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Review Article
Maladaptive Reward-Learning and Impulse Control Disorders in Patients with Parkinson’s Disease: A Clinical Overview and Pathophysiology Update
Jee-Young Lee1, Beom Seok Jeon2
Journal of Movement Disorders 2014;7(2):67-76.
Published online: October 30, 2014

1Department of Neurology, Seoul National University-Seoul Metropolitan Government Boramae Medical Center, College of Medicine, Seoul National University, Seoul, Korea

2Department of Neurology, Seoul National University Hospital, College of Medicine, Seoul National University, Seoul, Korea

Corresponding author: Jee-Young Lee, MD, PhD, Department of Neurology, Seoul National University-Seoul Metropolitan Government, Boramae Medical Center, 20 Boramaero 5-gil, Dongjak-gu, Seoul 156-707, Korea Tel: +82-2-870-2476 Fax: +82-2-831-2826 E-mail:
• Received: September 3, 2014   • Revised: September 14, 2014   • Accepted: September 14, 2014

Copyright © 2014 The Korean Movement Disorder Society

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Impulse control disorders (ICD) in Parkinson’s disease (PD) are a disabling non-motor symptom with frequencies of 13–35% among patients receiving dopamine replacement therapy. ICD in PD is strongly associated with dopaminergic drug use, especially non-ergot dopamine agonists (DA). However, individual susceptibility and disease-related neural changes are also important contributors to the development of ICD. Discrepancies between nigrostriatal and mesolimbic dopaminergic degeneration and non-physiological administration of dopaminergic drugs may induce abnormal ’hyperstimulation’ of the mesolimbic system, which alters reward-learning behaviors in PD patients. In addition, DA can make patients more impulsive during decision-making and seek risk-taking behaviors. DA intake is also related to the biased representation of rewards. Ultimately, loss of negative feedback control due to dysfunctional frontostriatal connections is necessary for the establishment of ICD in PD. The subsequent behavioral and neural changes are affected by PD treatment and disease progression; thus, proper treatment guidelines for physicians are needed to prevent the development of ICD. Future studies aimed at producing novel therapeutics to control the risk factors for ICD or treat ICD behaviors in PD are warranted. This review summarizes recent advances from epidemiological and pathophysiological studies on ICD in PD. Management principles and limitations of current therapeutics are briefly discussed.
Parkinson’s disease (PD) is the second most common neurodegenerative disorder in the elderly population. Clinical features of PD are characterized by a progressive motor syndrome of resting tremor, rigidity, bradykinesia, and postural instability; however, it is often accompanied by a variety of non-motor symptoms, including sleep, sensory, psychiatric, cognitive, and autonomic disturbances. Although PD was first described in 1817, levodopa was introduced in late 1960s and since this time, chronic dopamine replacement therapy has become the gold standard medical treatment of PD.
In spite of the remarkable anti-parkinsonian efficacy of levodopa in PD, abnormal psychiatric and behavioral symptoms were observed in PD patients soon after its introduction [1-7]. Typically those symptoms included psychosis, delusion, paranoia, hypomania, mood cycling, anxiety, aggression, impulsive behavior, hypersexuality, agitation, and restlessness [8]. Some patients were engaged in meaningless repetitive tasks which resembles the “punding” described in cocaine abusers [7]. Others exhibited mood swings based on the medication-ON and -OFF states or showed compulsive drug seeking behaviors [9]. Giovannoni et al. [9]. described these behavioral disturbances as a hedonistic homeostatic dysregulation syndrome, which was later to be re-defined as dopamine dysregulation syndrome (DDS) [10]. These kinds of behaviors eventually led to financial and social problems and were disastrous to patients and their families [10]. Impulse control disorders (ICD) are one of these psychiatric and behavioral disturbances in PD. Its relationship to dopaminergic drugs has been recognized after numerous reports on pathological gambling in PD patients taking dopamine agonists beginning in the 1990s [11,12]. ICD-like behaviors in PD patients also included compulsive shopping, hypersexuality, and binge eating that met the DSM-IV criteria of ICD [13]. Systematic surveys have shown that all of these behaviors were highly prevalent in PD patients when compared with the general population [14,15]. The prevalence of ICD in PD patients taking drugs is approximately 13.6% in North America [14] and 10.1% in South Korea [15]. Approximately one quarter of patients with ICD have two or more behaviors [14,15]. The prevalence of behavioral disturbances, including both compulsive drug use (DDS) and punding-like behaviors, is reported to be up to 15.5–35% in studies using the newly validated screening tool ‘QUIP’ for ICD in PD [16-19]. ICD often co-exists with DDS but can be present in isolation.
The characteristic features of ICD in PD are often related to simple actions that do not require complex cognitive thought processing. They are linked to immediate rewards and repetitive in nature with insuppressible internal urges. Thus, ICD-related behavioral disturbances in PD are currently not only considered to be confined to pathological gambling, shopping, hypersexuality, and binge eating but also include a broad spectrum of disorders that are obsessive compulsive in nature and related to impaired impulse control, such as kleptomania, trichotillomania and problematic Internet use [20]. Repetitive and compulsive behaviors, known as ‘punding’, can include habitual but non-goal oriented-behaviors, such as hobbyism, cleaning, repairing, compulsive writing, and categorizing information, artistic drawing, craft-making, singing, playing a musical instrument, playing cards, and fishing [21]. These behaviors often co-exist with ICD in PD patients. Another characteristic behavior is the excessive intake of levodopa beyond the required dose which is necessarily accompanied by drug-seeking behavior typically observed in drug addicts [21]. Daily levodopa intake exceeds 3000 or 4000 mg despite severe dyskinesia and DDS has been observed in nearly all cases [13]. Punding can be frequently observed in patients with excessive levodopa intake behavior [22], suggesting a shared pathophysiological mechanism for these compulsive motoric phenomenon [23]. Because of the rapid increase in knowledge about behavioral disturbances in PD, physicians and researchers can confuse terminologies. In general, ‘ICD’, ‘punding’, and ‘excessive intake of levodopa’ are terminologies focused on the specific type of behavioral disturbances, while ‘DDS’ indicates a clinically significant problematic state that is caused by a ‘levodopa addiction’. Predictive factors for DDS and punding in PD remain largely unknown, and the management of these symptoms remains a challenge. Unlike DDS and punding, there have been recent advances in our understanding of the risk factors and the pathophysiology for ICD; thus, this review focuses on the ICD in PD.
Other than dopaminergic drug therapy, epidemiologic studies have reported that a younger age at onset, left sided dominance of parkinsonian symptoms, and male sex are possibly related to ICD risk (Table 1). However, a recent large-scale case-control study that matched medication dosages failed to confirm the significance of all of these factors [24].
Dopamine agonists
Based on current epidemiological research, dopamine agonists are the strongest risk factor for ICD in PD. The first report on ICD was in patients using pramipexole [25], a non-ergot dopamine agonist with a relatively high affinity to limbic dopamine receptor D3 over D2, which raised the possibility of new class dopamine agonists having the ability to induce ICD. ICD was also reported in patients with restless leg syndrome [26], progressive supranuclear palsy [27], and fibromyalgia [28] treated with dopamine agonists that show a high affinity for D3. Because the mesolimbic system plays a central role in the pathophysiology of ICD and non-ergot dopamine agonists can hyper-stimulate limbic dopamine receptors, these drugs are considered to have a high probability for inducing ICD. However, subsequent studies showed that the class of dopamine agonists does not matter. ICD typically occurs in dopamine agonist users of any kind at a frequency 10-fold higher than non-users [15,29]. The risk of ICD increases with higher dosages [15,30]. In a prospective cohort study, the incidence of ICD increased based on the duration of dopamine agonist exposure [31]. However, there was a huge variability during the follow-up [31], and controversies remained regarding the ‘dosage effect’ of dopamine agonists [23]. A recent study suggested that another non-ergot dopamine agonist, the rotigotine transdermal patch, causes ICD less frequently [32]. Large systematic studies are needed to confirm these findings.
Individual susceptibility to ICD
Not all patients who use dopamine agonists develop ICD, and some patients who do not take dopamine agonist develop ICD [15]. Thus, individual susceptibility likely plays a significant role in the appearance of ICD in PD (Table 1).

