Over the past several decades, and particularly during the last 10 to 15 years, there has been a rapid increase in the accessibility of legalized gambling in the United States and other parts of the world. Few studies have systematically explored the relationships between patterns of gambling and health status. Existing data support the notion that some gambling behaviors, particularly problem and pathological gambling, are associated with nongambling health problems. The purpose of this article is to provide a perspective on the relationship between gambling behaviors and substance use disorders, review the data regarding health associations and screening and treatment options for problem and pathological gambling, and suggest a role for generalist physicians in assessing problem and pathological gambling. A rationale for conceptualization of pathological gambling as an addictive disorder and a model proposing stress as a possible mediating factor in the relationship between gambling and health status are presented. More research is needed to investigate directly the biological and health correlates associated with specific types of gambling behaviors and to define the role for generalist physicians in the prevention and treatment of problem and pathological gambling.
addiction; pathological gambling; treatment; prevention; substance abuse
Pathological gambling (PG) has recently been considered as a “behavioral” or non-substance addiction. A comparison of characteristics of PG and substance use disorders (SUDs) has clinical ramifications and could help advance future research on these conditions. Specific relationships with impulsivity and compulsivity may be central to understanding PG and SUDs.
To compare and contrast research findings in PG and SUDs pertaining to neurocogntive tasks, brain function and neurochemistry, with a focus on impulsivity and compulsivity.
Multiple similarities were found between PG and SUDs, including poor performance on neurocognitive tasks, specifically with respect to impulsive choice and response tendencies and compulsive features (e.g., response perseveration and action with diminished relationship to goals or reward). Findings suggest dysfunction involving similar brain regions, including the ventromedial prefrontal cortex (PFC) and striatum and similar neurotransmitter systems, including dopaminergic and serotonergic. Unique features exist which may in part reflect influences of acute or chronic exposures to specific substances.
Both similarities and differences exist between PG and SUDs. Understanding these similarities more precisely may facilitate treatment development across addictions, whereas understanding differences may provide insight into treatment development for specific disorders. Individual differences in features of impulsivity and compulsivity may represent important endophenotypic targets for prevention and treatment strategies.
Iowa Gambling Task; delay discounting; neuroimaging; alcohol; cocaine; dopamine; serotonin; glutamate; frontal cortex; striatum
Gambling is a prevalent recreational behaviour. Approximately 5% of adults have been estimated to experience problems with gambling. The most severe form of gambling, pathological gambling (PG), is recognized as a mental health condition. Two alternate non-mutually exclusive conceptualizations of PG have considered it as an obsessive-compulsive spectrum disorder and a ‘behavioural’ addiction. The most appropriate conceptualization of PG has important theoretical and practical implications. Data suggest a closer relationship between PG and substance use disorders than exists between PG and obsessive-compulsive disorder. This paper will review data on the neurobiology of PG, consider its conceptualization as a behavioural addiction, discuss impulsivity as an underlying construct, and present new brain imaging findings investigating the neural correlates of craving states in PG as compared to those in cocaine dependence. Implications for prevention and treatment strategies will be discussed.
gambling; addiction; impulsivity; impulse control disorder; brain imaging; functional magnetic resonance imaging
The Iowa Gambling Task (IGT) is widely used in investigations of decision making. A growing number of studies have linked performance on this task to personality differences, with the aim of explaining the large degree of variability in healthy individuals' performance of the task. However, this line of research has yielded inconsistent results. In the present study, we tested whether increasing the conflict between short-term and long-term gains in the IGT can clarify personality-related modulations of decision making. We assessed performance on the original IGT as a function of the personality traits typically involved in risky decision making (i.e., impulsivity, sensation seeking, sensitivity to reward and punishment). The impact of these same personality traits was also evaluated on a modified version of the task in which the difference in immediate reward magnitude between disadvantageous and advantageous decks was increased, while keeping the net gain fixed. The results showed that only in this latter IGT variant were highly impulsive individuals and high sensation seekers lured into making disadvantageous choices. The opposite seems to be the case for participants who were highly sensitive to punishment, although further data are needed to corroborate this finding. The present preliminary results suggest that the IGT variant used in this study could be more effective than the original task at identifying personality effects in decision making. Implications for dispositional and situational effects on decision making are discussed.
