The purpose of this work is to identify a role of the pineal gland/suprachiasmatic nucleus system in adolescent idiopathic scoliosis (AIS) aetiology and pathogenesis. To analyze electroencephalograms of 292 children with AIS and in 46 healthy subjects, a processing method was used to assess three-dimensional coordinates of electric equivalent dipole sources (EEDSs) within the brain. Amounts of EEDSs in the pineal gland and suprachiasmatic nucleus (SCN) area were assessed in different age groups and during the progress of orthopaedic pathology. It was shown that children with AIS, compared with healthy children, were characterized by a higher level of electric activity (as judged by EEDS values) in the pineal gland area. It was also revealed that the number of EEDS in the pineal gland area increases significantly with increased severity of spinal deformation, while their number in the suprachiasmatic nucleus (SCN) area decreases compared with the number in healthy peers. Changes in electric activity and changes in the pineal gland and SCN area suggest that mechanisms of AIS aetiology and pathogenesis involve functional disturbances in brain areas responsible for the formation and maintenance of normal biorhythms, including osteogenesis and bone growth. 1. Background Adolescent idiopathic scoliosis (AIS) is a disease of unknown aetiology, characterized by a complex three-dimensional deformation of the spinal column as the most common paediatric orthopaedic pathology. Its incidence, according to different sources, varies from 2 to 6% of the total paediatric population, while 3 in 1000 adolescents require severe reconstructive spinal surgery [1]. AIS is characterized by its relationship with the pubertal period, its much higher incidence in adolescent girls as compared with boys (from 1？:？7 to 1？:？10 according to various authors), and poor prediction of the course of the disease. The process of deformation can stop spontaneously without treatment at some point, but it can also progress rapidly up to an angle of 70 degrees or more [1, 2]. Although the first mention of scoliosis goes back as far as Hippocrates (c. 460–370 BC), to date there is no factual, scientifically feasible theory of AIS aetiology and pathogenesis [3]. Accordingly, there are no reliable methods for predicting the extent and rate of spinal deformation, nor for its effective treatment and prevention. One of the main reasons for this state is the lack of an effective model reproducing all the specific features of the pathological process in animals. The disease therefore is difficult to
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