Compulsive features in behavioural addictions: the case of pathological gambling (2012)

Addiction. 2012 Oct;107(10):1726-34. doi: 10.1111/j.1360-0443.2011.03546.x. Epub 2011 Oct 10.

el-Guebaly N1, Mudry T, Zohar J, Tavares H, Potenza MN.



To describe, in the context of DSM-V, how a focus on addiction and compulsion is emerging in the consideration of pathological gambling (PG).


A systematic literature review of evidence for the proposed re-classification of PG as an addiction.


Findings include: (i) phenomenological models of addiction highlighting a motivational shift from impulsivity to compulsivity associated with a protracted withdrawal syndrome and blurring of the ego-syntonic/ego-dystonic dichotomy; (ii) common neurotransmitter (dopamine, serotonin) contributions to PG and substance use disorders (SUDs); (iii) neuroimaging support for shared neurocircuitries between ‘behavioural’ and substance addictions and differences between obsessive-compulsive disorder (OCD), impulse control disorders (ICDs) and SUDs; (iv) genetic findings more closely related to endophenotypic constructs such as compulsivity and impulsivity than to psychiatric disorders; (v) psychological measures such as harm avoidance identifying a closer association between SUDs and PG than with OCD; (vi) community and pharmacotherapeutic trials data supporting a closer association between SUDs and PG than with OCD. Adapted behavioural therapies, such as exposure therapy, appear applicable to OCD, PG or SUDs, suggesting some commonalities across disorders.


PG shares more similarities with SUDs than with OCD. Similar to the investigation of impulsivity, studies of compulsivity hold promising insights concerning the course, differential diagnosis and treatment of PG, SUDs, and OCD.

Keywords: Compulsivity, Impulsivity, Addiction, Pathological Gambling, Endophenotypes


Debate exists regarding the appropriateness of considering pathological gambling (PG) as an impulse control, obsessive-compulsive-spectrum or addictive disorder (1;2) as features of impulsivity, compulsivity, and addiction are observed in PG (3). This debate is timely as the Diagnostic and Statistical Manual of Mental Disorders

(DSM-5) develops (4;5). Proposed changes include the reclassification of PG from the Impulse Control Disorders (ICDs) category to one of “Addiction and Related Disorders” (1) and obsessive-compulsive disorder (OCD) from the anxiety disorder category to one of obsessive-compulsive spectrum disorders (OCSDs) (6), where ICDs characterized by excessive shopping, internet use, or sexual behaviour could be included (7). Emerging from these proposed changes is an increasing focus on addiction and compulsion in the consideration of ICDs within the new nomenclature. Here we examine the potential overlap of compulsivity and addiction in relation to PG, substance use disorders (SUDs), and OCD along phenomenological and neurobiological lines, and discuss treatment implications.

Commonalities between definitions and criteria

A feature of substance dependence in the DSM-IV-TR is that “use is continued despite knowledge of having a persistent or recurrent physical or psychological problem” (8). The term addiction avoids confusion relating to non-addictive forms of dependence (e.g., as observed in people taking beta-adrenergic antagonists for hypertension). With components related to diminished self-control and craving (9), addiction involves compulsive drug use despite adverse consequences (10), suggesting addictions are not limited to drug use (11;12). Similar to drug addictions, PG can include repeated unsuccessful efforts to control, cut back, or stop gambling; feeling restless or irritable when attempting to cut down or stop gambling; and diminished ability to resist an impulse to gamble despite serious or adverse consequences of the gambling behaviours (8).

Compulsivity in OCD involves performing unpleasantly repetitive acts in a habitual manner to prevent perceived negative consequences, leading to functional impairment (13;14;15). The traditional psychopathology perspective associates compulsive behaviours to obsessions, cognitions which as whole are characterized by unrelenting doubts about one’s own perceptions and behaviours, hesitation, feelings of incompleteness and overestimation of risk. Such features are proposed to have their roots in personality, the so-called anankastic trait. The perennial nature of the trait would answer for the recurrent need to repeat specific behaviours to domesticate an eternal subjective disquiet, thus delineating a compulsivity construct (16). Parallels in phenomenology related to OCD, ICDs and substance addictions may involve engagement in seemingly compulsive behaviours to prevent or reduce distress (8), anxiety or stress prior to participation in the behaviours, and relief during and following performance of the behaviours (9).

Phenomenological aspects of compulsivity

a. Is there a motivational shift?

Several models of addiction conceptualize a progression from impulsivity to compulsivity, transitioning from initial positive reinforcement motivations to later negative reinforcement and automaticity mechanisms (9;1721). A protracted withdrawal syndrome may occur, generating motivational aspects of dependence, through negative emotional states (e.g., dysphoria, anxiety, irritability) when access to the drug or addictive behaviour is prevented. This negative affective state may contribute to compulsivity through negative reinforcement (9;20;22).

b. How distinct is the ego-syntonic/ego-dystonic dichotomy?

While there may be similar compulsive features in PG, OCD, and substance addiction, there are also differences. Substance and behavioural addictions like PG have been described as ego-syntonic, meaning they are often preceded by feelings of “pleasure, gratification, or relief at the time of committing the act” (8). In OCD, compulsive behaviours are often completed to suppress or neutralize thoughts and reduce tension and anxiety related to obsessions (8). These compulsions are typically considered ego-dystonic in nature. Thus, the motivations underlying compulsive behaviours in addictions and OCD may differ. However, addictive behaviours may become less ego-syntonic and more ego-dystonic over time, as the behaviour or effects of the substance becomes less pleasurable and more habitual or compulsive (9;20;2224). Similarly, reference to the compulsions in OCD as integrally “unpleasant” may not always be the case, as in childhood OCD, or the relief individuals may obtain after “cleaning just right” or the satisfaction attached to arranging until “mission accomplished” (25).

c. Tolerance and Withdrawal

The occurrence of tolerance may be another similarity between substance addiction, PG, and OCD, with a drive to increase the intensity of the repetitive behaviour over time (26;27). An urge or craving while abstaining from the behaviours may have similarity with cravings during drug withdrawal in substance addictions (1). The transition of drug use to addiction has also been considered with respect to neuroplasticity, where with repeated exposure to drugs of abuse an incentive salience state “wanting,” linked to compulsive use, replaces a “liking” or hedonic response (28).

Neurobiological underpinnings of compulsivity

a. Neurotransmitters

Multiple neurotransmitter systems contribute to substance addiction and PG, many of which are implicated in OCD; however, data suggest differences in the nature of the involvement of these systems in PG and OCD (23).

