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Ordinary sensations from inside the body are important causes and consequences of our affective states and behaviour, yet the roles of neurotransmitters in interoceptive processing have been unclear. With a within-subjects design, this experiment tested the impacts of acute increases of endogenous extracellular serotonin on the neural processing of attended internal sensations and the links of these effects to anxiety using a selective serotonin reuptake inhibitor (SSRI) (20 mg CITALOPRAM) and a PLACEBO. Twenty-one healthy volunteers (fourteen female, mean age 23.9) completed the Visceral Interoceptive Attention (VIA) task while undergoing functional magnetic resonance imaging (fMRI) with each treatment. The VIA task required focused attention on the heart, stomach, or visual sensation. The relative neural interoceptive responses to heart sensation [heart minus visual attention] (heart-IR) and stomach sensation [stomach minus visual attention] (stomach-IR) were compared between treatments. Visual attention subtraction controlled for the general effects of CITALOPRAM on sensory processing. CITALOPRAM was associated with lower interoceptive processing in viscerosensory (the stomach-IR of bilateral posterior insular cortex) and integrative/affective (the stomach-IR and heart-IR of bilateral amygdala) components of interoceptive neural pathways. In anterior insular cortex, CITALOPRAM reductions of heart-IR depended on anxiety levels, removing a previously known association between anxiety and the region's response to attended heart sensation observed with PLACEBO. Preliminary post hoc analysis indicated that CITALOPRAM effects on the stomach-IR of the amygdalae corresponded to acute anxiety changes. This direct evidence of general and anxiety-linked serotonergic influence on neural interoceptive processes advances our understanding of interoception, its regulation, and anxiety.

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The stomach-derived hormone ghrelin motivates food search and stimulates food consumption, with highest plasma concentrations before a meal and lowest shortly after. However, ghrelin also appears to affect the value of non-food rewards such as interaction with rat conspecifics, and monetary rewards in humans. The present pre-registered study investigated how nutritional state and ghrelin concentrations are related to the subjective and neural responses to social and non-social rewards. In a cross-over feed-and-fast design, 67 healthy volunteers (20 women) underwent functional magnetic resonance imaging (fMRI) in a hungry state and after a meal with repeated plasma ghrelin measurements. In task 1, participants received social rewards in the form of approving expert feedback, or non-social computer reward. In task 2, participants rated the pleasantness of compliments and neutral statements. Nutritional state and ghrelin concentrations did not affect the response to social reward in task 1. In contrast, ventromedial prefrontal cortical activation to non-social rewards was reduced when the meal strongly suppressed ghrelin. In task 2, fasting increased activation in the right ventral striatum during all statements, but ghrelin concentrations were neither associated with brain activation nor with experienced pleasantness. Complementary Bayesian analyses provided moderate evidence for a lack of correlation between ghrelin concentrations and behavioral and neural responses to social rewards, but moderate evidence for an association between ghrelin and non-social rewards. This suggests that ghrelin's influence may be restricted to non-social rewards. Social rewards implemented via social recognition and affirmation may be too abstract and complex to be susceptible to ghrelin's influence. In contrast, the non-social reward was associated with the expectation of a material object that was handed out after the experiment. This may indicate that ghrelin might be involved in anticipatory rather than consummatory phases of reward.

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RATIONALE: Interoception is the signalling, perception, and interpretation of internal physiological states. Many mental disorders associated with changes of interoception, including depressive and anxiety disorders, are treated with selective serotonin reuptake inhibitors (SSRIs). However, the causative link between SSRIs and interoception is not yet clear. OBJECTIVES: To ascertain the causal effect of acute changes of serotonin levels on cardiac interoception. METHODS: Using a within-participant placebo-controlled design, forty-seven healthy human volunteers (31 female, 16 male) were tested on and off a 20 mg oral dose of the commonly prescribed SSRI, citalopram. Participants made judgements on the synchrony between their heartbeat and auditory tones and then expressed confidence in each judgement. We measured three types of interoceptive cognition. RESULTS: Citalopram increased cardiac interoceptive insight, measured as correspondence of self-reported confidence to the likelihood that interoceptive judgements were actually correct. This effect was driven by enhanced confidence for correct interoceptive judgements and was independent of measured cardiac and reported subjective effects of the drug. CONCLUSIONS: An acute change of serotonin levels can increase insight into the reliability of inferences made from cardiac interoceptive sensations.

