Bernd Figner

Lateral prefrontal cortex and self-control in intertemporal choice.

Disruption of function of left, but not right, lateral prefrontal cortex (LPFC) with low-frequency repetitive transcranial magnetic stimulation (rTMS) increased choices of immediate rewards over larger delayed rewards. rTMS did not change choices involving only delayed rewards or valuation judgments of immediate and delayed rewards, providing causal evidence for a neural lateral-prefrontal cortex–based self-control mechanism in intertemporal choice.

Increased Capacity to Delay Reward in Anorexia Nervosa

Individuals with anorexia nervosa (AN) are often characterized as possessing excessive self-control and are unusual in their ability to reduce or avoid the consumption of palatable foods. This behavior promotes potentially life-threatening weight loss and suggests disturbances in reward processing. We studied whether individuals with AN showed evidence of increased self-control by examining the tendency to delay receipt of a monetary, non-food related, reward. Underweight AN (n = 36) and healthy controls (HC, n = 28) completed a monetary intertemporal choice task measuring delay discounting factor. Individuals with AN reduced the value of a monetary reward over time significantly less than HC (F[1,61] = 5.03; p = 0.029). Secondary analyses indicated that the restricting subtype of AN, in particular, showed significantly less discounting than HC (F[1,46] = 8.3; p = 0.006). These findings indicate that some individuals with AN show less temporal discounting than HC, suggestive of enhanced self-control that is not limited to food consumption. This is in contrast to other psychiatric disorders, for example, substance abuse, which are characterized by greater discounting. Though preliminary, these findings suggest that excessive self-control may contribute to pathological processes and individuals with AN may have neuropsychological characteristics that enhance their ability to delay reward and thereby may help to maintain persistent food restriction.

On Weight and Waiting: Delay Discounting in Anorexia Nervosa Pretreatment and Posttreatment

BACKGROUND Individuals with anorexia nervosa (AN) override the drive to eat, forgoing immediate rewards in favor of longer-term goals. We examined delay discounting and its neural correlates in AN before and after treatment to test a potential mechanism of illness persistence. METHODS Inpatients with AN (n = 59) and healthy control subjects (HC, n = 39) performed a delay discounting task at two time points. A subset (n = 30 AN, n = 22 HC) participated in functional magnetic resonance imaging scanning during the task. The task consisted of a range of monetary choices with variable delay times, yielding individual discount rates-the rate by which money loses value over time. RESULTS Before treatment, the AN group showed a preference for delayed over earlier rewards (i.e., less steep discount rates) compared with HC; after weight restoration, AN did not differ from HC. Underweight AN showed slower response times for earlier versus delayed choices; this reversed with treatment. Underweight AN showed abnormal neural activity in striatum and dorsal anterior cingulate; normalization of behavior was associated with increased activation in reward regions (striatum and dorsal anterior cingulate) and decision-making regions (dorsolateral prefrontal cortex and parietal cortex). CONCLUSIONS The undernourished state of AN may amplify the tendency to forgo immediate rewards in favor of longer-term goals. The results suggest that behavior that looks phenotypically like excessive self-control does not correspond with enhanced prefrontal recruitment. Rather, the results point to alterations in cingulostriatal circuitry that offer new insights on the potential role of abnormalities in decision-making neural systems in the perpetuation of AN.

Why Some People Discount More than Others: Baseline Activation in the Dorsal PFC Mediates the Link between COMT Genotype and Impatient Choice

Individuals differ widely in how steeply they discount future rewards. The sources of these stable individual differences in delay discounting (DD) are largely unknown. One candidate is the COMT Val158Met polymorphism, known to modulate prefrontal dopamine levels and affect DD. To identify possible neural mechanisms by which this polymorphism may contribute to stable individual DD differences, we measured 73 participants’ neural baseline activation using resting electroencephalogram (EEG). Such neural baseline activation measures are highly heritable and stable over time, thus an ideal endophenotype candidate to explain how genes may influence behavior via individual differences in neural function. After EEG-recording, participants made a series of incentive-compatible intertemporal choices to determine the steepness of their DD. We found that COMT significantly affected DD and that this effect was mediated by baseline activation level in the left dorsal prefrontal cortex (DPFC): (i) COMT had a significant effect on DD such that the number of Val alleles was positively correlated with steeper DD (higher numbers of Val alleles means greater COMT activity and thus lower dopamine levels). (ii) A whole-brain search identified a cluster in left DPFC where baseline activation was correlated with DD; lower activation was associated with steeper DD. (iii) COMT had a significant effect on the baseline activation level in this left DPFC cluster such that a higher number of Val alleles was associated with lower baseline activation. (iv) The effect of COMT on DD was explained by the mediating effect of neural baseline activation in the left DPFC cluster. Our study thus establishes baseline activation level in left DPFC as salient neural signature in the form of an endophenotype that mediates the link between COMT and DD.

