Abstract
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.
Highlights
Binge-eating disorder (BED), a serious public health issue, has been gaining recognition as the most widespread of the eating disorder types [1] [2]
We present one case of chronic binge-eating disorder (BED) and highlight the EEG scans pre- and post-LDX treatment
BED is described by the DSM-V as recurrent and uncontrollable episodes of compulsive eating with marked physical and psychological distress [3]
Summary
Binge-eating disorder (BED), a serious public health issue, has been gaining recognition as the most widespread of the eating disorder types [1] [2]. The signal dominance of the Dopamine Type-1 Receptor neurons (D1R) found in the DLS of those with binge-eating behaviour showed increased habit-forming functioning when triggered by palatable foods [14] Overstimulation of these dopaminergic pathways were found to bring about insensitivity to the outcomes of these habitual actions surrounding food intake, and contributed to the loss of pleasure, and deficits in the motivation that cause action [14]. As palatable food intake has been found to activate the reward circuit and release DA in PFC pathways, the modulation of TAAR1 in these areas have been proposed as a remedial option for addictive disorders including BED [8] [15]. Via LDX and its resulting restoration of 5-HT activity, a reduction of compulsive eating behaviours in those with BED is seen [6] [8] [19]
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