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The role of working memory for cognitive control in anorexia nervosa versus substance use disorder

Frontiers in Psychology
DOI: 10.3389/fpsyg.2017.01651
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Abstract

Prefrontal cortex executive functions, such as working memory (WM) interact with limbic processes to foster impulse control. Such an interaction is referred to in a growing body of publications by terms such as cognitive control, cognitive inhibition, affect regulation, self-regulation, top-down control, and cognitive-emotion interaction. The rising trend of research into cognitive control of impulsivity, using various related terms reflects the importance of research into impulse control, as failure to employ cognitions optimally may eventually result in mental disorder. Against this background, we take a novel approach using an impulse control spectrum model - where anorexia nervosa (AN) and substance use disorder (SUD) are at opposite extremes - to examine the role of WM for cognitive control. With this aim, we first summarize WM processes in the healthy brain in order to frame a systematic review of the neuropsychological, neural and genetic findings of AN and SUD. In our systematic review of WM/cognitive control, we found n = 15 studies of AN with a total of n = 582 AN and n = 365 HC participants; and n = 93 studies of SUD with n = 9106 SUD and n = 3028 HC participants. In particular, we consider how WM load/capacity may support the neural process of excessive epistemic foraging (cognitive sampling of the environment to test predictions about the world) in AN that reduces distraction from salient stimuli. We also consider the link between WM and cognitive control in people with SUD who are prone to 'jumping to conclusions' and reduced epistemic foraging. Finally, in light of our review, we consider WM training as a novel research tool and an adjunct to enhance treatment that improves cognitive control of impulsivity.