Time ambiguity during intertemporal decision-making is aversive, impacting choice and neural value coding

&NA; We are often presented with choices that differ in their more immediate versus future consequences. Interestingly, in everyday‐life, ambiguity about the exact timing of such consequences frequently occurs, yet it remains unknown whether and how time‐ambiguity influences decisions and their underlying neural correlates. We developed a novel intertemporal fMRI choice task in which participants make choices between sooner‐smaller (SS) versus later‐larger (LL) monetary rewards with systematically varying levels of time‐ambiguity. Across trials, delay information of the SS, the LL, or both rewards was either exact (e.g., in 5 weeks), of low ambiguity (4 week range: e.g., in 3–7 weeks), or of high ambiguity (8 week range: e.g., in 1–9 weeks). Choice behavior showed that the majority of participants preferred options with exact delays over those with ambiguous delays, indicating time‐ambiguity aversion. Consistent with these results, the ventromedial prefrontal cortex showed decreased activation during ambiguous versus exact trials. In contrast, intraparietal sulcus activation increased during ambiguous versus exact trials. Furthermore, exploratory analyses suggest that more time‐ambiguity averse participants show more insula and dorsolateral prefrontal cortex activation during subjective value (SV)‐coding of ambiguous versus exact trials. Lastly, the best‐fitting computational choice models indicate that ambiguity impacts the SV of options via time perception or via an additive ambiguity‐related penalty term. Together, these results provide the first behavioral and neural signatures of time‐ambiguity, pointing towards a unique profile that is distinct from impatience. Since time‐ambiguity is ubiquitous in real‐life, it likely contributes to shortsighted decisions above and beyond delay‐discounting. HighlightsWe investigate time‐ambiguity: uncertainty about when an outcome will occur.Time‐ambiguity is aversive, impacting choice behavior and reducing subjective value.Time‐ambiguity shows a neurobehavioral signature distinct from that of impatience.Time‐ambiguity is associated with increased IPS and decreased vmPFC activation.Individual time‐ambiguity preferences appear to modulate dlPFC and insula activity.

Having attention-deficit/hyperactivity disorder and substance use disorder: A review of the literature

The co-occurence of attention-deficit/hyperactivity disorder (ADHD) and substance use disorders (SUDs) is a relatively new topic in the field of psychiatric comorbidity. Accordingly, the ADHD syndrome is a relatively new diagnostic category: the category was first introduced in ICD-8 (1968) [1] as Hyperkinetic Syndrome and then in DSM-III (1980) [2] as Attention-Deficit Disorder and subsequently changed from revision to revision until it was called Attention-Deficit/Hyperactivity Disorder in DSM-IV [3]. As of now, there is no diagnostic entity regarding adult ADHD in the diagnostic manual ICD-10 of the World Health Organization [4]. Despite these diagnostic deficiencies, comorbidity of ADHD and SUD has received considerable attention in the scientific community in the recent years. This is not surprising given the diverse close connections between the two disorders (for an overview, see Sullivan and Rudnik-Levin [5]): symptoms of ADHD and SUDs can be very similar, making it difficult to diagnostically differentiate between the two disorders and to assess ADHD in the presence of a known SUD. Another concern is that the treatment of ADHD needs special considerations in persons with a SUD. And – coming to the main issue of this article – persons with ADHD seem to be at increased risk for developing a SUD: studies [6] have shown that individuals with ADHD have an earlier onset of substance abuse and exhibit a pattern of more frequent or more intense substance use than persons with SUDs without comorbid ADHD.