Depression


Depression is the number one cause of disability worldwide. In Australia, it is estimated that 1 million adults experience depression in any given year (BeyondBlue). Over half of people who experience depression will experience anxiety at the same time. On average, 1 in 5 women and 1 in 8 men in Australia will experience depression at least once during their life, and for some that will be quite minor symptoms while for others it will be severe.

So how can Neurofeedback help?

Very simply explained, people who have depression also show asymmetry in their frontal lobe. Specifically, the left frontal lobe has significantly less activation in people with depression than in people without depression. This was first researched in the 70s, so that research into NF and depression date back over 45 years. The initial studies looked at parietal alpha and asymmetries. Later studies in the 80s and 90s also looked at frontal alpha asymmetry, finding a relative hyper-activation of the right frontal cortex that was not found in the parietal cortex. It has been suggested that this is related to ‘approach’ and ‘withdrawal’ behaviours. Decreased left-sided frontal activation is thought to be associated with a deficit in the approach system (which can generate positive moods), hence people with these deficits are more prone to depressive disorders. Right-sided frontal activation is related to withdrawal related emotion such as anxiety disorders. Interestingly this right sided activation was associated with selective spatial deficits, which are often reported to accompany depression, and may account for the issues with the decoding of nonverbal behaviour in people with depression.

There have been some questions of stability of frontal alpha over time suggesting several measures may be worthwhile. It is thought that this stability may be related to the fact that alpha is usually seen in occipital and parental areas, and can often be very low in frontal regions- possibly too low to result in a reliable asymmetry comparison. rTMS, a way of stimulating the brain through magnetic current, has been shown to be helpful in depression by stimulating the left frontal cortex, or inhibiting the right frontal cortex.

Neurofeedback allows us to increase left frontal lobe activation, which has been found to result in a large reduction of depressive symptoms, even sometimes resulting in a complete absence of depression by the end of the neurofeedback treatment (Hammond, 2005).

 

depression

Supporting Research

Underlying pathophysiological mechanisms have been identified in depression and research has shown that neurofeedback can target these physiological mechanisms in order to reduce depressive symptoms. Recent research in 2016 by Wang and colleagues investigated the efficacy of neurofeedback on alpha asymmetry in patients with major depressive disorder. Patients were randomly assigned to either a neurofeedback training group or control group. Over 6 weeks, the people in the neurofeedback group received training for 1 hour each week. The training saw those who responded to the neurofeedback training decrease their scores in both depression and anxiety when comparing pre and post measures. The findings highlight the benefits of neurofeedback on left and right frontal activity asymmetry in patients with major depressive disorder. One suggestion for non-responders to treatment in the neurofeedback group, was that the patients may have needed more sessions of training. Appropriate clinical application can be drawn from those who responded to treatment in the neurofeedback group.

In 2016, Cheon, Koo and Choi, evaluated the effect of neurofeedback on depressive symptoms and electrophysiological disturbances in patients with major depressive disorder. Twenty participants suffering from depression were recruited to participate in an 8-week, prospective, open-label study, to assess the efficacy of left prefrontal beta with alpha/theta training. The treatment protocol was twice or three times a week training of beta at F3 with alpha/theta at Pz for 8 weeks. It was found that depressive symptoms improved significantly (as determined by scores on self-report questionnaires) after neurofeedback treatment. Despite some limitations, such as, small sample size and lack of a control group for comparison, this study indicates that neurofeedback may have significant effects in patients with major depressive disorder.

In 2016,  Kaur and Singh from Punjab University (in India) focused their research on spectral analysis of EEG signals for tomographic neurofeedback. Score standardised low resolution electromagnetic tomography (sLORETA) was applied over 16 sessions to a patient with depression. The research found that sLORETA neurofeedback training increased alpha, impacted the theta/beta ratio and decreased beta in a patient with depression, suggesting tomographic neurofeedback could have a positive effect on depressive symptoms.

In 2015, Ramirez and colleagues introduced a new approach using neurofeedback. The approach focused on alleviating depression in elderly populations and required participants to manipulate expressive parameters in musical performances. The researchers found that musical neurofeedback training led to decreased depressive symptoms and decreased alpha activity in the frontal lobe in elderly individuals. Differences between pre and post BDI depression scores were found to be significant suggesting a positive effect of neurofeedback treatment on depressive symptoms in this population group.

