Известия высших учебных заведений: Прикладная нелинейная динамика (Jun 2020)
Thalamo-cortical dysrhythmia and its diagnostic principles
Abstract
Aim. In the brain of mammals and humans, several widespread neuronal networks are capable of generating spontaneous rhythmic activity. Among them is the thalamo-cortical network, which involves neurons of the thalamus (diencephalon) and in the neocortex and characterized by hierarchical organization. The thalamo-cortical network generates alpha rhythms with a frequency of about 8...14 Hz. Various neurological and psychiatric disorders are known to associate with similar disturbances of thalamo-cortical rhythms, i.e. the thalamo-cortical dysrhythmia. In particular, absence epilepsy, a non-convulsive form of epilepsy caused by disturbances of the thalamo-cortical system. Absence seizures involve brief and sudden lapses of consciousness (i.e., the state of «absence») associated with high-amplitude spike-wave discharges in the encephalogram. The current paper describes morphology of the thalamo-cortical system and diagnostic principles of the thalamo-cortical dysrhythmia. Methods. WAG/Rij rats with genetic predisposition to absence epilepsy were used as a model of the thalamo-cortical dysrhythmia. Electrical brain activity was recorded from the surface of neocortex using implanted electrodes (electrocorticogram, ECoG). Time-frequency analysis of rhythmic activity in ECoG was performed using continuous wavelet transform and the fast Fourier transform. Results. The following hallmarks of the thalamo-cortical dysrhythmia were defined. (1) During the slow-wave sleep, the spectral power in ECoG was shifted from slow to fast frequencies. (2) Short-lasting episodes of 3...12 Hz rhythmic activity with the amplitude maximum in delta (3...4 Hz) and theta (5...9 Hz) ranges were present in the frontal ECoG. (3) The so-called «pro-epileptic» 5...9 Hz oscillations were present in the frontal ECoG. Conclusion. The most pronounced manifestation of the thalamo-cortical dysrhythmia was found in ECoG during the slow-wave sleep. The dysrhythmic mechanism mostly affected short-lasting slow-wave oscillations with a frequency of 3...4 Hz and 5...9 Hz in combination with disturbances of the time-frequency structure of ECoG.
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