Abstract
Typical adolescents have increased limbic engagement unchecked by regulatory medial prefrontal cortex (PFC) activity as well as heightened self-focus. The resulting emotion dysregulation and self-focused rumination make adolescents more susceptible to depression and suicide attempts. Heightened self-focus converges with mental illness among depressed adolescents, who deploy exaggerated attention to negative self-relevant stimuli and neglect positive ones as part of depression’s phenomenology. This results in rigid negative self-representations during an identity formative period with potential lifetime repercussions. Current empirically supported treatments fail to allay recurrent depression. Evidence-based interventions for illnesses linked to suicide ideation and attempts (e.g., depression) underperform across the lifespan. This could be because current treatments are not successful in altering pervasive negative self-representations and affect dysregulation, which is known to be a risk factor of chronic depression. This study departs from the premise that increasing positive self-processing might be protective against chronic depression particularly during adolescence. The present research is a novel investigation of neurofeedback as a potential treatment alternative for adolescent depression. To enhance positive self-processing, we used the happy self-face as a cue to initiate neurofeedback from the bilateral amygdala and hippocampus and adolescents attempted to upregulate that limbic activity through the recall of positive autobiographical memories. We identified limbic functional circuitry engaged during neurofeedback and links to short-term symptoms’ change in depression and rumination. We found that depressed youth showed greater right amygdala to right frontocortical connectivity and lower left amygdala to right frontocortical connectivity compared to healthy controls during neurofeedback vs. control conditions. Depressed youth also showed significant symptom reduction. Connectivity between the right amygdala and frontocortical regions was positively correlated with rumination and depression change, but connectivity between frontocortical regions and the left amygdala was negatively correlated with depression change. The results suggest that depressed youth might engage implicit emotion regulation circuitry while healthy youth recruit explicit emotion regulation circuits during neurofeedback. Our findings support a compensatory approach (i.e., target the right amygdala) during future neurofeedback interventions in depressed youth. Future work ought to include a placebo condition or group.
Highlights
Adolescence is a period of increased risk for developing depression, and early onset is associated with a poorer prognosis, higher symptom severity, and comorbidity, along with higher suicidality rates (Sung et al, 2013)
Depressed youth showed greater right amygdala to right frontocortical connectivity compared to healthy adolescents during FB vs. count-backward, they showed lower left amygdala to right frontocortical connectivity compared to healthy controls
There were no increases in connectivity between the prefrontal cortex (PFC) and the averaged left and right amygdala seeds, all the results pertained to differences between the left or right amygdala connectivity patterns between the groups
Summary
Adolescence is a period of increased risk for developing depression, and early onset is associated with a poorer prognosis, higher symptom severity, and comorbidity, along with higher suicidality rates (Sung et al, 2013). Given that suicide—a severe outcome of depression in youth—is the second leading cause of adolescent death in the United States (Murphy et al, 2018) and that persistent depression is a risk for adolescent attempts (Goldstein et al, 2012), the need for developing novel and effective treatments for adolescent depression is imperative This is critical as it has been shown that whereas current treatments such as medication and psychotherapy aid in recovering from depressive episodes, they often fail to prevent recurring episodes (Rush et al, 2008; Maalouf and Brent, 2012; Schwartz-Lifshitz et al, 2012; De Silva et al, 2013; O’Connor et al, 2013; Hetrick et al, 2016; Weisz et al, 2017; Cha et al, 2018), resulting in a compounded economic burden for families and health systems (Wang et al, 2003) and higher risks for suicide attempts (Pezawas et al, 2003; Witte et al, 2009; Jonsson et al, 2011). Due to heightened cortico-limbic plasticity (Gee et al, 2013), this developmental period is a window of opportunity to train the substrates of affect regulation and self-processing via novel procedures such as neurofeedback
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