Concepts on the pathogenesis of adolescent idiopathic scoliosis. Bone growth and mass, vertebral column, spinal cord, brain, skull, extra-spinal left-right skeletal length asymmetries, disproportions and molecular pathogenesis.

dc.contributor.authorBurwell, R.
dc.contributor.authorDangerfield, P.
dc.contributor.authorFreeman, B.
dc.date.issued2008
dc.description.abstractThere is no generally accepted scientific theory for the causes of adolescent idiopathic scoliosis (AIS). Encouraging advances thought to be related to AIS pathogenesis have recently been made in several fields including anthropometry of bone growth, bone mass, spinal growth modulation, extra-spinal left-right skeletal length asymmetries and disproportions, magnetic resonance imaging of vertebral column, spinal cord, brain, skull, and molecular pathogenesis. These advances are leading to the evaluation of new treatments including attempts at minimally invasive surgery on the spine and peri-apical ribs. Several concepts of AIS are outlined indicating their clinical applications but not their research potential. The concepts, by derivation morphological, molecular and mathematical, are addressed in 15 sections: 1) initiating and progressive factors; 2) relative anterior spinal overgrowth; 3) dorsal shear forces that create axial rotational instability; 4) rotational preconstraint; 5) uncoupled, or asynchronous, spinal neuro-osseous growth; 6) brain, nervous system and skull; 7) a novel neuro-osseous escalator concept based on a putative abnormality of two normal polarized processes namely, a) increasing skeletal dimensions, and b) the CNS body schema – both contained within a neuro-osseous timing of maturation (NOTOM) concept; 8) transverse plane pelvic rotation, skeletal asymmetries and developmental theory; 9) thoraco-spinal concept; 10) origin in contracture at the hips; 11) osteopenia; 12) melatonin deficiency; 13) systemic melatonin-signaling pathway dysfunction; 14) platelet calmodulin dysfunction; and 15) biomechanical spinal growth modulation. From these concepts, a collective model for AIS pathogenesis is formulated. The central concept of this model includes the body schema of the neural systems, widely-studied in adults, that control normal posture and coordinated movements with frames of reference in the posterior parietal cortex. The escalator concept has implications for the normal development of upright posture, and the evolution in humans of neural control, the trunk and unique bipedal gait.
dc.description.statementofresponsibilityR. Geoffrey Burwell, Peter H. Dangerfield and Brian J.C. Freema
dc.description.urihttp://www.ncbi.nlm.nih.gov/pubmed/18401079
dc.identifier.citationStudies in Health Technology and Informatics, 2008; 135:3-52
dc.identifier.issn0926-9630
dc.identifier.issn1879-8365
dc.identifier.orcidFreeman, B. [0000-0003-0237-9707]
dc.identifier.urihttp://hdl.handle.net/2440/53457
dc.language.isoen
dc.publisherIOS Press
dc.subjectSkull
dc.subjectSpine
dc.subjectBrain
dc.subjectHumans
dc.subjectScoliosis
dc.subjectAnthropometry
dc.subjectBone Development
dc.subjectAdolescent
dc.subjectFemale
dc.subjectMale
dc.subjectPostural Balance
dc.titleConcepts on the pathogenesis of adolescent idiopathic scoliosis. Bone growth and mass, vertebral column, spinal cord, brain, skull, extra-spinal left-right skeletal length asymmetries, disproportions and molecular pathogenesis.
dc.typeJournal article
pubs.publication-statusPublished

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