Despite reasonable knowledge of pathological gambling (PG), little is known of its cognitive antecedents. We evaluated decision-making and impulsivity characteristics in people at risk of developing PG using neuropsychological tests. Non-treatment seeking volunteers (18-29 years) who gamble ≥5 times/year were recruited from the general community, and split into two groups: those “at risk” of developing PG (n=74) and those social, non-problem gamblers (n=112). Participants undertook the Cambridge Gamble and Stop-signal tasks and were assessed with the Mini-International Neuropsychiatric Interview and the Yale Brown Obsessive Compulsive Scale Modified for Pathological Gambling. On the Cambridge Gamble task, the at- risk subjects gambled more points overall, were more likely to go bankrupt, and made more irrational decisions under situations of relative risk ambiguity. On the Stop-signal task, at- risk gamblers did not differ from the social, non-problem gamblers in terms of motor impulse control (stop-signal reaction times). Findings suggest that selective cognitive dysfunction may already be present in terms of decision-making in at-risk gamblers, even before psychopathology arises. These findings implicate selective decision-making deficits and dysfunction of orbitofronto-limbic circuitry in the chain of pathogenesis between social, non-problematic and pathological gambling.
Pathological Gambling; Pathogenesis; Addiction; Cognitive Dysfunction; Cognition; Inhibition
As a behavioral addiction with clinical and phenomenological similarities to substance addiction, recreational and pathological gambling represent models for studying the neurobiology of addiction, without the confounding deleterious brain effects which may occur from chronic substance abuse.
A community sample of individuals aged 18–65 years who gamble was solicited through newspaper advertising. Subjects were grouped a priori into three groups (no-risk, at-risk, and pathological gamblers) based on a diagnostic interview. All subjects underwent a psychiatric clinical interview and neurocognitive tests assessing motor impulsivity and cognitive flexibility. Subjects with a current axis I disorder, history of brain injury/trauma, or implementation or dose changes of psychoactive medication within 6 weeks of study enrollment were excluded.
A total of 135 no-risk, 69 at-risk and 46 pathological gambling subjects were assessed. Pathological gamblers were significantly older, and exhibited significant deficiencies in motor impulse control (stop-signal reaction times), response speed (median ‘go’ trial response latency) and cognitive flexibility [total intra-dimensional/extra-dimensional (IDED) errors] versus controls. The finding of impaired impulse control and cognitive flexibility was robust in an age-matched subgroup analysis of pathological gamblers. The no-risk and at-risk gambling groups did not significantly differ from each other on task performance.
Impaired response inhibition and cognitive flexibility exist in people with pathological gambling compared with no-risk and at-risk gamblers. The early identification of such illness in adolescence or young adulthood may aid in the prevention of addiction onset of such disabling disorders.
Cognition; gambling; impulsivity
Gambling, including pathological gambling and problem gambling, has received increased attention from clinicians and researchers over the past three decades since gambling opportunities have expanded around the world. Gambling disorders affect 0.2–5.3% of adults worldwide, although measurement and prevalence varies according to the screening instruments and methods used, and availability and accessibility of gambling opportunities. Several distinct treatment approaches have been favorably evaluated, such as cognitive behavioral and brief treatment models and pharmacological interventions. Although promising, family therapy and support from Gamblers Anonymous are less well empirically supported. Gambling disorders are highly comorbid with other mental health and substance use disorders, and a further understanding is needed of both the causes and treatment implications of this disorder. This article reviews definition, causes and associated features with substance abuse, screening and diagnosis, and treatment approaches.
Addiction; gambling; substance use
Impulsivity is a hallmark of problem gambling. However, impulsivity is not a unitary construct and this study investigated the relationship between problem gambling severity and two facets of impulsivity: impulsive action (impaired ability to withhold a motor response) and impulsive choice (abnormal aversion for the delay of reward).
The recruitment includes 65 problem gamblers and 35 normal control participants. On the basis of DSM-IV-TR criteria, two groups of gamblers were distinguished: problem gamblers (n = 38) and pathological gamblers (n = 27) with similar durations of gambling practice. Impulsive action was assessed using a response inhibition task (the stop-signal task). Impulsive choice was estimated with the delay-discounting task. Possible confounds (e.g., IQ, mood, ADHD symptoms) were recorded.
Both problem and pathological gamblers discounted reward at a higher rate than their controls, but only pathological gamblers showed abnormally low performance on the most demanding condition of the stop-signal task. None of the potential confounds covaried with these results.