Personality traits

Impulsivity and novelty seeking traits are consistently reported as risk factors for ICD [24,33,34]. Depression, anxiety, aggression, irritability, obsessive-compulsive traits, and alexithymia are also potential risk factors [24,35,36]. These personality traits are also closely related to addictive disorders in the general population. One study reported that the degree of impulsivity in drug-naïve PD patients was lower than healthy controls, and the frequency of ICD in drug naïve PD patients was not different from that of healthy controls [37]. Thus, these data suggest that dopamine replacement therapy can make patients more impulsive than their premorbid state.
Individuals with a past history of smoking, alcoholism or drug abuse, and a family history of alcohol or drug abuse are vulnerable to ICD after the initiation of dopaminergic treatment [24,34,38].

Genetic susceptibility

Impulse control disorder is considered to be a behavioral addiction and vulnerability to this disorder involves complex traits. These traits typically show a common susceptibility to both drug addiction and ICD. Many genetic and family studies have been conducted in drug addicts or pathologic gamblers from the non-PD population, and candidate genes code receptors, transporters, and enzymes involved in the dopamine, serotonin and glutamatergic systems in the brain [39]. Unfortunately, there have been only a few studies regarding the genetic susceptibility to ICD in PD. Among the dopamine receptor genes, the most frequently investigated is DRD2. In the general population, addictive disorders are significantly influenced by the presence of a DRD2 Taq1A variant that is linked to low receptor availability [40,41]. In contrast, two studies in the PD population consistently reported that this variant was not associated with ICD [42,43]. The different genetic influences between ‘ICD in PD’ and ‘addiction in the general population’ may be related to a different pathophysiology or false negative results in PD ICD studies because of small sample sizes or population stratification.
Lee et al. [42] reported that ICD is significantly associated with being a carrier of the DRD3 gene S9G variant and glutamate N-methyl-D-aspartate receptor type 2B gene C366G variant regardless of clinical status on dopamine agonist use, duration of treatment, PD onset and current patient age. The D3 receptor is predominantly expressed in the mesolimbic system and is thought to exert inhibitory actions [44,45]. An alternative splice variant in this receptor is associated with high novelty responding [46], and the upregulation of D3 expression is associated with behavioral sensitization to ethanol in animal experiments [47]. Another interesting finding is that the serotonergic system may also have a role in the appearance of ICD. In a PD population treated with low doses of dopaminergic drugs, a serotonin receptor type 2A gene T102C variant was associated with a dose-dependent increased risk of ICD [48]. Further studies are needed to explore the genetic mechanisms behind ICD in PD.

