Deep TMS Over the Anterior Cingulate Cortex | BrainsWay

Deep Transcranial Magnetic Stimulation Over the Medial Prefrontal and Anterior Cingulate Cortex Alters Brain Connectivity and Reduces Relapses to Alcohol Use

Journal: Biological Psychiatry 85(10):S108 (2019)

Authors: M Harel, N Barnea-Ygael, H Shalev, I Besser, M Salti, R Kampe, M Heilig, A Zangen

Background:

Alcohol use disorder (AUD) is a highly prevalent disorder with limited treatment options, partially due to limited understanding of its basic neuropathology. Nevertheless, abnormal neuronal activity in the medial prefrontal and anterior cingulate cortices (mPFC and ACC, respectively) have been suggested to play central roles in alcohol craving, reduced inhibitory control and relapse to alcohol use in AUD.

Objective:

The authors attempted to reduce craving levels and relapse rates in short-term abstinent AUD subjects using deep transcranial magnetic stimulation (Deep TMS™) over the mPFC and ACC following daily provocations of alcohol craving.

Methods:

In this double-blind, sham-controlled, randomized clinical trial we evaluate clinical and neurobiological effects induced by high-frequency (10Hz) Deep TMS over 3 weeks of treatment and 12 weeks of follow-up. Clinical response is determined using self-report levels of craving and alcohol consumption validated by urine measures, while fMRI is employed to identify alterations in brain connectivity.

Results:

Interim results comparing the real (n=16) and sham (n=14) treatment groups during follow-up indicate significantly reduced craving levels and relapse rates (measured based on percentage of binge alcohol drinking days) in the real group relative to the sham group. In addition, real treatment prevented an increase in rest connectivity between ACC and the medial frontal cortex during the 3 weeks of treatment. Such increased connectivity was suggested to correlate with cue induced craving and relapse rates.

Conclusions:

Deep TMS treatment appears to reduce craving levels and relapse rates in AUD and to modify restingstate connectivity in relevant brain areas.