Trial reportBrain topography2026
Dopaminergic Drugs Modulate Resting-State EEG Microstates in Healthy Participants.
Trial report in Brain topography, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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0 citing papers in PubMed.
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in the temporal parameters of EEG microstates are observed in various psychiatric illnesses, including psychotic disorders. These changes have also been observed in individuals with a clinical or genetic high risk for psychosis. It is unclear whether dopamine abnormalities, distinctive of psychotic disorders, contribute to microstate alterations. Fifty-eight healthy participants (M: F = 32:26) took part in a single-dose drug challenge study. Using a randomized, double-blind, cross-over, and placebo-controlled design, participants received the dopamine precursor L-DOPA (100 mg), the dopamine antagonist haloperidol (2 mg), and a placebo. Resting-state (10 min, eyes-closed) 64-channel EEG was recorded at peak drug effects. We calculated temporal parameters (coverage, duration, and occurrence) of 5 microstate classes (A-E) and compared them between drug conditions using linear mixed-effect models. Significant group x class interactions were observed for all parameters. Compared to placebo, parameters of microstate B were decreased under L-DOPA (duration and occurrence) and haloperidol (coverage, duration, and occurrence). Coverage and occurrence of microstate C were reduced under L-DOPA compared to haloperidol and placebo. Parameters of microstate E were reduced under L-DOPA compared to haloperidol (coverage and occurrence) and placebo (coverage, duration, and occurrence). Both haloperidol and L-DOPA increased all parameters of microstate D, compared to placebo. Our results show that resting-state EEG microstates are modulated by dopaminergic drugs. However, extrapolations from healthy controls to patients with psychotic disorders are complicated by various factors. Further studies should investigate the (long-term) effects of haloperidol and other antipsychotics on EEG microstates in patients with psychotic disorders.
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