Disease-related neural changes in PD

The mesolimbic dopaminergic system plays a central role in the induction and establishment of addictive behaviors [49]. Thus, the chronic exogenous administration of dopaminergic drugs may induce ICD by aberrant stimulation of this system. A remaining question is whether the same dosages of drugs induce ICD in PD patients more frequently than healthy controls. A study using dynamic dopamine transporter (DAT) positron emission tomography (PET) scanning recently revealed that the mesolimbic to nigrostriatal DAT binding potential ratios were higher in PD when compared with normal controls. The ratios were approximately 3 times higher than those of healthy controls due to the profound degeneration of nigral dopaminergic neurons projecting to striatum in PD patients [50]. Thus, PD patients could be easily affected by exogenous dopaminergic drugs, and the effect could be synergistically increased if those drugs have high affinities to limbic dopamine receptors.
The pathophysiological mechanisms of ICD in PD are not fully understood; however, it may be a phased process, as compared to levodopa-induced dyskinesias which is supposed to undergo priming-induction-establishment processes. The priming process may begin with characteristic pathological features of PD and the chronic administration of dopaminergic drugs. The major feature of this process would be alterations in reward-learning behaviors. Some patients who have particular susceptibility to ICD may go on to induction process and during this process dopamine agonists possibly exert a central role. Lastly, ICD would be established by impairments in inhibitory networks and behavioral monitoring systems related to dysfunctional fronto-striatal connections.
Altered reward reinforcement learning in PD patients
Dopamine in the mesolimbic system has a significant role in motivation and learning behaviors. It acts as a pleasurable neurotransmitter and mediates teaching signals during reward-reinforcement learning processes [51]. Dopamine also represents incentive sailence [52]. In the ventral striatum, dopamine release is discretely coded to the probability and uncertainty of rewards [53]. There is a phasic dopamine surge in response to unexpected rewards, whereas there is phasic dopamine suppression in the absence of expected rewards [53]. In parallel, there is tonic dopamine release during the expectation of rewards with the highest degree to the highest uncertainty [53]. Although these observations are obtained from primate experiments, dopamine release in the human brain is thought to be regulated in a similar way. Thus, modulation of dopaminergic signals can affect reward-seeking behaviors in humans. For example, subjects treated with L-DOPA have a greater propensity to choose the most rewarding action relative to subjects treated with dopamine receptor blockers [54]. PD patients usually undergo several challenges to their reward-learning machinery during the course of the disease, including the progressive loss of the dopaminergic system, non-physiological administration of exogenous dopamine and dopamine receptor agonists, and excessive dopamine levels caused by high dose medications. In combination, these conditions alter the physiological regulation of dopamine release that occurs during the reward-reinforcement learning process. As a result, PD patients have different learning and reward seeking behaviors from healthy controls. PD patients showed exactly opposite learning patterns during their medication-ON and -OFF states [55]. PD patients achieved more efficient learning by positive reinforcement during their medication-ON state (carrot), whereas their best performance through negative feedback (stick) was during their medication-OFF state [55]. The learning pattern during the medication-OFF state was also observed in drugnaïve PD patients [56] and even in SNCA duplication carriers (genetic carriers for familial PD) [57]. The sensitivity to rewards and punishment becomes more disrupted in PD patients on chronic dopaminergic treatment. Briefly, they develop increased sensitivity to rewards and insensitivity to punishments, a phenomenon demonstrated by performance differences during modified and original versions of the Iowa Gambling Tasks [58].
Biased representation of rewards on risk taking behaviors and impulsive decision making in PD patients with ICD
It seems that dopamine agonists enhance a deviated learning pattern in PD patients who are beginning to express ICD. Dopamine agonists enhance the rate of gain-specific learning and increase striatal activity to δ of prediction error observed in patients with pathological gambling or problem shopping [59]. Thus, PD patients with ICD can experience a persistent “better than expected” outcome while taking dopamine agonists [59].
Dopamine agonists also enhance risk taking behaviors in PD patients with ICD. While taking dopamine agonists, these patients have a bias towards risky choices independent of the effect of loss aversion [60]. Voon et al. [60] has shown that neural activity in brain areas associated with risk representation, such as the ventral striatum, orbitofrontal cortex and anterior cingulate cortex, are decreased in these patients. In a study using the Balloon Analogue Risk Task [61], resting state regional blood flow at ventral striatum was decreased in PD patients with ICD when compared with those that did not have ICD; in addition, there was no activation in the right ventral striatum during risk taking (with unknown probability of the risk). Pathological gamblers in the general population showed a similar activity pattern of relatively diminished ventral striatal activity during simulated gambling [62].
Impulsive decision making is a typical feature of people with ICD. This feature seems to be closely related to the action of dopamine agonists. Administration of dopamine agonists is significantly associated with greater impulsive choices, faster reaction time, faster decision conflict reaction time and executive dysfunction in PD patients with ICD [63].
Plastic changes in the presynaptic and postsynaptic dopaminergic systems and sensitization in PD patients with ICD
Several functional imaging studies have shown that dopaminergic neural systems undergo plastic changes as ICD develops in PD patients (Table 2). The postsynaptic D2 receptor availability at the ventral striatum is lower in PD patients with ICD than those without ICD [64]. This characteristic resembles the low D2 receptor availability observed in drug addicts [65]. On the other hand, presynaptic DAT binding in the ventral striatum is relatively reduced in PD patients with ICD compared with those without ICD [50,66,67], and reduced DAT binding predicts the future risk for ICD [68]. There are only three studies that explored extrastriatal dopaminergic systems. One study used a [11C]FLB-457 {(S)-N-[(1-ethyl-2-pyrrolidinyl)methyl]-5-bromo-2,3-dimethoxybenzamide} PET [69] to explore postsynaptic fibers, and the other studies used N-(3-[18F]fluoropropyl)-2β-carbomethoxy-3β-(4-iodophenyl) nortropane ([18F]FP-CIT) PET [50] and [18F]fluorodopa PET [70] to explore presynaptic fibers. In PD patients with pathological gambling, the D2-autoreceptor occupancy in the midbrain was reduced and the D2/D3 receptor occupancy in the orbitofrontal and anterior cingulate cortex was low [69]. The ventromedial prefrontal DAT uptake and medial orbitofrontal decarboxylase activity were relatively high in patients with ICD at resting state [50,70]. PD is a progressive neurodegenerative disorder; therefore, these binding differences may be secondary to differences in the degree of degeneration [71]. However, studies on dopamine releasability suggest that these findings may be related to a neural plastic change towards the induction of ICD. Cue-induced dopamine release in the ventral striatum is greater in PD patients with ICD than those without ICD [64,72]. Interestingly, an experiment on PD patients with DDS revealed that ventral striatal dopamine release was more sensitized in these subjects, and the magnitude of dopamine release correlated with “wanting” but not “liking” [73]. Thus, incentive sensitization is the pathophysiological mechanism of DDS and ICD-like behaviors in PD, and mesolimbic dopamine release is important for the motivational aspect of these behavioral disturbances. A similar pattern of incentive sensitization is observed in drug addicts [74]. Thus, DDS in PD may share a common mechanism with addictive disorders in the general population.
Dysfunctional fronto-striatal networks in PD patients with ICD
The orbitofrontal and anterior cingulate cortex play a role in punishment-based decision making, the suppression of previously rewarded behavior (i.e., negative feedback) and the monitoring of functions to avoid negative consequences [75]. An early study with [18F]fluorodeoxyglucose PET showed a deactivation of these areas in PD patients during Iowa Gambling Task [76], suggesting dysfunctional limbic frontal networks are present in PD patients. A later study using [15O]H2O PET clearly demonstrated apomorphine-induced deactivation of these two areas during a gambling task in PD patients with pathological gambling [77]. Disconnection between the striatum and lateral orbitofrontal and anterior cingulate cortex was also reported in PD patients with pathological gambling by a path modeling analysis [78]. These findings suggest a dysfunctional inhibitory fronto-striatal network is another important feature of PD patients with ICD. A dysfunctional prefrontal cortex is a hallmark of addicts in the general population [79] that leads to impaired response inhibition and salience attribution in addiction cycles of intoxication, binging, withdrawal and craving [79].
Currently, there is no treatment guideline established for the management of ICD in PD. However, the principle of proper management is to treat the disorder as a behavioral complication of dopaminergic therapy. Although we may encounter conflicts in individual patients between the parkinsonian motor symptoms and behavioral problems, attempts to discontinue or decrease the dosages of dopamine agonists or switching to the use of levodopa are necessary. Comorbid psychiatric symptoms, such as depression and anxiety, should not be neglected. Proper treatments often require multidisciplinary approaches, including psychiatric consultation.
One study reported that all of their 18 subjects experienced full or partial remission of ICD symptoms after discontinuation or decreasing the dose of dopamine agonists [80]. However, there is a risk of dopamine agonist withdrawal syndrome (DAWS) [81]. DAWS is similar to a drug-withdrawal syndrome and is characterized by anxiety, panic attacks, depression, dysphoria, agitation, insomnia, irritability and drug cravings that are often accompanied by autonomic symptoms, such as orthostatic hypotension, diaphoresis and nausea. DAWS was reported in up to 20% of patients taking high doses dopamine agonists [81]. In addition, patients may develop severe apathy after withdrawal of dopaminergic drugs because of underlying disease-associated mesolimbic denervation [82].
One cross-over trial of amantadine showed a promising effect on reducing the severity of gambling behaviors in PD [83]; however, the results were refuted by other investigators and controversy remains as to the effect of amantadine. Actually the frequency of ICD behavior was significantly higher in amantadine users when compared with non-users in two large cohorts (relative risk for ICD is approximately 1.7) [84,85].
Deep brain stimulation (DBS) is an attractive therapeutic option in severe cases. However, the collective literature on DBS showed that some patients improve but others do not [86-93]. Unexpectedly, some patients develop ICD after DBS, despite dosage reduction or no intake of dopaminergic drugs [94-96]. Although these DBS studies are not specifically designed to investigate the effect of DBS on ICD, it is raised why de novo ICD cases occur after DBS [97]. Frank et al. [98]. assessed decision-making in PD patients using a computer game and found that DBS of the subthalamic nucleus makes patients more impulsive in high-conflict decisions, whereas dopaminergic drugs interfere with the ability to learn from negative experience. The subthalamic nucleus has been suggested to act on response inhibition as a central brake [99], which may be either a ‘proactive inhibition’ or a ‘reactive inhibition’. One study showed that subthalamic nucleus stimulation was associated with alterations in brain areas involved in both mechanisms [100], and the ventral portion of the subthalamic nucleus is specifically responsible for response inhibition [99]. To control motor symptoms, dopaminergic drug therapy and DBS would be a necessary evil for PD patients; thus, close monitoring for the appearance of ICD is required during the course of the disease.
Intrajejunal continuous levodopa infusion has been shown to be effective in 8 patients with severe motor complications, ICD and dopamine dysregulation syndrome [101]. In this small open label trial, all types of ICD behaviors, except for punding, improved after 6 months of treatment [101]. This treatment appears attractive because both motor complications and psychiatric symptoms can be controlled. However, large-scale double-blind studies are needed before any conclusions can be made. Recent trials on cognitive behavioral therapy [102] and on the administration of opioid antagonists [103,104] suggest a new treatment option; however, further studies are needed to confirm the efficacy of these therapies.
Impulse control disorder is a relatively common behavioral complication of dopamine replacement therapy in PD and is quite disabling to patients and their caregivers. In addition to dopaminergic drugs, individual susceptibility and disease-related neural changes contribute to the appearance of ICD. Based on the pathophysiological mechanisms of ICD in PD, establishment of proper treatment guidelines to prevent ICD and development of therapeutics to control risk factors of ICD and other problematic behaviors are warranted.

