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ObjectiveTo describe the incidence of, and clinical and neurobiological risk factors for, new-onset impulse control disorder (ICD) symptoms and related behaviours in early Parkinson disease (PD).MethodsThe Parkinson's Progression Markers Initiative is an international, multicenter, prospective study of de novo patients with PD untreated at baseline and assessed annually, including serial dopamine transporter imaging (DAT-SPECT) and ICD assessment (Questionnaire for Impulsive-Compulsive Disorders in Parkinson's Disease short form, QUIP). Participants were included if they screened negative on the QUIP at baseline. Kaplan-Meier curves and generalised estimating equations examined frequency and predictors of incident ICD symptoms.ResultsParticipants were seen at baseline (n=320), year 1 (n=284), year 2 (n=217) and year 3 (n=96). Estimated cumulative incident rates of ICD symptoms and related behaviours were 8% (year 1), 18% (year 2) and 25% (year 3) and increased each year in those on dopamine replacement therapy (DRT) and decreased in those not on DRT. In participants on DRT, risk factors for incident ICD symptoms were younger age (OR=0.97, p=0.05), a greater decrease in right caudate (OR=4.03, p=0.01) and mean striatal (OR=6.90, p=0.04) DAT availability over the first year, and lower right putamen (OR=0.06, p=0.01) and mean total striatal (OR=0.25, p=0.04) DAT availability at any post-baseline visit.ConclusionsThe rate of incident ICD symptoms increases with time and initiation of DRT in early PD. In this preliminary study, a greater decrease or lower DAT binding over time increases risk of incident ICD symptoms, conferring additional risk to those taking DRT.Clinical trial registrationNCT01141023.

Aims/hypothesis No studies have evaluated whether the frequently observed associations between depression and diabetes could reflect the presence of comorbid psychiatric conditions and their associations with diabetes. We therefore examined the associations between a wide range of pre-existing Diagnostic Statistical Manual, 4th edition (DSM-IV) mental disorders with self-reported diagnosis of diabetes. Methods We performed a series of cross-sectional face-to-face household surveys of community-dwelling adults ( n  = 52,095) in 19 countries. The World Health Organization Composite International Diagnostic Interview retrospectively assessed lifetime prevalence and age at onset of 16 DSM-IV mental disorders. Diabetes was indicated by self-report of physician’s diagnosis together with its timing. We analysed the associations between all mental disorders and diabetes, without and with comorbidity adjustment. Results We identified 2,580 cases of adult-onset diabetes mellitus (21 years +). Although all 16 DSM-IV disorders were associated with diabetes diagnosis in bivariate models, only depression (OR 1.3; 95% CI 1.1, 1.5), intermittent explosive disorder (OR 1.6; 95% CI 1.1, 2.1), binge eating disorder (OR 2.6; 95% CI 1.7, 4.0) and bulimia nervosa (OR 2.1; 95% CI 1.3, 3.4) remained after comorbidity adjustment. Conclusions/interpretation Depression and impulse control disorders (eating disorders in particular) were significantly associated with diabetes diagnosis after comorbidity adjustment. These findings support the focus on depression as having a role in diabetes onset, but suggest that this focus may be extended towards impulse control disorders. Acknowledging the comorbidity of mental disorders is important in determining the associations between mental disorders and subsequent diabetes.

Impulse Control Disorders (ICDs) are increasingly recognized as a significant non-motor complication in Parkinson’s disease (PD), impacting patients and their caregivers. ICDs in PD are primarily associated with dopaminergic treatments, particularly dopamine agonists, though not all patients develop these disorders, indicating a role for genetic and other clinical factors. Studies over the past few years suggest that the mesocorticolimbic reward system, a core neural substrate for impulsivity, is a key contributor to ICDs in PD. Recent advances in neuroimaging have begun to unravel the neurobiological diversity of ICD subtypes. Moreover, recent studies provide valuable insights into the clinical and biologic risk factors for ICDs that could be used as indicators for the development of future preventive strategies or targeted interventions. Indeed, current treatment strategies, which often involve reducing or discontinuing dopamine agonists, are limited in efficacy. Emerging therapies, including behavioral interventions and continuous drug delivery methods, show promise, though further research is needed. This paper provides an updated review of ICD prevalence, mechanisms, assessment, and novel management approaches.