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An abnormality in inference, resulting in distorted internal models of the world, has been argued to be a common mechanism underlying the heterogeneous psychopathology in schizophrenia. However, findings have been mixed as to wherein the abnormality lies and have typically failed to find convincing relations to symptoms. The limited and inconsistent findings may have been due to methodological limitations of the experimental design, such as conflating other factors (e.g. comprehension) with the inferential process of interest, and a failure to adequately assess and model the key aspects of the inferential process. Here, we investigated probabilistic inference based on multiple sources of information using a new digital version of the beads task, framed in a social context. Thirty-five patients with schizophrenia or schizoaffective disorder with a wide range of symptoms and 40 matched healthy control subjects performed the task, where they guessed the colour of the next marble drawn from a jar based on a sample from the jar as well as the choices and the expressed confidence of four people, each with their own independent sample (which was hidden from participant view). We relied on theoretically motivated computational models to assess which model best captured the inferential process and investigated whether it could serve as a mechanistic model for both psychotic and negative symptoms. We found that 'circular inference' best described the inference process, where patients over-weighed and overcounted direct experience and under-weighed information from others. Crucially, overcounting of direct experience was uniquely associated with most psychotic and negative symptoms. In addition, patients with worse social cognitive function had more difficulties using others' confidence to inform their choices. This difficulty was related to worse real-world functioning. The findings could not be easily ascribed to differences in working memory, executive function, intelligence or antipsychotic medication. These results suggest hallucinations, delusions and negative symptoms could stem from a common underlying abnormality in inference, where directly experienced information is assigned an unreasonable weight and taken into account multiple times. By this, even unreliable first-hand experiences may gain disproportionate significance. The effect could lead to false perceptions (hallucinations), false beliefs (delusions) and deviant social behaviour (e.g. loss of interest in others, bizarre and inappropriate behaviour). This may be particularly problematic for patients with social cognitive deficits, as they may fail to make use of corrective information from others, ultimately leading to worse social functioning.

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BACKGROUND: Gathering and evaluating information leads to better decisions, but often at cost. The balance between information seeking and exploitation features in neurodevelopmental, mood, psychotic and substance-related disorders. Serotonin's role has been highlighted by experimental reduction of its precursor, tryptophan. AIMS: We tested the boundaries and applicability of this role by asking whether changes to information sampling would be observed following acute doses of serotonergic and catecholaminergic clinical treatments. We used a variant of the Information Sampling Task (IST) to measure how much information a person requires before they make a decision. This task allows participants to sample information until satisfied to make a choice. METHODS: In separate double-blind placebo-controlled experiments, we tested 27 healthy participants on/off 20 mg of the serotonin reuptake inhibitor (SRI) citalopram, and 22 participants on/off 40 mg of the noradrenergic reuptake inhibitor atomoxetine. The IST variant minimised effects of temporal impulsivity and loss aversion. Analyses used a variety of participant prior expectations of sampling spaces in the IST, including a new prior that accounts for learning of likely states across trials. We analysed behaviour by a new method that also accounts for baseline individual differences of risk preference. RESULTS: Baseline preferences demonstrated risk aversion. Citalopram decreased the expected utility of choices and probability of being correct based on informational content of samples collected, suggesting participants collected less useful information before making a choice. Atomoxetine did not influence information seeking. CONCLUSION: Acute changes of serotonin activity by way of a single SRI dose alter information-seeking behaviour.

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Schizophrenia is often associated with distinctive or odd social behaviours. Previous work suggests this could be due to a general reduction in conformity; however, this work only assessed the tendency to publicly agree with others, which may involve a number of different mechanisms. In this study, we specifically investigated whether patients display a reduced tendency to adopt other people's opinions (socially learned attitude change). We administered a computerized conformity task, assumed to rely on reinforcement learning circuits, to 32 patients with schizophrenia or schizo-affective disorder and 39 matched controls. Each participant rated 153 faces for trustworthiness. After each rating, they were immediately shown the opinion of a group. After approximately 1 hour, participants were unexpectedly asked to rate all the faces again. We compared the degree of attitude change towards group opinion in patients and controls. Patients presented equal or more social influence on attitudes than controls. This effect may have been medication induced, as increased conformity was seen with higher antipsychotic dose. The results suggest that there is not a general decline in conformity in medicated patients with schizophrenia and that previous findings of reduced conformity are likely related to mechanisms other than reinforcement based social influence on attitudes.

