As most psychiatric disorders, anxiety and depression are conditions whose severity can be represented over continuums that range from subclinical manifestations (expectancy/fear without proper justification and low mood, respectively) to full-blown biosocial disabilities. From an endophenotypic perspective, alpha band (8-12 Hz) asymmetry in the left frontal cortex has emerged as the most prominent electroencephalographic (EEG) correlate of both anxiety and depression in right-handed people, followed by excessive band power in beta 1 (12-20 Hz) and beta 2 waves (20-30 Hz) in the right parietal lobe.1
Shared features also extend to the genetic level, where the presence of copies of the short variation of the 5-HTTLPR polymorphism increases the risk of both anxiety and depression.
EEG neurofeedback is an operant conditioning technique in which subjects learn to self-regulate and modify their brain activity through a feedback loop. In the recent past, induction of healthy alpha asymmetry2,3
and regulation of alpha power bands4
have been successfully used to treat anxiety and depression, whereas increasing the power of sensorimotor rhythm (SMR) bands - a sort of EEG activity ranging from 12-15 Hz over the sensorimotor cortex - has been used successfully to improve memory and sleep quality.5
We report the case of a 29-year-old woman, with no previous psychiatric history, who presented with anxiety symptoms, sleep problems, and mild cognitive impairments which she associated to a contingent situation she was facing. We assessed pre- and post-EEG data using a protocol reported elsewhere.3
Anxiety and depression symptoms were assessed using Beck scales (Beck Anxiety Inventory [BAI] and Beck Depression Inventory [BDI]), and sleep quality, with the Pittsburgh Sleep Quality Index (PSQI). Cognitive measures were also administered. A summary of results is presented in Table 1.
The training protocol lasted 20 sessions, during which the subject was trained to increase beta 1 (12-15 Hz) at C4 with eyes open, followed by closed-eyes training designed to increase the alpha/beta 3 ratio (9.5-12 Hz/23-38 Hz) at P4. There was marked improvement of anxiety, depression, and sleep quality, as well as some improvement in executive functions (Table 1). From an endophenotypic viewpoint, there was an overall increase in beta 1, low alpha (8-10 Hz), and high alpha (10-12 Hz) powers and a decrease in beta 2 (a stress biomarker). Low and high alpha changes from the pre-treatment baseline were particularly prominent at P4, increasing from 8.9 to 14% and from 12.2 to 26.2% respectively. These results are encouraging and suggest that neurofeedback can be used as an adjunct in the treatment of subclinical anxiety and, perhaps, other psychiatric conditions, with minimal risk and low technology costs.
The use of an alpha/beta 3 ratio neurofeedback protocol is not well documented in the literature, and seems to have potential efficacy for reducing anxiety and associated symptoms. In this case, the combination of two protocols - SMR followed by alpha/beta 3 ratio - led to an overall improvement in the symptoms reported by the patient. To the best of our knowledge, this is the first time such a combination has been used. Although our initial findings are promising, caution is needed in their interpretation, and these results should be replicated in larger, controlled clinical trial settings. Moreover, the specific effects of SMR and of alpha/beta 3 training for anxiety should be investigated separately.ACKNOWLEDGEMENTS
JSG receives a scholarship from Coordenaçao de Aperfeiçoamento de Pessoal de Nível Superior (CAPES). AMD has received a grant from Fundaçao de Amparo à Pesquisa do Estado de Sao Paulo (FAPESP; protocol no. 2015/3931-0).DISCLOSURE
The authors report no conflicts of interest.REFERENCES
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