NEUROPHYSIOLOGICAL ASPECTS OF THE EARLY DIAGNOSIS AND ASSESSMENT OF PROGRESS AND RESULTS IN TREATMENT OF ADOLESCENT IDIOPATHIC SCOLIOSIS (AIS).

Abstract

Radiological diagnosis is not the only tool in detection, monitoring of progress and making easy to undertake a decision about the surgical scoliosis correction. The below presented algorithm of scoliosis monitoring with complex and repetitive (comparative) neurophysiological examinations facilitates the doctor’s decision about method of the conservative treatment or just the moment of surgical intervention [3, 14]. Neurogenic changes in muscles can be found in early stages of the spine deformation – usually when the Cobb’s angle is over 100 [1]. Vertebral rotation and curvature progression follow simultaneously leading to deformation of the spinal cord together with the local ventral roots compression and sometimes inflammation of them. The structure of the grey matter especially in the ventral horn changes its form more on the convex side of scoliosis. Cell bodies together with the axonal hillocks in the motoneuronal pools show deformations comparing to the analogical area of the concave side. This produce discrete unilateral axonopathy in both efferent fibers of peroneal and tibial nerves in scoliotic patients at the age of about 10. This can be found in electroneurographical (ENG) recordings of M and F potentials even at the angle of scoliosis of 100 [10, 14]. Both parameters of the amplitudes and conduction velocities in M-wave studies are decreased and the frequency of F wave recording is diminished what suggests pathological asymmetrical changes just at the level of the ventral root. That is why electromyographical (EMG) recordings show asymmetrical, according to the ventral root somatotopical innervation, selective (found only in some muscles) deficits in frequency and amplitude of motor units action potentials, predominantly in girls. These girls have scoliosis accelerating the most with angle changes of 50 per year [2] that rapidly deepens the neurogenic changes.

Other significant evaluation of the scoliosis acceleration is using the somatosensory evoked potentials (SEPs) for recording progression of pathology in the afferent transmission within the long ascending spinal cord pathways running in dorsal, dorsolateral and lateral funiculi [4, 5]. Changes in parameters more amplitude than conduction velocity from SEPs studies recorded at the cervical level are more visible on the concave than convex side of scoliosis. These changes are correlated with increasing the Cobb’s angle at the apical thoracic vertebrae (Th7–8) while peripheral sensory transmission remains only slightly disturbed [6, 7]. These changes were found to be twice greater when recording of SEPs was performed over cranially on the contralateral side of the scalp to the stimulation site at the ankle (tibial nerve than peroneal nerve fibers excitation) both in mothers and their daughters [4]. This points at the strong inhibition of the afferent transmission at the level of the brain stem (probably thalamus or medial lemniscus). During the comparative SEPs recordings at the cervical level, when parameters of waves change dramatically (or even they disappear), this may suggest that the lateral angle of scoliosis exceeded 450 with great acceleration of the torsion [9]. Somatosensory evoked potential recordings during the surgical correction of scoliosis showed only rarely the immediate improvement of the afferent transmission [7, 8, 11]. However, they make sure a surgeon about lack of blockade within the spinal pathways which comes from derotation and distraction procedures performed on the spine during implantation of the corrective instrumentation. First visible results of improvement in the SEPs parameters recorded postoperatively are usually seen a week after the surgery [14].

The above analogical phenomena but referring to the efferent transmission 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 nerves and muscles of upper and lower extremities [12,13, 15].

Usually when AIS reaches the Cobb’s angle of 200 at the age of 25 and does not progress more it can be assumed, that its development is finished. In these patients the signs of neurogenic changes found in EMG examinations performed in lower extremities, paravertebral and gluteal muscles do not progress, too [14].