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EEG spectral power and coherence were analyzed under waking baseline condition in 19 high (HH) and 12 low (LH) hypnotizable subjects. In HH subjects, the theta1 and theta2 spectral power was higher than in LH. The major new finding of this study is that coherence between distributed brain regions was sharply elevated in HH subjects within the theta and alpha frequency bands. In contrast, spectral power and coherence of beta2 and gamma1 bands were higher in LH subjects as compared to HH subjects. However, the long distance coherence between frontal and posterior areas within beta-gamma frequency ranges was higher in HH subjects. It might be supposed that HH subjects are engaged in imaginal mental activity whereas LH ones are mainly engaged in linguistic activity. The neurophysiological basis of the obtained EEG differences is discussed.

Contingent negative variation (CNV) topography, hemispheric asymmetry and time-course were investigated in healthy subjects and non-medicated paranoid schizophrenic patients in two antisaccade paradigms with the short (800-1000 ms) and long (1200-1400 ms) durations of the fixation period. EEG and electrooculogram (EOG) were recorded. Saccade characteristics and mean amplitudes of slow cortical potentials time-locked to peripheral target were analyzed in 23 healthy volunteers and 19 schizophrenic patients. Compared to healthy control subjects, schizophrenic patients had significantly slower antisaccades and committed significantly more erroneous saccades in the both antisaccade tasks. The prolongation of the fixation period resulted in noticeable decrease of error percent in patients group. The analysis of CNV time-course has revealed two distinct stages in both groups. The early CNV stage was represented by a negative wave with the maximal amplitude over midline fronto-central area, and the late stage was characterized by increased CNV amplitude at the midline and left parietal electrode sites. In healthy subjects the simultaneous activation of frontal and parietal areas was observed in the paradigm with the shorter fixation interval; the increase of the fixation period produced consecutive activation of these areas. Schizophrenic patients' CNV amplitude was generally smaller than that of healthy subjects. The most pronounced between-group differences of the negative shift amplitude were revealed at frontal electrode sites during the early CNV stage in both modifications of the antisaccade task. The deficit of frontal activation revealed in patients at the early stage of antisaccade preparatory set in both antisaccadic paradigms may be related to pathogenesis of paranoid schizophrenia.

The precision and electromyographic characteristics of single-joint voluntary movements of the human foot, of the programmed and tracking types, were studied, along with the characteristics of rhythmic activity of motor units before and during 120-day antiorthostatic hypokinesia. This latter was accompanied by significant decreases in the precision of the control system, evident as decreases in the number of discriminable force gradations, increases in the absolute and differential thresholds for movements of the programmed type, and sharp increases in the variability of integrated EMG traces from the working muscles during tracking movements. The direction and dynamics of changes in the activity of motor units at different stages of antiorthostatic hypokinesia were different: during the first 14-30 days (stage I), there was a sharp increase in the variability of interspike intervals and an increase in the extent of synchronization of motor unit activity; from day 30 onwards (stage II), there was a reproducible decrease in the duration of interspike intervals, along with disappearance of the synchronization of motor units, while the high level of variability of spike activity persisted. The results obtained here suggest that impairments of precision during stages I and II of antiorthostatic hypokinesia are different in nature and are associated with reflex responses to support unloading at stage I and with atrophic processes in muscles in stage II.

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