Cheon and colleagues in 2015 carried out naturalistic study in a clinical setting to investigate the effects of neurofeedback on adult psychiatric patients. Seventy-seven patients were involved in the study. The neurofeedback protocol was adjusted according to each patient’s individual psychiatric complaints and the most common disorder was depression among other psychiatric complaints such as anxiety. For patients with depression, adjusting abnormal frontal cortex asymmetery between the left and right hemisphere was important in reducing depressive symptoms regardless of the specific neurofeedback protocol method prescribed for each participant. The findings showed that neurofeedback was successful in alleviating clinical symptoms of psychiatric disorders such as depression.

In 2015, Mirski and colleagues (from various institutions in Poland, USA, Russia and Norway), proposed to investigate the efficacy of an individually tailored neurofeedback protocol using anodal tDCs/ neurofeedback. A 45 year old female patient had previously undergone an operation of the meningioma, and complained of pain, anxiety, trouble sleeping, inattention and had withdrawn from work. Neuropsychological testing revealed this patient had post-operative depression. The research aimed to assess this tailored neurofeedback treatment protocol efficacy on post-operative depression. The research found that the patient was able to recover from her post-operative depression and returned to work following 20 sessions of the combined neurofeedback/DCS protocol.

In 2014, Young and associates found that real-time fMRI neurofeedback training of amygdala activity in individuals with major depression led to an improved ability to self-regulate the amygdala response. Participants in the experimental condition were able to up-regulate their amygdala response during positive memory recall. Pre and post scans showed significant increases of happiness ratings and significant decreases of anxiety ratings when compared to control group results. The results showed an improvement in mood and promising implications for fMRI neurofeedback training as a therapeutic application in the treatment of major depressive disorder.

In a controlled trial conducted by Escolano and colleagues in 2014, participants were allocated to either a neurofeedback test group or control group. This study was aimed at investigating a neurofeedback intervention on working-memory function in depressed patients. The protocol employed was targeted to increase the upper alpha power of the parieto-occipital area of the scalp. The neurofeedback test group participated in 8 training sessions and the results compared to the non-intervention control group. Cognitive variables including working memory, attention and executive function were measured pre and post training. The test group receiving the neurofeedback training showed improvement in performance as well as processing speed in working memory functioning. Enhanced upper alpha power was also observed in patients following neurofeedback training. A positive correlation was reported between improvement in processing speed and beta power increase. The results are supportive of this neurofeedback treatment protocol for working memory function in depressed patients.

In 2014, Lucas Koberda from Tellahassee Neurobalance Center (in USA) found that LORETA Z-score neurofeedback training led to improvements in depressive symptoms in individuals diagnosed with depression. Two cases were presented, one at 15 years of age and the second 40 years. The younger participant presented with anxiety, palpitations and dysregulation of the AC subcallosal region showing an increase in beta activity. After 15 sessions of neurofeedback therapy this dysregulation was corrected. In the second case, the patient has sustained memory impairment due to depresssion and had not been responding to conventional treatments. After 10 sessions of neurofeedback this patient was able to show improvement in cognitive domains particularly memory, information processing speed and visual spacial domain. Successful neurofeedback treatment also enabled this patient to return to work after a significant period of unemployment.

In 2014, Choobforoushzadeh and colleagues conducted a randomised trial on 24 Multiple Sclerosis patients showing symptoms of fatigue and depression. Patients were randomly allocated to two treatment groups; a neurofeedback treatment that underwent 16 sessions of training or a normal treatment group. Evaluations were measured at baseline, end of trials and at 2 month follow-up, differences in scores between the groups were examined. Using the Hospital Anxiety and Depression Scale for the outcome measures of depression, the study found that neurofeedback reduced symptoms of depression in patients with MS, compared to the standard treatment. These effects were maintained at the 2-month follow-up. These findings suggest that neurofeedback can aid in the treatment of depression in a variety of disorders and conditions.

