## 1 Introduction  
The causes of idiopathic scoliosis have not been explained to date. There is no universally accepted theory of scoliosis etiopathogenesis. There is a consensus that idiopathic scoliosis is multifactorial. Extensive literature in this field describes abnormalities at the level of systems, organs, tissues, cells, particles, and genes, without prejudging their primary or secondary nature [1]. In an etiopathogenice sense, scoliosis is only a symptom, an external expression of an unrecognized pathology that can occur in different places of the spine [2]. Although scoliosis is obviously a distortion of posture and body structure, it is also the effect of its compensatory abilities, allowing the preservation of the position of the head and shoulder girdle over the pelvis [3]. The final shape of the body is the result of deforming processes and compensatory reactions. It is justifiable to talk about etiological factors, and not about a specific theory, e.g., genetic or metabolic scoliosis [4]. Currently, the multi-factor concept in this genetically conditioned pathology of the central nervous system has the most supporters. This pathology applies, in particular, to the broadly understood postural system [5]. It affects, most likely, the system of deep back muscles (ereactor spinae), on the growing spine of a child with individually variable and multifactorial susceptibility to distortion [6]. Progression of scoliosis is associated with growth and biomechanical factors. Among theories on the etiology of scoliosis, the concept of disturbances in the balance of muscle tension is of special importance. In maintaining the course of fibers of individual muscles in scoliosis,an important role is played by the thoracolumbar fascia, which presses the erector spinae muscle to the spine and prevents greater dislocations [7]. The uneven tension of the erector spinae visible on both sides and at different levels of the spine, visible in the surface electromyography (SEMG) amplitude record, is related to the mass movement of this muscle. The main mass of the erector spinae muscle lies in the groove restricted by spinal processes of the vertebrae on one side and the arch lamellae, the transverse processes, and the vertebral segments of the ribs on the other side [8]. The shape of this groove varies on the convex and concave sides of the curve, hence, the muscle system on both sides is different. Due to dislocations on the concave side resulting from spinous processes and the deviation towards the back because of lateral processes, the longest erector spinae muscle is displaced and is most often emphasized in the form of convex protrusion, sometimes up to the concave side. The liicostalis muscle is associated with the paraspinal rib sections. The ribs in the rear hump are set in a plane similar to the sagittal one. The liicostalis muscle at the top of the curve undergoes sagittal rotation in the course of the curvature, because above and below the hump, it lies in the frontal plane. The lateral fibers of this muscle attach to the ribs at the points of their angular bend in the area of the hump. The shift of the longest erector spinae muscle to the concave side and the rotation of the hippocampal muscle at the top of the curve causes a narrowing of their mass. On the concave side of the curve, the course of the erector spinae muscles is also changed. These muscles are arranged along the string of the curvature, and therefore, the longest back muscle, and especially the liicostalis muscle on the concave side, are flattened and widened. In severe curvatures of the spine, macrophobia atrophy of the muscle fibers on the concave side and overgrowth with adipose tissue can be found [9]. In the lumbar section, there is a similar pattern of muscles on the convex and concave sides of the curve. The short erector spinae muscles forming the transversospinal system show smaller macro-lesions than the long muscles.