Elsevier

Biological Psychology

Volume 87, Issue 3, July 2011, Pages 379-385
Biological Psychology

Frontal EEG asymmetry and symptom response to cognitive behavioral therapy in patients with social anxiety disorder

https://doi.org/10.1016/j.biopsycho.2011.04.009Get rights and content

Abstract

Although previous studies have shown that socially anxious individuals exhibit greater relative right frontal electroencephalogram (EEG) activity at rest, no studies have investigated whether improvements in symptoms as a result of treatment are associated with concomitant changes in resting brain activity. Regional EEG activity was measured at rest in 23 patients with social anxiety disorder (SAD) before and after cognitive behavioral therapy (CBT). Results indicated that patients shifted significantly from greater relative right to greater relative left resting frontal brain activity from pre- to posttreatment. Greater left frontal EEG activity at pretreatment predicted greater reduction in social anxiety from pre- to posttreatment and lower posttreatment social anxiety after accounting for pretreatment symptoms. These relations were specific to the frontal alpha EEG asymmetry metric. These preliminary findings suggest that resting frontal EEG asymmetry may be a predictor of symptom change and endstate functioning in SAD patients who undergo efficacious psychological treatment.

Highlights

► Regional EEG activity measured in patients with social anxiety disorder (SAD) before and after cognitive behavioral therapy (CBT). ► Resting EEG frontal alpha asymmetry changes significantly from pre- to posttreatment from greater right to greater left. ► Greater resting left frontal EEG alpha activity at pretreatment predicts both symptom reduction and endstate functioning during CBT for SAD.

Introduction

Social anxiety disorder (SAD) is characterized by extreme fear and avoidance of social and performance situations (American Psychiatric Association, 2000). With a lifetime prevalence estimated to be as high as 12%, SAD is the third most common psychological disorder (Kessler et al., 2005). SAD has an early onset, a chronic course, and a debilitating impact on quality of life in interpersonal, emotional, and occupational domains. Numerous controlled trials have demonstrated that cognitive behavioral therapy (CBT) is efficacious in the treatment of SAD (Moscovitch et al., 2009, Smits and Hofmann, 2009), with approximately 50–70% of patients experiencing significant symptom reduction after 12 weeks of therapy (Swinson et al., 2006).

Despite the proven efficacy of CBT in reducing symptoms of social anxiety, little is known about the impact of CBT interventions on the neural mechanisms underlying social anxiety. Imaging studies on the neurobiological effects of CBT among patients with depression as well as those with anxiety disorders have shown significant treatment-related changes across broadly distributed brain regions (Porto et al., 2009, Roffman et al., 2005). However, only one previous study has investigated the association between symptom improvement during CBT and corresponding brain changes in patients with a principal diagnosis of SAD (Furmark et al., 2002), and this study used positron emission tomography (PET).

The search for neural mechanisms underlying CBT interventions for SAD is of considerable theoretical and practical importance. Intervention studies provide us with a means by which to examine how environmental influences impact brain–behavior relations. Studies may also be useful in terms of identifying aspects of neuronal function at pretreatment that may predict endstate functioning, thereby leading to improvements in the prognosis and treatment of SAD.

Of particular interest to the present study are models that link frontal brain asymmetry to individual differences in affective style and emotion processing. Davidson and Fox have theorized that the frontal lobes are differentially involved in positive versus negative affective states and corresponding motivated behaviors (Davidson, 2000, Fox, 1991), with left frontal areas of the brain mediating the experience of positive emotions (e.g., joy, happiness, etc.) and approach behaviors, and right frontal areas of the brain mediating the experience of negative emotions (e.g., fear, sadness, etc.) and withdrawal behaviors. Moreover, patterns of frontal electroencephalogram (EEG) asymmetry may serve as an index of risk for a variety of emotion-related disorders, including depression and anxiety. A number of studies over the past three decades have supported these theoretical predictions (see Coan and Allen, 2004). Non-clinical samples of adults selected for high levels of shyness (Schmidt, 1999) and social anxiety (Beaton et al., 2008), or clinically diagnosed with SAD (Davidson et al., 2000) have been shown to exhibit significant relative elevations in right frontal brain activity when assessed during resting states or periods of acute emotional provocation.

