Introduction. Postural and motor activities are the results of interactions of smaller inhibitory and larger facilitating structures of the central nervous system (CNS). In the case of dysbalance of inhibitory and facilitating structures during CNS evolution, the asymmetry of postural activities can appear. This asymmetry remains hidden in the early periods of evolution and becomes apparent in the periods of quick growth and increased hormonal and metabolic activities. Genetic and neural factors have proven to be significant in the cause of idiopathic scoliosis (IS), so we propose a neural developmental hypothesis of this disease. Methods. We evaluated a cohort of 19 patients, all of whom were girls with a mean age of 14·7 years (range 13–18) with right idiopathic thoracic curve (mean Cobb angle 53·5°, range 37–72°; of the apical vertebra from T7 to T9). Heart and pulmonary functions were evaluated by heart ECHO and spiroergometry. Results. Normal heart and pulmonary functions support the opinion that heart and pulmonary changes are not the causative factors in IS. The CNS is specialised computer, so we can found hardware and software damages and faults, resulting in asymmetric function of postural motor muscles. Hardware damage–structural changes from brain cortex to spinal cord–can be of genetic, perinatal, or aquired origin (possibly up to 2 years of age). Software damage–repeated asymmetric positions–can cause an increased plasticity period (quick evolution) of CNS pathological programmes of postural reactions in children at risk of IS–uprighting. Conclusions. Children at risk of IS have postural reaction and postural evolution (quick uprighting) pathology, which can be diagnosed during the first year of age by Vojta diagnostic system. The treatment can be effective only in the period of increased plasticity and development of the CNS, mainly in the first 6 months of age. The symmetric positions and symmetric sensory, and proprioceptive input and motor activities can affect CNS evolution. By slowing down the uprighting the CNS has time to repair the damaged software or replace the damaged connections/programmes. In this way we could minimise structural damage. Developmental
Clinical and radiological data were reviewed for all patients
with mucopolysaccharidoses (MPS) with thoracolumbar kyphosis managed
non-operatively or operatively in our institution. In all 16 patients were included (eight female: eight male; 50%
male), of whom nine had Hurler, five Morquio and two Hunter syndrome.
Six patients were treated non-operatively (mean age at presentation
of 6.3 years; 0.4 to 12.9); mean kyphotic progression +1.5o/year;
mean follow-up of 3.1 years (1 to 5.1) and ten patients operatively (mean
age at presentation of 4.7 years; 0.9 to 14.4); mean kyphotic progression
10.8o/year; mean follow-up of 8.2 years; 4.8 to 11.8)
by circumferential arthrodesis with posterior instrumentation in
patients with flexible deformities (n = 6).Aims
Methods