These results suggest that, whereas abnormal impulsive choice characterizes all problem gamblers, pathological gamblers' impairments in impulsive action may represent an important developmental pathway of pathological gambling.
Impairments in self-regulatory behaviour reflect a deficit in executive functioning and decision-making, as well as higher levels of self-reported impulsivity, and may be involved in the development and maintenance of addictive disorders. We sought to explore the association between self-reported impulsivity and neurocognitive measures, and their association with treatment outcome in pathologic gambling.
We assessed patients with pathologic gambling using executive functioning and decision-making tests and self-report measures of impulsivity. Patients underwent cognitive–behavioural therapy (CBT) for pathologic gambling.
We included 88 patients (8% women) in our study. High self-reported extravagance was associated with poor performance in the Iowa Gambling Task (IGT)-ABCD version. High impulsiveness, low disorderliness, high exploratory excitability (trend), poor backward block span and poor IGT-EFGH scores (trend) predicted dropout. We observed no self-reported or neurocognitive predictors of relapse or number of treatment sessions attended.
Most participants were slot-machine gamblers seeking treatment. No follow-up data and no control group were included in the study. The missing sample (i.e., individuals who were recruited and assessed in the pretreatment stage but who chose not to begin treatment) had higher extravagance scores than the final sample.
Neurocognitive reward sensitivity was related to self-reported overspending behaviour. Self-regulatory impairments (especially rash impulsiveness and punishment sensitivity) and executive dysfunction predicted only dropout of CBT in participants with pathologic gambling. Different neurocognitive processes and personality traits might mediate treatment response to psychological therapy of pathologic gambling according to the specific target variable assessed.
Failures in cortical control of fronto-striatal neural circuits may underpin impulsive and compulsive acts. In this narrative review, we explore these behaviors from the perspective of neural processes and consider how these behaviors and neural processes contribute to mental disorders such as obsessive–compulsive disorder (OCD), obsessive–compulsive personality disorder, and impulse-control disorders such as trichotillomania and pathological gambling. We present findings from a broad range of data, comprising translational and human endophenotypes research and clinical treatment trials, focussing on the parallel, functionally segregated, cortico-striatal neural projections, from orbitofrontal cortex (OFC) to medial striatum (caudate nucleus), proposed to drive compulsive activity, and from the anterior cingulate/ventromedial prefrontal cortex to the ventral striatum (nucleus accumbens shell), proposed to drive impulsive activity, and the interaction between them. We suggest that impulsivity and compulsivity each seem to be multidimensional. Impulsive or compulsive behaviors are mediated by overlapping as well as distinct neural substrates. Trichotillomania may stand apart as a disorder of motor-impulse control, whereas pathological gambling involves abnormal ventral reward circuitry that identifies it more closely with substance addiction. OCD shows motor impulsivity and compulsivity, probably mediated through disruption of OFC-caudate circuitry, as well as other frontal, cingulate, and parietal connections. Serotonin and dopamine interact across these circuits to modulate aspects of both impulsive and compulsive responding and as yet unidentified brain-based systems may also have important functions. Targeted application of neurocognitive tasks, receptor-specific neurochemical probes, and brain systems neuroimaging techniques have potential for future research in this field.
impulsive; compulsive; endophenotypes; serotonin; dopamine; Cognition; Psychiatry & Behavioral Sciences; Animal models; Biological Psychiatry; OCD; impulsivity; compulsivity; translational
Two studies were conducted to test and explain the relation of mindfulness to the severity of gambling outcomes among frequent gamblers. In both studies, dispositional mindfulness related to less severe gambling outcomes as measured by a DSM-IV-based screen for pathological gambling, even after controlling for gambling frequency and dispositional self-control. Study 2 extended this finding in showing that the association between mindfulness and lower pathological gambling was partially mediated by better performance on two risk-taking tasks that capture overconfidence, risky bet acceptance, and myopic focus on reward. These studies suggest a role for mindfulness in lessening the severity of gambling problems and making adaptive decisions, especially in risk-relevant contexts.