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BACKGROUND: Historically, research investigating neural correlates of mentalizing deficits in schizophrenia has focused on patients who have been ill for several years with lengthy exposure to medication. Little is known about the neural and behavioral presentations of theory-of-mind deficits in schizophrenia, shortly after the first episode of psychosis. METHODS: We investigated social cognition in 17 recently diagnosed first-episode schizophrenia (FES) patients with little or no exposure to antipsychotic medication and 1:1 matched healthy controls. We recorded behavioral and neural responses to the Animated Triangles Task (ATT), which is a nonverbal validated mentalizing task that measures the ascription of intentionality to the movements of objects. RESULTS: FES patients under-interpreted social cues and over-interpreted nonsocial cues. These effects were influenced by current intelligence (IQ). Control group and FES neural responses replicated earlier findings in healthy adults. However, a region of anterior medial prefrontal cortex (amPFC) of FES patients showed a different response pattern to that of controls. Unlike healthy controls, patients increased activity in this social cognition region while studying "random" movements of shapes, as compared to the study of movements normally interpreted as "intentional". CONCLUSIONS: Mentalizing deficits in FES consists of hypo- and hypermentalizing. The neural pattern of FES patients is consistent with deficits in the ability to switch off mentalizing processes in potentially social contexts, instead increasing them when intentionality is not forthcoming. Overall, results demonstrate complexities of theory of mind deficits in schizophrenia that should be considered when offering social cognitive training programs.

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Imitation plays a key role in social learning and in facilitating social interactions and likely constitutes a basic building block of social cognition that supports higher-level social abilities. Recent findings suggest that patients with schizophrenia have imitation impairments that could contribute to the social impairments associated with the disorder. However, extant studies have specifically assessed voluntary imitation or automatic imitation of emotional stimuli without controlling for potential confounders. The imitation impairments seen might therefore be secondary to other cognitive, motoric, or emotional deficits associated with the disorder. To overcome this issue, we used an automatic imitation paradigm with nonemotional stimuli to assess automatic imitation and the top-down modulation of imitation where participants were required to lift one of 2 fingers according to a number shown on the screen while observing the same or the other finger movement. In addition, we used a control task with a visual cue in place of a moving finger, to isolate the effect of observing finger movement from other visual cueing effects. Data from 33 patients (31 medicated) and 40 matched healthy controls were analyzed. Patients displayed enhanced imitation and intact top-down modulation of imitation. The enhanced imitation seen in patients may have been medication induced as larger effects were seen in patients receiving higher antipsychotic doses. In sum, we did not find an imitation impairment in schizophrenia. The results suggest that previous findings of impaired imitation in schizophrenia might have been due to other cognitive, motoric, and/or emotional deficits.

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The decision to share resources is fundamental for cohesive societies. Humans can be motivated to give for many reasons. Some generosity incurs a definite cost, with no extrinsic reward to the act, but instead provides intrinsic satisfaction (labelled here as 'altruistic' giving). Other giving behaviours are done with the prospect of improving one's own situation via reciprocity, reputation, or public good (labelled here as 'strategic' giving). These contexts differ in the source, certainty, and timing of rewards as well as the inferences made about others' mental states. We executed a combined statistical map and coordinate-based fMRI meta-analysis of decisions to give (36 studies, 1150 participants). Methods included a novel approach for accommodating variable signal dropout between studies in meta-analysis. Results reveal consistent, cross-paradigm neural correlates of each decision type, commonalities, and informative differences. Relative to being selfish, altruistic and strategic giving activate overlapping reward networks. However, strategic decisions showed greater activity in striatal regions than altruistic choices. Altruistic giving, more than strategic, activated subgenual anterior cingulate cortex (sgACC). Ventromedial prefrontal cortex (vmPFC) is consistently involved during generous decisions and processing across a posterior to anterior axis differentiates the altruistic/strategic context. Posterior vmPFC was preferentially recruited during altruistic decisions. Regions of the 'social brain' showed distinct patterns of activity between choice types, reflecting the different use of theory of mind in the two contexts. We provide the consistent neural correlates of decisions to give, and show that many will depend on the source of incentives.

