Comorbid anxiety moderates the relationship between depression history and prefrontal EEG asymmetry. (29th July 2017)

• Record Type: Journal Article
• Authors: Nusslock, Robin; Shackman, Alexander J.; McMenamin, Brenton W.; Greischar, Lawrence L.; Davidson, Richard J.; Kovacs, Maria
• Other Names: Allen John J.B. guestEditor.; Keune Philipp M. guestEditor.; Schönenberg Michael guestEditor.; Nusslock Robin guestEditor.
• Is Part Of: Psychophysiology. Volume 55:Number 1(2018)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2017-07-29
• Subjects: anxiety -- comorbidity -- depression -- frontal EEG asymmetry; Psychophysiology -- Periodicals; 612.8
• DOI: 10.1111/psyp.12953
• Languages: English
• ISSNs: 0048-5772

Abstract

Abstract: The internalizing spectrum of psychiatric disorders—depression and anxiety—are common, highly comorbid, and challenging to treat. Individuals with childhood onset depression have a particularly poor prognosis. There is compelling evidence that individuals with depression display reduced resting‐state EEG activity at sensors overlying the left prefrontal cortex, even during periods of remission, but it remains unknown whether this asymmetry is evident among individuals with a comorbid anxiety disorder. Here, we demonstrate that women with a history of childhood onset depression and no anxiety disorder ( n = 37) show reduced left lateral frontal activity compared to psychiatrically healthy controls ( n = 69). In contrast, women with a history of childhood onset depression and pathological levels of anxious apprehension ( n = 18)—as indexed by a current generalized anxiety disorder, obsessive compulsive disorder, or separation anxiety disorder diagnosis—were statistically indistinguishable from healthy controls. Collectively, these observations suggest that anxious apprehension can mask the relationship between prefrontal EEG asymmetry and depression. These findings have implications for understanding (a) prefrontal EEG asymmetry as a neurophysiological marker of depression, (b) the comorbidity of depression and anxiety, and (c) failures to replicate the relationship between prefrontal EEG asymmetry and depression. More broadly, they set the stage for developing refined interventions for internalizing psychopathology.