Comorbid anxiety moderates the relationship between depression history and prefrontal EEG asymmetry

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.

Frontal EEG alpha asymmetry and emotion: From neural underpinnings and methodological considerations to psychopathology and social cognition

“…Finally, the relationship of frontal asymmetry to psychopathology will be facilitated by moving beyond viewing diagnostic entities as homogeneous constructs. Future studies should examine frontal alpha asymmetry's relationship to specific symptoms ( Nelson et al, ), to clusters of features ( Keune et al, ; Nusslock et al, ), or to transdiagnostic dimensions reflecting fundamental processes ( Nelson et al, ) that may underlie a variety of psychopathology (Insel et al, ; Patrick & Hajcak, ).…”

“…Related, Nusslock et al () report that only individuals with a history of childhood onset depression and no comorbid anxiety disorder show reduced left‐frontal activity compared to psychiatrically healthy controls. In contrast, women with a history of depression and pathological levels of anxious apprehension—as indexed by a current generalized anxiety disorder, obsessive‐compulsive disorder, or separation anxiety disorder—were statistically indistinguishable from controls.…”

EEG biomarkers in depression: paving the way for stratified psychiatry

“…To our knowledge, this is the first study to assess the temporal stability of FAA in a large sample. This supports previous studies showing that FAA mainly depends on a considerable number of trait-like features, insensitive to antidepressant treatment, age, sex or depression severity (Allen et al, 2004;Arns et al, 2016;Bruder et al, 2008;Carvalho et al, 2011;Deldin & Chiu, 2005;Feldmann et al, 2018;Gollan et al, 2014;Keune et al, 2011;Nusslock et al, 2018;Spronk et al, 2008;Sutton & Davidson, 1997;Tomarken et al, 1992;Van der Vinne et al, 2017;Vuga et al, 2006). Similarly, Segrave and colleagues (2011) showed no evidence for antidepressant elicited changes in FAA when comparing a small group of depressed patients on ADs with unmedicated patients.…”

“…Cross-sectionally, several studies showed that FAA is independent of depression severity, both between patients (Allen et al, 2004;Arns et al, 2016;Feldmann et al, 2018;Gollan et al, 2014;Nusslock et al, 2018;Van der Vinne et al, 2017;Vuga et al, 2006) and within patients, including remission (Carvalho et al, 2011). This contrasts the findings by Grünewald et al (2018) and Keune et al (2011), where a higher level of depression complaints correlated with more left-sided FAA (albeit only in the control group of Grünewald et al).…”

“…We hypothesized that analysis of week-8 medicated EEG data would result in the same treatment prediction results as baseline unmedicated data did. Bruder et al, 2008Debener et al, 2000Deldin & Chiu, 2005Gollan et al, 2014Keune et al, 2011Spronk et al, 2008Vuga et al, 2006Davidson et al, 2003Hagemann, et al, 2002Hagemann, et al, 2005³ Sutton & Davidson, 1997Tenke et al, 2017³ Tomarken et al, 1992Carvalho et al, 2011Feldmann et al, 2018Gotlib et al, 1998Grünewald et al, 2018Nusslock et al, 2018 3.2 METHODS AND MATERIALS…”