A pilot study carried out by Choi and colleagues in 2011, found that asymmetry neurofeedback training increased left frontal dominance which led to the alleviation of depressive symptoms in individuals with depression. The neurofeedback training was shown to have profound effect upon emotion and cognition. Following treatment cognitive tests revealed improved performance in executive functioning when compared to placebo group which showed no such improvement. This demonstrates the impact of neurofeedback on underlying physiological asymmetry associated with depression which can improve depressive symptoms and cognition. The findings have been consistent with previous research.

A paper published in 2005(a) by D. Croydon Hammond outlines the internal meachanisms in why asymmetry has been associated with depression and how neurofeedback has an affect on depressive symptoms through this brain mechanism. It is noted that the left hemisphere of the prefrontal cortex is associated with an advantage for positive emotion and the right negative emotion. In depression there has been observed an impairment in the left prefrontal function, this imbalance can implicate a vulnerability to depression Hammond writes. In a second research paper from Hammond in 2005(b) focused on the biological aspects of depression, findings showed that neurofeedback is as effective (if not more) than regular medications in the reduction of depressive symptoms. The study further showed that the benefit of neurofeedback are more long-lasting than those of medication. This approach to treatment in depression has been highlighted as a noninvasive intervention and is not associated with major side effects related to other treatments such as medication.

Using the Roshi, a double channel unit integrating neurofeedback and photic stimulation treatment, D. Croydon Hammond in the year 2000 reported a reduction in depressive symptoms including somatic symptoms, anxiety and rumination. The treatment targeted left hemisphere beta training in a individual with severe medication resistant depression. The patient underwent 30 sessions of training. After the first five sessions the patient reported feeling less depressed and at the end of the full treatment, objective measures confirmed the significant improvements in depression and related symptoms. Benefits evident in the patient showed they had become more active, more socially involved and less withdrawn and these were maintained at eight and half month follow-up.

In a single case study Carolyn Earnest in 1999, presented findings of the first account of neurofeedback efficacy for depression on an adolescent. She (the patient) was diagnosed with a single episode of chronic depressive disorder at the age of 14. This patient received 67 episodes of neurofeedback training over a 10 month period. The protocol used was an asymmetry protocol to increase the activation in the left hemisphere and decrease activation in the right hemisphere and was carried out alongside psychotherapy sessions. Positive results were observed in the patient’s progress through the treatment and learned to increase differences in right and left hemisphere activation. The assessment of depression using The Beck Depression Inventory scores showed a significant decrease from 11 at the beginning of the neurofeedback training to 3 at the end of the trial. The findings of the study attributed these positive findings to the neurofeedback training. Interestingly, the psychotherapist involved in this case reported that the neurofeedback training prevented further mental illness in the individual. This case outlines the potential benefit of neurofeedback for depression in adolescents as well as adults.

Baehr, Rosenfeld and Baehr in 1997 presented two case studies of depressed women who each received more than 34 sessions of neurofeedback training. The researches applied an alpha asymmetry protocol. They wanted to find out if the patients could learn to increase the activity of the left frontal hemisphere or decrease right side activation in order to reduce their depression. The first patient in these case studies was able the differences in right and left frontal brain activation. After twenty-five sessions of alpha asymmetry neurofeedback training this patient claimed to no longer feel depressed and could identify different emotions evoked by depression and those normal to worry or sadness associated with adverse life events. A retest at five month follow-up showed that she had continued to maintain the learnt asymmetry differences. Similar to the first patient, the second patient also achieved the ability to distinguish between right and left hemisphere activation. She made significant gains in her functioning. In both cases neither medication or psychotherapy had been effective at helping them overcome their depression until a neurofeedback protocol had been added to their treatment.

 

 

References

Baehr, E., & Baehr, R. (1997). The use of brainwave biofeedback as an adjunctive therapeutic treatment for depression: Three case studies. Biofeedback25(1), 10-11.

Baehr, E., Rosenfeld, J. P., & Baehr, R. (1997). The clinical use of an alpha asymmetry protocol in the neurofeedback treatment of depression: Two case studies. Journal of neurotherapy2(3), 10-23.

Baehr, E., Rosenfeld, J. P., Baehr, R., & Earnest, C. (1998). Comparison of two EEG asymmetry indices in depressed patients vs. normal controls. International Journal of Psychophysiology31(1), 89-92.

