Baseline frontostriatal‐limbic connectivity predicts reward‐based memory formation

Reward mediates the acquisition and long‐term retention of procedural skills in humans. Yet, learning under rewarded conditions is highly variable across individuals and the mechanisms that determine interindividual variability in rewarded learning are not known. We postulated that baseline functional connectivity in a large‐scale frontostriatal‐limbic network could predict subsequent interindividual variability in rewarded learning. Resting‐state functional MRI was acquired in two groups of subjects (n = 30) who then trained on a visuomotor procedural learning task with or without reward feedback. We then tested whether baseline functional connectivity within the frontostriatal‐limbic network predicted memory strength measured immediately, 24 h and 1 month after training in both groups. We found that connectivity in the frontostriatal‐limbic network predicted interindividual variability in the rewarded but not in the unrewarded learning group. Prediction was strongest for long‐term memory. Similar links between connectivity and reward‐based memory were absent in two control networks, a fronto‐parieto‐temporal language network and the dorsal attention network. The results indicate that baseline functional connectivity within the frontostriatal‐limbic network successfully predicts long‐term retention of rewarded learning. Hum Brain Mapp 35:5921–5931, 2014. © 2014 Wiley Periodicals, Inc.     

Excessive hoarding in Parkinson's disease

Hoarding is seen in several psychiatric conditions, but has not been specifically assessed in Parkinson's disease (PD). This study investigates hoarding tendency amongst patients with PD, and its association with impulsive‐compulsive spectrum behaviors (ICBs). We compare clinical features, measures of hoarding, impulse buying, self‐control, obsessive‐compulsive symptoms, depression, and anxiety in 39 patients with PD with ICBs (PD + ICB), 61 patients with PD without ICBs (PD ? ICB), and 50 healthy controls. A much higher proportion of PD + ICB (27.8%) than PD ? ICB (3.5%) were hoarders (P = 0.001). 6% of healthy controls were hoarders. Compulsive shoppers scored higher than other varieties of ICB on excessive acquisition measures. Hoarding correlated positively with impulsive buying, obsessive‐compulsive symptoms, PD duration, and negatively with self‐control measures. Using multivariate regression analyzes, the presence of ICBs and measures of impulsive buying were the only variables independently associated with hoarding in PD. The association of hoarding with other ICBs and low trait impulse control suggests that excessive hoarding is related to the spectrum of impulsive behaviors in PD. © 2010 Movement Disorder Society     

Parkinson's disease duration determines effect of dopaminergic therapy on ventral striatum function

We investigated the hypothesis that variation in endogenous dopamine (DA) across brain regions explains dissimilar effects of dopaminergic therapy on aspects of cognition in early Parkinson's disease (PD). Extensive degeneration of DA‐producing cells in the substantia nigra cause dorsal striatum (DS) DA deficiency and movement abnormalities. Particularly in early PD, this contrasts with relative sparing of the dopaminergic cells of the ventral tegmental area (VTA). 1 The hypothesis predicts that DS‐mediated cognitive functions are deficient at baseline and improved by DA replacement, whereas functions depending upon VTA‐innervated brain regions are normal off medication and worsen with treatment. The latter pattern presumably owes to overdose of relatively DA‐replete VTA‐supplied brain regions with medication levels titrated to DS‐mediated motor symptoms. 2 , 3 As PD progresses, however, VTA degeneration increases. Impairment in cognitive operations performed by VTA‐innervated brain regions, such as the ventral striatum (VS), is expected. We compared the performance of early and late PD patients, on and off dopaminergic medication, relative to age‐matched controls, on reward learning, previously shown to implicate the VS. As expected, in early PD, stimulus‐reward learning was normal off medication, but worsened with DA replacement. At more advanced disease stages, PD patients learned stimulus‐reward contingencies more poorly than controls and early PD patients off medication. Furthermore, dopaminergic medication did not worsen reward learning in late PD patients, in line with the dopamine overdose hypothesis. Unlike its effect on DS‐mediated functions, however, DA‐replacement therapy did not improve reward learning in late PD patients. © 2012 Movement Disorder Society     

Brain PET substrate of impulse control disorders in Parkinson's disease: A metabolic connectivity study