ObjectiveIn this multicentre open-label trial, we compared behavioural and neuropsychiatric symptoms in Parkinson’s disease (PD) patients with impulse control disorders (ICD) treated with dopamine agonists before and 12 weeks after substituting dopamine agonists with an equivalent dose of levodopa/carbidopa slow-release formulation.MethodsBaseline characteristics of 50 PD patients with ICD were compared with those of 60 medicated and 40 drug-naive PD control groups. Neuropsychiatric trait changes in the PD-ICD group were investigated 12 weeks after the intervention. ICD behaviours were assessed via modified Minnesota Impulsive Disorders Interview (mMIDI), whereas parkinsonian severity and neuropsychiatric characters were systematically assessed with the Unified PD Rating Scale (UPDRS) and a predefined neuropsychological assessment battery.ResultsAt baseline, ICD patients showed higher scores in the Neuropsychiatric Inventory and anxiety, anger and obsessive-compulsive traits compared with both PD control groups. In contrast, the three PD groups showed indifference in the impulsivity scales. At 12 weeks post intervention, ICD behaviours significantly improved (p<0.001, Δ modified MIDI score=‒5.27 ± 5.75) along with the UPDRS II daily activity scores (p=0.02, Δ=‒2.07 ± 4.53). Behavioural disinhibition tended to improve (p=0.06), although no significant changes were observed in the Neuropsychiatric Inventory and personality trait scores. Dopamine agonist withdrawal syndrome developed in 5.3% of the PD-ICD group.ConclusionsThis study provides class IV evidence suggesting that switching from dopamine agonists to levodopa/carbidopa slow-release formulations alleviated ICD behaviours in PD patients leading to improvement in daily activities whereas neuropsychiatric traits associated with ICD persisted after the 12-week therapy.Trial registration numberNCT01683253.

Background Impulse control disorders (ICDs) are frequently encountered in Parkinson’s disease (PD). Objectives We aimed to assess whether clonidine, an α2-adrenergic receptor agonist, would improve ICDs. Methods We conducted a multicentre trial in five movement disorder departments. Patients with PD and ICDs ( n  = 41) were enrolled in an 8-week, randomised (1:1), double-blind, placebo-controlled study of clonidine (75 μg twice a day). Randomisation and allocation to the trial group were carried out by a central computer system. The primary outcome was the change at 8 weeks in symptom severity using the Questionnaire for Impulsive-Compulsive Disorders in Parkinson’s Disease–Rating Scale (QUIP-RS) score. A reduction of the most elevated subscore of the QUIP-RS of more than 3 points without any increase in the other QUIP-RS dimension defined success. Results Between 15 May 2019 and 10 September 2021, 19 patients in the clonidine group and 20 patients in the placebo group were enrolled. The proportion difference of success in reducing QUIP-RS at 8 weeks, was 7% (one-sided upper 90% CI 27%) with 42.1% of success in the clonidine group and 35.0% in the placebo group. Compared to patients in the placebo group, patients in the clonidine group experienced a greater reduction in the total QUIP-RS score at 8 weeks (11.0 points vs. 3.6). Discussion Clonidine was well tolerated but our study was not enough powerful to demonstrate significant superiority compared to placebo in reducing ICDs despite a greater reduction of total QUIP score at 8 weeks. A phase 3 study should be conducted. Trial Registration The study was registered (NCT03552068) on clinicaltrials.gov on June 11, 2018.

Objective: Irritability in disruptive mood dysregulation disorder (DMDD) may be associated with a biased tendency to judge ambiguous facial expressions as angry. We conducted three experiments to explore this bias as a treatment target. We tested: 1) whether youth with DMDD express this bias; 2) whether judgment of ambiguous faces can be altered in healthy youth by training; and 3) whether such training in youth with DMDD is associated with reduced irritability and associated changes in brain function. Methods: Participants in all experiments made happy versus angry judgments of faces that varied along a happy to angry continuum. These judgments were used to quantify a “balance point,” the facial expression at which a participant's judgment switches from predominantly happy to predominantly angry. We first compared balance points in youth with DMDD (n = 63) versus healthy youth (n = 26). We then conducted a double-blind, randomized controlled trial of active versus sham balance-point training in 19 healthy youth. Finally, we piloted open, active balance-point training in 14 youth with DMDD, with 10 completing an implicit functional MRI (fMRI) face-emotion processing task. Results: Relative to healthy youth, DMDD youth manifested a shifted balance point, expressed as a tendency to classify ambiguous faces as angry rather than happy. In both healthy and DMDD youth, active training is associated with a shift in balance point toward more happy judgments. In DMDD, evidence suggests that active training may be associated with decreased irritability and changes in activation in the lateral orbitofrontal cortex. Conclusions: These results set the stage for further research on computer-based treatment targeting interpretation bias of angry faces in DMDD. Such treatment may decrease irritability and alter neural responses to subtle expressions of happiness and anger.