Serotonin (5-HT) contributes to behavioural inhibition and dopamine (DA) to learning, motivation, and the salience of stimuli, including rewards (29). Pharmacological challenges of 5-HT and dopamine systems (3034) suggest differences in the nature of the involvement of these systems in OCD as compared to PG and SUDs. Following a challenge with a serotonergic agonist like meta-chlorophenyl piperazine (m-CPP), OCD patients report an exacerbation of OC symptoms (33). Individuals with PG are more likely to report a euphoric or “high” response to m-CPP, similar to responses seen in alcohol dependent subjects (31).

b. Neurocircuitry

Neuroimaging data support a shared neurocircuitry of behavioral and substance addictions that appears differentially involved in OCD (20). Frontostriatal circuitry contributes to impulsive choice in substance addiction (18) and PG (35;36). Dysfunction of striato-thalamo-cortical circuitry, implicated in perseverative behaviours, may account for compulsive drug use in addiction (37).

Frontal–striatal circuits are implicated in OCD, ICDs in Parkinson’s disease (PD), and cocaine-seeking behaviours (38). In one model (38), a ventral prefrontal system concerned with emotive factors interacts with a dorsal prefrontal executive functioning system. In ICDs in PD, an imbalance between limbic and motor cortical systems, in part related to PD pathology and/or the DA replacement therapies used to treat the disorder, may exist (39). In drug addiction, an imbalance of the ventral and motor systems may be flexible in time, moving from involvement of ventral to dorsal circuitry (4042).

Cravings in substance and behavioral addictions have been associated with diminished ventral striatal activation (43), similar to findings during reward processing or simulated gambling in PG and alcoholism (44;45). Gambling task participation may elicit greater DA release in the ventral striatum in individuals with PD and PG than in individuals with PD alone (46), a response similar to that elicited by drugs or drug-associated cues in drug-addicted individuals (47) or in PD subjects who excessively take DA replacement drugs (48). Increased activation of frontostriatal circuitry has been observed following cue exposure in OCD (49), whereas diminished activation has been seen in PG (50), highlighting the need for concurrent investigation of PG, OCD, drug dependent and control subjects (23).

Koob and Volkow (9) argue that impulsivity dominates the early stages of addiction, and impulsivity combined with compulsivity dominates the later stages. They propose three stages of the addiction cycle: ‘binge/intoxication’, ‘withdrawal/negative affect’, and ‘preoccupation/anticipation’ (craving). In their model, the ventral tegmental area and ventral striatum contribute substantially to the binge/intoxication stage, the extended amygdala (including regions of amygdala, stria terminalis and nucleus accumbens) contributes substantially to the withdrawal/negative affect stage, and the preoccupation/anticipation stage involves a widely distributed network involving the orbitofrontal cortex–dorsal striatum, prefrontal cortex, basolateral amygdala, and hippocampus. The insula contributes to craving, the cingulate gyrus, dorsolateral prefrontal, and inferior frontal cortices to poor inhibitory control, and a protracted withdrawal syndrome with a negative affect state to compulsivity (9;22).

Consideration of protracted withdrawal in PG is warranted as psychological withdrawal has been reported in PG (1;51). Additionally, gambling in response to emotional dysregulation (24) and coping with stress have been cited as precedents of engaging in PG (52). Similarly, drug-taking in drug addiction and compulsive behaviours in OCD may be performed to reduce distress (8).

Lubman et al. (53) caution, that while there are similarities in clinical features and behavioural deficits associated with inhibitory control in both addiction and OCD, functional activity within inhibitory regions is markedly dissimilar, reflecting differences in core cognitive processes relevant to each disorder (5356). An under-activity of the inhibitory system in addiction may be associated with limited future regard and diminished ability to resist engaging in drug-related behaviours, whereas in OCD, the system may be over-active, perhaps because individuals are overly concerned about future consequences (53).

c. Genetic vulnerability and endophenotypes

Candidate gene studies of PG suggest links to SUDs and poor inhibitory control (23). Some but not other studies have implicated the Taq-A1 polymorphism of the gene encoding the DA D2 receptor (5759). Variants of the 5HT transporter gene have been implicated in both OCD and PG, but the nature of the associations differ (23), with the long allele found in association with OCD and the short allele found in association with PG (60;61).

In support of OCSDs, a cluster analysis conducted in patients with OCD identified 3 separate clusters (62). The clusters were termed: reward deficiency (including trichotillomania, Tourette’s disorder, pathological gambling, and hypersexual disorder); impulsivity (including compulsive shopping, kleptomania, eating disorders, self-injury, and intermittent explosive disorder); and somatic (including body dysmorphic disorder and hypochondriasis). None were associated with any particular genetic variant studied. Future genetic investigations should consider behavioral dimensions (compulsivity and impulsivity) and endophenotypes (63). Endophenotypes have the potential to measure objective trait markers that are either simpler to assess than complex phenotypic behavioral diseases or may represent constructs more closely aligned with biological underpinnings of psychiatric disorders (64). Because endophenotype research in psychiatry is relatively new, limited data are available (65).

An abnormally reduced activation of several cortical regions, including the orbitofrontal cortex during reversal learning in OCD patients and their clinically unaffected close relatives, has been identified. In a study assessing inhibitory controlprocesses, OCD probands and unaffectedfirst-degree relatives showed cognitiveinflexibility (extradimensional set shifting) and motor impulsivity(stop-signal reaction times). These deficits may represent endophenotypesfor OCD and related conditions (65;66).

In a motor inhibition paradigm (the stop-signal task – SST), both OCD patients and their unaffected first-degree relatives exhibited impaired motor inhibitory control, indexed by prolonged latency of the stop signal reaction time (SSRT), and longer latency was associated with both decreased gray-matter volume in the orbitofrontal cortex and right inferior frontal cortex (areas conventionally associated with OCD and SST activation, respectively) and increased gray-matter volume in areas of the striatum, cingulate, and parietal cortex (67). These results argue for the first structural MRI endophenotype mediating familial, and possibly genetic, risk for OCD-related impulsivity. Data suggest that such an endophenotype may also be relevant to PG and SUDs (24).