MINDFULNESS; OVERCONFIDENCE; RISK-TAKING; GAMBLING; DECISION-MAKING
To examine whether gambling cue reactivity is cue-specific, 47 scratch-off lottery players and 47 horse race gamblers were presented with video clips of their preferred and non-preferred modes of gambling, and two control stimuli including an exciting car race and a mental stressor task while heart rates, excitement, and urge to gamble were being measured. Heart rates for both groups of gamblers were highest to the mental stressor and did not differ in response to the other three cues. Excitement for both groups was highest in response to the action cues (horse race and car chase). Urge to gamble was significantly higher for each group to their preferred mode of gambling. A post-hoc exploratory analysis comparing social gamblers (n=54) and probable pathological gamblers (n=40) revealed a similar pattern of responses. However, pathological gamblers reported overall significantly higher urges to gamble than social gamblers. As urges have been shown to play a pivotal role in addictive behaviors and relapse, the current findings may have implications for the development of gambling problems and relapse after successful treatment.
cue-reactivity; gambling; heart rate; excitement; urge
Abnormal cue reactivity is a central characteristic of addiction, associated with increased activity in motivation, attention and memory related brain circuits. In this neuroimaging study, cue reactivity in problem gamblers (PRG) was compared with cue reactivity in heavy smokers (HSM) and healthy controls (HC). A functional magnetic resonance imaging event-related cue reactivity paradigm, consisting of gambling, smoking-related and neutral pictures, was employed in 17 treatment-seeking non-smoking PRG, 18 non-gambling HSM, and 17 non-gambling and non-smoking HC. Watching gambling pictures (relative to neutral pictures) was associated with higher brain activation in occipitotemporal areas, posterior cingulate cortex, parahippocampal gyrus and amygdala in PRG compared with HC and HSM. Subjective craving in PRG correlated positively with brain activation in left ventrolateral prefrontal cortex and left insula. When comparing the HSM group with the two other groups, no significant differences in brain activity induced by smoking cues were found. In a stratified analysis, the HSM subgroup with higher Fagerström Test for Nicotine Dependence scores (FTND M = 5.4) showed higher brain activation in ventromedial prefrontal cortex, rostral anterior cingulate cortex, insula and middle/superior temporal gyrus while watching smoking-related pictures (relative to neutral pictures) than the HSM subgroup with lower FTND scores (FTND M = 2.9) and than non-smoking HC. Nicotine craving correlated with activation in left prefrontal and left amygdala when viewing smoking-related pictures in HSM. Increased regional responsiveness to gambling pictures in brain regions linked to motivation and visual processing is present in PRG, similar to neural mechanisms underlying cue reactivity in substance dependence. Increased brain activation in related fronto-limbic brain areas was present in HSM with higher FTND scores compared with HSM with lower FTND scores.
Addiction; cue reactivity; fMRI; impulse control disorder; nicotine dependence; pathological gambling
Surface-level differences in the reward and punishment variants, specifically greater long-term decision making in the punishment variant of the Iowa Gambling Task (IGT) observed in previous studies led to the present comparison of long-term decision making in the two IGT variants (n = 320, male = 160). It was contended that risk aversion triggered by a positive frame of the reward variant and risk seeking triggered by a negative frame of the punishment variant appears as long-term decision making in the two IGT variants. Apart from the frame of the variant as a within-subjects factor (variant type: reward and punishment), the order in which the frame was triggered (order type: reward–punishment or punishment–reward), and the four types of instructions that delineated motivation toward reward from that of punishment (reward, punishment, reward and punishment, and no-hint) were hypothesized to have an effect on foresighted decision making in the IGT. As expected, long-term decision making differed across the two IGT variants suggesting that the frame of the variant has an effect on long-term decision making in the IGT (p < 0.001). The order in which a variant was presented, and the type of the instructions that were used both had an effect on long-term decision making in the two IGT variants (p < 0.05). A post hoc test suggested that the instructions that differentiated between reward and punishment resulted in greater foresight than the commonly used IGT instructions that fail to distinguish between reward and punishment. As observed in previous studies, there were more number of participants (60%) who showed greater foresight in the punishment variant than in the reward variant (p < 0.001). The results suggest that foresight in IGT decision making is sensitive to reward and punishment frame in an asymmetric manner, an observation that is aligned with the behavioral decision making framework. Benefits of integrating findings from behavioral studies in decision neuroscience are discussed, and a need to investigate cultural differences in the IGT studies is pointed out.
