Neurofeedback and Depression
Updated: Jul 8
Major depressive disorder (MDD) is a severely disabling disorder resulting in the deterioration of daily function and lowering the quality of life. (American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 2000). Neurofeedback for depression is based on well-established EEG research indicating that the left frontal area is more associated with positive affect, while the right frontal area is more involved with negative emotion (Davidson, 2004), in which asymmetric neurofeedback training is required to improve depressive symptoms.
The Neural Imbalance:
A biological predisposition for depression exists when there is an asymmetry in brain wave activity, such that there is excessive left frontal alpha (8-12 Hz) reflecting less activation and failure to suppress the subcortical structures that mediate depression (Walker et al., 2007). Indeed research has shown that when the left frontal region is “stuck” in an alpha idling rhythm, there is both reduced positive affect and more withdrawal behavior.
One neurofeedback protocol for modifying this suboptimal brain state involves modifying the left-right alpha balance at electrodes F3 and F4 (with a Cz reference). Research supports the efficacy of this ALAY (“alpha asymmetry”) protocol (Choi et al., 2011; Peeters et al., 2014), including evidence indicating changes in the asymmetry and depressive symptoms endure 1 and 5 years after the end of treatment (Baehr et al., 2001).
Another neurofeedback protocol directly targets reducing left frontal alpha rather than modifying the left-right alpha balance (Walker et al., 2007). This protocol involves enhancing left-frontal beta (typically 15-18 Hz) and inhibiting left-frontal theta or alpha to yield greater activation, which, in turn, generally triggers improved mood. Studies have shown that enhancing beta and inhibiting theta or alpha at C3 reduced depressive symptoms in most patients (Walker et al., 2007).
In a recent study, most MDD participants who received 1-hour/week ALAY intervention for 6 weeks regulated their asymmetry and showed improvement in depressive symptoms, though 43% were non-responders (Wang et al., 2016). Notably, although pharmacologic intervention yields remission of depression, it does not affect the frontal alpha asymmetry, suggesting that individuals who receive such intervention continue to have this biomarker for future depression.
Using the alternative reported protocol, a recent controlled trial, Liu (Liu, 2017) applied the enhanced beta/inhibit alpha protocol at F3 in 32 college students with MDD. In addition to regulating brainwaves, the neurofeedback intervention was protective, significantly reducing the recurrence and intensity of depressive symptoms for 3 weeks post-intervention; in contrast, depressive symptoms increased in active control participants.
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