Complementary dimensions of compulsivity

a. Psychological measures

Individuals with OCD score high on measures of harm avoidance (68;68), whereas those with PG more closely approximate those with SUDs, scoring high on measures of impulsivity and novelty seeking (20;50;69). However, some individuals with OCD display high levels of cognitive impulsiveness (70), and individuals with PG or OCD have demonstrated high levels of both impulsivity and harm avoidance, suggesting a complex relationship between impulsivity and compulsivity (23;71). Within OCSDs, Hollander and Wong (72) proposed an organizing axis (the Impulsive-Compulsive spectrum) in which psychiatric disorders lie along a spectrum with OCD at the compulsivity extreme and antisocial personality disorder at the impulsive extreme. However, the co-occurrence of impulsivity and compulsivity traits in several addictive disorders challenges this uni-dimensional model. A study of PG and OCD (71) proposed unfolding the Impulsive-Compulsive spectrum into two orthogonal dimensions, yielding three psychopathological domains: predominantly impulsive, predominantly compulsive (OCD), and impulsive-compulsive (PG).

Decision-making is relevant to PG, OCD, and SUDs (23). Similar differences in decision-making reflecting a propensity to make disadvantageous choices during gambling task performance have been found between control subjects and those with PG (73), OCD (74), and SUDs (75). However, other studies have found decision-making to be intact in OCD despite impairment on other tasks (76;77). The lack of convergence of these findings may reflect the heterogeneity of OCD, and further research is needed investigating compulsivity and decision-making.

b. Co-occurring disorders

Clinical and community samples indicate that PG co-occurs with multiple axis I and II disorders, with particularly strong associations with SUDs (7881). Unfortunately, diagnostic assessments of OCD have not been consistently obtained. In the St. Louis Epidemiologic Catchment Area (ECA) study, whereas elevated odds ratios (ORs) were observed between problem/pathological gambling and SUDs, a non-elevated OR of 0.6 was observed between problem/pathological gambling and OCD (82).

Although PG and OCD might not have a strong connection, they share comorbidities. In the National Comorbidity Survey Replication, a subsample of 2073 respondents was assessed for OCD (83). More than one quarter of respondents reported experiencing lifetime obsessions or compulsions, but only small proportions of respondents met DSM-IV criteria for lifetime (2.3%) or 12-month (1.2%) OCD. OCD was associated with substantial comorbidity, with the strongest associations with internalizing (anxiety and mood) disorders and elevated odds for ICDs and SUDs. Together, these findings suggest the need for measures of OCD, PG, and other substance and behavioural addictions in population surveys and further investigation of their relationships.

Response to treatment

a. Pharmacotherapies

Although no drug is formally indicated for PG, three main classes have been investigated: opioid antagonists, mood stabilizers, and serotonin reuptake inhibitors (SRIs) (84;85). Opioid antagonists such as naltrexone reduce drinking frequency and likelihood of relapse to heavy drinking (86;87). Opioid antagonists also appear efficacious in the treatment of PG (1;8890). As response to opioid antagonist treatment appears particularly robust amongst individuals with a family history of alcoholism (91), a treatment-relevant addiction-related endophenotype, perhaps related to craving or urges, is suggested.

The treatment-related similarities between PG and SUDs constrast with OCD findings. Naltrexone does not influence OCD severity (92) and may exacerbate symptoms (93;94). Mood stabilizers like lithium may be helpful in treating PG (9597) but not OCD (98). Antipsychotic drugs antagonizing DA D2-like receptors (haloperidol, risperidone and olanzapine) have shown efficacy as augmenting agents in OCD (99), but have demonstrated negative findings in placebo-controlled trials in PG (100102) and increase motivations to gamble in PG (103).

SRIs are indicated for treating OCD (99) but have had mixed results for PG and SUDs (23). Some randomized control trials have found fluvoxamine and paroxetine to be superior to placebo in the treatment of PG (104;105), and others have not (106;107). Differential effects of pharmacotherapy on PG suggest targeting co-occurring disorders, such as anxiety (108), when treating PG (79;109), and concurrent decreases in both PG and the co-occurring domains have been observed (96;108).

A double-blind, placebo-controlled, counterbalanced study of an atypical stimulant (modafinil) in PG suggested two subgroups (103). Subjects with high impulsivity showed a decrease in motivation to gamble, risky decision-making, impulsivity, and responses to gambling-related lexical stimuli. Those with low impulsivity showed increased scores on all these measures, suggesting a bidirectional effect of modafinil that differentiates between high and low impulsive individuals with PG. This finding suggests heterogeneity in PG, which could explain seemingly conflicting results in clinical trials. Other data suggest that impulsivity may represent an important treatment target in PG (110;111). Emerging data also suggest roles for glutamatergic therapies in the treatment of OCD, PG, and SUDs (99;112;113), possibly through targeting compulsivity-related measures (e.g., cognitive inflexibility) (114), although results should be interpreted cautiously.

b. Behavioural Interventions

Behavioral therapies efficacious in treating SUDs may also be helpful for PG and OCD (115;116). Behavioural and motivational therapies, including Motivational Interviewing (MI) and Cognitive Behaviour Therapy (CBT) have been shown to be effective in treating SUDs and PG (85;117120). Attendance in Gamblers Anonymous (GA), modeled after Alcoholics Anonymous (AA), has been associated with better outcome for people participating in professional gambling treatment (121). OCD has been typically treated through exposure/response prevention strategies (122;123), and theoretically similar imaginal desensitization approaches have support in PG (124127).

Summary and Conclusions

Significant overlap exists between PG and SUDs with compulsivity representing a potentially important endophenotype. Although OCD and addictions may share some similarities, they appear neurobiologically different, have lower than expected comorbidity rates and differ with respect to responses to treatments (128). However, like impulsivity, compulsivity as an endophenotypic construct is important to examine in future studies of ICDs, SUDs and OCD (42;129;130).

Regarding the putative behavioural addictions, PG may be the only disorder with enough existing data to progress with classification as an addiction (1). Behavioural addictions represent an important focus of future research. Behavioural addictions may be similar to or different from each other at phenotypical and neurobiological levels with existing data suggesting both (131). It is likely that as with OCD and other psychiatric disorders, each behavioural addiction will represent a heterogeneous disorder (132;133). Such heterogeneity should be recognized while investigating the precise categorizations of the disorders and the development of optimally effective prevention and treatment strategies. Neurobiological advances may help understand heterogeneities and guide treatment development. Cognitive and behavioral approaches mindful of specific symptom clusters and recognizing the symptomatic evolution of the impulsivity-compulsivity constructs may lead to enhanced effectiveness. Recent models of impulsivity suggest the construct is not uni-dimensional (134;135). Compulsivity is likely to be multi-dimensional, with components reflecting motivationally driven, repetitive performance of behaviors. Compulsivity, like impulsivity, may represent an important endophenotype for ICDs, SUDs and OCD (42;129;130. As endophenotype represent intermediary constructs between complex disorders and genotypes, they may track more closely to biological constructs and be improved targets for prevention and treatment interventions.