Iowa gambling task; reward–punishment; instructions; decision making; framing effect
Delay discounting describes the decline in the value of a reinforcer as the delay to that reinforcer increases. A review of the available studies revealed that steep delay discounting is positively correlated with problem or pathological gambling. One hypothesis regarding this correlation derives from the discounting equation proposed by Mazur (1989). According to the equation, steeper discounting renders the difference between fixed-delayed rewards and gambling-like variable-delayed rewards larger; with the latter being more valuable. The present study was designed to test this prediction by first assessing rats’ impulsive choices across four delays to a larger-later reinforcer. A second condition quantified strength of preference for mixed- over fixed-delays, with the duration of the latter adjusted between sessions to achieve indifference. Strength of preference for the mixed-delay alternative is given by the fixed delay at indifference (lower fixed-delay values reflect stronger preferences). Percent impulsive choice was not correlated with the value of the fixed delay at indifference and, therefore, the prediction of the hyperbolic model of gambling was not supported. A follow-up assessment revealed a significant decrease in impulsive choice after the second condition. This shift in impulsive choice could underlie the failure to observe the predicted correlation between impulsive choice and degree of preference for mixed- over fixed delays.
Delay discounting; impulsivity; delay; gambling; rat
Our ability to measure the cognitive components of complex decision-making across species has greatly facilitated our understanding of its neurobiological mechanisms. One task in particular, reversal learning, has proven valuable in assessing the inhibitory processes that are central to executive control. Reversal learning measures the ability to actively suppress reward-related responding and to disengage from ongoing behavior, phenomena that are biologically and descriptively related to impulsivity and compulsivity. Consequently, reversal learning could index vulnerability for disorders characterized by impulsivity, such as proclivity for initial substance abuse, as well as the compulsive aspects of dependence.
Though we describe common variants and similar tasks, we pay particular attention to discrimination reversal learning, its supporting neural circuitry, neuropharmacology and genetic determinants. We also review the utility of this task in measuring impulsivity and compulsivity in addictions.
We restrict our review to instrumental, reward-related reversal learning studies, as they are most germane to addiction.
The research reviewed here suggests that discrimination reversal learning may be used as a diagnostic tool for investigating the neural mechanisms that mediate impulsive and compulsive aspects of pathological reward-seeking and –taking behaviors. Two interrelated mechanisms are posited for the neuroadaptations in addiction that often translate to poor reversal learning: frontocorticostriatal circuitry dysregulation and poor dopamine (D2 receptor) modulation of this circuitry. These data suggest new approaches to targeting inhibitory control mechanisms in addictions.
orbitofrontal cortex; striatum; decision-making; dopamine; serotonin; psychostimulant; methamphetamine; noradrenaline; response control
Gambling offers opportunities for basic research and theory, and has hugely important applied implications. As I have said recently: “The current view of pathological gambling as an addiction cries out for a functional analysis of the controlling variables and for strategies of behavioral intervention.” (Fantino, 2008). This view echoed that of Dixon (2007), who called out for behavior analysts to apply their very relevant skills to discovering the causes of gambling disorders. To understand the behavior of gambling, one must understand the basic processes and variables involved in making the decisions gamblers make. Behavior analysts, those experimental psychologists who approach psychological phenomena from a behavioral (or functional) perspective, have long concentrated on the choices organisms make. Thus, they should be in a strong position to contribute to our appreciation of the factors controlling gambling. In this paper we will examine some of the advances already made, and also propose some directions for future research.
Pathological Gambling (PG) is an impulse control disorder often comorbid with other psychopathology, particularly bipolar spectrum disorders, attention deficit/hyperactivity disorder, obsessive-compulsive disorder (OCD) and substance abuse. This paper reviews the published literature on the pharmacological management of PG, highlighting how clinical and subclinical comorbid psychopathology influences the choice of pharmacological treatment.
Using Medline, the authors reviewed relevant articles published on this topic from1995 to 2005, focusing on the best-designed studies for inclusion.
Much of the literature on PG-treatment presupposes different theories regarding this disorder. Data suggest the utility of differentiating the pharmacotherapy of pathological gamblers in light of their comorbid profile, specifically assessing for comorbid bipolar, ADHD, OCD, and substance abuse disorders.
Decisions about pharmacological treatment of PG should take into account current and previous comorbid disorders which influence treatment selection.
