Abstract
There is no generally accepted scientific theory for the causes of adolescent idiopathic scoliosis (AIS). As part of its mission to widen understanding of scoliosis etiology, the International Federated Body on Scoliosis Etiology (IBSE) introduced the electronic focus group (EFG) as a means of increasing debate on knowledge of important topics. This has been designated as an on-line Delphi discussion. The Statement for this debate was written by Dr WCW Chu and colleagues who examine the spinal cord to vertebral growth interaction during adolescence in scoliosis. Using the multi-planar reconstruction technique of magnetic resonance imaging they investigated the relative length of spinal cord to vertebral column including ratios in 28 girls with AIS (mainly thoracic or double major curves) and 14 age-matched normal girls. Also evaluated were cerebellar tonsillar position, somatosensory evoked potentials (SSEPs), and clinical neurological examination. In severe AIS compared with normal controls, the vertebral column is significantly longer without detectable spinal cord lengthening. They speculate that anterior spinal column overgrowth relative to a normal length spinal cord exerts a stretching tethering force between the two ends, cranially and caudally leading to the initiation and progression of thoracic AIS. They support and develop the Roth-Porter concept of uncoupled neuro-osseous growth in the pathogenesis of AIS which now they prefer to term 'asynchronous neuro-osseous growth'. Morphological evidence about the curve apex suggests that the spinal cord is also affected, and a 'double pathology' is suggested. AIS is viewed as a disorder with a wide spectrum and a common neuroanatomical abnormality namely, a spinal cord of normal length but short relative to an abnormally lengthened anterior vertebral column. Neuroanatomical changes and/or abnormal neural function may be expressed only in severe cases. This asynchronous neuro-osseous growth concept is regarded as one component of a larger concept. The other component relates to the brain and cranium of AIS subjects because abnormalities have been found in brain (infratentorial and supratentorial) and skull (vault and base). The possible relevance of systemic melatonin-signaling pathway dysfunction, platelet calmodulin levels and putative vertebral vascular biology to the asynchronous neuro-osseous growth concept is discussed. A biomechanical model to test the spinal component of the concept is in hand. There is no published research on the biomechanical properties of the spinal cord for scoliosis specimens. Such research on normal spinal cords includes movements (kinematics), stress-strain responses to uniaxial loading, and anterior forces created by the stretched cord in forward flexion that may alter sagittal spinal shape during adolescent growth. The asynchronous neuro-osseous growth concept for the spine evokes controversy. Dr Chu and colleagues respond to five other concepts of pathogenesis for AIS and suggest that relative anterior spinal overgrowth and biomechanical growth modulation may also contribute to AIS pathogenesis.
Highlights
In the absence of any accepted scientific theory for the etiology of idiopathic scoliosis treatment remains pragmatic with a very incomplete scientific basis
The research is part of a series of studies [5,6,7,8,9,10,11] to evaluate the hypothesis that in adolescent idiopathic scoliosis (AIS) there is a systemic disturbance of growth [12,13,14,15] manifest in each of the appendicular skeleton, vertebral column and skull that points to a problem of axial skeletal growth control [7]
Our study suggests the presence of tethering and increased tension along the longitudinal axis of spinal cord results in morphological changes of cross-sectional shape and relative position of the cord – an observation which is obvious in the apical region In conclusion, there is indirect evidence that the cord in AIS is "abnormal" and we hypothesize that both vertebral column and spinal cord are affected in AIS (Moderator, spinal forward flexion and extension affect spinal cord shape (Figure 2) as may the apical hypokyphosis of thoracic AIS)
Summary
In the absence of any accepted scientific theory for the etiology of idiopathic scoliosis treatment remains pragmatic with a very incomplete scientific basis. As the brain inside the cranium is fixed while the lower nerve roots exit normally via the neural foraminae in the lengthened vertebral column, we speculate the relative shorter cord is under a stretching tethering force from the two ends, both cranially and caudally This might explain why the prevalence of low-lying tonsils was increased in AIS patients with marked scoliotic curves. 13 The uncoupled, or asynchronous, neuro-osseous growth concept accommodates - a) the general skeletal overgrowth abnormality as applied to the spine, b) the left-right asymmetries of the appendicular skeleton, and c) speculates that a spinal cord abnormality with growth 'insufficiency' leads to 'a stretching tethering force from the two ends, both cranially and caudally' which causes the initiation and progression of thoracic AIS
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