The
subcallosal cingulate gyrus CG25 which consists of BA25 as well as parts of
BA24 and
BA32 has been implicated as playing an important role in
major depression and has been the target of
deep brain stimulation to treat the disorder. One study found that BA25 is metabolically overactive in
treatment-resistant depression. A different study found that metabolic hyperactivity in this area is associated with poor therapeutic response of persons with
major depressive disorder to
cognitive-behavioral therapy and
venlafaxine. In 2005
Helen S. Mayberg and collaborators described how they successfully treated a number of depressed people—individuals virtually catatonic with depression despite years of talk therapy, drugs, and electroconvulsive therapy—with pacemaker-like electrodes (
deep brain stimulation) in area 25. In 2013, Walker and Lawson conducted neurofeedback research with 183 subjects experiencing drug resistant depression. The neurofeedback specifically targeted Brodmann area 25. The treatment consisted of 6 neurofeedback sessions that were 20min long each over the course of 3 weeks. 1 year after the treatment 84% of subjects experienced over a 50% reduction in depression symptoms. 9% reported a 20-50% reduction in depression symptoms. 7% reported a 0-20% improvement. 1% initially reported positive effects, but had a depression relapse before the year follow up completed. There were no side effects or complications reported from the treatment. A study found that
transcranial magnetic stimulation is more clinically effective treating depression when targeted specifically to
Brodmann area 46, because this area has intrinsic functional connectivity (negative correlation) with area 25. Another study has found that the responses of area 25 to viewing sad stimuli are affected by
cortisol. This suggests that depression related changes in the activity in area 25 could be due to
hypothalamic–pituitary–adrenal axis dysregulation. ==Image==