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.2013 Mar 25:2:448-58.
doi: 10.1016/j.nicl.2013.03.011. eCollection 2013.

Neural mechanisms of symptom improvements in generalized anxiety disorder following mindfulness training

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Neural mechanisms of symptom improvements in generalized anxiety disorder following mindfulness training

Britta K Hölzel et al. Neuroimage Clin..

Abstract

Mindfulness training aims to impact emotion regulation. Generalized anxiety disorder (GAD) symptoms can be successfully addressed through mindfulness-based interventions. This preliminary study is the first to investigate neural mechanisms of symptom improvements in GAD following mindfulness training. Furthermore, we compared brain activation between GAD patients and healthy participants at baseline. 26 patients with a current DSM-IV GAD diagnosis were randomized to an 8-week Mindfulness Based Stress Reduction (MBSR, N = 15) or a stress management education (SME, N = 11) active control program. 26 healthy participants were included for baseline comparisons. BOLD response was assessed with fMRI during affect labeling of angry and neutral facial expressions. At baseline, GAD patients showed higher amygdala activation than healthy participants in response to neutral, but not angry faces, suggesting that ambiguous stimuli reveal stronger reactivity in GAD patients. In patients, amygdala activation in response to neutral faces decreased following both interventions. BOLD response in ventrolateral prefrontal regions (VLPFC) showed greater increase in MBSR than SME participants. Functional connectivity between amygdala and PFC regions increased significantly pre- to post-intervention within the MBSR, but not SME group. Both, change in VLPFC activation and amygdala-prefrontal connectivity were correlated with change in Beck Anxiety Inventory (BAI) scores, suggesting clinical relevance of these changes. Amygdala-prefrontal connectivity turned from negative coupling (typically seen in down-regulation of emotions), to positive coupling; potentially suggesting a unique mechanism of mindfulness. Findings suggest that in GAD, mindfulness training leads to changes in fronto-limbic areas crucial for the regulation of emotion; these changes correspond with reported symptom improvements.

Keywords: Amygdala; Beck Anxiety Inventory; Connectivity; Emotion regulation; Generalized anxiety disorder; Intervention; Longitudinal; Mindfulness; Prefrontal cortex; Stress; Ventrolateral prefrontal cortex.

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Figures

Fig. 1
Fig. 1
When labeling the affect, compared to the gender of facial expressions, healthy participants (N = 26) show decreased activation in the left amygdala (A; p = 0.0121, multiple comparison corrections within area of bilateral amygdalae), the right rostral ACC (C; p = 0.0314; multiple comparison corrections within mask of the frontal cortex/insula), and left inferior parietal cortex (B; p = 0.0321, multiple comparison corrections for entire brain for this and all following clusters) and increased activation in the left lateral occipital (B; p = 0.0087), left fusiform (B; p = 0.0099), and right lingual cortex (C; p = 0.0105).
Fig. 2
Fig. 2
GAD patients (N = 26) show greater activation in a cluster in the right amygdala when viewing neutral facial expressions when compared to healthy participants (N = 26; p = 0.0001; size = 440 mm3; multiple comparison corrections within area of bilateral amygdalae; cluster overlaid over a FreeSurfer subcortical parcellation image).
Fig. 3
Fig. 3
MBSR participants (N = 15) show stronger increases in brain activation in clusters in the right pars opercularis (A; p = 0.0156; multiple comparison corrections within mask of the frontal cortex/insula) and left pars triangularis (B; p = 0.0015), i.e., ventrolateral prefrontal regions when viewing neutral emotional expressions than SME participants (N = 11). Extracted averaged values from the clusters in the right pars opercularis (C), and the left pars triangularis (D) for the MBSR (black) and SME (blue) groups when viewing neutral facial expressions at pre- and post-interventions (error bars indicate standard errors). Signal in the cluster in the left pars triangularis is correlated with scores on the Beck Anxiety Inventory (BAI) at post-intervention (E; ρ = − .645, p < .001, uncorrected) and the pre–post intervention change in this cluster is correlated with the change in BAI (F; ρ = − .617, p = .001, uncorrected).
Fig. 4
Fig. 4
MBSR participants (N = 15) show stronger pre–post increases than SME participants (N = 11) in two clusters in the right VLPFC when viewing angry facial expressions (A; pars opercularis: p = 0.0003; rostral middle frontal gyrus: p = 0.0018; multiple comparison corrections within mask of the frontal cortex/insula). Extracted averaged signal for the MBSR (black) and SME (blue) groups at pre- and post-interventions in the right rostral middle frontal gyrus, reaching into the pars opercularis (B) and right pars opercularis, reaching into the pars triangularis and insula (C; error bars indicate standard errors).
Fig. 5
Fig. 5
Functional connectivity between the seed region in the right amygdala and several regions in the frontal cortex increased from pre- to post-intervention in GAD patients who underwent the MBSR program (N = 15), but not in those who underwent the SME class (N = 11). Anatomical location displayed on an inflated surface with FreeSurfer cortex parcellations (top row), regression coefficients extracted from the clusters from the MBSR (black) and SME (blue) participants at pre- and post-interventions (middle row) and scatter plots of regression coefficients (y-axis) and Beck Anxiety Inventory (BAI, x-axis) for MBSR and SME participants at post (bottom row) for the left rostral anterior cingulate cortex (ACC, column A, pre- to post increase in connectivity: p = 0.0002, multiple comparison corrections within mask of the frontal cortex/insula; correlation with BAI scores: ρ = − .229, ns, uncorrected), right superior frontal cortex (column B, pre–post increase: p = 0.04; correlation: ρ = − .470, p = .015), right rostral middle frontal cortex (column C, pre–post increase: p = 0.03; correlation: ρ = − .572, p = .002), and left rostral middle frontal cortex (column D, pre–post increase: p = 0.01; correlation: ρ = − .646, p < .001).
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References

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