Abstract
Nachemson [2] drawing upon the theses of Sahlstrand [3] and Lidström [4] articulated the view there are more girls than boys with progressive AIS for the following reason. The maturation of postural mechanisms in the nervous system is complete about the same time in boys and girls. Girls enter their skeletal adolescent growth spurt with immature postural mechanisms – so if they have a predisposition to develop a scoliosis curve, the spine deforms. In contrast, boys enter their adolescent growth spurt with mature postural mechanisms so they are protected from developing a scoliosis curve. We term Nachemson’s concept the neuro-osseous timing of maturation (NOTOM) hypothesis [1,5] The earlier sexual and skeletal maturation of girls may have an evolutionary basis through natural selection. Curve progression in AIS is associated with acceleration of the adolescent growth spurt [6]. Postural sway involves proprioceptive, vestibular and visual input to the central nervous system. In normal children there is a significant reduction in postural sway amplitude between six to nine years and 10–14 years [7,8]. In 1071 normal children aged 6–14 years postural sway is more stable in girls from 6–9 years and over 10 years there is no sex effect [9]; all these findings fit the Nachemson concept. But in view of a subsequent report on 64 normal children aged 3–17 years showing the change with age is limited to boys [10] the age and sex effect of postural sway in healthy children needs further evaluation. In AIS children stabilometry findings are conflicting and observed greater postural sway may be secondary to the curve. In the siblings of scoliotics Lidström et al [11] concluded that postural aberration is a factor in the aetiology of AIS.
Conclusion: The NOTOM hypothesis suggests a treatment to prevent progression of late-juvenile idiopathic scoliosis, early-AIS, and some secondary scolioses. It is based on delaying the onset of the adolescent growth spurt and puberty as used therapeutically in children with idiopathic precocious puberty (IPP)[12]. The proposal is to administer a gonadorelin analogue which in the pituitary down-regulates receptors to hypothalamic gonadotropin-releasing hormone (GnRH) causing a fall in both luteinizing hormone (LH) and follicle-stimulating stimulating hormone (FSH); in turn this causes a fall in oestrogens and androgens and thereby delays or stops menarche and slows bone growth – as in girls and boys with IPP [13]. Expert paediatric opinion is supportive. King [14] has suggested the use of a gonadorelin analogue (Lupron) to delay the onset of the adolescent growth spurt in progressive AIS.
Correspondence should be addressed to Jeremy C T Fairbank at The Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX7 7LD, UK
