Neuromodulation for the treatment of eating disorders and obesity

Abstract

Eating disorders and obesity adversely affect individuals both medically and psychologically, leading to reduced life expectancy and poor quality of life. While there exist a number of treatments for anorexia, morbid obesity and bulimia, many patients do not respond favorably to current behavioral, medical or bariatric surgical management. Neuromodulation has been postulated as a potential treatment for eating disorders and obesity. In particular, deep brain stimulation and transcranial non-invasive brain stimulation have been studied for these indications across a variety of brain targets. Here, we review the neurobiology behind eating and eating disorders as well as the current status of preclinical and clinical neuromodulation trials for eating disorders and obesity.

Keywords: anorexia nervosa; bulimia; deep brain stimulation; eating disorders; non-invasive brain stimulation; obesity; transcranial direct current stimulation; transcranial magnetic stimulation.

Figure 1.

Reward pathways and interactions. This schematic illustrates the hypothalamic–mesocorticolimbic pathways and potential anatomical targets involved with reward, cognitive control, motivation and the learning/memory circuits. Reward and saliency involve the ventral tegmental area, nucleus accumbens and caudate. The orbitofrontal cortex and subgenual cingulate cortex are thought to be involved in motivation and drive. The learning/memory circuit, which includes the amygdala, hippocampus and putamen, are also components in eating neurobiology. Inhibitory control has been known to involve the dorsolateral prefrontal cortex, ventromedial prefrontal cortex, and the anterior cingulate cortex. The arrows signify the direction of signal transmission. ACC, anterior cingulate cortex; NAc, nucleus accumbens; OFC, orbitofrontal cortex; PFC, prefrontal cortex; SCC, subgenual cingulate cortex; VTA, ventral tegmental area.