Conflicts of Interest

The authors have no financial conflicts of interest.

This work was partially supported by a grant from the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2011-0014451).
Table 1.
Risk factors for impulse control disorders in patients with Parkinson’s disease
Drugs Dopamine agonist, high dose, oral non-ergot drugs
Personality traits Novelty seeking trait, impulsivity, obsessive-compulsive trait
Psychiatric symptoms Depression, anxiety, aggression, irritability, alexithymia
Past history Smoking, alcohol use disorder, addiction or substance use disorder
Family history Alcohol use disorder, substance use disorder
Genetic predisposition DRD3, GRIN2B, HTR2A
Dopaminergic system Low dopamine transporter densities at ventral striatum
Clinical features of PD* Young age at onset, male gender, predominant parkinsonism on left side

* controversial.

PD: Parkinson’s disease, DRD3: dopamine receptor D3 gene, GRIN2B: glutamate N-methyl-D-aspartate receptor type 2B gene, HTR2A: serotonin receptor type 2A gene.

Table 2.
Suggested synaptic plastic changes in the mesolimbic and mesocortical dopaminergic systems in PD patients with impulse control disorders
Ventral striatum Mesocortex
D2 auto-Rc Probably low -
DAT Low High
D2/D3 Rc occupancy High Low
Synaptic DA High Low
DA release Sensitized Unknown

PD: Parkinson’s disease, DA: dopamine, Rc: receptor, DAT: dopamine transporter.

