CLINICAL AND PATHOGENETIC FEATURES OF MILD TRAUMATIC BRAIN INJURY DISTANT PERIOD

Abstract

Plastic and energetic reorganization of brain after its traumatic injury lasts for many years, and impaired adaptive neuroplasticity can lead to progressive development. In the long term, even with a minor injury, the organic neurological symptoms are mitigated and autonomic and psychopathological disorders come to the fore, which are the main cause of social and occupational maladaptation of patients. To identify and analyze the clinical and pathogenetic features of the long−term period of mild traumatic brain injury, 100 patients aged 20−60 years who underwent it 1−5 years ago were examined. Patients underwent clinical−neurological, neuropsychological and biochemical studies. The reparative capacity of brain was assessed by determining the content of neurotrophic factors in the serum: brain−derived neurotrophic factor (BDNF), nerve growth factor (beta−NGF) and protein−promoter of apoptosis Bcl−2 by enzyme−linked immunosorbent assay. The results of the study confirm the idea that mild traumatic brain injury most often affects the mid−stem structures of the brain, which play a leading role in ensuring the human body adaptation. Clinically, this was manifested by asthenic, autonomic and neurocognitive disorders, which is a reflection of persistent neuronal dysfunction. Decreased BDNF expression and increased beta−NGF in the long term may be a marker of neuronal dysfunction, a persistent disorder of adaptive neuroplasticity that is closely associated with emotional and neurocognitive disorders. The level of Bcl−2 remains consistently high, significantly higher than control values, even with prolonging duration of the post−traumatic period. This feature is likely to be of regulatory character as an apoptosis inhibitor. Key words: mild traumatic brain injury, pathogenesis, clinic, diagnosis, neuroplasticity.