Pathological Gambling; Impulse Control Disorders; Comorbidity; Compulsive-Impulsive Spectrum; Subthreshold symptoms
Impaired decision-making is a core problem in several psychiatric disorders including attention-deficit/hyperactivity disorder, schizophrenia, obsessive–compulsive disorder, mania, drug addiction, eating disorders, and substance abuse as well as in chronic pain. To ensure progress in the understanding of the neuropathophysiology of these disorders, animal models with good construct and predictive validity are indispensable. Many human studies aimed at measuring decision-making capacities use the Iowa gambling task (IGT), a task designed to model everyday life choices through a conflict between immediate gratification and long-term outcomes. Recently, new rodent models based on the same principle have been developed to investigate the neurobiological mechanisms underlying IGT-like decision-making on behavioral, neural, and pharmacological levels. The comparative strengths, as well as the similarities and differences between these paradigms are discussed. The contribution of these models to elucidate the neurobehavioral factors that lead to poor decision-making and to the development of better treatments for psychiatric illness is considered, along with important future directions and potential limitations.
Iowa gambling task; animal model; validity; dopamine; serotonin; neurobiology
Gambling is a widespread form of entertainment that may afford unique insights into the interaction between cognition and emotion in human decision-making. It is also a behaviour that can become harmful, and potentially addictive, in a minority of individuals. This article considers the status of two dominant approaches to gambling behaviour. The cognitive approach has identified a number of erroneous beliefs held by gamblers, which cause them to over-estimate their chances of winning. The psychobiological approach has examined case-control differences between groups of pathological gamblers and healthy controls, and has identified dysregulation of brain areas linked to reward and emotion, including the ventromedial prefrontal cortex (vmPFC) and striatum, as well as alterations in dopamine neurotransmission. In integrating these two approaches, recent data are discussed that reveal anomalous recruitment of the brain reward system (including the vmPFC and ventral striatum) during two common cognitive distortions in gambling games: the near-miss effect and the effect of personal control. In games of chance, near-misses and the presence of control have no objective influence on the likelihood of winning. These manipulations appear to harness a reward system that evolved to learn skill-oriented behaviours, and by modulating activity in this system, these cognitive distortions may promote continued, and potentially excessive, gambling.
gambling; addiction; risk; reward; cognition; emotion
Although pathological gambling (PG) is relatively common, pharmacotherapy research for PG is limited. Memantine, an N-methyl d-aspartate receptor antagonist, appears to reduce glutamate excitability and improve impulsive decision making, suggesting it may help individuals with PG.
This study sought to examine the safety and efficacy of Memantine in PG.
Twenty-nine subjects (18 females) with DSM-IV PG were enrolled in a 10-week open-label treatment study of memantine (dose ranging from 10 to 30 mg/day). Subjects were enrolled from January 2009 until April 2010. Change from baseline to study endpoint on the Yale Brown Obsessive Compulsive Scale Modified for Pathological Gambling (PG-YBOCS) was the primary outcome measure. Subjects underwent pre- and post-treatment cognitive assessments using the stop-signal task (assessing response impulsivity) and the intra-dimensional/extra-dimensional (ID/ED) set shift task (assessing cognitive flexibility).
Twenty-eight of the 29 subjects (96.6%) completed the 10-week study. PG-YBOCS scores decreased from a mean of 21.8±4.3 at baseline to 8.9±7.1 at study endpoint (p<0.001). Hours spent gambling per week and money spent gambling both decreased significantly (p<0.001). Subjects also demonstrated a significant improvement in ID/ED total errors (p=0.037) at study endpoint. The mean effective dose of memantine was 23.4±8.1 mg/day. The medication was well-tolerated. Memantine treatment was associated with diminished gambling and improved cognitive flexibility.
These findings suggest that pharmacological manipulation of the glutamate system may target both gambling and cognitive deficits in PG. Placebo-controlled, double-blind studies are warranted in order to confirm these preliminary findings in a controlled design.
Cognition; Glutamate; Impulsivity; Treatment; Pharmacology; Addiction
Pathological gambling (PG) is categorized as an impulse control disorder (ICD). Phenomenological, neurobiological and pharmacological data suggest similarities in the pathophysiologies of substance use disorders (SUDs) and PG. Both behavioral and pharmacological approaches, including those that have been empirically validated for SUDs, have shown promise in the treatment of PG. Findings from biological studies of PG are reviewed, and treatment approaches based on controlled studies are summarized.