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Expectation of reward can be shaped by the observation of actions and expressions of other people in one's environment. A person's apparent confidence in the likely reward of an action, for instance, makes qualities of their evidence, not observed directly, socially accessible. This strategy is computationally distinguished from associative learning methods that rely on direct observation, by its use of inference from indirect evidence. In twenty-three healthy human subjects, we isolated effects of first-hand experience, other people's choices, and the mediating effect of their confidence, on decision-making and neural correlates of value within ventromedial prefrontal cortex (vmPFC). Value derived from first-hand experience and other people's choices (regardless of confidence) were indiscriminately represented across vmPFC. However, value computed from agent choices weighted by their associated confidence was represented with specificity for ventromedial area 10. This pattern corresponds to shifts of connectivity and overlapping cognitive processes along a posterior-anterior vmPFC axis. Task behavior and self-reported self-reliance for decision-making in other social contexts correlated. The tendency to conform in other social contexts corresponded to increased activation in cortical regions previously shown to respond to social conflict in proportion to subsequent conformity (Campbell-Meiklejohn et al., 2010). The tendency to self-monitor predicted a selectively enhanced response to accordance with others in the right temporoparietal junction (rTPJ). The findings anatomically decompose vmPFC value representations according to computational requirements and provide biological insight into the social transmission of preference and reassurance gained from the confidence of others. SIGNIFICANCE STATEMENT: Decades of research have provided evidence that the ventromedial prefrontal cortex (vmPFC) signals the satisfaction we expect from imminent actions. However, we have a surprisingly modest understanding of the organization of value across this substantial and varied region. This study finds that using cues of the reliability of other peoples' knowledge to enhance expectation of personal success generates value correlates that are anatomically distinct from those concurrently computed from direct, personal experience. This suggests that representation of decision values in vmPFC is suborganized according to the underlying computation, consistent with what we know about the anatomical heterogeneity of the region. These results also provide insight into the observational learning process by which someone else's confidence can sway and reassure our choices.

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Changed reward functions have been proposed as a core feature of stimulant addiction, typically observed as reduced neural responses to non-drug-related rewards. However, it was unclear yet how specific this deficit is for different types of non-drug rewards arising from social and non-social reinforcements. We used functional neuroimaging in cocaine users to investigate explicit social reward as modeled by agreement of music preferences with music experts. In addition, we investigated non-social reward as modeled by winning desired music pieces. The study included 17 chronic cocaine users and 17 matched stimulant-naive healthy controls. Cocaine users, compared with controls, showed blunted neural responses to both social and non-social reward. Activation differences were located in the ventromedial prefrontal cortex overlapping for both reward types and, thus, suggesting a non-specific deficit in the processing of non-drug rewards. Interestingly, in the posterior lateral orbitofrontal cortex, social reward responses of cocaine users decreased with the degree to which they were influenced by social feedback from the experts, a response pattern that was opposite to that observed in healthy controls. The present results suggest that cocaine users likely suffer from a generalized impairment in value representation as well as from an aberrant processing of social feedback.

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In mental health practice, both pharmacological and non-pharmacological treatments are aimed at improving neuropsychological symptoms, including cognitive and emotional impairments. However, at present there is no established neuropsychological test battery that comprehensively covers multiple affective domains relevant in a range of disorders. Our objective was to generate a standardized test battery, comprised of existing, adapted and novel tasks, to assess four core domains of affective cognition (emotion processing, motivation, impulsivity and social cognition) in order to facilitate and enhance treatment development and evaluation in a broad range of neuropsychiatric disorders. The battery was administered to 200 participants aged 18-50 years (50% female), 42 of whom were retested in order to assess reliability. An exploratory factor analysis identified 11 factors with eigenvalues greater than 1, which accounted for over 70% of the variance. Tasks showed moderate to excellent test-retest reliability and were not strongly correlated with demographic factors such as age or IQ. The EMOTICOM test battery is therefore a promising tool for the assessment of affective cognitive function in a range of contexts.

