Journal: Brain Stimulation (2016)
Authors: Menolascinoa S, Belgina M, Fishera L, Ranuma E
Background:
A patient with lifelong treatment-resistant mood disorder and social anxiety was treated successfully with intranasal ketamine for several months until side effects became intolerable. During a recurrence of depression, treatment with dTMS led to full and durable recovery. The authors used QEEG to directly observe changes in brain activity, finding that the two treatment modalities both normalized excess corticolimbic activity.
Methods:
The authors used QEEG as a state biomarker to observe the immediate effect of ketamine, before and after administration intranasally. Months later, during acute recurrence of depression (MADRS = 46), we treated with dTMS (18 Hz, daily) recording QEEG before TMS and again in remission.
Results:
The pre-ketamine QEEG (state of social anxiety) showed corticolimbic overactivity at 14–15 Hz throughout the frontal region of the brain. Ten minutes post-ketamine, QEEG showed that over-activity was normalized. Months later, in a recurrence of depression, his QEEG (state of acute depression) revealed a very similar pattern of corticolimbic overactivity. The post-TMS QEEG (state of full remission) showed near normalization of this corticolimbic circuitry. The patient noted: “TMS really shut down the internal dialogue feedback loop much the same way ketamine did.”
Conclusions:
Post-TMS QEEG appears remarkably similar to post-ketamine QEEG with normalization of beta activity in frontal area. This suggests that the two treatments both exert antidepressant effects by normalizing excess activity in the corticolimbic circuitry.
