Discussion
Tourette syndrome, PTSD, obsessive-compulsive disorder, trauma
CORTEX, TOURETTE SYNDROME
In the current study, we demonstrated the effect of amygdala neurofeedback training in PTSD for improving control over amygdala activity following trauma recall.Our finding of better amygdala control after training converges with data from previous fMRI neurofeedback studies targeting the same region. In one study, PTSD patients were successfully trained to lower bilateral amygdala activation during exposure to personal trauma-related words [Reductions in PTSD symptoms were seen in both groups in this trial. The active group had greater symptom improvements than the control group, but this group difference was not significant. The lack of group difference in clinical change may be due to our relatively small sample size and to the robust clinical improvements associated with exposure therapy alone - both groups were exposed to personalized trauma scripts over the course of the study which is potentially therapeutic for the patients [Both our clinical and brain imaging outcome measures bear an intriguing pattern of continuing improvement at later assessment timepoints. This observation is consistent with the clinical data from our other neurofeedback studies that used similar training protocols, one in obsessive-compulsive disorder and one in Tourette syndrome [In addition, the clinical promise of amygdala neurofeedback training for PTSD is amplified by ongoing work in the Hendler lab: they have developed an EEG technique for targeting amygdala activity, referred to as EEG Fingerprinting of amygdala activity [Of course, amygdala activity training is only one of many possible approaches for treating PTSD with neurofeedback. In addition to dysregulation of this limbic area, the prefrontal cortex is also implicated in generating symptoms. In rodents, the basal lateral area of amygdala was known to bidirectionally project to the medial prefrontal cortex, a pathway that is central to fear learning and extinction [In summary, our three sessions of neurofeedback training induced improvements in control over amygdala activity in PTSD patients, and improvements in amygdala control in the active group significantly exceeded those in the control group. However, the clinical data did not demonstrate significantly greater symptom reduction in the active group compared to the control group, likely due to the limited sample size and strong clinical response in the control group in this study. The trajectory of changes seen in both the brain and clinical data suggest neuroplastic changes may develop after the training and highlight the potential for long-term impacts of this intervention.