Figures

  • FIGURE 1 | The impulse control spectrum model of eating disorders by Brooks et al. (2012b, 2016). This model describes the common comorbid neuropsychological traits, some neural and genetic markers of restraint versus impulsivity, as related to eating behavior. SUD is regarded, based on studies reviewed in this paper, to correspond to similar processes as binge eating disorder (Volkow and Baler, 2015), at the opposite end of the spectrum to restricting anorexia nervosa. Normalcy – or normal appetite/impulse control – is deemed to be in the middle of the spectrum. OCPD, obsessive-compulsive personality disorder; DLPFC, dorsolateral prefrontal cortex; OFC, orbitofrontal cortex; MPFC, medial prefrontal cortex; ACC, anterior cingulate cortex; COMT, catechol-O-methyl-transferase; 5HT2A, 5-hydroxy-tryptophan-2A (serotonin receptor 2A gene); BDNF, brain derived neurotrophic factor. Of note: anxiety is hypothesized to be experienced when the system is imbalanced.
  • FIGURE 2 | (A) Neurobiological depiction of the WM model. Red square represents the prefrontal cortex (in orange) and the central executive; left blue square represents the language network underling the phonological loop, namely speech production (Broca’s area in the frontal cortex) and speech comprehension (Wernicke’s area in the temporal cortex); the middle blue square represents the visual network underlying the visuospatial sketchpad and semantics, incorporating the dorsal (“where”) and the ventral (“what”) pathway; the right blue square represents the episodic buffer and short term memory, supported by activation of the hippocampus. Prefrontal cortex image from Wikimedia courtesy of Gray (1918): Brodmann areas 8 = primary motor cortex (eye fields), 9 = dorsolateral, 10 = frontopolar, 11 = orbitofrontal, 44/45 = inferior frontal (Broca’s area), 46 = dorsolateral, 47 = orbitofrontal. Broca’s/Wernicke’s area image from Wikimedia courtesy of Anatomy and Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/; Dorsal and ventral visual stream image from Wikimedia courtesy of Anatomy and Physiology, Connexions Web site; Hippocampus image from Wikimedia courtesy of Gray, 1918. (B) The original WM model by Baddeley and Hitch (1974), reproduced via Wikimedia.
  • FIGURE 3 | Libet’s half-second study. External stimulus of the cortex and internal experience. At least 500 ms was needed of cortical stimulation before subjective experience.
  • FIGURE 4 | (A) Schematic diagram of the backward masking technique. A salient image (e.g., food) is presented for 23 ms, prior to a mosaic screen. The mosaic functions as a backward mask to interrupt the processing of the salient stimulus rendering it subliminal. Adorned on the mosaic image is a red letter, which changes during consecutive cycles, and represents either a target or non-target image during the N-back task. For 1-back, the target letter is the same as the previously presented letter, whereas for 2-back the target letter is the same as the letter presented two letters previously. Image courtesy of Dr. Samantha Brooks’ Ph.D. thesis (Published via University of London, King’s College, London, June 2010). (B) Using a schematic diagram of the classic WM model by Baddeley and Hitch (1974), reproduced via Wikimedia, to hypothesize as to the sequence of events that is associated with competitive interference during subliminal priming when cognitive load is low, and reduced competitive interference when cognitive load is high in healthy subjects (see Uher et al., 2014). (1) During the subliminal presentation of arousing stimuli (e.g., food and aversive image), which have been frequently encountered before (e.g., food) or that evolutionarily we are primed to find salient (e.g., aversive image of bloody bodies), the hippocampus is activated after the visual stimulus, via V1 and thalamus has increased dopamine release in the mesolimbic pathway. Direct connection to the prefrontal cortex from the hippocampus ensures that cognitive systems are primed to attend to this stimulus for further processing.
  • FIGURE 5 | Summary of the research questions still to be answered in the field of neural correlates of WM and cognitive control.
  • FIGURE 6 | Schematic diagram of the dopamine absorber and dopamine pump analogy. Image of dopamine uptake pump by permission from http://www.nida.nih.gov/pubs/teaching/teaching2/Teaching2.html. Image of eye by permission from http://www.clipartpanda.com/categories/blue-eyes-clipart. Image of ear by permission from http://www.clipartkid.com/ear-cliparts/. Image of mouth by permission from http://www.clipartkid.com/mouth-cliparts/.Image of “1” reward badge by permission from http://www.clker.com/cliparts/B/Z/b/k/v/7/award-symbol-md.png. Image of red prefrontal cortex by permission from https://commons.wikimedia.org/wiki/Category:Prefrontal_cortex#/media/File:Prefrontal_cortex_(left)_-_lateral_view.png. (A) Dopamine absorber analogy (anorexia nervosa): excessive, deliberative activation of the prefrontal cortex (sponge), by way of repetitive cognitive ruminations, absorbs increased endogenous dopamine release via the basal ganglia (reward symbol) via epigenetic upregulation of receptor systems. Repetitive phonological and visuospatial rehearsal (eyes, ears, mouth), held in mind by prefrontal cortex delay interneurons strengthens the saliency (and therefore the ability to stimulate basal ganglia dopamine release) and relevance of imagined images. To prevent habituation over time, imagined images become more detailed and complex to stimulate required levels of dopamine for prefrontal cortex absorption. (B) Dopamine pump analogy (substance use disorder): excessive activation of basal ganglia dopaminergic system (uptake pump) by way of consumption of substances increases the release and re-uptake of dopamine. This in turn biases repetitive phonological and visuospatial rehearsal (eyes, ears, mouth) in favor of the stimulus that is associated with increased dopamine release (e.g., food and drugs). Excessive dopamine arriving at the prefrontal cortex weakens top-down control and encourages exogenous dopamine release stimulation. In both analogies, there is a propensity for increased dopamine in the prefrontal cortex, which leads to epigenetic effects, inflexible cognitive style and chronic disorder, as well as risk for the development of psychosis.

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CITATION STYLE

APA

Brooks, S. J., Funk, S. G., Young, S. Y., & Schiöth, H. B. (2017, September 22). The role of working memory for cognitive control in anorexia nervosa versus substance use disorder. Frontiers in Psychology. Frontiers Media S.A. https://doi.org/10.3389/fpsyg.2017.01651

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