Impulse control disorders (ICDs) have received increased attention in Parkinson's disease (PD) because of potentially dramatic consequences. Their physiopathology, however, remains incompletely understood. An overstimulation of the mesocorticolimbic system has been reported, while a larger network has recently been suggested. The aim of this study is to specifically describe the metabolic PET substrate and related connectivity changes in PD patients with ICDs. Eighteen PD patients with ICDs and 18 PD patients without ICDs were evaluated using cerebral 18F‐fluorodeoxyglucose positron emission tomography. SPM‐T maps comparisons were performed between groups and metabolic connectivity was evaluated by interregional correlation analysis (IRCA; p < .005, uncorrected; k > 130) and by graph theory (p < .05). PD patients with ICDs had relative increased metabolism in the right middle and inferior temporal gyri compared to those without ICDs. The connectivity of this area was increased mostly with the mesocorticolimbic system, positively with the orbitofrontal region, and negatively with both the right parahippocampus and the left caudate (IRCA). Moreover, the betweenness centrality of this area with the mesocorticolimbic system was lost in patients with ICDs (graph analysis). ICDs are associated in PD with the dysfunction of a network exceeding the mesocorticolimbic system, and especially the caudate, the parahippocampus, and the orbitofrontal cortex, remotely including the right middle and inferior temporal gyri. This latest area loses its central place with the mesocorticolimbic system through a connectivity dysregulation.     

Limbic grey matter changes in early Parkinson's disease

The purpose of this study was to investigate local and network‐related changes of limbic grey matter in early Parkinson's disease (PD) and their inter‐relation with non‐motor symptom severity. We applied voxel‐based morphometric methods in 538 T1 MRI images retrieved from the Parkinson's Progression Markers Initiative website. Grey matter densities and cross‐sectional estimates of age‐related grey matter change were compared between subjects with early PD (n = 366) and age‐matched healthy controls (n = 172) within a regression model, and associations of grey matter density with symptoms were investigated. Structural brain networks were obtained using covariance analysis seeded in regions showing grey matter abnormalities in PD subject group. Patients displayed focally reduced grey matter density in the right amygdala, which was present from the earliest stages of the disease without further advance in mild‐moderate disease stages. Right amygdala grey matter density showed negative correlation with autonomic dysfunction and positive with cognitive performance in patients, but no significant interrelations were found with anxiety scores. Patients with PD also demonstrated right amygdala structural disconnection with less structural connectivity of the right amygdala with the cerebellum and thalamus but increased covariance with bilateral temporal cortices compared with controls. Age‐related grey matter change was also increased in PD preferentially in the limbic system. In conclusion, detailed brain morphometry in a large group of early PD highlights predominant limbic grey matter deficits with stronger age associations compared with controls and associated altered structural connectivity pattern. This provides in vivo evidence for early limbic grey matter pathology and structural network changes that may reflect extranigral disease spread in PD. Hum Brain Mapp 38:3566–3578, 2017. © 2017 The Authors Human Brain Mapping Published by Wiley Periodicals, Inc.     

Decreased limbic and increased fronto‐parietal connectivity in unmedicated patients with obsessive‐compulsive disorder

Obsessive‐compulsive disorder (OCD) is characterized by recurrent intrusive thoughts and ritualized, repetitive behaviors, or mental acts. Convergent experimental evidence from neuroimaging and neuropsychological studies supports an orbitofronto‐striato‐thalamo‐cortical dysfunction in OCD. Moreover, an over excitability of the amygdala and over monitoring of thoughts and actions involving the anterior cingulate, frontal and parietal cortex has been proposed as aspects of pathophysiology in OCD. We chose a data driven, graph theoretical approach to investigate brain network organization in 17 unmedicated OCD patients and 19 controls using resting‐state fMRI. OCD patients showed a decreased connectivity of the limbic network to several other brain networks: the basal ganglia network, the default mode network, and the executive/attention network. The connectivity within the limbic network was also found to be decreased in OCD patients compared to healthy controls. Furthermore, we found a stronger connectivity of brain regions within the executive/attention network in OCD patients. This effect was positively correlated with disease severity. The decreased connectivity of limbic regions (amygdala, hippocampus) may be related to several neurocognitive deficits observed in OCD patients involving implicit learning, emotion processing and expectation, and processing of reward and punishment. Limbic disconnection from fronto‐parietal regions relevant for (re)‐appraisal may explain why intrusive thoughts become and/or remain threatening to patients but not to healthy subjects. Hyperconnectivity within the executive/attention network might be related to OCD symptoms such as excessive monitoring of thoughts and behavior as a dysfunctional strategy to cope with threat and uncertainty. Hum Brain Mapp 35:5617–5632, 2014. © 2014 Wiley Periodicals, Inc.     

