This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Burwell, R.G. Articles by Moulton, A. PubMed Articles by Burwell, R.G. Articles by Moulton, A.

A NEURODEVELOPMENTAL CONCEPT FOR ADOLESCENT IDIOPATHIC SCOLIOSIS (AIS): MATURATIONAL DELAY OF THE CNS BODY SCHEMA ("BODY IN THE BRAIN")

¹ The Centre for Spinal Studies and Surgery, Queen’s Medical Centre, Nottingham, UK , ² Department of Human Anatomy & Cell Biology & Royal Liverpool Children’s Hospital, University of Liverpool, UK , ³ Department of Orthopaedic Surgery, King’s Mill Hospital, Mansfield, UK (Supported by AO).

The possibility that AIS aetiology involves undetected neuromuscular dysfunction is considered likely by several workers [1,2]. Yet in the extensive neuroscience research of idiopathic scoliosis certain neurodevelopmental concepts have been neglected. These include [3]:

1. a CNS body schema ("body in the brain") for posture and movement control generated during development and growth by establishing a long-lasting memory, and
   
2. pruning of cortical synapses at puberty.
   

During normal development the CNS has to adapt to the rapidly growing skeleton of adolescence, and in AIS to developing spinal asymmetry from whatever cause. Examination of publications relating to the CNS body schema, parietal lobe and temporo-parietal junction [4,5] led us to a new concept: namely, that a delay in maturation of the CNS body schema during adolescence with an early AIS deformity at a time of rapid spinal growth results in the CNS attempting to balance the deformity in a trunk that is larger than the information on personal space (self) already established in the brain by that time of development. It is postulated that this CNS maturational delay allows scoliosis curve progression to occur – unless the delay is temporary when curve progression would cease. The maturational delay may be primary in the brain or secondary to impaired sensory input from end-organs [6], nerve fibre tracts [2,7,8] or central processing [9,10]. The motor component of the concept could be evaluated using transcranial magnetic stimulation [11].

Conclusion: Any maturational delay of the CNS body schema could impair postural mechanisms in girls and boys with or without early AIS deformity. The "body in the brain" concept adds a particular CNS mechanism (maturational delay) to the neuro-osseous timing of maturation (NOTOM) hypothesis for the pathogenesis of AIS [12,13]. The NOTOM hypothesis states that there are more girls than boys with progressive AIS because of different developmental timing of skeletal maturation and postural maturation between the sexes in adolescence [12,13].

Correspondence should be addressed to Jeremy C T Fairbank at The Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX7 7LD, UK