Although no studies to date have investigated patterns of change in frontal EEG activity among individuals with SAD before and after CBT, preliminary research has demonstrated that frontal EEG asymmetry can be balanced following therapeutic interventions. For example, in a recent randomized controlled study, patients with posttraumatic stress disorder who received CBT exhibited decreased right frontal EEG activity from pre- to posttreatment relative to those assigned to a waitlist control condition (Rabe et al., 2008).1 Across a number of other studies, significant modifications of EEG alpha asymmetry (increased relative left or decreased relative right frontal EEG activity) have been observed in depressed adolescents who received massage and music therapy (Jones and Field, 1999), in healthy individuals (Davidson et al., 2003) as well as those with a history of suicidal depression (Barnhofer et al., 2007) exposed to an 8-week mindfulness meditation program, and in depressed individuals undergoing repetitive transcranial magnetic stimulation treatment (Funk and George, 2008; but see Spronk et al., 2008). Moreover, the administration of acute cortisol and prednisone, which generate anxiogenic effects, has been shown to increase right frontal EEG alpha activity among healthy participants (Schmidt et al., 1999, Tops et al., 2005). Finally, a study that examined frontal asymmetry in young adults at two time points 1 year apart (Blackhart et al., 2006) found that greater relative right frontal EEG resting activity at time 1 was significantly associated with higher levels of trait anxiety (controlling for symptoms of depression) at time 2, suggesting that EEG asymmetry may predict the development of future anxiety symptoms. Similarly, Beaton et al. (2008) found that a nonclinical sample of socially anxious undergraduate students demonstrated greater relative right frontal EEG activity at rest, but only after accounting for symptoms of depressed mood.

We investigated whether CBT was associated with changes in frontal EEG asymmetry in individuals with SAD and whether pretreatment EEG had utility in terms of predicting posttreatment functioning. Patients with a principal diagnosis of generalized SAD completed 12 sessions of standardized group CBT. At pre- and posttreatment, resting regional EEG activity was recorded as part of a larger study (see Miskovic et al., 2011). We hypothesized that: (i) at pretreatment, SAD patients would exhibit greater right than left frontal resting EEG activity; (ii) patients would shift significantly from greater right to greater relative left frontal brain activity from pre- to posttreatment; and (iii) greater pretreatment left frontal EEG asymmetry would uniquely predict greater treatment-related decreases in symptoms of social anxiety. Given the documented links between depression and frontal EEG asymmetry (e.g., Henriques and Davidson, 1990, Schaffer et al., 1983), the high rate of comorbidity between SAD and depressive disorders (Brown et al., 2001), and the significant degree of overlap observed in clinical samples between symptoms of social anxiety and depression (Brown and Barlow, 2009), we accounted for symptoms of depression in our analyses.

Section snippets

Participants

Thirty three outpatients were recruited for this study. Eight of these individuals discontinued treatment and their participation in the study. Two participants had extreme scores on EEG α spectral power (±3 SD from mean) and were thus excluded from the analysis, leaving 23 (12 male) eligible Caucasian, right-handed participants for the current analysis. All participants were assessed and treated at the Anxiety Treatment and Research Centre (ATRC), an urban Canadian anxiety treatment clinic

Effectiveness of CBT on symptom change

Paired t-tests (pre- versus posttreatment) on patients’ CGI severity scores indicated that illness severity decreased significantly from pretreatment to posttreatment as rated by both the independent, blind clinician, t(18) = 3.98, p = .001 (M = 5.05 ± 0.78 versus 4.37 ± 1.11), and the group therapist, t(22) = 6.10, p < .001 (M = 5.30 ± .82 versus 3.83 ± 1.15). As expected, patients’ self-reported social anxiety and depression symptoms at pre- versus posttreatment also indicated a significant decrease in both the

Discussion

We investigated changes in the pattern of frontal EEG asymmetry among patients with SAD who completed 12 sessions of group CBT. In conjunction with symptom amelioration from pre- to posttreatment, significant electrocortical changes occurred that were characterized by a shift from greater relative right to left frontal alpha EEG asymmetry at rest. These findings are consistent with the growing literature demonstrating that frontal EEG asymmetry is sensitive to the effects of therapeutic

Acknowledgements

This research was supported by an Ontario Mental Health Foundation New Investigator Fellowship and funding from the Canada Research Chairs Program awarded to David A. Moscovitch, and by NSERC and SSHRC Operating Grants awarded to Louis A. Schmidt.

We are grateful to Jessica Senn, Sue McKee, and to the clinicians and staff at the Anxiety Treatment and Research Centre, for their invaluable contributions to this study.

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