Reduced functional connectivity within the limbic cortico‐striato‐thalamo‐cortical loop in unmedicated adults with obsessive‐compulsive disorder

Cortico‐striato‐thalamo‐cortical (CSTC) loops project from the cortex to the striatum, then from the striatum to the thalamus via the globus pallidus, and finally from the thalamus back to the cortex again. These loops have been implicated in Obsessive‐Compulsive Disorder (OCD) with particular focus on the limbic CSTC loop, which encompasses the orbitofrontal and anterior cingulate cortices, as well as the ventral striatum. Resting state functional‐connectivity MRI (rs‐fcMRI) studies, which examine temporal correlations in neural activity across brain regions at rest, have examined CSTC loop connectivity in patients with OCD and suggest hyperconnectivity within these loops in medicated adults with OCD. We used rs‐fcMRI to examine functional connectivity within CSTC loops in unmedicated adults with OCD (n = 23) versus healthy controls (HCs) (n = 20). Contrary to prior rs‐fcMRI studies in OCD patients on medications that report hyperconnectivity in the limbic CSTC loop, we found that compared with HCs, unmedicated OCD participants had reduced connectivity within the limbic CSTC loop. Exploratory analyses revealed that reduced connectivity within the limbic CSTC loop correlated with OCD symptom severity in the OCD group. Our finding of limbic loop hypoconnectivity in unmedicted OCD patients highlights the potential confounding effects of antidepressants on connectivity measures and the value of future examinations of the effects of pharmacological and/or behavioral treatments on limbic CSTC loop connectivity. Hum Brain Mapp 35:2852–2860, 2014. © 2013 Wiley Periodicals, Inc .     

Decreased ventral striatal activity with impulse control disorders in Parkinson's disease

A range of impulse control disorders (ICDs) are reported to occur in Parkinson's disease (PD). However, alterations in brain activity at rest and during risk taking occurring with ICDs in PD are not well understood. We used both arterial spin labeling perfusion functional magnetic resonance imaging (fMRI) to directly quantify resting cerebral blood flow (CBF) and blood oxygenation level dependent (BOLD) fMRI to measure neural responses to risk taking during performance on the Balloon Analogue Risk Task (BART). Eighteen PD patients, either with a diagnosis of one or more ICDs (N = 9) or no lifetime ICD history (N = 9), participated. BOLD fMRI data demonstrated that PD patients without an ICD activate the mesocorticolimbic pathway during risk taking. Compared with non‐ICD patients, ICD patients demonstrated significantly diminished BOLD activity in the right ventral striatum during risk taking and significantly reduced resting CBF in the right ventral striatum. ICDs in PD are associated with reduced right ventral striatal activity at rest and diminished striatal activation during risk taking, suggesting that a common neural mechanism may underlie ICDs in individuals with PD and those without PD. Thus, treatments for ICDs in non‐PD patients warrant consideration in PD patients with ICDs. © 2010 Movement Disorder Society     

Intrinsic brain connectivity predicts impulse control disorders in patients with Parkinson's disease