  • 1. Barbeau A. L-dopa therapy in Parkinson’s disease: a critical review of nine years’ experience. Can Med Assoc J 1969;101:59–68.
  • 2. Celesia GG, Barr AN. Psychosis and other psychiatric manifestations of levodopa therapy. Arch Neurol 1970;23:193–200.ArticlePubMed
  • 3. Goodwin FK. Psychiatric side effects of levodopa in man. JAMA 1971;218:1915–1920.ArticlePubMed
  • 4. Damãsio AR, Lobo-Antunes J, Macedo C. Psychiatric aspects in Parkinsonism treated with L-dopa. J Neurol Neurosurg Psychiatry 1971;34:502–507.ArticlePubMedPMC
  • 5. Quinn NP, Toone B, Lang AE, Marsden CD, Parkes JD. Dopa dose-dependent sexual deviation. Br J Psychiatry 1983;142:296–298.ArticlePubMed
  • 6. Uitti RJ, Tanner CM, Rajput AH, Goetz CG, Klawans HL, Thiessen B. Hypersexuality with antiparkinsonian therapy. Clin Neuropharmacol 1989;12:375–383.ArticlePubMed
  • 7. Friedman JH. Punding on levodopa. Biol Psychiatry 1994;36:350–351.Article
  • 8. Lim SY, Evans AH, Miyasaki JM. Impulse control and related disorders in Parkinson’s disease: review. Ann N Y Acad Sci 2008;1142:85–107.ArticlePubMed
  • 9. Giovannoni G, O’Sullivan JD, Turner K, Manson AJ, Lees AJ. Hedonistic homeostatic dysregulation in patients with Parkinson’s disease on dopamine replacement therapies. J Neurol Neurosurg Psychiatry 2000;68:423–428.ArticlePubMedPMC
  • 10. Lawrence AD, Evans AH, Lees AJ. Compulsive use of dopamine replacement therapy in Parkinson’s disease: reward systems gone awry? Lancet Neurol 2003;2:595–604.ArticlePubMed
  • 11. Seedat S, Kesler S, Niehaus DJ, Stein DJ. Pathological gambling behaviour: emergence secondary to treatment of Parkinson’s disease with dopaminergic agents. Depress Anxiety 2000;11:185–186.ArticlePubMed
  • 12. Dodd ML, Klos KJ, Bower JH, Geda YE, Josephs KA, Ahlskog JE. Pathological gambling caused by drugs used to treat Parkinson disease. Arch Neurol 2005;62:1377–1381.ArticlePubMed
  • 13. Voon V, Potenza MN, Thomsen T. Medication-related impulse control and repetitive behaviors in Parkinson’s disease. Curr Opin Neurol 2007;20:484–492.ArticlePubMed
  • 14. Weintraub D, Koester J, Potenza MN, Siderowf AD, Stacy M, Voon V, et al. Impulse control disorders in Parkinson disease: a cross-sectional study of 3090 patients. Arch Neurol 2010;67:589–595.ArticlePubMed
  • 15. Lee JY, Kim JM, Kim JW, Cho J, Lee WY, Kim HJ, et al. Association between the dose of dopaminergic medication and the behavioral disturbances in Parkinson disease. Parkinsonism Relat Disord 2010;16:202–207.ArticlePubMed
  • 16. Weintraub D, Hoops S, Shea JA, Lyons KE, Pahwa R, Driver-Dunckley ED, et al. Validation of the questionnaire for impulsive-compulsive disorders in Parkinson’s disease. Mov Disord 2009;24:1461–1467.ArticlePubMedPMC
  • 17. Kim J, Kim M, Kwon do Y, Seo WK, Kim JH, Baik JS, et al. Clinical characteristics of impulse control and repetitive behavior disorders in Parkinson’s disease. J Neurol 2013;260:429–437.ArticlePubMed
  • 18. Lim SY, Tan ZK, Ngam PI, Lor TL, Mohamed H, Schee JP, et al. Impulsive-compulsive behaviors are common in Asian Parkinson’s disease patients: assessment using the QUIP. Parkinsonism Relat Disord 2011;17:761–764.ArticlePubMed
  • 19. Callesen MB, Weintraub D, Damholdt MF, Møller A. Impulsive and compulsive behaviors among Danish patients with Parkinson’s disease: prevalence, depression, and personality. Parkinsonism Relat Disord 2014;20:22–26.ArticlePubMed
  • 20. Wu K, Politis M, O’Sullivan SS, Lawrence AD, Warsi S, Lees A, et al. Problematic Internet use in Parkinson’s disease. Parkinsonism Relat Disord 2014;20:482–487.ArticlePubMed
  • 21. Evans AH, Strafella AP, Weintraub D, Stacy M. Impulsive and compulsive behaviors in Parkinson’s disease. Mov Disord 2009;24:1561–1570.ArticlePubMed
  • 22. Evans AH, Katzenschlager R, Paviour D, O’Sullivan JD, Appel S, Lawrence AD, et al. Punding in Parkinson’s disease: its relation to the dopamine dysregulation syndrome. Mov Disord 2004;19:397–405.ArticlePubMed
  • 23. Voon V, Mehta AR, Hallett M. Impulse control disorders in Parkinson’s disease: recent advances. Curr Opin Neurol 2011;24:324–330.ArticlePubMedPMC
  • 24. Voon V, Sohr M, Lang AE, Potenza MN, Siderowf AD, Whetteckey J, et al. Impulse control disorders in Parkinson disease: a multicenter case--control study. Ann Neurol 2011;69:986–996.ArticlePubMed
  • 25. Grosset KA, Macphee G, Pal G, Stewart D, Watt A, Davie J, et al. Problematic gambling on dopamine agonists: not such a rarity. Mov Disord 2006;21:2206–2208.ArticlePubMed
  • 26. Voon V, Schoerling A, Wenzel S, Ekanayake V, Reiff J, Trenkwalder C, et al. Frequency of impulse control behaviours associated with dopaminergic therapy in restless legs syndrome. BMC Neurol 2011;11:117.ArticlePubMedPMCPDF
  • 27. O’Sullivan SS, Djamshidian A, Ahmed Z, Evans AH, Lawrence AD, Holton JL, et al. Impulsive-compulsive spectrum behaviors in pathologically confirmed progressive supranuclear palsy. Mov Disord 2010;25:638–642.ArticlePubMed
  • 28. Holman AJ. Impulse control disorder behaviors associated with pramipexole used to treat fibromyalgia. J Gambl Stud 2009;25:425–431.ArticlePubMed
  • 29. Weintraub D, Siderowf AD, Potenza MN, Goveas J, Morales KH, Duda JE, et al. Association of dopamine agonist use with impulse control disorders in Parkinson disease. Arch Neurol 2006;63:969–973.ArticlePubMedPMC
