No abstract

The stabilometric results reflect the stages of the formation of the persistent pathological static/locomotor stereotype and compensatory mechanisms for the low extremity dysfunction.

Prolonged observations of 157 children with spastic forms of childhood cerebral palsy (CCP) were used to construct a mathematical regression model for motor development in relation to the severity of the course and outcome of the condition. Mathematical relationships were established reflecting dysneuroontogenesis of the suprasegmental regulatory systems. Data obtained from complex electroencephalogram and electroneuromyogram studies, along with assessments of autonomic nervous system function, demonstrated a role for intra-and intersystem disintegration of the limboreticular complex in decreases adaptive capacity and rehabilitation potential of patients with CCP. This was used to identify the principles of a pathogenetically based adaptive-regulatory approach to the rehabilitation of this category of patients, based on the need to correct the functional state of non-specific brain systems to create the neurodynamic suprasegmental and segmental adaptive-energetic and adaptive-immunoregulatory prerequisites for forming and supporting specific psychomotor functions.

Questioning on sleep disturbances and polygraphic investigations of sleep and active state in 31 children with temporal epilepsy has been carried out. According to literature available and original observations, the novel classification of sleep disturbances in children is offered. Sleep disturbances are divided into permanent and paroxysmal. Paroxysms are divided into typical hypnic (non-epileptic), sleep-related "border" paroxysms and typical sleep-related epileptic attacks.

In the first 24 h, the overstrain of the neuroendocrine system in response to strong stress influence of the trauma was noted in all patients. In patients with fatal outcome, an increase in cortisol in the first 24 h was excessive and lactate level was significantly higher during the observational period compared to the patients with favorable outcome. The peak of mortality was at 1-5 days when the stress level indicators, contents of ACTH, cortisol and lactate reached maximal values indicating the stress-induces overstrain of the hypothalamic- pituitary-adrenal axis and promoting the development of brain tissue hypoxia.