This paper was conceived with the help of a travel grant funded by the Alberta Gaming Research Institute and in part supported by NIH grants R01 DA019039, R01 DA020908, RL1 AA017539, RC1 DA028279, and P20 DA027844, the VA VISN1 MIRECC, and the National Center for Responsible Gaming and its Institute for Research on Gambling Disorders.


Concise Statement: The involvement of compulsivity in impulse control disorders (particularly pathological gambling), obsessive-compulsive disorder and substance addictions is examined. While the endophenotypic construct of impulsivity has been investigated and described with respect to these disorders, that of compulsivity has been less well-studied. Neurobiological and clinical implications are discussed.


Declaration of Interest:

Dr. Nady el-Guebaly has no financial conflict of interest to report with respect to the content of this manuscript.

Tanya Mudry has no financial conflict of interest to report with respect to the content of this manuscript.

Dr. Zohar has received research funding and speaking fees from Lundbeck as well as research funding and consultancy fees from Servier.

Dr. Tavares has received research support from Cristalia, Roche, and Sandoz in his role as President of Brazil’s National Association on Pathological Gambling and Other Impulse Control Disorders.

Dr. Potenza has received research support from the Mohegan Sun Casino, the National Center for Responsible Gaming and its affiliated Institute for Research on Gambling Disorders (both gambling industry funded organisations); has consulted for and advised Boehringer Ingelheim; has consulted for and has financial interests in Somaxon; and Forest Laboratories, Ortho-McNeil, Oy-Control/Biotie, Glaxo-SmithKline and Psyadon pharmaceuticals.