  • 30. Joutsa J, Martikainen K, Vahlberg T, Kaasinen V. Effects of dopamine agonist dose and gender on the prognosis of impulse control disorders in Parkinson’s disease. Parkinsonism Relat Disord 2012;18:1079–1083.ArticlePubMed
  • 31. Bastiaens J, Dorfman BJ, Christos PJ, Nirenberg MJ. Prospective cohort study of impulse control disorders in Parkinson’s disease. Mov Disord 2013;28:327–333.ArticlePubMedPMC
  • 32. Garcia-Ruiz PJ, Martinez Castrillo JC, Alonso-Canovas A, Herranz Barcenas A, Vela L, Sanchez Alonso P, et al. Impulse control disorder in patients with Parkinson’s disease under dopamine agonist therapy: a multicentre study. J Neurol Neurosurg Psychiatry 2014;85:840–844.ArticlePubMed
  • 33. Isaias IU, Siri C, Cilia R, De Gaspari D, Pezzoli G, Antonini A. The relationship between impulsivity and impulse control disorders in Parkinson’s disease. Mov Disord 2008;23:411–415.ArticlePubMed
  • 34. Voon V, Thomsen T, Miyasaki JM, de Souza M, Shafro A, Fox SH, et al. Factors associated with dopaminergic drug-related pathological gambling in Parkinson disease. Arch Neurol 2007;64:212–216.ArticlePubMed
  • 35. Pontone G, Williams JR, Bassett SS, Marsh L. Clinical features associated with impulse control disorders in Parkinson disease. Neurology 2006;67:1258–1261.ArticlePubMed
  • 36. Goerlich-Dobre KS, Probst C, Winter L, Witt K, Deuschl G, Möller B, et al. Alexithymia-an independent risk factor for impulsive-compulsive disorders in Parkinson’s disease. Mov Disord 2014;29:214–220.ArticlePubMed
  • 37. Antonini A, Siri C, Santangelo G, Cilia R, Poletti M, Canesi M, et al. Impulsivity and compulsivity in drug-naïve patients with Parkinson’s disease. Mov Disord 2011;26:464–468.ArticlePubMed
  • 38. ValenÇa GT, Glass PG, Negreiros NN, Duarte MB, Ventura LM, Mueller M, et al. Past smoking and current dopamine agonist use show an independent and dose-dependent association with impulse control disorders in Parkinson’s disease. Parkinsonism Relat Disord 2013;19:698–700.ArticlePubMed
  • 39. Kreek MJ, Nielsen DA, Butelman ER, LaForge KS. Genetic influences on impulsivity, risk taking, stress responsivity and vulnerability to drug abuse and addiction. Nat Neurosci 2005;8:1450–1457.ArticlePubMedPDF
  • 40. Haile CN, Kosten TR, Kosten TA. Genetics of dopamine and its contribution to cocaine addiction. Behav Genet 2007;37:119–145.ArticlePubMed
  • 41. Comings DE, Rosenthal RJ, Lesieur HR, Rugle LJ, Muhleman D, Chiu C, et al. A study of the dopamine D2 receptor gene in pathological gambling. Pharmacogenetics 1996;6:223–234.ArticlePubMed
  • 42. Lee JY, Lee EK, Park SS, Lim JY, Kim HJ, Kim JS, et al. Association of DRD3 and GRIN2B with impulse control and related behaviors in Parkinson’s disease. Mov Disord 2009;24:1803–1810.ArticlePubMed
  • 43. Vallelunga A, Flaibani R, Formento-Dojot P, Biundo R, Facchini S, Antonini A. Role of genetic polymorphisms of the dopaminergic system in Parkinson’s disease patients with impulse control disorders. Parkinsonism Relat Disord 2012;18:397–399.ArticlePubMed
  • 44. Waters N, Svensson K, Haadsma-Svensson SR, Smith MW, Carlsson A. The dopamine D3-receptor: a postsynaptic receptor inhibitory on rat locomotor activity. J Neural Transm Gen Sect 1993;94:11–19.ArticlePubMed
  • 45. Richtand NM. Behavioral sensitization, alternative splicing, and d3 dopamine receptor-mediated inhibitory function. Neuropsychopharmacology 2006;31:2368–2375.ArticlePubMedPMCPDF
  • 46. Pritchard LM, Logue AD, Taylor BC, Ahlbrand R, Welge JA, Tang Y, et al. Relative expression of D3 dopamine receptor and alternative splice variant D3nf mRNA in high and low responders to novelty. Brain Res Bull 2006;70:296–303.ArticlePubMedPMC
  • 47. Harrison SJ, Nobrega JN. A functional role for the dopamine D3 receptor in the induction and expression of behavioural sensitization to ethanol in mice. Psychopharmacology (Berl) 2009;207:47–56.ArticlePubMed
  • 48. Lee JY, Jeon BS, Kim HJ, Park SS. Genetic variant of HTR2A associates with risk of impulse control and repetitive behaviors in Parkinson’s disease. Parkinsonism Relat Disord 2012;18:76–78.ArticlePubMed
  • 49. Brewer JA, Potenza MN. The neurobiology and genetics of impulse control disorders: relationships to drug addictions. Biochem Pharmacol 2008;75:63–75.ArticlePubMedPMC
  • 50. Lee JY, Seo SH, Kim YK, Yoo HB, Kim YE, Song IC, et al. Extrastriatal dopaminergic changes in Parkinson’s disease patients with impulse control disorders. J Neurol Neurosurg Psychiatry 2014;85:23–30.ArticlePubMed
  • 51. Schultz W, Dayan P, Montague PR. A neural substrate of prediction and reward. Science 1997;275:1593–1599.ArticlePubMed
  • 52. Berridge KC. The debate over dopamine’s role in reward: the case for incentive salience. Psychopharmacology (Berl) 2007;191:391–431.ArticlePubMed
  • 53. Fiorillo CD, Tobler PN, Schultz W. Discrete coding of reward probability and uncertainty by dopamine neurons. Science 2003;299:1898–1902.ArticlePubMed
  • 54. Pessiglione M, Seymour B, Flandin G, Dolan RJ, Frith CD. Dopamine-dependent prediction errors underpin rewardseeking behaviour in humans. Nature 2006;442:1042–1045.ArticlePubMedPMCPDF
  • 55. Frank MJ, Seeberger LC, O’reilly RC. By carrot or by stick: cognitive reinforcement learning in parkinsonism. Science 2004;306:1940–1943.ArticlePubMed