Baehr, E., Rosenfeld, J. P., & Baehr, R. (2001). Clinical use of an alpha asymmetry neurofeedback protocol in the treatment of mood disorders: Follow-up study one to five years post therapy. Journal of neurotherapy4(4), 11-18.

Bell, I. R., Schwartz, G. E., Hardin, E. E., Baldwin, C. M., & Kline, J. P. (1998). Differential resting quantitative electroencephalographic alpha patterns in women with environmental chemical intolerance, depressives, and normals. Biological psychiatry43(5), 376-388.

Cheon, E. J., Koo, B. H., Seo, W. S., Lee, J. Y., Choi, J. H., & Song, S. H. (2015). Effects of neurofeedback on adult patients with psychiatric disorders in a naturalistic setting. Applied psychophysiology and biofeedback40(1), 17-24.

Cheon, E. J., Koo, B. H., & Choi, J. H. (2016). The Efficacy of Neurofeedback in Patients with Major Depressive Disorder: An Open Labeled Prospective Study. Applied psychophysiology and biofeedback41(1), 103-110.

Choi, S. W., Chi, S. E., Chung, S. Y., Kim, J. W., Ahn, C. Y., & Kim, H. T. (2011). Is alpha wave neurofeedback effective with randomized clinical trials in depression? A pilot study. Neuropsychobiology63(1), 43-51.

Choobforoushzadeh, A., Neshat-Doost, H., Molavi, H., & Abedi, M. (2015). Effect of neurofeedback training on depression and fatigue in patients with multiple sclerosis. Appled Psychophysiology Biofeedback, 40(1), 1-8.

Deldin, P. J., & Chiu, P. (2005). Cognitive restructuring and EEG in major depression. Biological psychology70(3), 141-151.

DeRubeis, R. J., Siegle, G. J., & Hollon, S. D. (2008). Cognitive therapy versus medication for depression: treatment outcomes and neural mechanisms. Nature Reviews Neuroscience9(10), 788-796.

Dias, Á. M., & van Deusen, A. (2011). A new neurofeedback protocol for depression. The Spanish journal of psychology14(01), 374-384.

Earnest, C. (1999). Single case study of EEG asymmetry biofeedback for depression: An independent replication in an adolescent. Journal of Neurotherapy3(2), 28-35.

Escolano, C., Navarro-Gil, M., Garcia-Campayo, J., Congedo, M., De Ridder, D., & Minguez, J. (2014). A controlled study on the cognitive effect of alpha neurofeedback training in patients with major depressive disorder. Frontiers in behavioral neuroscience8, 296.

Eskandari, Z., Taremian, F., Nazari, M., Bakhtiari, M., Momtazi, S., & Rezaei, M. (2014). Effectiveness of neurofeedback treatment to decrease severity symptoms in major depressive disorder. Journal of Zanjan University of Medical Sciences and Health Sciences, 22(92), 86-95.

Hamilton, J. P., Glover, G. H., Hsu, J. J., Johnson, R. F., & Gotlib, I. H. (2011). Modulation of subgenual anterior cingulate cortex activity with real‐time neurofeedback. Human brain mapping32(1), 22-31.

Hamilton, J. P., Glover, G. H., Bagarinao, E., Chang, C., Mackey, S., Sacchet, M. D., & Gotlib, I. H. (2016). Effects of salience-network-node neurofeedback training on affective biases in major depressive disorder. Psychiatry Research: Neuroimaging249, 91-96.

Hammond, D. C. (2000). Neurofeedback treatment of depression with the Roshi. Journal of Neurotherapy4(2), 45-56.

Hammond, D. C. (2005a). Neurofeedback with anxiety and affective disorders. Child and adolescent psychiatric clinics of North America14(1), 105-123.

Hammond, D. C. (2005b). Neurofeedback treatment of depression and anxiety. Journal of Adult Development12(2-3), 131-137.

Kaur, C., & Singh, P. (2016). Toward EEG spectral analysis of tomographic neurofeedback for depression. Advances in Intelligent Systems and Computing, 479, 97-103.

Koberda, L. (2014). Z-score LORETA neurofeedback as a potential therapy in depression/anxiety and cognitive dysfunction. Z score Neurofeedback: Clinical applications. Elsevier: Academic press.

