EEG abnormalities are not associated with poor antidepressant treatment outcome - A NeuroPharm study

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EEG brain abnormalities, such as slowing and isolated epileptiform discharges (IEDs), has previously been associated with non-response to antidepressant treatment with escitalopram and venlafaxine, suggesting a potential need for treatment with anticonvulsant property in some patients. The current study aims to replicate the reported association of EEG abnormality and treatment outcomes in an open-label trial of escitalopram for major depressive disorder (MDD) and explore its relationship to mood and cognition. Pretreatment, 6 min eyes-closed resting-state 256-channel EEG was recorded in 91 patients with MDD (age 18–57) who were treated with 10–20 mg escitalopram for 12 weeks; patients could switch to duloxetine after four weeks. A certified clinical neurophysiologist rated the EEGs.

IED and EEG slowing was seen in 13.2%, and in 6.6% there were findings with unclear significance (i.e., Wicket spikes and theta activity). We saw no group-difference in remission or response rates after 8 and 12 weeks of treatment or switching to duloxetine. Patients with EEG abnormalities had higher pretreatment mood disturbances driven by greater anger (p=.039) and poorer verbal memory (p=.012). However, EEG abnormality was not associated with improved mood or verbal memory after treatment. Our findings should be interpreted in light of the rarity of EEG abnormalities and the sample size. While we cannot confirm that EEG abnormalities are associated with non-response to treatment, including escitalopram, abnormal EEG activity is associated with poor mood and verbal memory. The clinical utility of EEG abnormality in antidepressant treatment selection needs careful evaluation before deciding if useful for clinical implementation.
OriginalsprogEngelsk
TidsskriftEuropean Neuropsychopharmacology
Vol/bind79
Sider (fra-til)59-65
Antal sider7
ISSN0924-977X
DOI
StatusUdgivet - 2024

Bibliografisk note

Funding Information:
KRJ and VGF were supported by the Research Fund of the Mental Health Services - Capital Region of Denmark . CTI was supported by Augustinus Fonden (19–0219) and the University of Macau ( SRG2023–00040-ICI ). KRJ, VGF, and CTI were also supported by The Lundbeck Foundation alliance BrainDrugs ( R279–2018–1145 ). The funding was unrestricted and did not involve decisions regarding the study's design, data collection, analyses, interpretation, or writing.

Funding Information:
The data analysed in this study is subject to the following licenses/restrictions: A Cimbi database application is required to access the dataset through the following procedures: https://cimbi.dk/index.php/documents/category/3-cimbi-database. KRJ and VGF were supported by the Research Fund of the Mental Health Services - Capital Region of Denmark. CTI was supported by Augustinus Fonden (19–0219) and the University of Macau (SRG2023–00040-ICI). KRJ, VGF, and CTI were also supported by The Lundbeck Foundation alliance BrainDrugs (R279–2018–1145). The funding was unrestricted and did not involve decisions regarding the study's design, data collection, analyses, interpretation, or writing. KRJ and CTI contributed to the study's conception and design and wrote the manuscript's initial draft. OUC performed the clinical EEG evaluations, and KRJ and CTI performed the statistical analyses. VGF, MBJ and GMK conceptualised the Neuropharm study and the data was collected by CTI, VND, KKF. All authors contributed to the interpretation of the analyses and the manuscript revision and have approved the submitted version. We gratefully acknowledge investigators from the NeuroPharm-1 study, collaborating general practitioners, and the Center for Referral and Diagnostics, Mental Health Services, Capital Region of Copenhagen, for helping recruit patients.

Publisher Copyright:
© 2023 The Author(s)

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