This epitomises the spine of the scoliosis patient who is growing faster with a spinal template similar to other family members allowing idiopathic scoliosis to express itself genetically. It is the opposite condition to idiopathic hyperkyphosis (Scheuermann's disease), but this deformity is rotationally stable, thus remaining in the sagittal plane. The presence of an adjacent area of lordo-scoliosis below the region of hyperkyphosis testifies to the common nature of the pathogenesis of idiopathic scoliosis and Scheuermann's disease. It is the area of compensatory hyperlordosis below the Scheuermann's area that has obligatorily buckled and represents a human model supporting the lordosis theory, as does surgically tethering the back of the young growing human spine, which crankshafts accelerated progression. Similarly the only successful animal model of the formation of idopathic follows creation of a lordotic spinal segment in an otherwise kyphotic spine. For centuries, engineers have recognised that the mechanical behaviour of a column under load is influenced by geometry, as well as by material properties; it is clear that the spinal column also obeys these well-described laws.
无论出于何种原因，左右不对称吸引了不合理比例的研究精力。例如，继发于腿长不等的非结构性脊柱侧弯确实是左右不对称问题，但结构性脊柱侧弯是涉及所有平面的复杂三维畸形。生物力学、生物学和临床证据清楚表明，问题在于前后不对称而非左右不对称。生物因素的重要性在于它们能够使脊柱达到并超过其屈曲阈值。因此，更高且更细长的脊柱更容易弯曲，并且由于在矢状面更僵硬，有利于向其他平面移动。这体现了脊柱侧弯患者的脊柱情况，其生长速度更快，脊柱模板与其他家庭成员相似，使得特发性脊柱侧弯能够通过基因表现出来。这与特发性脊柱后凸（休曼病）情况相反，但这种畸形在旋转方面是稳定的，因此保持在矢状面。在脊柱后凸区域下方存在相邻的脊柱前凸 - 脊柱侧弯区域证明了特发性脊柱侧弯和休曼病发病机制的共同性质。正是休曼病区域下方的代偿性脊柱前凸区域必然发生了屈曲，代表了支持脊柱前凸理论的人体模型，就像对年轻生长中的人类脊柱后部进行手术束缚会导致曲轴效应加速进展一样。同样，特发性脊柱侧弯形成的唯一成功动物模型是在原本后凸的脊柱中创建一个脊柱前凸节段。几个世纪以来，工程师们已经认识到，柱体在负载下的力学行为受几何形状以及材料特性的影响；很明显，脊柱也遵循这些已被充分描述的规律。
