AIS: Etiology, Pathogenesis. Facts and Reflections

This article has conceptual character. Authors paid attention to one of the paradoxes of AIS-it’s being mono-form in the shape of a 3D deformation at any etiology (polietiology). The explanation of this paradox and its reason was found while performing a mathematical modeling of a 3D deformation. The developed model as "matrix", allowed not only to reestimate a number of known features of real AIS, but also to see the patterns in its development which weren't known earlier. Authors claim that AIS is a compensatory reaction of an organism to the unique circumstance - non-conjugation (non-synchronization) of longitudinal development of a spinal cord and its bone-disc-ligamentousmuscular "sheath". The fact of existence of two types of AIS - typical (lordoscoliosis) and atypical (kyphoscoliosis) serves as the major argument in favor of such conclusion. Speaking of lordoscoliosis, we should know, that the "sheath" has the excess of longitudinal size, and concerning kyphoscoliosis - insufficient longitudinal size. Results of studying an endocrine regulation of a bone formation at patients with both types of AIS allowed the authors to establish features of an osteotropic hormonal profile which is usually directly correlated both with a clinical picture, and with nature of a spine column deformation progress. Causes interest authors interpretation of the melatonin theory of a pathogenesis of AIS. The authors explanation of the origin of phenomenon’s EMG is intriguing - they explain it through high electrical activity of muscles on apex frontal curve. In the final part of this article new classification of AIS origin is offered for discussion - hormonal, spinal and central.