Changing a "progressive" factor into a "corrective" factor: the effect of intervertebral disc modulation in treatment of idiopathic scoliosis

Abstract

BMI is a surrogate measure for body fat and circulating leptin levels. The finding that girls with relatively lower BMI have significantly later menarche, and a significant excess of TAs, suggests a relation to energy homeostasis through the hypothalamus. The hypothesis we suggest for the pathogenesis of severe TA in girls and boys has the same mechanism as that proposed recently for AIS girls, namely: severe TAs are initiated by a genetically-determined selectively increased hypothalamic sensitivity (up-regulation, i.e. increased sensitivity) to leptin with asymmetry as an adverse response to stress (hormesis), mediated bilaterally mainly to the growing trunk via the sympathetic nervous system (leptin-hypothalamic-sympathetic nervous system (LHS) concept). The putative autonomic dysfunction is thought to be increased by any lower circulating leptin levels associated with relatively lower BMIs. Sympathetic nervous system activation with asymmetry leads to asymmetries in ribs and/or vertebrae producing severe TA when beyond the capacity of postural mechanisms of the somatic nervous system to control the shape distortion of the trunk. A test of this hypothesis testing skin sympathetic responses, as in the Rett syndrome, is suggested.

Are the Spinal Changes in the Course of Scoliogeny Primary but Secondary?

“…The study of the radiographical assessment of our referred school scoliosis screening children suffering mild IS showed that the deformity starts at the level of the intervertebral disc, then the vertebra body, as a result of the plasticity of the intervertebral disc [8,9]. Three years later, this finding was confirmed in another report [15].…”

“…It was discovered that the younger children with truncal asymmetry who were referred to the scoliosis clinic often times had a perfectly straight spine with no vertebral rotation, despite the presence of a thoracic hump [7]. The scoliotic spine first deforms at the level of the intervertebral disc, not the vertebrae [8,9].…”

“…The used methods of imaging, the ethics based on describing the requested imaging, their reliability study, the ages of children, and the degree of deformity are analyzed in detail in our earlier publications, refs. [7][8][9][10]12,13,22,38,41,[47][48][49][50][51][52]110].…”

Early onset scoliosis: What the primary care provider needs to know and implications for practice

“…The Hueter–Volkman law, which is the rationale for the management of scoliosis during skeletal growth, explains this “vicious cycle” of asymmetrical growth. The law assumes that growth follows a biomechanical mode of deformity progression in which increased axial compression decelerates growth and reduced axial compression accelerates growth in the skeletally immature (Grivas, Vasiliadis, Rodopoulos, Bardakos, & Gatos, 2009). The Hueter–Volkmann theory is the basis for explaining the relationship in which wedging of the IVD contributes to the progression of IS.…”

Maturation of the vertebral ring apophysis is delayed in girls with adolescent idiopathic scoliosis compared to the normal population

“…For growth to proceed harmoniously, the developing mechanical properties of the disc must remain in synchronicity with these rapidly increasing loads [3]. In case of a mismatch between increasing asymmetrical spinal loading, and mechanical maturation of the IVD, spinal deformity may develop [3,[8][9][10][11].…”