AI Article Synopsis

  • The sleep-wake learning cycle is crucial for understanding human interaction with the environment and its relation to CNS diseases like epilepsy.
  • A study involved 178 epilepsy patients and healthy volunteers, examining the effects of prolonged sleep deprivation through clinical and EEG methods, while also observing brain changes in rats subjected to sleep deprivation.
  • The findings indicate that sleep deprivation leads to significant neuroplasticity impairments in the CNS, contributing to epilepsy development, suggesting further research on neuroplasticity modulators for treatment is necessary.

Article Abstract

Aim: Learning cycle «sleep-wake» is of great theoretical and practical importance because it allows to understand the general patterns of adaptive mechanisms of human interaction with the environment (neuroplasticity), violations of which are the basis of many diseases of the CNS, including epilepsy.

Material And Methods: Complex clinical and electroencephalographic (video-EEG monitoring with mandatory recording of sleep) study was carried out before and after prolonged sleep deprivation (for at least 1 day) of 178 patients with locally due to epilepsy (LEi). 45 healthy volunteers were examined in the control group as well as the patients with epilepsy. The work was carried out to compare the results of clinical and neurological and electrophysiological studies during sleep deprivation (SD) in patients with LEi and in healthy individuals with neurohistological and electron microscopic patterns of changes in the brain of rats in an experiment with 48-hour SD.

Results And Conclusion: Discovered in the CNS of rats after SD morphological changes such as pleyokoniya of mitochondria, damage in the blood-brain barrier, signs of exhaustion astrocytes, glial cells and the change of the nuclei of gliocytes and some neurons of the type of apoptosis and karyorrhexis and destruction of synapses reveal a violation of the fundamental mechanisms of neuroplasticity. The results allow us to consider the SD patients as a damaging factor for the central nervous system, provoking the development of epileptic seizures and epilepsy, and the SD in laboratory animals can be used as a model for further study of the mechanisms of neuroplasticity. In addition the findings greatly complement current understanding of the mechanisms of neuroplasticity and pathogenesis of epilepsy, and justify the need for the study of therapeutic efficacy of modulators of neuroplasticity (transcranial magnetic stimulation, ipidacrin etc.) in the complexe treatment of patients with the this specified profile.

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Source
http://dx.doi.org/10.17116/jnevro20161167159-65DOI Listing

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