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    Physiol Behav. 2007 Sep 10;92(1-2):141-7. Epub 2007 May 23.

    The human EEG--physiological and clinical studies.

    Source

    Karolinska Institutet, Clinical Neurophysiology, Karolinska University Hospital, Stockholm, Sweden. tom.brismar@ki.se

    Abstract

    The present review summarizes the research in EEG performed by our group during the last 5 years. Our studies have been focussed on two areas: studies of variability and correlations in the oscillations during resting conditions of normal subjects, and the abnormalities related to type 1 diabetes. Recordings in normal subjects showed that also under standardized conditions with regular cycles of closed and open eyes, there is a temporal variability of the spectral components in EEG that necessitates samples>124 s in order to achieve estimates of alpha power with a coefficient of variation<0.1 in all recording channels (brain regions). The temporal variability in alpha and beta power demonstrates long-range temporal correlations, i.e., periods of large power (alpha or beta) are more likely to be followed by large power, and vice versa. The long-range temporal correlations were reproducible, especially during the closed-eyes condition, stronger in males than females, and not age dependent. In patients with type 1 diabetes, the alpha and beta power components were both decreased with similar nadirs in the posterior temporal regions, and the slow spectral components were increased in the frontal regions. The cognitive function was presently not studied but in a group of adolescents with diabetes we found a correlation between the presence of slow activity and the number of hypoglycaemic episodes. The loss of alpha and beta power was highly correlated which initiated a study of the normal alpha-beta correlation. A significant 1:2 phase synchronization was present between alpha and beta oscillations with a phase lag of about pi/2 in all electrode derivations. The strong frequency relationship between the resting beta and alpha oscillations suggested that they are generated by a common mechanism.

    PMID:
    17585964
    [PubMed - indexed for MEDLINE]

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