Reference List

1. Grant JE, Potenza MN, Weinstein A, Gorelick DA. Introduction to behavioral addictions. The American Journal of Drug and Alcohol Abuse. 2010;35(5):233–41. [PMC free article] [PubMed]
2. Wareham JD, Potenza MN. Pathological gambling and substance use disorders. The American Journal of Drug and Alcohol Abuse. 2000;36(5):242–7. [PMC free article] [PubMed]
3. el-Guebaly N, Mudry T. Problematic Internet use and the diagnostic journey. World Psychiatry. 2010;9(2):93–4. [PMC free article] [PubMed]
4. Holden C. Behavioral Addictions Debut in Proposed DSM-V. Science. 2010 Feb 19;327(5968):935. [PubMed]
5. American Psychiatric Association. DSM-5: The future of psychiatric diagnosis. DSM-5 development website. 2010 Nov 26; Available from: URL:
6. Hollander E, Benzaquen SD. The obsessive-compulsive spectrum disorders. International Review of Psychiatry. 1997;9:99–110.
7. Lejoyeux M, Weinstein A. Compulsive Buying. The American Journal of Drug and Alcohol Abuse. 2010;36(5):248–53. [PubMed]
8. American Psychiatric Association. Diagnostic and statistical nanual of mental disorders. Arlington, VA: American Psychiatric Association; 2000. IV-TR ed.
9. Koob GF, Volkow ND. Neurocircuitry of addiction. Neuropharmacology. 2010;35:217–38. [PMC free article] [PubMed]
10. O’Brien CP, Volkow N, Li TK. What’s in a word? Addiction versus dependence in DSM-V. Am J Psychiatry. 2006;163:764–765. [PubMed]
11. Holden C. ‘Behavioral’ addictions: Do they exist? Science. 2001;294:980–982. [PubMed]
12. Holden C. Psychiatry. Behavioral addictions debut in proposed DSM-V. Science. 2010;327:935. [PubMed]
13. Hollander E, Cohen LJ. Impulsivity and compulsivity. Washington, D.C: American Psychiatric Press; 1996.
14. Chamberlain SR, Fineberg NA, Blackwell AD, Robbins TW, Sahakian BJ. Motor inhibition and cognitive flexibility in obsessive-compulsive disorder and trichotillomania. American Journal of Psychiatry. 2006;163:1282–4. [PubMed]
15. World Health Organization. International Classification of Diseases (10th Revision) World Health Organization website. 2010 Nov 26; Available from: URL:
16. Rasmussen SA, Eisen JL. Epidemiological and clinical features of obsessive-compulsive disorder. In: Jenike MA, Baer LB, Minichielo, editors. Obsessive-Compulsive Disorders: Theory and Management. 2. Chicago, I.L: Year Book Medical; 1990. pp. 39–60.
17. Koob GF. Brain stress systems in the amygdala and addiction. Brain Research. 2009;1293:61–75. [PMC free article] [PubMed]
18. Everitt B, Robbins TW. Neural systems of reinforcement for drug addiction: From actions to habits to compulsion. Nature Neuroscience. 2005;8:1481–9. [PubMed]
19. Zohar J, Fostick L, Juven-Wetzler E. Obsessive compulsive disorder. In: Belder M, Andreasen N, Lopez-Ibor J, Geddes J, editors. New Oxford Textbook of Psychiatry. 2. New York: Oxford University Press; 2009. pp. 765–73.
20. Brewer JA, Potenza MN. The neurobiology and genetics of impulse control disorders: Relationships to drug addictions. Biochemical Pharmacology. 2008;75:63–75. [PMC free article] [PubMed]
21. Koob GF, Le Moal M. Drug abuse: Hedonic homeostatic dysregulation. Science. 1997;278:52–8. [PubMed]
22. Koob GF, Le Moal M. Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology. 2001;24:97–129. [PubMed]
23. Potenza MN, Koran LM, Pallanti S. The relationship between impulse-control disorders and obsessive-compulsive disorder: a current understanding and future research directions. Psychiatry Research. 2009;170(1):22–31. [PMC free article] [PubMed]
24. de Castro V, Fong T, Rosenthal RJ, Tavares H. A comparison of craving and emotional states between pathological gamblers and alcoholics. Addictive Behaviors. 2007;32:1555–64. [PubMed]
25. Zohar J, Hollander E, Stein DJ, Westenberg HG. The Cape Town Consensus Group. Consensus statement CNS Spectrums: The International Journal of Neuropsychiatric Medicine. 2007;12(2 Suppl 3):59–63. [PubMed]
26. Blanco C, Moreyra P, Nunes EV, Saiz-Ruiz J, Ibanez A. Pathological gambling: Addiction or compulsion? Seminars in Clinical Neuropsychiatry. 2001;6(3):167–76. [PubMed]
27. Grant JE, Brewer JA, Potenza MN. The neurobiology of substance and behavioral addictions. CNS Spectrums. 2006;11(12):924–30. [PubMed]
28. Robinson TE, Berridge KC. The neural basis of drug craving: An incentive-sensitization theory of addiction. Brain Research Reviews. 1993;18(3):247–91. [PubMed]
29. Fineberg NA, Potenza MN, Chamberlain SR, Berlin HA, Menzies L, Bechara A, et al. Probing compulsive and impulsive behaviors, from animal models to endophenotypes: A narrative review. Neuropsychopharmacology. 2010;35(3):591–604. [PMC free article] [PubMed]
30. Chambers RA, Taylor JR, Potenza MN. Developmental neurocircuitry of motivation in adolescence: A critical period of addiction vulnerability. American Journal Psychiatry. 2003;160:1041–1052. [PMC free article] [PubMed]
31. Potenza MN, Hollander E. Pathological gambling and impulse control disorders. In: Davis KL, Charney D, Coyle JT, Nemeroff C, editors. Neuropsychopharmacology: The 5th generation of progress. Baltimore, MD: Lippincott Williams and Wilkins; 2002. pp. 1725–41.
32. Pauls DL, Mundo E, Kennedy JL. The pathophysiology and genetics of obsessive-compulsive disorder. In: Davis K, Charney D, Coyle JT, Nemeroff C, editors. Neuropsychopharmacology: The 5th generation of progress. Baltimore, MD: Lippincott Williams and Wilkins; 2002. pp. 1609–19.
33. Gross-Isseroff R, Cohen R, Sasson Y, Voet H, Zohar J. Serotonergic dissection of obsessive compulsive symptoms: a challenge study with m-chlorophenylpiperazine and sumatriptan. Neuropsychobiology. 2004;50(3):200–5. [PubMed]
34. Denys D, de Geus F, van Megan HJ, Westenberg HG. A double-blind, randomized, placebo-controlled trial of quetiapine addition in patients with obsessive-compulsive disorder refractory to serotonin reuptake inhibitors. Journal of Clinical Psychiatry. 2004;65:1040–8. [PubMed]
35. Potenza MN. Should addictive disorders include non-substance-related conditions? Addiction. 2006;101(Suppl):142–51. [PubMed]
36. Williams WA, Potenza MN. The neurobiology of impulse control disorders. Revista Brasileira de Psiquiatria. 2008;30(Suppl 1):S24–S30. [PMC free article] [PubMed]
37. Volkow ND, Fowler JS. Addiction, a disease of compulsion and drive: Involvement of the orbitofrontal cortex. Cerebral Cortex. 2000;10(3):318–25. [PubMed]
38. van den Heuvel OA, der Werf YD, Verhoef KM, de Wit S, Berendse HW, Wolters ECh, et al. Frontal-striatal abnormalities underlying behaviours in the compulsive-impulsive spectrum. Journal of Neurological Science. 2010;289(1–2):55–9. [PubMed]