Background: Impulse control disorders can be triggered by dopamine replacement therapies in patients with PD. Using resting‐state functional MRI, we investigated the intrinsic brain network connectivity at baseline in a cohort of drug‐naive PD patients who successively developed impulse control disorders over a 36‐month follow‐up period compared with patients who did not. Methods: Baseline 3‐Tesla MRI images of 30 drug‐naive PD patients and 20 matched healthy controls were analyzed. The impulse control disorders' presence and severity at follow‐up were assessed by the Questionnaire for Impulsive‐Compulsive Disorders in Parkinson's Disease Rating Scale. Single‐subject and group‐level independent component analysis was used to investigate functional connectivity differences within the major resting‐state networks. We also compared internetwork connectivity between patients. Finally, a multivariate Cox regression model was used to investigate baseline predictors of impulse control disorder development. Results: At baseline, decreased connectivity in the default‐mode and right central executive networks and increased connectivity in the salience network were detected in PD patients with impulse control disorders at follow‐up compared with those without. Increased default‐mode/central executive internetwork connectivity was significantly associated with impulse control disorders development (P < 0.05). Conclusions: Our findings demonstrated that abnormal brain connectivity in the three large‐scale networks characterizes drug‐naive PD patients who will eventually develop impulse control disorders while on dopaminergic treatment. We hypothesize that these divergent cognitive and limbic network connectivity changes could represent a potential biomarker and an additional risk factor for the emergence of impulse control disorders. © 2017 International Parkinson and Movement Disorder Society     

Invariant inhibition to calculate prediction errors?

The ventral tegmental area (VTA) has a pivotal role in motivated behavior. Much of the research on the VTA has focused on the mesocorticolimbic dopamine projections and their role in the computation of a ‘reward prediction error’ (RPE) for reward-guided learning. In a recent study, Zhou et al. report that VTA GABA neurons, the axons of which innervate the ventral pallidum (VP), have a unique role in signaling reward value to the basal ganglia and guiding reward seeking.     

Striatal Dopamine and Reward Prediction Error Signaling in Unmedicated Schizophrenia Patients

Increased striatal dopamine synthesis capacity has consistently been reported in patients with schizophrenia. However, the mechanism translating this into behavior and symptoms remains unclear. It has been proposed that heightened striatal dopamine may blunt dopaminergic reward prediction error signaling during reinforcement learning. In this study, we investigated striatal dopamine synthesis capacity, reward prediction errors, and their association in unmedicated schizophrenia patients (n = 19) and healthy controls (n = 23). They took part in FDOPA-PET and underwent functional magnetic resonance imaging (fMRI) scanning, where they performed a reversal-learning paradigm. The groups were compared regarding dopamine synthesis capacity (Ki^cer), fMRI neural prediction error signals, and the correlation of both. Patients did not differ from controls with respect to striatal Ki^cer. Taking into account, comorbid alcohol abuse revealed that patients without such abuse showed elevated Ki^cer in the associative striatum, while those with abuse did not differ from controls. Comparing all patients to controls, patients performed worse during reversal learning and displayed reduced prediction error signaling in the ventral striatum. In controls, Ki^cer in the limbic striatum correlated with higher reward prediction error signaling, while there was no significant association in patients. Ki^cer in the associative striatum correlated with higher positive symptoms and blunted reward prediction error signaling was associated with negative symptoms. Our results suggest a dissociation between striatal subregions and symptom domains, with elevated dopamine synthesis capacity in the associative striatum contributing to positive symptoms while blunted prediction error signaling in the ventral striatum related to negative symptoms.     

Probabilistic classification learning with corrective feedback is associated with in vivo striatal dopamine release in the ventral striatum,while learning without feedback is not

The basal ganglia (BG) mediate certain types of procedural learning, such as probabilistic classification learning on the ‘weather prediction task’ (WPT). Patients with Parkinson's disease (PD), who have BG dysfunction, are impaired at WPT‐learning, but it remains unclear what component of the WPT is important for learning to occur. We tested the hypothesis that learning through processing of corrective feedback is the essential component and is associated with release of striatal dopamine. We employed two WPT paradigms, either involving learning via processing of corrective feedback (FB) or in a paired associate manner (PA). To test the prediction that learning on the FB but not PA paradigm would be associated with dopamine release in the striatum, we used serial ¹¹C‐raclopride (RAC) positron emission tomography (PET), to investigate striatal dopamine release during FB and PA WPT‐learning in healthy individuals. Two groups, FB, (n = 7) and PA (n = 8), underwent RAC PET twice, once while performing the WPT and once during a control task. Based on a region‐of‐interest approach, striatal RAC‐binding potentials reduced by 13–17% in the right ventral striatum when performing the FB compared to control task, indicating release of synaptic dopamine. In contrast, right ventral striatal RAC binding non‐significantly increased by 9% during the PA task. While differences between the FB and PA versions of the WPT in effort and decision‐making is also relevant, we conclude striatal dopamine is released during FB‐based WPT‐learning, implicating the striatum and its dopamine connections in mediating learning with FB. Hum Brain Mapp 35:5106–5115, 2014. © 2014 The Authors. Human Brain Mapping Published by Wiley Periodicals, Inc.     