  • 56. Bódi N, Kéri S, Nagy H, Moustafa A, Myers CE, Daw N, et al. Reward-learning and the novelty-seeking personality: a between- and within-subjects study of the effects of dopamine agonists on young Parkinson’s patients. Brain 2009;132(Pt 9):2385–2395.ArticlePubMedPMCPDF
  • 57. Kéri S, Moustafa AA, Myers CE, Benedek G, Gluck MA. {alpha}-Synuclein gene duplication impairs reward learning. Proc Natl Acad Sci U S A 2010;107:15992–15994.ArticlePubMedPMC
  • 58. Kobayakawa M, Tsuruya N, Kawamura M. Sensitivity to reward and punishment in Parkinson’s disease: an analysis of behavioral patterns using a modified version of the Iowa gambling task. Parkinsonism Relat Disord 2010;16:453–457.ArticlePubMed
  • 59. Voon V, Pessiglione M, Brezing C, Gallea C, Fernandez HH, Dolan RJ, et al. Mechanisms underlying dopaminemediated reward bias in compulsive behaviors. Neuron 2010;65:135–142.ArticlePubMedPMC
  • 60. Voon V, Gao J, Brezing C, Symmonds M, Ekanayake V, Fernandez H, et al. Dopamine agonists and risk: impulse control disorders in Parkinson’s disease. Brain 2011;134(Pt 5):1438–1446.ArticlePubMedPMCPDF
  • 61. Rao H, Mamikonyan E, Detre JA, Siderowf AD, Stern MB, Potenza MN, et al. Decreased ventral striatal activity with impulse control disorders in Parkinson’s disease. Mov Disord 2010;25:1660–1669.ArticlePubMedPMC
  • 62. Reuter J, Raedler T, Rose M, Hand I, Gläscher J, Büchel C. Pathological gambling is linked to reduced activation of the mesolimbic reward system. Nat Neurosci 2005;8:147–148.ArticlePubMedPDF
  • 63. Voon V, Reynolds B, Brezing C, Gallea C, Skaljic M, Ekanayake V, et al. Impulsive choice and response in dopamine agonist-related impulse control behaviors. Psychopharmacology (Berl) 2010;207:645–659.ArticlePubMedPMC
  • 64. Steeves TD, Miyasaki J, Zurowski M, Lang AE, Pellecchia G, Van Eimeren T, et al. Increased striatal dopamine release in Parkinsonian patients with pathological gambling: a [11C] raclopride PET study. Brain 2009;132(Pt 5):1376–1385.ArticlePubMedPMCPDF
  • 65. Lee B, London ED, Poldrack RA, Farahi J, Nacca A, Monterosso JR, et al. Striatal dopamine d2/d3 receptor availability is reduced in methamphetamine dependence and is linked to impulsivity. J Neurosci 2009;29:14734–14740.ArticlePubMedPMC
  • 66. Cilia R, Ko JH, Cho SS, van Eimeren T, Marotta G, Pellecchia G, et al. Reduced dopamine transporter density in the ventral striatum of patients with Parkinson’s disease and pathological gambling. Neurobiol Dis 2010;39:98–104.ArticlePubMed
  • 67. Voon V, Rizos A, Chakravartty R, Mulholland N, Robinson S, Howell NA, et al. Impulse control disorders in Parkinson’s disease: decreased striatal dopamine transporter levels. J Neurol Neurosurg Psychiatry 2014;85:148–152.ArticlePubMedPMC
  • 68. Vriend C, Nordbeck AH, Booij J, van der Werf YD, Pattij T, Voorn P, et al. Reduced dopamine transporter binding predates impulse control disorders in Parkinson’s disease. Mov Disord 2014;29:904–911.ArticlePubMed
  • 69. Ray NJ, Miyasaki JM, Zurowski M, Ko JH, Cho SS, Pellecchia G, et al. Extrastriatal dopaminergic abnormalities of DA homeostasis in Parkinson’s patients with medicationinduced pathological gambling: a [11C] FLB-457 and PET study. Neurobiol Dis 2012;48:519–525.ArticlePubMedPMC
  • 70. Joutsa J, Martikainen K, Niemelä S, Johansson J, Forsback S, Rinne JO, et al. Increased medial orbitofrontal [18F]fluorodopa uptake in Parkinsonian impulse control disorders. Mov Disord 2012;27:778–782.ArticlePubMed
  • 71. Lee CS, Samii A, Sossi V, Ruth TJ, Schulzer M, Holden JE, et al. In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson’s disease. Ann Neurol 2000;47:493–503.ArticlePubMed
  • 72. O’Sullivan SS, Wu K, Politis M, Lawrence AD, Evans AH, Bose SK, et al. Cue-induced striatal dopamine release in Parkinson’s disease-associated impulsive-compulsive behaviours. Brain 2011;134(Pt 4):969–978.ArticlePubMedPDF
  • 73. Evans AH, Pavese N, Lawrence AD, Tai YF, Appel S, Doder M, et al. Compulsive drug use linked to sensitized ventral striatal dopamine transmission. Ann Neurol 2006;59:852–858.ArticlePubMed
  • 74. Leyton M, Boileau I, Benkelfat C, Diksic M, Baker G, Dagher A. Amphetamine-induced increases in extracellular dopamine, drug wanting, and novelty seeking: a PET/ [11C]raclopride study in healthy men. Neuropsychopharmacology 2002;27:1027–1035.ArticlePubMed
  • 75. Goldstein RZ, Tomasi D, Rajaram S, Cottone LA, Zhang L, Maloney T, et al. Role of the anterior cingulate and medial orbitofrontal cortex in processing drug cues in cocaine addiction. Neuroscience 2007;144:1153–1159.ArticlePubMedPMC
  • 76. Thiel A, Hilker R, Kessler J, Habedank B, Herholz K, Heiss WD. Activation of basal ganglia loops in idiopathic Parkinson’s disease: a PET study. J Neural Transm 2003;110:1289–1301.ArticlePubMed
  • 77. van Eimeren T, Pellecchia G, Cilia R, Ballanger B, Steeves TD, Houle S, et al. Drug-induced deactivation of inhibitory networks predicts pathological gambling in PD. Neurology 2010;75:1711–1716.ArticlePubMedPMC
  • 78. Cilia R, Cho SS, van Eimeren T, Marotta G, Siri C, Ko JH, et al. Pathological gambling in patients with Parkinson’s disease is associated with fronto-striatal disconnection: a path modeling analysis. Mov Disord 2011;26:225–233.ArticlePubMed
  • 79. Goldstein RZ, Volkow ND. Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications. Nat Rev Neurosci 2011;12:652–669.ArticlePubMedPMCPDF
  • 80. Mamikonyan E, Siderowf AD, Duda JE, Potenza MN, Horn S, Stern MB, et al. Long-term follow-up of impulse control disorders in Parkinson’s disease. Mov Disord 2008;23:75–80.ArticlePubMedPMC
