scispace - formally typeset
W

Wilhelmus Drinkenburg

Researcher at Janssen Pharmaceutica

Publications -  115
Citations -  3599

Wilhelmus Drinkenburg is an academic researcher from Janssen Pharmaceutica. The author has contributed to research in topics: Electroencephalography & Allosteric modulator. The author has an hindex of 33, co-authored 112 publications receiving 2925 citations. Previous affiliations of Wilhelmus Drinkenburg include Janssen-Cilag & Johnson & Johnson.

Papers
More filters
Journal ArticleDOI

Disorder specificity despite comorbidity: Resting EEG alpha asymmetry in major depressive disorder and post-traumatic stress disorder

TL;DR: Electroencephalographic data under resting state, eyes closed conditions in patients with major depressive disorder and post-traumatic stress disorder are compared to examine the specificity of brain laterality in these disorders to partially support the diagnostic applicability of the theoretical frameworks.
Journal ArticleDOI

Neurophysiological predictors of non-response to rTMS in depression

TL;DR: In this paper, a multi-site open-label study assessing pre-treatment EEG and ERP measures associated with non-response to rTMS treatment was conducted, and the non-responders were characterized by increased fronto-central theta EEG power, a slower anterior individual alpha peak frequency, a larger P300 amplitude, and decreased pre-frontal delta and beta cordance.
Journal ArticleDOI

Guidelines for the recording and evaluation of pharmaco-EEG data in man: the International Pharmaco-EEG Society (IPEG).

TL;DR: The present updated guidelines reflect the consensus of a global panel of EEG experts and are intended to assist investigators using pharmaco-EEG in clinical research, by providing clear and concise recommendations and thereby enabling standardisation of methodology and facilitating comparability of data across laboratories.
Journal ArticleDOI

Effects of diazepam and zolpidem on EEG beta frequencies are behavior-specific in rats.

TL;DR: It is hypothesized that the large increase in beta-3/gamma activity caused by diazepam and zolpidem is a compensatory mechanism that allows for behavioral activation, despite pharmacologically induced sedation.