Olfactory performance and resting state functional connectivity in non‐demented drug naïve patients with Parkinson's disease

Olfactory performance in Parkinson's disease (PD) is closely associated with subsequent cognitive decline. In the present study, we analyzed the olfaction‐dependent functional connectivity with a hypothesis that olfactory performance would influence functional connectivity within key brain areas of PD. A total of 110 nondemented drug‐naïve patients with PD were subdivided into three groups of high score (PD‐H, n = 23), middle score (PD‐M, n = 64), and low score (PD‐L, n = 23) based on olfactory performance. We performed the resting‐state functional connectivity with seed region of interest in the posterior cingulate cortex (PCC) and caudate. An analysis of functional connectivity revealed that PD‐L patients exhibited a significant attenuation of cortical functional connectivity with the PCC in the bilateral primary sensory areas, right frontal areas, and right parietal areas compared to PD‐H or PD‐M patients. Meanwhile, PD‐L patients exhibited a significant enhancement of striatocortical functional connectivity in the bilateral occipital areas and right frontal areas compared to PD‐H or PD‐M patients. In the voxel‐wise correlation analysis, olfactory performance was positively associated with cortical functional connectivity with the PCC in similar areas of attenuated cortical connectivity in PD‐L patients relative to PD‐H patients. On the other hand, the cortical functional connectivity with the caudate was negatively correlated with olfactory performance in similar areas of increased connectivity in PD‐L patients relative to PD‐H patients. The present study demonstrated that resting state functional connectivity exhibits a distinctive pattern depending on olfactory performance, which might shed light on a meaningful relationship between olfactory impairment and cognitive dysfunction in PD. Hum Brain Mapp 36:1716–1727, 2015. © 2014 Wiley Periodicals, Inc.     

Chronic alcohol intake abolishes the relationship between dopamine synthesis capacity and learning signals in the ventral striatum

Drugs of abuse elicit dopamine release in the ventral striatum, possibly biasing dopamine‐driven reinforcement learning towards drug‐related reward at the expense of non‐drug‐related reward. Indeed, in alcohol‐dependent patients, reactivity in dopaminergic target areas is shifted from non‐drug‐related stimuli towards drug‐related stimuli. Such ‘hijacked’ dopamine signals may impair flexible learning from non‐drug‐related rewards, and thus promote craving for the drug of abuse. Here, we used functional magnetic resonance imaging to measure ventral striatal activation by reward prediction errors (RPEs) during a probabilistic reversal learning task in recently detoxified alcohol‐dependent patients and healthy controls (N = 27). All participants also underwent 6‐[¹⁸F]fluoro‐DOPA positron emission tomography to assess ventral striatal dopamine synthesis capacity. Neither ventral striatal activation by RPEs nor striatal dopamine synthesis capacity differed between groups. However, ventral striatal coding of RPEs correlated inversely with craving in patients. Furthermore, we found a negative correlation between ventral striatal coding of RPEs and dopamine synthesis capacity in healthy controls, but not in alcohol‐dependent patients. Moderator analyses showed that the magnitude of the association between dopamine synthesis capacity and RPE coding depended on the amount of chronic, habitual alcohol intake. Despite the relatively small sample size, a power analysis supports the reported results. Using a multimodal imaging approach, this study suggests that dopaminergic modulation of neural learning signals is disrupted in alcohol dependence in proportion to long‐term alcohol intake of patients. Alcohol intake may perpetuate itself by interfering with dopaminergic modulation of neural learning signals in the ventral striatum, thus increasing craving for habitual drug intake.     

