About the use of omega-electroencephalography to estmate functional and metabolic state of nervous tissue of the brain during hyperventilation

Objectives. The aim of this study was to investigate diagnostic capabilities of a new electrophysiological method  of omega-electroencephalography in the  estimation  of change  in functional  and metabolic  state  of the cells of nervous tissue during ischemic adaptation.

Materials and methods.  Brain ischemia was modeled  based on a hyperventilation test  (HVT). Recording  and  analysis  were  made  on  concomitant changes  in direct  current potential level (DCPL) and EEG in 38 derivations  for the same test person  in a fourfold-replicated HVT.

Results. Brain ischemia that  occurs  during volitional  hyperventilation was initially followed by DCPL negativation   (negative  shift)  (0.5–1  mV) and  increase  in amplitude  of all EEG  waves. Cessation  of HVT and return to  initial  DCPL were followed by positivation  (positive  shift) of DCPL (about  1 mV), combined  also with  high-amplitude EEG waves. Adaptation to  hypoxia and  ischemia,  modeled  using replication-based HVT,  and  improvement  of brain  resistance  to these  unfavorable  factors  manifested  themselves first in a short-term  electropositive deviation of DCPL at the start  of the test followed by DCPL positivation  reduction and then in complete substitution of electronegative response  to  positive  shift in DCPL (about  0.5 mV) during  the test.

Conclusion. The analysis of concomitant changes in DCPL and EEG during and after hyperventilation and literature data  analysis suggests that  HVT  was initially  responded  to  by depolarization in neocortical nerve  cells, combined  with  intensification  of  neuronal  activity. Activation  of compensatory mechanisms,  resulting  in improvement  of nerve  cell resistance  to ischemic conditions,  is associated  with  ischemic depolarization followed by hyperpolarization, and  enhancing  adaptive  capabilities  of brain  cells manifest  themselves  in substitution of cell membrane  depolarization to hyperpolarization in response to unfavorable  factor,  also combined with intense neuronal  activity.

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