pathological gambling (PG); impulse control disorders (ICDs); substance use disorders (SUDs)
Genetic variation at the serotonin transporter-linked polymorphic region (5-HTTLPR) is associated with altered amygdala reactivity and lack of prefrontal regulatory control. Similar regions mediate decision-making biases driven by contextual cues and ambiguity, for example the “framing effect.” We hypothesized that individuals hemozygous for the short (s) allele at the 5-HTTLPR would be more susceptible to framing. Participants, selected as homozygous for either the long (la) or s allele, performed a decision-making task where they made choices between receiving an amount of money for certain and taking a gamble. A strong bias was evident toward choosing the certain option when the option was phrased in terms of gains and toward gambling when the decision was phrased in terms of losses (the frame effect). Critically, this bias was significantly greater in the ss group compared with the lala group. In simultaneously acquired functional magnetic resonance imaging data, the ss group showed greater amygdala during choices made in accord, compared with those made counter to the frame, an effect not seen in the lala group. These differences were also mirrored by differences in anterior cingulate–amygdala coupling between the genotype groups during decision making. Specifically, lala participants showed increased coupling during choices made counter to, relative to those made in accord with, the frame, with no such effect evident in ss participants. These data suggest that genetically mediated differences in prefrontal-amygdala interactions underpin interindividual differences in economic decision making.
Impulse control disorders such as pathological gambling (PG) are a serious and common adverse effect of dopamine (DA) replacement medication in Parkinson’s disease (PD). Patients with PG have increased impulsivity and abnormalities in striatal DA, in common with behavioural and substance addictions in the non-PD population. To date, no studies have investigated the role of extrastriatal dopaminergic abnormalities in PD patients with PG. We used the PET radiotracer, [11C] FLB-457, with high-affinity for extrastriatal DA D2/3 receptors. 14 PD patients on DA agonists were imaged while they performed a gambling task involving real monetary reward and a control task. Trait impulsivity was measured with the Barratt Impulsivity Scale (BIS). Seven of the patients had a history of PG that developed subsequent to DA agonist medication. Change in [11C] FLB-457 binding potential (BP) during gambling was reduced in PD with PG patients in the midbrain, where D2/D3 receptors are dominated by autoreceptors. The degree of change in [11C] FLB-457 binding in this region correlated with impulsivity. In the cortex, [11C] FLB-457 BP was significantly greater in the anterior cingulate cortex (ACC) in PD patients with PG during the control task, and binding in this region was also correlated with impulsivity. Our findings provide the first evidence that PD patients with PG have dysfunctional activation of DA autoreceptors in the midbrain and low DA tone in the ACC. Thus, altered striatal and cortical DA homeostasis may incur vulnerability for the development of PG in PD, linked with the impulsive personality trait.
PMID: 22766031 CAMSID: cams2373
Parkinson’s disease; Dopamine agonists; Pathological gambling; Impulsivity
Research on self-serving biases in judgments and decision-making suggests that individuals first evaluate the outcomes they get, and then the procedures by which these outcomes were obtained. Evidence also suggests that the appraisal of the former (outcome favorability) can bias the appraisal of the latter (procedural fairness). We investigated the nature of the emotions that are elicited by these appraisals by using a new paradigm in which participants performed a choice task between pairs of competing gambles against a virtual opponent. Conflicts (when the participant selected the same gamble as his virtual opponent) were resolved by a neutral arbitrator who either confirmed the participant’s choice (“pro-self”) or attributed his gamble to the virtual opponent (“pro-competitor”). Trials in which the participant and his virtual opponent selected different gambles (“no-conflict”) served as a control condition. In order to validate this new task, emotional reactions to the outcomes of the gambles were measured using self-reports, skin conductance responses, and facial electromyography (zygomaticus, corrugator, and frontalis). In no-conflict trials, effects of counterfactual thinking and social comparison resulted in (i) increased happiness as well as SCR and zygomaticus activity for wins compared to losses (valence effect) and for high compared to low gains (magnitude effect), and (ii) increased anger, regret, disappointment, and envy for losses compared to wins (valence effect). More importantly, compared to no-conflict trials and to pro-self awards with similar outcomes, pro-competitor awards increased subjective reports of anger for unfavorable outcomes, and increased happiness and guilt for favorable outcomes. Although the outcomes were independent from the arbitrators’ decisions, and both the arbitrators’ decisions and the outcomes were kept equally likely, individuals tended to attribute their outcomes to unfair arbitrators, reacting emotionally, especially when the modification of their initial choice for a gamble led to a negative outcome.
conflict; arbitration; emotion; appraisals; procedural justice; distributive justice; outcome favorability; self-serving bias