Resting‐state functional connectivity of the bed nucleus of the stria terminalis in post‐traumatic stress disorder and its dissociative subtype

The bed nucleus of the stria terminals (BNST) is a subcortical structure involved in anticipatory and sustained reactivity to threat and is thus essential to the understanding of anxiety and stress responses. Although chronic stress and anxiety represent a hallmark of post‐traumatic stress disorder (PTSD), to date, few studies have examined the functional connectivity of the BNST in PTSD. Here, we used resting state functional Magnetic Resonance Imaging (fMRI) to investigate the functional connectivity of the BNST in PTSD (n = 70), its dissociative subtype (PTSD + DS) (n = 41), and healthy controls (n = 50). In comparison to controls, PTSD showed increased functional connectivity of the BNST with regions of the reward system (ventral and dorsal striatum), possibly underlying stress‐induced reward‐seeking behaviors in PTSD. By contrast, comparing PTSD + DS to controls, we observed increased functional connectivity of the BNST with the claustrum, a brain region implicated in consciousness and a primary site of kappa‐opioid receptors, which are critical to the dynorphin‐mediated dysphoric stress response. Moreover, PTSD + DS showed increased functional connectivity of the BNST with brain regions involved in attention and salience detection (anterior insula and caudate nucleus) as compared to PTSD and controls. Finally, BNST functional connectivity positively correlated with default‐mode network regions as a function of state identity dissociation, suggesting a role of BNST networks in the disruption of self‐relevant processing characterizing the dissociative subtype. These findings represent an important first step in elucidating the role of the BNST in aberrant functional networks underlying PTSD and its dissociative subtype.     

Reduced neural connectivity but increased task‐related activity during working memory in de novo Parkinson patients

Objective: Patients with Parkinson's disease (PD) often suffer from impairments in executive functions, such as working memory deficits. It is widely held that dopamine depletion in the striatum contributes to these impairments through decreased activity and connectivity between task‐related brain networks. We investigated this hypothesis by studying task‐related network activity and connectivity within a sample of de novo patients with PD, versus healthy controls, during a visuospatial working memory task. Methods: Sixteen de novo PD patients and 35 matched healthy controls performed a visuospatial n‐back task while we measured their behavioral performance and neural activity using functional magnetic resonance imaging. We constructed regions‐of‐interest in the bilateral inferior parietal cortex (IPC), bilateral dorsolateral prefrontal cortex (DLPFC), and bilateral caudate nucleus to investigate group differences in task‐related activity. We studied network connectivity by assessing the functional connectivity of the bilateral DLPFC and by assessing effective connectivity within the frontoparietal and the frontostriatal networks. Results: PD patients, compared with controls, showed trend‐significantly decreased task accuracy, significantly increased task‐related activity in the left DLPFC and a trend‐significant increase in activity of the right DLPFC, left caudate nucleus, and left IPC. Furthermore, we found reduced functional connectivity of the DLPFC with other task‐related regions, such as the inferior and superior frontal gyri, in the PD group, and group differences in effective connectivity within the frontoparietal network. Interpretation: These findings suggest that the increase in working memory‐related brain activity in PD patients is compensatory to maintain behavioral performance in the presence of network deficits. Hum Brain Mapp 36:1554–1566, 2015. © 2015 Wiley Periodicals, Inc.     

Ventral striatal prediction error signaling is associated with dopamine synthesis capacity and fluid intelligence

Fluid intelligence represents the capacity for flexible problem solving and rapid behavioral adaptation. Rewards drive flexible behavioral adaptation, in part via a teaching signal expressed as reward prediction errors in the ventral striatum, which has been associated with phasic dopamine release in animal studies. We examined a sample of 28 healthy male adults using multimodal imaging and biological parametric mapping with (1) functional magnetic resonance imaging during a reversal learning task and (2) in a subsample of 17 subjects also with positron emission tomography using 6‐[¹⁸F]fluoro‐L‐DOPA to assess dopamine synthesis capacity. Fluid intelligence was measured using a battery of nine standard neuropsychological tests. Ventral striatal BOLD correlates of reward prediction errors were positively correlated with fluid intelligence and, in the right ventral striatum, also inversely correlated with dopamine synthesis capacity (FDOPA K). When exploring aspects of fluid intelligence, we observed that prediction error signaling correlates with complex attention and reasoning. These findings indicate that individual differences in the capacity for flexible problem solving relate to ventral striatal activation during reward‐related learning, which in turn proved to be inversely associated with ventral striatal dopamine synthesis capacity. Hum Brain Mapp, 2013. © 2012 Wiley Periodicals, Inc.     

