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EEG θ rhythm in preterm and full-term infants at the age of five months in endogenous attention
Authors:T. A. Stroganova  I. N. Posikera  M. V. Pisarevskii  M. M. Tsetlin
Affiliation:(1) Institute of Psychology, Russian Academy of Education, Moscow, 103009, Russia
Abstract:EEG indicators of endogenous attention (EnA) were studied in healthy infants carried to term and extremely preterm infants at a corrected age of five months. The cortical topography of the spectral amplitudes of the EEG θ rhythm was studied during long-term attention of the children to a new visual stimulus (exogenous attention, ExA) and during the retention of anticipatory attention under the conditions of constant appearance and disappearance of a stimulus in the paradigm of visual expectation (EnA). The relationship between reactive changes in the EEG θ rhythm during the retention of EnA and the behavioral parameters of the infant’s ability to retain this type of attention was also assessed. In five-month-old infants, the retention of EnA, in contrast to simpler types of attention to an exogenous stimulus, was accompanied by the appearance of a highly synchronized EEG θ rhythm (3.6–5.2 Hz) with a topical amplitude maximum in the lower temporal associative areas of the cortex. The ability to maintain EnA in children of this age is directly related to the reactive increase in the θ rhythm in the lower temporal areas of the cortex during the retention of EnA as compared to ExA. The deficit of EnA control in healthy extremely preterm (HEP) infants was associated with a relative deficit of the functional synchronization of the θ rhythm in the lower temporal areas of the cortex during the retention of EnA compared to full-term infants. In HEP infants, a decreased synchronization of the θ rhythm was equally typical of EnA and ExA. However, its cortical location depended on the type of attention. The functional nature of the θ rhythm inhibition in HEP infants suggests that this abnormality was related to alterations in the neurotransmitter interactions between the limbic and cortical structures, rather than to structural defects. These alterations could be one of the causes of the partial deficit of EnA in HEP infants.
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