39. Leeman RF, Potenza NM. Impulse control disorders in Parkinson’s disease: clinical characteristics and implications. Neuropsychiatry. 2011;1(2):133–147. [PMC free article] [PubMed]
40. Everitt BJ, Robbins TW. Neural systems of reinforcement for drug addiction: From actions to habits to compulsion. Nature Neuroscience. 2005;8:1481–9. [PubMed]
41. Brewer JA, Potenza MN. The neurobiology and genetics of impulse control disorders: relationships to drug addictions. Biochemical Pharmacology. 2008;75:63–75. [PMC free article] [PubMed]
42. Dalley JW, Everitt BJ, Robbins TW. Impulsivity, compulsivity, and top-down cognitive control. Neuron. 2011;69:680–694. [PubMed]
43. Potenza MN. The neurobiology of pathological gambling and drug addiction: An overview and new findings. Philosophical Transactions: Biological Sciences. 2008;363(1507):3181–9. [PMC free article] [PubMed]
44. Reuter J, Raedler T, Rose M, Hand I, Glascher J, Buchel C. Pathological gambling is linked to reduced activation of the mesolimbic reward system. Nature Neuroscience. 2005;8(2):147–8. [PubMed]
45. Wrase J, Kahnt T, Schlagenhauf F, Beck A, Cohen MX, Knutson B, et al. Different neural systems adjust motor behavior in response to reward and punishment. Neuroimage. 2007;36(4):1253–62. [PubMed]
46. Steeves TD, Miyasaki J, Zurowski M, Lang AE, Pellecchia G, VanEimeren T, et al. Increased striatal dopamine release in Parkinsonian patients with pathological gambling: A [11C] raclopride PET study. Brain. 2009;132:1376–85. [PMC free article] [PubMed]
47. Bradberry CW. Cocaine sensitization and dopamine mediation of cue effects in rodents, monkeys, and humans: Areas of agreement, disagreement, and implications for addiction. Psychopharmacology. 2007;191:705–17. [PubMed]
48. Evans AH, Pavese N, Lawrence AD, Tai YF, Appel S, Doder M, et al. Compulsive drug use linked to sensitized ventral striatal dopamine transmission. Annals of Neurology. 2006;59(5):852–8. [PubMed]
49. Mataix-Cols D, van den Heuvel OA. Common and distinct neural correlates of obsessive-compulsive disorder and related disorders. Psychiatric Clinics of North America. 2006;29:391–410. [PubMed]
50. Potenza MN, Leung HC, Blumberg HP, Peterson BS, Fulbright RK, Lacadie CM, et al. An fMRI stroop task study of ventromedial prefrontal cortical function in pathological gamblers. American Journal of Psychiatry. 2003;160(11):1990–4. [PubMed]
51. Rosenthal RJ, Lesieur HR. Self-reported withdrawal symptoms and pathological gambling. American Journal on Addictions. 1992;1(2):150–4.
52. Lightsey OR, Hulsey CD. Impulsivity, coping, stress, and problem gambling among university students. Journal of Counseling Psychology. 2002;49(2):202–11.
53. Lubman DI, Yucel M, Pantelis C. Addiction, a condition of compulsive behaviour? Neuroimaging and neuropsychological evidence of inhibitory dysregulation. Addiction. 2004;99(12):1491–502. [PubMed]
54. Nordahl TE, Benkelfat C, Semple WE, Gross M, King AC, Cohen RM. Cerebral glucose metabolic rates in obsessive compulsive disorder. Neuropsychopharmacology. 1989;2:23–8. [PubMed]
55. Volkow ND, Wang G-J, Overall JE, Hitzemann R, Fowler JS, Pappas NR, et al. Regional brain metabolic response to lorazepam in alcoholics during early and late alcohol detoxification. Alcohol and Clinical Experimental Research. 1997;21:1278–84. [PubMed]
56. Maruff P, Purcell R, Pantelis C. Obsessive compulsive disorder. In: Harrison JE, Owen AM, editors. Cognitive deficits in brain disorders. London: Martin Dunitz; 2002. pp. 249–72.
57. Comings DE. The molecular genetics of pathological gambling. CNS Spectrums. 1998;3(6):20–37.
58. Rodriguez-Jimenez R, Avila C, Ponce G, Ibanez MI, Rubio G, Jimenez-Arriero MA, et al. The Taq1A polymorphism linked to the DRD2 gene is related to lower attention and less inhibitory control in alcoholic patients. European Psychiatry. 2006;21:66–9. [PubMed]
59. Lobo DS, Souza RP, Tong RP, Casey DM, Hodgins DC, Smith GJ, et al. Association of functional variants in the dopamine D2- like receptors with risk for gambling behaviors in healthy Caucasian subjects. Biological Psychology. 2010;85:33–7. [PubMed]
60. Ibanez A, Blanco C, de Castro IP, Fernandez-Piqueras J, Saiz-Ruiz J. Genetics of pathological gambling. Journal of Gambling Studies. 2003;19:11–22. [PubMed]
61. Hemmings SMJ, Stein DJ. The current status of association studies in obsessive-compulsive disorder. Psychiatric Clinics of North America. 2006;29:411–44. [PubMed]
62. Lochner C, Hemmings SMJ, Kinnear CJD, Niehaus J, Nel DG, Corfield VA, et al. Cluster analysis of obsessive-compulsive spectrum disorder in patients with obsessive-compulsive disorder: clinical and genetic correlates. Comprehensive Psychiatry. 2005;46:14–9. [PubMed]
63. Baca-Garcia E, Salgado BR, Segal HD, Lorenzo CV, Acosta MN, Romero MA, et al. A pilot genetic study of the continuum between compulsivity and impulsivity in females: the serotonin transporter promoter polymorphism. Progress in Neuro-psychopharmacology & Biological Psychiatry. 2005;29(5):713–7. [PubMed]
64. Gottesman II, Gould TD. The endophenotype concept in psychiatry: etymology and strategic intentions. American Journal of Psychiatry. 2003;160:636–45. [PubMed]
65. Chamberlain SR, Menzies L, Hampshire A, Suckling J, Fineberg NA, del Campo N, et al. Orbitofrontal dysfunction in patients with obsessive-compulsive disorder and their unaffected relatives. Science. 2008;321:421–2. [PubMed]
66. Chamberlain SR, Fineberg NA, Menzies LA, Menzies LA, Blackwell AD, Bullmore ET, et al. Impaired cognitive flexibility and motor inhibition in unaffected first-degree relatives of patients with obsessive-compulsive disorder. American Journal of Psychiatry. 2007;164:335–8. [PMC free article] [PubMed]
67. Menzies L, Achard S, Chamberlain SR, Fineberg N, Chen CH, del Campo N, et al. Neurocognitive endophenotypes of obsessive-compulsive disorder. Brain. 2007;130(12):3223–36. [PubMed]
68. Anholt GE, Emmelkamp PM, Cath DC, van OP, Nelissen H, Smit JH. Do patients with OCD and pathological gambling have similar dysfunctional cognitions? Behaviour Research & Therapy. 2004;42(5):529–37. [PubMed]
69. Hollander E, Wong CM. Body dysmorphic disorder, pathological gambling, and sexual compulsions. Journal of Clinical Psychiatry. 1995;56(Suppl 4):7–12. [PubMed]
69. Blaszczynski A, Steel Z, McConaghy N. Impulsivity in pathological gambling: the antisocial impulsivist. Addiction. 1997;92:75–87. [PubMed]
70. Ettelt S, Ruhrmann S, Barnow S, Buthz F, Hochrein A, Meyer K, et al. Impulsiveness in obsessive-compulsive disorder: results from a family study. Acta Psychiatrica Scandinavica. 2007;115(1):41–7. [PubMed]
