Pathogenesis of idiopathic scoliosis. The Nottingham concept.
There is no generally accepted scientific theory for the etiology of idiopathic scoliosis. Hence, current treatment is pragmatic and not based on knowledge of causation of the deformity. In Nottingham, we have evaluated data from studies of the hips, pelvis, spine, rib cage and trunk muscles in scoliotic (pre- and post operative) and control patients, cadavers and a mechanical model to formulate a new theory of etiology for idiopathic scoliosis (figs. 18 & 19 of ref. 15). Evidence is summarized for the view that idiopathic scoliosis results, in part, from a developmental abnormality in the central nervous system creating rib-vertebra angle asymmetry which leads to a cyclical failure of mechanisms of rotation control in the trunk; these involve rotation-inducing (pelvic) and rotation-defending (discal, ligamentous and costal) mechanisms acting mainly in gait. The mechanical breakdown of rotation occurs in association with a lateral spinal curvature and a lordotic segment to create the initial deformity of idiopathic scoliosis. Then, growth, both abnormal (secondary to vertebral hyper-pressures) and normal (linear spinal growth) with gravity adds to the initiating and continuing neuromuscular mechanisms to augment curve progression. This theory views the spine in the wider perspective of function in the trunk, evolution and development, all in relation to bipedalism. The goal of etiological research is ultimately to base a treatment on some knowledge of causation of the deformity.
Burwell
R G
RG
Department of Human Morphology, University of Nottingham Medical School, Queen's Medical Centre, U.K.
Cole
A A
AA
Cook
T A
TA
Grivas
T B
TB
Kiel
A W
AW
Moulton
A
A
Thirlwall
A S
AS
Upadhyay
S S
SS
Webb
J K
JK
Wemyss-Holden
S A
SA
D002490:Central Nervous System / Q000002:abnormalities / Q000196:embryology; D002648:Child; D005684:Gait; D006128:Growth; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D009068:Movement; D012600:Scoliosis / Q000196:embryology / Q000209:etiology* / Q000503:physiopathology; D013131:Spine / Q000196:embryology / Q000503:physiopathology