Repetitive Transcranial Magnetic Stimulation Reduces Cue-Induced Food Craving in Bulimic Disorders

Eynde, Fréderique Van den; Claudino, Angélica Medeiros; Mogg, Andrew; Horrell, Linda; Ståhl, Daniel; Ribeiro, Wagner Silva; Uher, Rudolf; Campbell, Iain C.; Schmidt, Ulrike

doi:10.1016/j.biopsych.2009.11.023

Cited by 155 publications

(149 citation statements)

References 20 publications

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“…Previous studies provide evidence of positive effects of neuromodulation techniques (i.e., repetitive transcranial magnetic stimulation [rTMS]) on eating disorder symptomatology in individuals with bulimic-type eating disorders. [51][52][53] Repetitive transcranial magnetic stimulation of the dorsolateral PFC in individuals with bulimic-type eating disorders resulted in lower cue-induced food cravings and could therefore reduce binge eating. A recently published study reported rTMSinduced decreases in cerebral oxygenation of the left dorsolateral PFC in patients with bulimia nervosa using near-infrared spectroscopy.…”

Section: Discussionmentioning

confidence: 99%

Neural signature of behavioural inhibition in women with bulimia nervosa

Skunde

Walther

Simon

et al. 2016

jpn

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Section: Discussionmentioning

confidence: 99%

Neural signature of behavioural inhibition in women with bulimia nervosa

Skunde

Walther

Simon

et al. 2016

jpn

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“…The role of the DLPFC in eating disorders has been explored in a clinical study in which participants with bulimic disorders where exposed to repetitive transcranial stimulation (TMS) of the DLPFC. These patients reported decreased craving immediately after TMS and fewer binge eating episodes in the 24 h following TMS, as compared to patients who received sham TMS [55]. Thus, craving for food and drugs appears to involve comparable neural substrates [56]table 2.…”

Section: Similarities Between Bed and Addiction In Humansmentioning

confidence: 99%

Towards an Animal Model of Food Addiction

Jong¹,

Vanderschuren²,

Adan³

2012

Obes Facts

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The dramatically increasing prevalence of obesity, associated with potentially life-threatening health problems, including cardiovascular diseases and type II diabetes, poses an enormous public health problem. It has been proposed that the obesity epidemic can be explained by the concept of ‘food addiction’. In this review we focus on possible similarities between binge eating disorder (BED), which is highly prevalent in the obese population, and drug addiction. Indeed, both behavioral and neural similarities between addiction and BED have been demonstrated. Behavioral similarities are reflected in the overlap in DSM-IV criteria for drug addiction with the (suggested) criteria for BED and by food addiction-like behavior in animals after prolonged intermittent access to palatable food. Neural similarities include the overlap in brain regions involved in food and drug craving. Decreased dopamine D2 receptor availability in the striatum has been found in animal models of binge eating, after cocaine self-administration in animals as well as in drug addiction and obesity in humans. To further explore the neurobiological basis of food addiction, it is essential to have an animal model to test the addictive potential of palatable food. A recently developed animal model for drug addiction involves three behavioral characteristics that are based on the DSM-IV criteria: i) extremely high motivation to obtain the drug, ii) difficulty in limiting drug seeking even in periods of explicit non-availability, iii) continuation of drug-seeking despite negative consequences. Indeed, it has been shown that a subgroup of rats, after prolonged cocaine self-administration, scores positive on these three criteria. If food possesses addictive properties, then food-addicted rats should also meet these criteria while searching for and consuming food. In this review we discuss evidence from literature regarding food addiction-like behavior. We also suggest future experiments that could further contribute to our understanding of behavioral and neural commonalities and differences between obesity and drug addiction.

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“…These results have led researchers to consider the prefrontal cortex as part of a neural circuit contributing to the pathophysiology of eating disorders (Kaye, Wagner, Fudge, & Paulus, 2011) and therefore an interesting candidate as cortical target for studies aiming at exploring the modulatory effects of non-invasive brain stimulation techniques on food-related behaviour (McClelland, Bozhilova, Campbell, & Schmidt, 2013). Indeed, medial and dorsolateral prefrontal cortices have been selected as target sites in studies with transcranial direct current stimulation (tDCS) or transcranial magnetic stimulation (TMS) showing that stimulation sessions reduced food craving in healthy participants (Fregni et al, 2008;Goldman et al, 2011;Uher et al, 2005) and pathological feelings and behaviour in participants with eating disorders (Downar, Sankar, Giacobbe, Woodside, & Colton, 2012;Van den Eynde et al, 2010;Van den Eynde, Guillaume, Broadbent, Campbell, & Schmidt, 2013). However, the mechanisms underlying the behavioural outcome and how stimulation of specific target areas could modulate attitudes towards food are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%