XXIst Congress of the European Society for Stereotactic and Functional Neurosurgery. Implementing Research in Clinical Applications. Maastricht, The Netherlands, September 17-20, 2014: Abstracts

Binge eating disorder (BED) has been postulated to arise from mesolimbic dopaminergic system changes, presumably homologous to those seen in drug addiction. Deep Brain Stimulation (DBS) is regarded as a relatively novel but promising surgical treatment of addiction. Because of potentially similar circuitries underlying drug addiction and BED, we aimed to investigate Nucleus Accumbens DBS as treatment option for BED. Methods: Wistar-rats had electrodes placed in the Nucleus Accumbens core (NAcc core) or lateral shell (NAcc lShell) or medial shell (NAcc mShell) and were adapted for several weeks to high fat food (HFF) binge eating protocol, with one-hour food deprivation preceding a one hour access to HFF (binge) at the penultimate hour before the dark phase. DBS was applied either before and/or during the binge and was varied in stimulation currents and frequencies. Results: With respect to the NAcc core, the most striking results were achieved when stimulating with a current of 250 μA before binge at 10Hz (intake = 61%, p=0.0076), while no effects were found when stimulation was performed during the binge. DBS in the NAcc lShell showed strongest suppression of the binge when stimulating with either 125 or 250 μA during binge at 50Hz (intake =56%, p=0.00331), but no effects were observed when stimulation was performed before the binge. No significant results were achieved when stimulating NAcc mShell. Conclusion: These data indicate that DBS of the NAcc core suppresses the “wanting” aspects of binging whereas DBS of the NAcc lShell suppresses “liking” aspects of binging. “Wanting” changes the food reward potency, and these aspects have indeed been found to reside in the NAcc core. Furthermore, incentive hotspots associated with “liking” have previously been identified in lateral parts of the NA. We conclude that DBS in the NAcc may be a promising tool for the treatment of BED in human patients