The brain regions associated with binge-eating disorder (BED) and those targeted by Lisdexamfetamine (LDX) overlap. The present paper reviews the psychobehavioural and neuropharmacological mechanisms at play in BED an...The brain regions associated with binge-eating disorder (BED) and those targeted by Lisdexamfetamine (LDX) overlap. The present paper reviews the psychobehavioural and neuropharmacological mechanisms at play in BED and compulsive eating behaviours, along with the mechanisms of action LDX is thought to play. We present one case of chronic BED and highlight the EEG scans pre- and post-LDX treatment. The normalization of the patient’s electroencephalogy (EEG) activity associated with BED after LDX supports theorized mechanisms of LDX action, further explaining its efficacy in treatment. A significant decrease in theta band power was observed in the patient after treatment with LDX. Specifically, this decrease was modulated by changes in the F8 electrode corresponding to the orbitofrontal cortex (OFC)—An area associated with deficits in inhibitory function, seen in addictions and BED. A better understanding of the psychobehavioural and neuropharmacological mechanisms involved in BED and LDX treatment has the potential to significantly enhance our knowledge of the underlying pathogenesis, potential prevention, and optimal treatment options for patients.展开更多
文摘The brain regions associated with binge-eating disorder (BED) and those targeted by Lisdexamfetamine (LDX) overlap. The present paper reviews the psychobehavioural and neuropharmacological mechanisms at play in BED and compulsive eating behaviours, along with the mechanisms of action LDX is thought to play. We present one case of chronic BED and highlight the EEG scans pre- and post-LDX treatment. The normalization of the patient’s electroencephalogy (EEG) activity associated with BED after LDX supports theorized mechanisms of LDX action, further explaining its efficacy in treatment. A significant decrease in theta band power was observed in the patient after treatment with LDX. Specifically, this decrease was modulated by changes in the F8 electrode corresponding to the orbitofrontal cortex (OFC)—An area associated with deficits in inhibitory function, seen in addictions and BED. A better understanding of the psychobehavioural and neuropharmacological mechanisms involved in BED and LDX treatment has the potential to significantly enhance our knowledge of the underlying pathogenesis, potential prevention, and optimal treatment options for patients.
