ABSTRACT
Our objective was to determine perisaccadic gamma range oscillations in the EEG during voluntary saccades in humans. We evaluated occipital perisaccadic gamma activity both in the presence and absence of visual input, when the observer was blindfolded. We quantified gamma power in the time periods before, during, and after horizontal saccades. The corresponding EEG was evaluated for individual saccades and the wavelet transformed EEG averaged for each time window, without averaging the EEG first. We found that, in both dark and light, parietal and occipital gamma power increased during the saccade and peaked prior to reaching new fixation. We show that this is not the result of muscle activity and not the result of visual input during saccades. Saccade direction affects the laterality of gamma power over posterior electrodes. Gamma power recorded over the posterior scalp increases during a saccade. The phasic modulation of gamma by saccades in darkness--when occipital activity is decoupled from visual input--provides electrophysiological evidence that voluntary saccades affect ongoing EEG. We suggest that saccade-phasic gamma modulation may contribute to short-term plasticity required to realign the visual space to the intended fixation point of a saccade and provides a mechanism for neuronal assembly formation prior to achieving the intended saccadic goal. The wavelet-transformed perisaccadic EEG could provide an electrophysiological tool applicable in humans for the purpose of fine analysis and potential separation of stages of 'planning' and 'action'.
Subject(s)
Darkness , Evoked Potentials, Visual/physiology , Light , Saccades , Visual Perception/physiology , Adolescent , Adult , Attention , Electroencephalography , Electromyography , Female , Humans , Linear Models , Male , Movement/physiology , Neuronal Plasticity/physiology , Reaction TimeABSTRACT
BACKGROUND: Power in the gamma band EEG increases during saccades in normal subjects. OBJECTIVE: To develop a potential method to quantify signs of cortical responsiveness in persistent vegetative state (PVS) we quantified gamma range EEG in association with conjugate slow ballistic eye movements (SBEM). METHODS: The EEG and the simultaneous electro-oculogram were recorded in 14 (8F/6M) PVS patients. Clinical scoring was based on the Glasgow Coma Scale (GCS) and Coma Rating Scale (CRS). The Wavelet Transform, followed by Hilbert transform was applied to the EEG and gamma power distribution was quantified relative to the timing of an eye movement. We correlated the clinical and the neurophysiological measures. RESULTS: Gamma activity was present in all PVS patients. Its power was modulated in association with eye movements only in less severely affected patients, with minimum power prior to, and maximum power during the eye movement. In severely affected patients there was no evidence of a temporal relationship between gamma power and the phase of the eye movement. CONCLUSIONS: Detecting changes in the time course of gamma power in relation to conjugate ballistic eye movements provides a quantitative neurophysiological method for prospective longitudinal studies to explore if the preservation of this CNS function relates to the potential for recovery in PVS patients.
