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POSSIBLE ORIGIN OF ADOLESCENT IDIOPATHIC SCOLIOSIS (AIS) BASING ON RESULTS OF CLINICAL NEUROPHYSIOLOGICAL INVESTIGATIONS.

¹ Department of Spinal Surgery, Orthopaedics and Traumatology ² Department of Pathophysiology of Locomotor Organs Karol Marcinkowski University School of Medical Sciences in Pozna, Poland

1. AIS has different image than paralytic scoliosis or scoliosis accompanying some diseases of the spinal cord in electromyographical and electroneurographical examinations (EMG and ENG). These differences are concerned to different progression, characteristic properties in skeletal system pathology or curves angles at the thoracic and lumbosacral spine.
   
2. There are always two sites in patients with AIS where changes in transmission from the motor cortex to the motoneuronal centres in lumbosacral region appear. These phenomena were shown in motor evoked potentials studies which were induced with the magnetic field (MEP) in areas of motor cortex and recorded from centres of cervical and lumbosacral spinal cord as well as from muscles of upper and lower extremities. Changes in efferent transmission are greater twice in recordings from muscles of lower extremities and in oververtebral recordings at L5-S1 regions what suggests, that secondary slowing down takes place at the level of the apical thoracic vertebrae of primary curve (mostly at Th7–8), predominantly on the concave than convex side of scoliosis. MEP study confirmed a previous finding with somatosensory evoked potentials (SEPs) similarly about two focuses of disturbances in of afferent transmission on the spinal centres-supraspinal centres pathway. MEP showed changes in the efferent transmission on the supraspinal centres-spinal motor generator pathway. Such changes are not observed in scolioses other than idiopathic.
   
3. Results of the complex neurophysiological studies suggest that the primary origin of AIS is the brain stem area at the level of thalamus where changes of afferent and efferent transmission are detected. There is a close relationship of this structure with the pineal gland and secretion of neurotransmitters at this level in correlation to disturbances in melatonin secretion and other neurohormones. Disorders in melatonin secretion and other neurohormones may induce a scoliosis what was shown in previous genetic and experimental neurophysiological studies on animals, together with cutting of the pineal stalk. Some aspects of this problem were also mentioned in our previous clinical neurophysiological studies [1–3].
   
4. Results of studies suggest that in patients with AIS, there are structural and functional changes in the area of thalamus, which cause disturbances in afferent and efferent transmission at this level. Pathology in the pineal secretion of neurohormones can be one of the factors influencing the formation and progression of AIS, as a disease of probably secondary origin to the functional changes in brain.
   
5. Results of MEP studies discussed in this report confirm that the primary origin of AIS takes place at the level of the brain stem but not in the spinal cord.
   

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