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. 2016 Jan 16:16:10.
doi: 10.1186/s12888-016-0714-z.

A debate on working memory and cognitive control: can we learn about the treatment of substance use disorders from the neural correlates of anorexia nervosa?

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A debate on working memory and cognitive control: can we learn about the treatment of substance use disorders from the neural correlates of anorexia nervosa?

Samantha J Brooks. BMC Psychiatry. .

Abstract

Background: Anorexia Nervosa (AN) is a debilitating, sometimes fatal eating disorder (ED) whereby restraint of appetite and emotion is concomitant with an inflexible, attention-to-detail perfectionist cognitive style and obsessive-compulsive behaviour. Intriguingly, people with AN are less likely to engage in substance use, whereas those who suffer from an ED with a bingeing component are more vulnerable to substance use disorder (SUD).

Discussion: This insight into a beneficial consequence of appetite control in those with AN, which is shrouded by the many other unhealthy, excessive and deficit symptoms, may provide some clues as to how the brain could be trained to exert better, sustained control over appetitive and impulsive processes. Structural and functional brain imaging studies implicate the executive control network (ECN) and the salience network (SN) in the neuropathology of AN and SUD. Additionally, excessive employment of working memory (WM), alongside more prominent cognitive deficits may be utilised to cope with the experience of negative emotions and may account for aberrant brain function. WM enables mental rehearsal of cognitive strategies while regulating, restricting or avoiding neural responses associated with the SN. Therefore, high versus low WM capacity may be one of the factors that unites common cognitive and behavioural symptoms in those suffering from AN and SUD respectively. Furthermore, emerging evidence suggests that by evoking neural plasticity in the ECN and SN with WM training, improvements in neurocognitive function and cognitive control can be achieved. Thus, considering the neurocognitive processes of excessive appetite control and how it links to WM in AN may aid the application of adjunctive treatment for SUD.

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Figures

Fig. 1
Fig. 1
The original working memory model by Baddeley [1]. Reproduced via open access Wikimedia: https://commons.wikimedia.org/wiki/File:Working-memory-en.svg
Fig. 2
Fig. 2
Bernie Baars’ Global Workspace Model incorporating working memory. Reproduced with permission via email communication from Professor Bernard Baars
Fig. 3
Fig. 3
Greg Gandenberger’s Bayesian Probabilistic Inference Model to explain how Bayesianism provides guidance for belief or action, particularly under conditions of uncertainty. Reproduced with permission via email from Gregory Gandenberger(http://gandenberger.org/category/philosophy-of-science/bayesianism/). 1) Likelihoodism is based on a belief system that an outcome will occur. 2) Frequentism is based on prior experience and the probability that an event will occur; 3) Bayesianism is based on updating belief system via frequency of exposure, and informs action tendencies in the presence of uncertainty
Fig. 4
Fig. 4
Neurobiological impulse-control model of temperamental dominance in ED [18]OCPD = Obsessive-Compulsive Personality Disorder; DLPFC = dorsolateral prefrontal cortex; OFC = orbitofrontal cortex; MPFC = medial prefrontal cortex; ACC = anterior cingulate cortex; COMT = catechol-o-methyltransferase; BDNF = Brain Derived Neurotrophic Factor; 5HT2A = 5-Hydroxy-Tryptophan-2A
Fig. 5
Fig. 5
A model of cognitive control of appetite. a The original Yerkes-Dodson Law [76], showing that optimal performance occurs when medium arousal is present, but that both low and high arousal can be detrimental to performance. Reproduced via open access Wikimedia: https://commons.wikimedia.org/wiki/File:Yerkes-Dodson_wet.png; b) Updated model to depict cognitive control of appetite, applicable to restricting anorexia nervosa and addictive behaviours such as SUD and binge eating. Low appetitive processes (e.g. due to satiation with substance/food or hijacked by negative emotion such as anxiety or anger) coincide with low cognitive control. High appetitive processes (e.g. reward sensitivity, real or perceived) coincide with low cognitive control because either reward responses impinge on executive functioning or executive functioning is overloaded. Optimal cognitive control (e.g. self-regulation and effective cognitive-emotion neural interactions) is suggested to occur when appetitive drive is within the medium range
Fig. 6
Fig. 6
Brain regions most implicated in addiction. a Prefrontal cortex volume is shown to be reduced in those with SUD, produced via unpublished data with permission from Dr Samantha Brooks; b) A cartoon of the basal ganglia, associated with arousal, motivation, primary process affective states. Together, the prefrontal cortex and areas of the basal ganglia form the cortico-striatal pathway, which is implicated in the neuropathology of SUD and AN

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