71. Tavares H, Gentil V. Pathological gambling and obsessive-compulsive disorder: Towards a spectrum of disorders of volition. Revista Brasileira de Psiquiatria. 2007;29(2):107–17. [PubMed]
72. Hollander E, Wong CM. Obsessive-compulsive spectrum disorders. J Clin Psychiatry. 1995;56(Suppl 4):3–6. [PubMed]
73. Cavedini P, Riboldi G, Keller R, D’Annucci A, Bellodi L. Frontal lobe dysfunction in pathological gambling. Biological Psychiatry. 2002;51:334–41. [PubMed]
74. Cavedini P, Riboldi G, D’Annucci A, Belotti P, Cisima M, Bellodi L. Decision making heterogeneity in obsessive-compulsive disorder: Ventromedial prefrontal cortex function predicts different treatment outcomes. Neuropsychologia. 2002;40:205–11. [PubMed]
75. Bechara A. Risky business: Emotion, decision-making, and addiction. Journal of Gambling Studies. 2003;19:23–51. [PubMed]
76. Chamberlain SR, Fineberg NA, Blackwell AD, Clark L, Robbins TW, Sahakian BJ. A neuropsychological comparison of obsessive-compulsive disorder and trichotillomania. Neuropsychologia. 2007;45:654–62. [PubMed]
77. Watkins LH, Sahakian BJ, Robertson MM, Veale DM, Rogers RD, Pickard KM, et al. Executive function in Tourette’s syndrome and obsessive compulsive disorder. Psychological Medicine. 2005;35:571–82. [PubMed]
78. Crockford DN, el-Guebaly N. Psychiatric comorbidity in pathological gambling: A critical review. Canadian Journal of Psychiatry. 1998;43:43–50. [PubMed]
79. Potenza MN. Impulse control disorders and co-occurring disorders: Dual diagnosis considerations. Journal of Dual Diagnosis. 2007;3:47–57.
80. Potenza MN, Xian H, Shah K, Scherrer JF, Eisen SA. Shared genetic contributions to pathological gambling and major depression in men. Archives of General Psychiatry. 2005;62(9):1015–21. [PubMed]
81. Petry NM, Stinson FS, Grant BF. Co-morbidity of DSM-IV pathological gambling and other psychiatric disorders: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Journal of Clinical Psychiatry. 2005;66:564–74. [PubMed]
82. Cunningham-Williams RM, Cottler LB, Compton WMI, Spitznagel EL. Taking chances: Problem gamblers and mental health disorders: Results from the St. Louis Epidemiologic Catchment Area study. American Journal of Public Health. 1998;88(7):1093–6. [PMC free article] [PubMed]
83. Ruscio AM, Stein DJ, Chiu WT, Kessler RC. The epidemiology of obsessive-compulsive disorder in the National Comorbidity Survey Replication. Molecular Psychiatry. 2010;15(1):53–63. [PMC free article] [PubMed]
84. Leung KS, Cottler LB. Treatment of pathological gambling. Current Opinion in Psychiatry. 2009;22(1):69–74. [PubMed]
85. Brewer JA, Grant JE, Potenza MN. The treatment of pathological gambling. Addictive Disorders and Their Treatment. 2008;7(1):1–13.
86. O’Malley SS, Jaffe AJ, Chang G, Schottenfeld RS, Meyer RE, Rounsaville B. Naltrexone and coping skills therapy for alcohol dependence: A controlled study. Archives of General Psychiatry. 1992;49:881–7. [PubMed]
87. Volpicelli JR, Alterman AI, Hayashida M, O’Brien CP. Naltrexone in the treatment of alcohol dependence. Archives of General Psychiatry. 1992;49(11):876–80. [PubMed]
88. Grant JE, Kim SW, Hartman BK. A double-blind, placebo-controlled study of the opiate antagonist naltrexone in the treatment of pathological gambling urges. Journal of Clinical Psychiatry. 2008;69(5):783–9. [PubMed]
89. Grant JE, Potenza MN, Hollander E, Cunningham-Williams R, Nurminen T, Smits G, et al. Multicenter investigation of the opioid antagonist nalmefene in the treatment of pathological gambling. American Journal of Psychiatry. 2006;163(2):303–12. [PubMed]
90. Kim SW, Grant JE, Adson DE, Shin YC. Double-blind naltrexone and placebo comparison study in the treatment of pathological gambling. Biological Psychiatry. 2001;49(11):914–21. [PubMed]
91. Grant JE, Kim SW, Hollander E, Potenza MN. Predicting response to opiate antagonists and placebo in the treatment of pathological gambling. Psychopharmacology (Berl) 2008;200:521–527. [PMC free article] [PubMed]
92. Revital A, Leah F, Ari G, Joseph Z. Naltrexone augmentation in OCD: A double-blind placebo-controlled cross-over study. Eur Neuropsychopharmacol. 2008;18(6):455–61. [PubMed]
93. Insel TR, Pickar D. Naloxone administration in obsessive-compulsive disorder: Report of two cases. American Journal of Psychiatry. 1983;140(9):1219–20. [PubMed]
94. Keuler DJ, Altemus M, Michelson D, Greenberg B, Murphy DL. Behavioral effects of naloxone infusion in obsessive-compulsive disorder. Biological Psychiatry. 1996;40(2):154–6. [PubMed]
95. Dannon PN, Lowengrub K, Gonopolski Y, Musin E, Kotler M. Topiramate versus fluvoxamine in the treatment of pathological gambling: A randomized, blind-rater comparison study. Clinical Neuropharmacology. 2005;28(1):6–10. [PubMed]
96. Hollander E, Pallanti S, Allen A, Sood E, Baldini RN. Does sustained-release lithium reduce impulsive gambling and affective instability versus placebo in pathological gamblers with bipolar spectrum disorders? American Journal of Psychiatry. 2005;162(1):137–45. [PubMed]
97. Pallanti S, Quercioli L, Sood E, Hollander E. Lithium and valproate treatment of pathological gambling: a randomized single-blind study. Journal of Clinical Psychiatry. 2002;63(7):559–64. [PubMed]
98. McDougle CJ, Price LH, Goodman WK, Charney DS, Heninger GR. A controlled trial of lithium augmentation in fluvoxamine-refractory obsessive-compulsive disorder: Lack of efficacy. Journal of Clinical Psychopharmacology. 1991;11(3):175–84. [PubMed]
99. Denys D. Pharmacotherapy of obsessive-compulsive disorder and obsessive-compulsive spectrum disorders. Psychiatric Clinics of North America. 2006;29(2):553–84. [PubMed]
100. Grant JE, Potenza MN. Impulse control disorders: Clinical characteristics and pharmacological management. Annals of Clinical Psychiatry. 2004;16(1):27–34. [PubMed]
101. Fong T, Kalechstein A, Bernhard B, Rosenthal R, Rugle L. A double-blind, placebo-controlled trial of olanzapine for the treatment of video poker pathological gamblers. Pharmacology, Biochemistry & Behavior. 2008;89(3):298–303. [PubMed]
102. McElroy SL, Nelson EB, Welge JA, Kaehler L, Keck PE., Jr Olanzapine in the treatment of pathological gambling: a negative randomized placebo-controlled trial. Journal of Clinical Psychiatry. 2008;69(3):433–40. [PubMed]
103. Zack M, Poulos CX. Effects of the atypical stimulant modafinil on a brief gambling episode in pathological gamblers with high vs. low impulsivity. Journal of Psychopharmacology. 2009;23(6):660–71. [PubMed]
