We used quantitative topographical electroencephalography (EEG) to determine the time course of changes in brain electrical activity after clonidine infusion. Twenty healthy male volunteers (aged 24 +/- 5 yr) were included in the randomized, double-blind, placebo-controlled (Group 1, placebo, n = 10; Group 2, 2.0 micrograms/kg clonidine, n = 10) study. EEG (17 electrodes, common average reference, fast Fourier transformation, band pass 0.4-35.0 Hz) output was recorded until 145 min after drug infusion. Subjects were intermittently stimulated by verbal commands. Clonidine-related changes resulted in attenuation of the physiological alpha fluctuations seen in untreated subjects and were most pronounced at parietooccipital (P4, O2) recording sites. This was associated with initial maximal increases in slow wave activity (delta) almost uniformly distributed over the whole cortex, restricting with time to occipital regions (O2). The EEG mapping technique may provide more specific information about clonidine-mediated sedative effects, indicating facilitations of EEG patterns that are not homogeneously distributed. These EEG changes cannot be explained by physiologic changes in vigilance or by normal sleep stages because they were not observed after placebo. EEG effects seem to be unrelated to changes in hemodynamics.
Implications: In healthy volunteers, placebo-controlled signal changes in the electroencephalogram were evaluated to quantify sedative drug effects after intravenous application of clonidine. A multichannel recording system and electroencephalogram mapping technique indicate fluctuations of electroencephalogram patterns that are not homogeneously distributed over the cortex associated with sedation.