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RATIONALE: Certain disorders, such as depression and anxiety, to which serotonin dysfunction is historically associated, are also associated with lower assessments of other people's trustworthiness. Serotonergic changes are known to alter cognitive responses to threatening stimuli. This effect may manifest socially as reduced apparent trustworthiness of others. Trustworthiness judgments can emerge from either direct observation or references provided by third parties. OBJECTIVE: We assessed whether explicit judgments of trustworthiness and social influences on those judgments are altered by changes within serotonergic systems. METHODS: We implemented a double-blind between-subject design where 20 healthy female volunteers received a single dose of the selective serotonin reuptake inhibitor (SSRI) citalopram (2 × 20 mg), while 20 control subjects (matched on age, intelligence, and years of education) received a placebo. Subjects performed a face-rating task assessing how trustworthy they found 153 unfamiliar others (targets). After each rating, the subjects were told how other subjects, on average, rated the same target. The subjects then performed 30 min of distractor tasks before, unexpectedly, being asked to rate all 153 faces again, in a random order. RESULTS: Compared to subjects receiving a placebo, subjects receiving citalopram rated targets as less trustworthy. They also conformed more to opinions of others, when others rated targets to be even less trustworthy than subjects had initially indicated. The two effects were independent of negative effects of citalopram on subjective state. CONCLUSIONS: This is evidence that serotonin systems can mediate explicit assessment and social learning of the trustworthiness of others.

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Methylphenidate (MPH) is a stimulant that increases extracellular levels of dopamine and noradrenaline. It can diminish risky decision-making tendencies in certain clinical populations. MPH is also used, without license, by healthy adults, but the impact on their decision-making is not well established. Previous work has found that dopamine receptor activity of healthy adults can modulate the influence of stake magnitude on decisions to persistently gamble after incurring a loss. In this study, we tested for modulation of this effect by MPH in 40 healthy human adults. In a double-blind experiment, 20 subjects received 20 mg of MPH, while 20 matched controls received a placebo. All were provided with 30 rounds of opportunities to accept an incurred loss from their assets or opt for a "double-or-nothing" gamble that would either avoid or double it. Rounds began with a variable loss that would double with every failed gamble until it was accepted, recovered, or reached a specified maximum. Probability of recovery on any gamble was low and ambiguous. Subjects receiving placebo gambled less as the magnitude of the stake was raised and as the magnitude of accumulated loss escalated over the course of the task. In contrast, subjects treated with MPH gambled at a consistent rate, well above chance, across all stakes and trials. Trait reward responsiveness also reduced the impact of high stakes. The findings suggest that elevated catecholamine activity by MPH can disrupt inhibitory influences on persistent risky choice in healthy adults.

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The ability to infer value from the reactions of other people is a common and essential ability with a poorly understood neurobiology. Commonly, social learning matches one's values and behavior to what is perceived as normal for one's social group. This is known as conformity. Conformity of value correlates with neural activity shared by cognitions that depend on optimum catecholamine levels, but catecholamine involvement in conformity has not been tested empirically. Methylphenidate (MPH) is an indirect dopamine and noradrenalin agonist, commonly used for the treatment of attention-deficit hyperactivity disorder for which it reduces undesirable behavior as evaluated by peers and authority figures, indicative of increased conformity. We hypothesized that MPH might increase conformity of value. In all, 38 healthy adult females received either a single oral 20 mg dose of MPH or placebo (PL). Each subject rated 153 faces for trustworthiness followed immediately by the face's mean rating from a group of peers. After 30 min and a 2-back continuous-performance working-memory task, subjects were unexpectedly asked to rate all the faces again. Both the groups tended to change their ratings towards the social norm. The MPH group exhibited twice the conformity effect of the PL group following moderate social conflict, but this did not occur following large conflicts. This suggests that MPH might enhance signals that would otherwise be too weak to evoke conformity. MPH did not affect 2-back performance. We provide a new working hypothesis of a neurocognitive mechanism by which MPH reduces socially disruptive behavior. We also provide novel evidence of catecholamine mediation of social learning [corrected].