  • 81. Rabinak CA, Nirenberg MJ. Dopamine agonist withdrawal syndrome in Parkinson disease. Arch Neurol 2010;67:58–63.ArticlePubMed
  • 82. Thobois S, Ardouin C, Lhommée E, Klinger H, Lagrange C, Xie J, et al. Non-motor dopamine withdrawal syndrome after surgery for Parkinson’s disease: predictors and underlying mesolimbic denervation. Brain 2010;133(Pt 4):1111–1127.ArticlePubMedPDF
  • 83. Thomas A, Bonanni L, Gambi F, Di Iorio A, Onofrj M. Pathological gambling in Parkinson disease is reduced by amantadine. Ann Neurol 2010;68:400–404.ArticlePubMed
  • 84. Weintraub D, Sohr M, Potenza MN, Siderowf AD, Stacy M, Voon V, et al. Amantadine use associated with impulse control disorders in Parkinson disease in cross-sectional study. Ann Neurol 2010;68:963–968.ArticlePubMed
  • 85. Lee JY, Kim HJ, Jeon BS. Is pathological gambling in Parkinson’s disease reduced by amantadine? Ann Neurol 2011;69:213– reply 214-215. ArticlePubMed
  • 86. Smeding HM, Goudriaan AE, Foncke EM, Schuurman PR, Speelman JD, Schmand B. Pathological gambling after bilateral subthalamic nucleus stimulation in Parkinson disease. J Neurol Neurosurg Psychiatry 2007;78:517–519.ArticlePubMedPMC
  • 87. Bandini F, Primavera A, Pizzorno M, Cocito L. Using STN DBS and medication reduction as a strategy to treat pathological gambling in Parkinson’s disease. Parkinsonism Relat Disord 2007;13:369–371.ArticlePubMed
  • 88. Lim SY, O’Sullivan SS, Kotschet K, Gallagher DA, Lacey C, Lawrence AD, et al. Dopamine dysregulation syndrome, impulse control disorders and punding after deep brain stimulation surgery for Parkinson’s disease. J Clin Neurosci 2009;16:1148–1152.ArticlePubMed
  • 89. Hälbig TD, Tse W, Frisina PG, Baker BR, Hollander E, Shapiro H, et al. Subthalamic deep brain stimulation and impulse control in Parkinson’s disease. Eur J Neurol 2009;16:493–497.ArticlePubMed
  • 90. Moro E. Impulse control disorders and subthalamic nucleus stimulation in Parkinson’s disease: are we jumping the gun? Eur J Neurol 2009;16:440–441.ArticlePubMed
  • 91. Broen M, Duits A, Visser-Vandewalle V, Temel Y, Winogrodzka A. Impulse control and related disorders in Parkinson’s disease patients treated with bilateral subthalamic nucleus stimulation: a review. Parkinsonism Relat Disord 2011;17:413–417.ArticlePubMed
  • 92. Moum SJ, Price CC, Limotai N, Oyama G, Ward H, Jacobson C, et al. Effects of STN and GPi deep brain stimulation on impulse control disorders and dopamine dysregulation syndrome. PLoS One 2012;7:e29768. ArticlePubMedPMC
  • 93. Shotbolt P, Moriarty J, Costello A, Jha A, David A, Ashkan K, et al. Relationships between deep brain stimulation and impulse control disorders in Parkinson’s disease, with a literature review. Parkinsonism Relat Disord 2012;18:10–16.ArticlePubMed
  • 94. Amami P, Dekker I, Piacentini S, Ferré F, Romito LM, Franzini A, et al. Impulse control behaviours in patients with Parkinson’s disease after subthalamic deep brain stimulation: de novo cases and 3-year follow-up. J Neurol Neurosurg Psychiatry 2014;pii: jnnp-2013-307214. Article
  • 95. Eusebio A, Witjas T, Cohen J, Fluchère F, Jouve E, Régis J, et al. Subthalamic nucleus stimulation and compulsive use of dopaminergic medication in Parkinson’s disease. J Neurol Neurosurg Psychiatry 2013;84:868–874.ArticlePubMed
  • 96. Kim YE, Kim HJ, Kim HJ, Lee JY, Yun JY, Kim JY, et al. Impulse control and related behaviors after bilateral subthalamic stimulation in patients with Parkinson’s disease. J Clin Neurosci 2013;20:964–969.ArticlePubMed
  • 97. Okun MS, Weintraub D. Should impulse control disorders and dopamine dysregulation syndrome be indications for deep brain stimulation and intestinal levodopa? Mov Disord 2013;28:1915–1919.ArticlePubMedPMC
  • 98. Frank MJ, Samanta J, Moustafa AA, Sherman SJ. Hold your horses: impulsivity, deep brain stimulation, and medication in parkinsonism. Science 2007;318:1309–1312.ArticlePubMed
  • 99. Hershey T, Campbell MC, Videen TO, Lugar HM, Weaver PM, Hartlein J, et al. Mapping Go-No-Go performance within the subthalamic nucleus region. Brain 2010;133(Pt 12):3625–3634.ArticlePubMedPMCPDF
  • 100. Ballanger B, van Eimeren T, Moro E, Lozano AM, Hamani C, Boulinguez P, et al. Stimulation of the subthalamic nucleus and impulsivity: release your horses. Ann Neurol 2009;66:817–824.ArticlePubMedPMC
  • 101. Catalán MJ, de Pablo-Fernández E, Villanueva C, Fernández-Diez S, Lapeña-Montero T, García-Ramos R, et al. Levodopa infusion improves impulsivity and dopamine dysregulation syndrome in Parkinson’s disease. Mov Disord 2013;28:2007–2010.ArticlePubMed
  • 102. Okai D, Askey-Jones S, Samuel M, O’Sullivan SS, Chaudhuri KR, Martin A, et al. Trial of CBT for impulse control behaviors affecting Parkinson patients and their caregivers. Neurology 2013;80:792–799.ArticlePubMedPMC
  • 103. Bosco D, Plastino M, Colica C, Bosco F, Arianna S, Vecchio A, et al. Opioid antagonist naltrexone for the treatment of pathological gambling in Parkinson disease. Clin Neuropharmacol 2012;35:118–120.ArticlePubMed
  • 104. Papay K, Xie SX, Stern M, Hurtig H, Siderowf A, Duda JE, et al. Naltrexone for impulse control disorders in Parkinson disease: a placebo-controlled study. Neurology 2014;83:826–833.ArticlePubMedPMC

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