104. Hollander E, DeCaria CM, Finkell JN, Begaz T, Wong CM, Cartwright C. A randomized double-blind fluvoxamine/placebo crossover trial in pathologic gambling. Biological Psychiatry. 2000;47(9):813–7. [PubMed]
105. Kim SW, Grant JE, Adson DE, Shin YC, Zaninelli R. A double-blind placebo-controlled study of the efficacy and safety of paroxetine in the treatment of pathological gambling. Journal of Clinical Psychiatry. 2002;63(6):501–7. [PubMed]
106. Blanco C, Petkova E, ez A, iz-Ruiz J. A pilot placebo-controlled study of fluvoxamine for pathological gambling. Annals of Clinical Psychiatry. 2002;14(1):9–15. [PubMed]
107. Grant JE, Kim SW, Potenza MN, Blanco C, Ibanez A, Stevens L, et al. Paroxetine treatment of pathological gambling: a multi-centre randomized controlled trial. International Clinical Psychopharmacology. 2003;18(4):243–9. [PubMed]
108. Grant JE, Potenza MN. Escitalopram treatment of pathological gambling with co-occurring anxiety: An open-label pilot study with double-blind discontinuation. International Clinical Psychopharmacology. 2006;21(4):203–9. [PubMed]
109. Hollander E, Kaplan A, Pallanti S. Pharmacological treatments. In: Grant JE, Potenza MN, editors. Pathological gambling: A clinical guide to treatment. Washington, DC: American Psychiatric Press; 2004. pp. 189–206.
110. Blanco C, Potenza MN, Kim SW, Ibáñez A, Zaninelli R, Saiz-Ruiz J, Grant JE. A pilot study of impulsivity and compulsivity in pathological gambling. Psychiatry Research. 2009;167:161–8. [PMC free article] [PubMed]
111. Potenza MN, Sofuoglu M, Carroll KM, Rounsaville BJ. Neuroscience of behavioral and pharmacological treatments for addictions. Neuron. 2011;69:695–712. [PMC free article] [PubMed]
112. Grant JE, Kim SW, Odlaug BL. N-Acetyl cysteine, a glutamate-modulating agent, in the treatment of pathological gambling: A pilot study. Biological Psychiatry. 2007;62(6):652–75. [PubMed]
113. Kalivas PW. The glutamate homeostasis hypothesis of addiction. Nature Reviews Neuroscience. 2009;10(8):561–72. [PubMed]
114. Grant JE, Chamberlain SR, Odlaug BL, Potenza MN, Kim SW. Memantine shows promise in reducing gambling severity and cognitive inflexibility in pathological gambling: A pilot study. Psychopharmacology (Berl) 2010;212:603–612. [PMC free article] [PubMed]
115. Miller WR, Leckman AL, Delaney HD, Tinkcom M. Long-term follow-up of behavioral self-control training. Journal of Studies on Alcohol. 1992;53(3):249–61. [PubMed]
116. Kadden RM, Litt MD, Cooney NL, Busher DA. Relationship between role-play measures of coping skills and alcoholism treatment outcome. Addictive Behaviors. 1992;17(5):425–37. [PubMed]
117. Sylvain C, Ladouceur R, Boisvert JM. Cognitive and behavioral treatment of pathological gambling: a controlled study. Journal of Consulting and Clinical Psychology. 1997;65:727–32. [PubMed]
118. Hodgins DC, Currie SR, el-Guebaly N. Motivational enhancement and self-help treatments for problem gambling. Journal of Clinical and Consulting Psychology. 2001;69:50–7. [PubMed]
119. Petry NM, Ammerman Y, Bohl J, Doersch A, Gay H, Kadden R, et al. Cognitive-behavioral therapy for pathological gamblers. Journal of Consulting & Clinical Psychology. 2006;74(3):555–67. [PubMed]
120. Grant JE, Potenza MN. Treatments for pathological gambling and other impulse control disorders. In: Gorman J, Nathan P, editors. A guide to treatments that work. Oxford, UK: Oxford University Press; 2007. pp. 561–77.
121. Petry NM. Gamblers anonymous and cognitive-behavioral therapies for pathological gamblers. Journal of Gambling Studies. 2005;21:27–33. [PubMed]
122. Hohagen F, Winkelmann G, Rasche R, Hand I, Konig A, Munchau N, et al. Combination of behaviour therapy with fluvoxamine in comparison with behaviour therapy and placebo. Results of a multicentre study. British Journal of Psychiatry. 1998;(Supplement 35):71–8. [PubMed]
123. Neziroglu F, Henricksen J, Yaryura-Tobias JA. Psychotherapy of obsessive-compulsive disorder and spectrum: Established facts and advances, 1995–2005. Psychiatric Clinics of North America. 2006;29(2):585–604. [PubMed]
124. Battersby M. The South Australian Statewide Gambling Therapy Service: Exposure as the model of therapy. Alberta Gaming Research Institute Conference; April 8–10, 2010; Banff, Alberta.
125. Oakes J, Battersby MW, Pols RG, Cromarty P. Exposure therapy for problem gambling via Videoconferencing: A case report. Journal of Gambling Studies. 2008;24(1):107–18. [PubMed]
126. Grant JE, Donahue CB, Odlaug BL, Kim SW, Miller MJ, Petry NM. Imaginal desensitisation plus motivational interviewing for pathological gambling: randomised controlled trial. British Journal of Psychiatry. 2009 Sep;195(3):266–7. [PMC free article] [PubMed]
127. Echeburua E, Baez C, Fernandez-Montalvo J. Comparative effectiveness of three therapeutic modalities in the psychological treatment of pathological gambling: Long-term outcome. Behavioural and Cognitive Psychotherapy. 1996;24:51–72.
128. Fineberg NA, Saxena S, Zohar J, Craig KJ. Obsessive-compulsive disorder: Boundary issues. CNS Spectrums. 2007;12(5):359–75. [PubMed]
129. Fineberg NA, Potenza MN, Chamberlain SR, Berlin HA, Menzies L, Bechara A, Sahakian BJ, Robbins TW, Bullmore ET, Hollander E. Probing compulsive and impulsive behaviors, from animal models to endophenotypes: A narrative review. Neuropsychopharmacology. 2010;35:591–604. [PMC free article] [PubMed]
130. Gottesman II, Gould TD. The endophenotype concept in psychiatry: Etymology and strategic intentions. Am J Psychiatry. 2003;160:636–45. [PubMed]
131. Voon V, Sohr M, Lang AE, Potenza MN, Siderowf AD, Whetteckey J, Weintraub D, Wunderlich GR, Stacy M. Impulse control disorders in parkinson disease: A multicenter case–control study. Annals of Neurology. 2011;69:1–11. [PubMed]
132. Milosevic A, Ledgerwood DM. The subtyping of pathological gambling: A comprehensive review. Clinical Psychology Review. 2010;30:988–998. [PubMed]
133. Ledgerwood DM, Petry NM. Subtyping pathological gamblers based on impulsivity, depression, and anxiety. Psychology of Addictive Behaviors. 2010;24:680–688. [PMC free article] [PubMed]
134. Meda SA, Stevens MC, Potenza MN, Pittman B, Gueorguieva R, Andrews MM, Thomas AD, Muska C, Hylton JL, Pearlson GD. Investigating the behavioral and self-report constructs of impulsivity domains using principal component analysis. Behav Pharmacol. 2009;20:390–9. [PMC free article] [PubMed]
135. Whiteside SP, Lynam DR, Miller JD, Reynolds SK. Validation of the UPPS impulsive behaviour scale: a four-factor model of impulsivity. Eur J Pers. 19:559–74.