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Dopaminergic treatments are associated with impulse control disorders such as pathological gambling in a subset of patients with Parkinson's Disease. While deep brain stimulation of the subthalamic nucleus has been reported to reduce symptoms of impulse control disorders in some Parkinson's Disease patients, little is known about its specific effects on gambling behaviour. In this experiment, we investigated the effects of deep brain stimulation of the subthalamic nucleus on one of the central features of pathological gambling: the tendency to chase losses. Loss-chasing is associated with impaired control over gambling behaviour and it is one of the most salient features of pathological gambling as it presents in the clinic. Twenty two patients with advanced idiopathic Parkinson's Disease and chronically implanted subthalamic nucleus electrodes for deep brain stimulation completed a simple laboratory model of loss-chasing behaviour twice: once with and once without stimulation. Exploratory analysis indicated that deep brain stimulation of the subthalamic nucleus increased the value of losses chased by patients with Parkinson's Disease when shifting from off- to on-stimulation. These effects were not attributable to changes in state affect or to the motor impairments produced by the withdrawal of deep brain stimulation of the subthalamic nucleus. The effects of the stimulation on the value of losses chased were more pronounced in female than in male patients and reduced in patients taking dopamine receptor agonists. Collectively, these results suggest that deep brain stimulation of the subthalamic nucleus can transiently alter the evaluation of accumulated losses during gambling episodes in idiopathic Parkinson's Disease.

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Continued gambling to recover losses--'loss chasing'--is a prominent feature of social and pathological gambling. However, little is known about the neuromodulators that influence this behavior. In three separate experiments, we investigated the role of serotonin activity, D(2)/D(3) receptor activity, and beta-adrenoceptor activity on the loss chasing of age and IQ-matched healthy adults randomized to treatment or an appropriate control/placebo. In Experiment 1, participants consumed amino-acid drinks that did or did not contain the serotonin precursor, tryptophan. In Experiment 2, participants received a single 176 µg dose of the D(2)/D(3) receptor agonist, pramipexole, or placebo. In Experiment 3, participants received a single 80 mg dose of the beta-adrenoceptor blocker, propranolol, or placebo. Following treatment, participants completed a computerized loss-chasing game. Mood and heart rate were measured at baseline and following treatment. Tryptophan depletion significantly reduced the number of decisions made to chase losses, and the number of consecutive decisions to chase, in the absence of marked changes in mood. By contrast, pramipexole significantly increased the value of losses chased and diminished the value of losses surrendered. Propranolol markedly reduced heart rate, but produced no significant changes in loss-chasing behavior. Loss chasing can be thought of as an aversively motivated escape behavior controlled, in part, by the marginal value of continued gambling relative to the value of already accumulated losses. Serotonin and dopamine appear to play dissociable roles in the tendency of individuals to gamble to recover, or to seek to 'escape' from, previous losses. Serotonergic activity seems to promote the availability of loss chasing as a behavioral option, whereas D(2)/D(3) receptor activity produces complex changes in the value of losses judged worth chasing. Sympathetic arousal, at least as mediated by beta-adrenoceptors, does not play a major role in laboratory-based loss-chasing choices.

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The opinions of others can easily affect how much we value things. We investigated what happens in our brain when we agree with others about the value of an object and whether or not there is evidence, at the neural level, for social conformity through which we change object valuation. Using functional magnetic resonance imaging we independently modeled (1) learning reviewer opinions about a piece of music, (2) reward value while receiving a token for that music, and (3) their interaction in 28 healthy adults. We show that agreement with two "expert" reviewers on music choice produces activity in a region of ventral striatum that also responds when receiving a valued object. It is known that the magnitude of activity in the ventral striatum reflects the value of reward-predicting stimuli. We show that social influence on the value of an object is associated with the magnitude of the ventral striatum response to receiving it. This finding provides clear evidence that social influence mediates very basic value signals in known reinforcement learning circuitry. Influence at such a low level could contribute to rapid learning and the swift spread of values throughout a population.

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BACKGROUND: Continued gambling to recover previous losses ("loss-chasing") is central to pathological gambling. However, very little is known about the neural mechanisms that mediate this behavior. METHODS: We used functional magnetic resonance imaging (fMRI) to examine neural activity while healthy adult participants decided to chase losses or decided to quit gambling to prevent further losses. RESULTS: Chasing losses was associated with increased activity in cortical areas linked to incentive-motivation and an expectation of reward. By contrast, quitting was associated with decreased activity in these areas but increased activity in areas associated with anxiety and conflict monitoring. Activity within the anterior cingulate cortex associated with the experience of chasing and then losing predicted decisions to stop chasing losses at the next opportunity. CONCLUSIONS: Excessive loss-chasing behavior in pathological gambling might involve a failure to appropriately balance activity within neural systems coding conflicting motivational states. Similar mechanisms might underlie the loss-of-control over appetitive behaviors in other impulse control disorders.

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