The relationship between impulsivity and impulse control disorders in Parkinson's disease

A range of behaviors presumed to be related to dopaminergic medications have been recently recognized in Parkinson's disease (PD). We evaluated 50 consecutive cognitively intact PD patients on stable dopamine agonist and levodopa therapy and 100 healthy controls for compulsive sexual behavior, compulsive buying, or intermittent explosive disorders assessed by the Minnesota Impulsive Disorders Interview (MIDI), pathological gambling (South Oaks Gambling Screen, SOGS), impulsivity (Barratt Impulsiveness Scale), compulsivity (Maudsley obsessional‐compulsive inventory), and depression scores (Geriatric Depression Scale). Overall 28% PD (14/50) and 20% healthy controls (20/100) reported at least one abnormal behavior at MIDI or pathological SOGS score. PD patients had higher scores than controls for impulsivity (P = 0.006), compulsivity (P < 0.001), and depression (P < 0.001). There was no correlation between impulsivity, compulsivity, and depression scores in PD. Male gender and higher impulsivity score, but not dose and kind of dopaminergic medications, were associated in PD with increased probability of impulsive disorders at MIDI. Impulse control disorders are also common in the control population. Individual susceptibility factors, such as high impulsivity and depression, underline abnormal behaviors in PD patients treated with stable dopaminergic therapy. © 2007 Movement Disorder Society     

Risk and learning in impulsive and nonimpulsive patients with Parkinson's disease

Relatively little is known about the interaction between behavioral changes, medication, and cognitive function in Parkinson's disease (PD). We examined working memory, learning and risk aversion in PD patients with and without impulsive or compulsive behavior (ICB) and compared the results with those in a group of age‐matched control subjects. Parkinson patients with PD+ICB had poorer working memory performance than either controls or PD patients without ICB. PD+ICB patients also showed decreased learning from negative feedback and increased learning from positive feedback in off compared with on dopaminergic medication. This interaction between medication status and learning was the opposite of that found in the PD patients without a diagnosis of ICB. Finally, the PD group showed increased risk preference on medication relative to controls, and the subgroup of PD+ICB patients with pathological gambling were overall more risk prone than the PD group. Thus, medication status and an impulsive behavioral diagnosis differentially affect several behaviors in PD. © 2010 Movement Disorder Society     

Are there ethnic differences in impulsive/compulsive behaviors in Parkinson’s disease?

Background and purpose: Recent studies have suggested increased prevalence of impulsive/compulsive behaviors (ICB) in patients with Parkinson’s disease (PD) as compared to general population in different ethnic groups. The spectrum of these behaviors includes dopamine dysregulation syndrome (DDS), punding, pathological gambling (PG), hypersexuality (HS), binge eating (BE), and compulsive shopping (CS). Methods: Two hundred and seventy‐eight consecutive patients with idiopathic PD regularly followed‐up at an outpatient clinic were interviewed and screened for the ICB between September 2008 and December 2008 using designated diagnostic criteria. All patients who screened positive for ICB or obsessive‐compulsive disorder (OCD) were further confirmed by an experienced psychiatrist. Results: Of all the studied patients, 15 patients confirmed to have ICB (lifetime prevalence: 5.60%), 3 (1.12%) were diagnosed to have DDS, 1 (0.37%) punding, 4 (1.49%) PG, 8 (2.99%) HS, 1 (0.37%) BE, 0 (0%) CS. OCD was found in one patient (0.37%). Conclusions: The prevalence of ICB is lower in Taiwan as compared with the Caucasians, with similar risk factors. The possible reasons include differences in ethnicity, environmental, cultural, and social factors as well as the dosage and selection of dopaminergic medications.