Koberda, J. L., Moses, A., Koberda, P., Winslow, J., & Koberda, L. (2014). Z-score LORETA neurofeedback as a potential therapy in depression/anxiety and cognitive dysfunction. Neuroconnection Spring, USA, 52-55.

Linden, D. E., Habes, I., Johnston, S. J., Linden, S., Tatineni, R., Subramanian, L., … & Goebel, R. (2012). Real-time self-regulation of emotion networks in patients with depression. PloS one7(6), e38115.

Lubar, J. F., Congedo, M., & Askew, J. H. (2003). Low-resolution electromagnetic tomography (LORETA) of cerebral activity in chronic depressive disorder. International Journal of Psychophysiology49(3), 175-185.

Mirski, A., Pąchalska, M., Moskała, M., Orski, M., Orska, M., Miąskiewicz, M., … & Kropotov, J. D. (2015). Neuromarkers of anxiety and depression in a patient after neuro-ophthalmic surgery of the meningioma–effect of individually-tailored tDCS and neurofeedback. Annals of Agricultural and Environmental Medicine, 22(4), 730-735..

Niv, S. (2013). Clinical efficacy and potential mechanisms of neurofeedback. Personality and Individual Differences54(6), 676-686.

Paquette, V., Beauregard, M., & Beaulieu-Prévost, D. (2009). Effect of a psychoneurotherapy on brain electromagnetic tomography in individuals with major depressive disorder. Psychiatry Research: Neuroimaging174(3), 231-239.

Peeters, F., Oehlen, M., Ronner, J., van Os, J., & Lousberg, R. (2014). Neurofeedback as a treatment for major depressive disorder–a pilot study. PloS one9(3), e91837.

Ramirez, R., Palencia-Lefler, M., Giraldo, S., & Vamvakousis, Z. (2015). Musical neurofeedback for treating depression in elderly people. Applied Psychology and Biofeedback, 40(1), 1-8.

Rosenfeld, J. P. (1997). EEG biofeedback of frontal alpha asymmetry in affective disorders. Biofeedback, 25(1), 8-25.

Rosenfeld, J. P. (2000). An EEG biofeedback protocol for affective disorders. Clinical EEG and Neuroscience31(1), 7-12.

Siegle, G. J., Thompson, W., Carter, C. S., Steinhauer, S. R., & Thase, M. E. (2007). Increased amygdala and decreased dorsolateral prefrontal BOLD responses in unipolar depression: related and independent features. Biological psychiatry61(2), 198-209.

Simkin, D. R., Thatcher, R. W., & Lubar, J. (2014). Quantitative EEG and neurofeedback in children and adolescents: anxiety disorders, depressive disorders, comorbid addiction and attention-deficit/hyperactivity disorder, and brain injury. Child and adolescent psychiatric clinics of North America23(3), 427-464.

Vuga, M., Fox, N. A., Cohn, J. F., George, C. J., Levenstein, R. M., & Kovacs, M. (2006). Long-term stability of frontal electroencephalographic asymmetry in adults with a history of depression and controls. International Journal of Psychophysiology59(2), 107-115.

Wang, S. Y., Lin, I. M., Peper, E., Chen, Y. T., Tang, T. C., Yeh, Y. C., … & Chu, C. C. (2016). The efficacy of neurofeedback among patients with major depressive disorder: preliminary study. NeuroRegulation3(3), 127.

Young, K. D., Zotev, V., Phillips, R., Misaki, M., Yuan, H., Drevets, W. C., & Bodurka, J. (2014). Real-time FMRI neurofeedback training of amygdala activity in patients with major depressive disorder. PloS one9(2), e88785.

Yuan, H., Young, K. D., Phillips, R., Zotev, V., Misaki, M., & Bodurka, J. (2014). Resting-state functional connectivity modulation and sustained changes after real-time functional magnetic resonance imaging neurofeedback training in depression. Brain connectivity4(9), 690-701.

Zotev, V., Yuan, H., Misaki, M., Phillips, R., Young, K. D., Feldner, M. T., & Bodurka, J. (2016). Correlation between amygdala BOLD activity and frontal EEG asymmetry during real-time fMRI neurofeedback training in patients with depression. NeuroImage: Clinical11, 224-238.