Effects of cranial electrotherapy stimulation on resting state brain activity.

Cranial electrotherapy stimulation (CES) is a U.S. Food and Drug Administration (FDA)-approved treatment for insomnia, depression, and anxiety consisting of pulsed, low-intensity current applied to the earlobes or scalp. Despite empirical evidence of clinical efficacy, its mechanism of action is largely unknown. The goal was to characterize the acute effects of CES on resting state brain activity. Our primary hypothesis was that CES would result in deactivation in cortical and subcortical regions. Eleven healthy controls were administered CES applied to the earlobes at subsensory thresholds while being scanned with functional magnetic resonance imaging in the resting state. We tested 0.5- and 100-Hz stimulation, using blocks of 22 sec "on" alternating with 22 sec of baseline (device was "off"). The primary outcome measure was differences in blood oxygen level dependent data associated with the device being on versus baseline. The secondary outcome measures were the effects of stimulation on connectivity within the default mode, sensorimotor, and fronto-parietal networks. Both 0.5- and 100-Hz stimulation resulted in significant deactivation in midline frontal and parietal regions. 100-Hz stimulation was associated with both increases and decreases in connectivity within the default mode network (DMN). Results suggest that CES causes cortical brain deactivation, with a similar pattern for high- and low-frequency stimulation, and alters connectivity in the DMN. These effects may result from interference from high- or low-frequency noise. Small perturbations of brain oscillations may therefore have significant effects on normal resting state brain activity. These results provide insight into the mechanism of action of CES, and may assist in the future development of optimal parameters for effective treatment.

An fMRI study of obesity, food reward, and perceived caloric density. Does a low-fat label make food less appealing?

We tested the hypothesis that obese individuals experience greater activation of the gustatory and somatosensory cortex, but weaker activation of the striatum, in response to intake and anticipated intake of high-fat chocolate milkshake versus an isocaloric milkshake labeled low-fat and a tasteless solution using functional magnetic resonance imaging (fMRI) with 17 obese and 17 lean young women. Obese relative to lean women showed greater activation in somatosensory (Rolandic operculum), gustatory (frontal operculum), and reward valuation regions (amgydala, ventralmedial prefrontal cortex (vmPFC) in response to intake and anticipated intake of milkshake versus tasteless solution, though there was little evidence of reduced striatal activation. Obese relative to lean women also showed greater activation in the Rolandic operculum, frontal operculum, and vmPFC in response to isocaloric milkshakes labeled regular versus low-fat. Results suggest that hyper-responsivity of somatosensory, gustatory, and reward valuation regions may be related to overeating and that top-down processing influence reward encoding, which could further contribute to weight gain.