BackgroundImpulse control disorders/other compulsive behaviours (‘ICD behaviours’) occur in Parkinson’s disease (PD), but prospective studies are scarce, and prevalence and clinical characteristics of patients are insufficiently defined.ObjectivesTo assess the presence of ICD behaviours over a 2-year period, and evaluate patients’ clinical characteristics.MethodsA prospective, non-interventional, multicentre study (ICARUS (Impulse Control disorders And the association of neuRopsychiatric symptoms, cognition and qUality of life in ParkinSon disease); SP0990) in treated Italian PD outpatients. Study visits: baseline, year 1, year 2. Surrogate primary variable: presence of ICD behaviours and five ICD subtypes assessed by modified Minnesota Impulsive Disorder Interview (mMIDI).Results1069/1095 (97.6%) patients comprised the Full Analysis Set. Point prevalence of ICD behaviours (mMIDI; primary analysis) was stable across visits: 28.6% (306/1069) at baseline, 29.3% (292/995) at year 1, 26.5% (245/925) at year 2. The most prevalent subtype was compulsive eating, followed by punding, compulsive sexual behaviour, gambling and buying disorder. Patients who were ICD positive at baseline were more likely to be male, younger, younger at PD onset, have longer disease duration, more severe non-motor symptoms (including mood and sexual function), depressive symptoms, sleep impairment and poorer PD-related quality of life. However, they did not differ from the ICD-negative patients in their severity of PD functional disability, motor performance and cognitive function.ConclusionsPrevalence of ICD behaviours was relatively stable across the 2-year observational period. ICD-positive patients had more severe depression, poorer sleep quality and reduced quality of life.

Little is known about the prevalence or correlates of DSM-IV pathological gambling (PG). Data from the US National Comorbidity Survey Replication (NCS-R), a nationally representative US household survey, were used to assess lifetime gambling symptoms and PG along with other DSM-IV disorders. Age of onset (AOO) of each lifetime disorder was assessed retrospectively. AOO reports were used to study associations between temporally primary disorders and the subsequent risk of secondary disorders. Most respondents (78.4%) reported lifetime gambling. Lifetime problem gambling (at least one Criterion A symptom of PG) (2.3%) and PG (0.6%) were much less common. PG was significantly associated with being young, male, and Non-Hispanic Black. People with PG reported first gambling significantly earlier than non-problem gamblers (mean age 16.7 v. 23.9 years, z=12.7, p<0.001), with gambling problems typically beginning during the mid-20s and persisting for an average of 9.4 years. During this time the largest annual gambling losses averaged US$4800. Onset and persistence of PG were predicted by a variety of prior DSM-IV anxiety, mood, impulse-control and substance use disorders. PG also predicted the subsequent onset of generalized anxiety disorder, post-traumatic stress disorder (PTSD) and substance dependence. Although none of the NCS-R respondents with PG ever received treatment for gambling problems, 49.0% were treated at some time for other mental disorders. DSM-IV PG is a comparatively rare, seriously impairing, and undertreated disorder whose symptoms typically start during early adulthood and is frequently secondary to other mental or substance disorders that are associated with both PG onset and persistence.

Background and objective Impulse control disorders (ICD), psychosis and delirium are part of the spectrum of behavioural changes associated with Parkinson’s disease (PD). The diagnostic and therapeutic management of these rather complex neuropsychiatric conditions has been updated in the clinical guideline by the German Society of Neurology (DGN). Methods Recommendations are based on a systematic literature reviews, other relevant guidelines and expert opinion. Results Patients receiving dopamine agonists (DA) therapy should be informed about the symptoms and risks of an ICD and should be routinely screened for ICD symptoms. In the presence of an ICD, DA should be reduced or discontinued and psychotherapeutic treatment may be considered. Non-oral therapies (levodopa/carbidopa intestinal gel infusion or deep brain stimulation) may also be an option for appropriate candidates. Psychosis in PD often has a gradual onset. Cognitive and affective disorders, psychiatric and medical comorbidities as well as polypharmacy are risk factors for a psychosis. Non-pharmacological treatments should be implemented as soon as possible and anti-parkinsonian medications should be adjusted/reduced if feasible. For psychosis associated with PD, quetiapine or clozapine should be used on an as-needed basis and for as short a time as is necessary, with safety monitoring. Delirium in PD may be underdiagnosed due to an overlap with chronic neuropsychiatric features of PD. Although transient by definition, delirium in PD can lead to permanent cognitive decline, motor impairment and increased mortality. Management of delirium includes pharmacological and non-pharmacological interventions. Conclusion The updated guideline encompasses the evidence-based diagnostic, non-pharmacological and pharmacological management of ICD, psychosis and delirium in PD.

This review summarizes neurobiological and genetic findings in behavioural addictions, draws parallels with findings pertaining to substance use disorders, and offers suggestions for future research. Articles concerning brain function, neurotransmitter activity, and family history and (or) genetic findings for behavioural addictions involving gambling, Internet use, video game playing, shopping, kleptomania, and sexual activity were reviewed. Behavioural addictions involve dysfunction in several brain regions, particularly the frontal cortex and striatum. Findings from imaging studies incorporating cognitive tasks have arguably been more consistent than cue-induction studies. Early results suggest white and grey matter differences. Neurochemical findings suggest roles for dopaminergic and serotonergic systems, but results from clinical trials seem more equivocal. While limited, family history and genetic data support heritability for pathological gambling and that people with behavioural addictions are more likely to have a close family member with some form of psychopathology. Parallels exist between neurobiological and genetic and family history findings in substance and nonsubstance addictions, suggesting that compulsive engagement in these behaviours may constitute addictions. To date, findings are limited, particularly for shopping, kleptomania, and sexual behaviour. Genetic understandings are at an early stage. Future research directions are offered.