Borderline personality disorder: no demonstrated additional clinical benefit from amygdala neurofeedback

Changing activity in a brain region does not necessarily mean improving symptoms. A randomized pilot trial in people with borderline personality disorder tested amygdala neurofeedback as an add-on to inpatient dialectical behavior therapy. Participants managed to reduce the targeted activity, without any demonstrated additional clinical benefit. However, the small sample limits the conclusions that can be drawn.

Illustration of the brain's amygdala, the region targeted by the neurofeedback evaluated in this trial on borderline personality disorder.
MindsetEditorial illustration, not study data.

An add-on tested during intensive psychotherapy

The trial included 36 people who still had clinically significant symptoms halfway through their dialectical behavior therapy. Random allocation assigned 23 participants to the group also receiving amygdala neurofeedback using real-time functional MRI, and 13 to the group continuing psychotherapy alone.

Here, neurofeedback uses a measure of brain activity to allow participants to practice modulating it. The hypothesis was that learning to reduce amygdala activity would lead to further improvements in emotion regulation. This biological hypothesis still needed to translate into a benefit in daily life.

The primary outcome was emotional instability, assessed through repeated measurements in daily life. The researchers also collected questionnaire responses and brain imaging measurements before and after the intervention, then at 3- and 6-month follow-ups.

Brain changes, without a consistent clinical advantage

Participants managed to reduce amygdala activity during neurofeedback. Some imaging measurements also showed changes after the intervention, including temporary reductions in activity in this region during an emotion regulation task.

But daily-life measurements did not show a consistent advantage from adding neurofeedback to psychotherapy. Negative emotions, inner tension and emotional instability improved over time, without a clearly established additional advantage for this group.

The questionnaires did not reveal any additional benefit either. Borderline symptom scores measured using the BSL-23 increased after discharge in both groups. The brain findings therefore cannot be presented as evidence of clinical improvement.

A finding limited by sample size and loss to follow-up

Post-treatment assessments were completed by 15 participants in the neurofeedback group and 9 in the control group. At the 6-month follow-up, the numbers were 12 and 7, respectively. These losses to follow-up, combined with the small initial sample, reduce the precision of the conclusions.

This trial does not demonstrate that neurofeedback is ineffective in all settings. It does not establish an additional clinical benefit when added to this intensive inpatient psychotherapy. Nor does it allow conclusions about its use alone or in other populations.

Limitations to keep in mind

Only the PubMed abstract was consulted, not the full text. The small sample and losses to follow-up limit the ability to detect an additional benefit. The abstract does not provide detailed estimates of clinical effects or safety data. Funding and conflicts of interest were not verified.

What we can take away

Neurofeedback enabled participants to modulate amygdala activity, but this pilot trial does not justify promising additional symptom benefits when it is added to intensive dialectical behavior therapy.

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