scholarly journals The sooner the better: clinical and neural correlates of impulsive choice in Tourette disorder

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cyril Atkinson-Clement ◽  
Astrid de Liege ◽  
Yanica Klein ◽  
Benoit Beranger ◽  
Romain Valabregue ◽  
...  
Keyword(s):  
Delay Discounting ◽  
Impulse Control ◽  
Ventral Striatum ◽  
Supplementary Motor Area ◽  
Insular Cortex ◽  
Impulse Control Disorders ◽  
Reward Processing ◽  
Motor Area ◽  
Diagnostic Feature ◽  
Tourette Disorder

AbstractReward sensitivity has been suggested as one of the central pathophysiological mechanisms in Tourette disorder. However, the subjective valuation of a reward by introduction of delay has received little attention in Tourette disorder, even though it has been suggested as a trans-diagnostic feature of numerous neuropsychiatric disorders. We aimed to assess delay discounting in Tourette disorder and to identify its brain functional correlates. We evaluated delayed discounting and its brain functional correlates in a large group of 54 Tourette disorder patients and 31 healthy controls using a data-driven approach. We identified a subgroup of 29 patients with steeper reward discounting, characterised by a higher burden of impulse-control disorders and a higher level of general impulsivity compared to patients with normal behavioural performance or to controls. Reward discounting was underpinned by resting-state activity of a network comprising the orbito-frontal, cingulate, pre-supplementary motor area, temporal and insular cortices, as well as ventral striatum and hippocampus. Within this network, (i) lower connectivity of pre-supplementary motor area with ventral striatum predicted a higher impulsivity and a steeper reward discounting and (ii) a greater connectivity of pre-supplementary motor area with anterior insular cortex predicted steeper reward discounting and more severe tics. Overall, our results highlight the heterogeneity of the delayed reward processing in Tourette disorder, with steeper reward discounting being a marker of burden in impulsivity and impulse control disorders, and the pre-supplementary motor area being a hub region for the delay discounting, impulsivity and tic severity.

scholarly journals Inhibitory control dysfunction in parkinsonian impulse control disorders

Brain ◽  
2020 ◽  
Author(s):  
Garance M Meyer ◽  
Charlotte Spay ◽  
Alina Beliakova ◽  
Gabriel Gaugain ◽  
Gianni Pezzoli ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inhibitory Control ◽  
Response Inhibition ◽  
Impulse Control ◽  
Supplementary Motor Area ◽  
Impulse Control Disorders ◽  
Motor Area ◽  
Beta Activity ◽  
Visuomotor Task

Abstract Impulse control disorders (ICDs) in Parkinson’s disease have been associated with dysfunctions in the control of value- or reward-based responding (choice impulsivity) and abnormalities in mesocorticolimbic circuits. The hypothesis that dysfunctions in the control of response inhibition (action impulsivity) also play a role in Parkinson’s disease ICDs has recently been raised, but the underlying neural mechanisms have not been probed directly. We used high-resolution EEG recordings from 41 patients with Parkinson’s disease with and without ICDs to track the spectral and dynamical signatures of different mechanisms involved in inhibitory control in a simple visuomotor task involving no selection between competing responses and no reward to avoid potential confounds with reward-based decision. Behaviourally, patients with Parkinson’s disease with ICDs proved to be more impulsive than those without ICDs. This was associated with decreased beta activity in the precuneus and in a region of the medial frontal cortex centred on the supplementary motor area. The underlying dynamical patterns pinpointed dysfunction of proactive inhibitory control, an executive mechanism intended to gate motor responses in anticipation of stimulation in uncertain contexts. The alteration of the cortical drive of proactive response inhibition in Parkinson’s disease ICDs pinpoints the neglected role the precuneus might play in higher order executive functions in coordination with the supplementary motor area, specifically for switching between executive settings. Clinical perspectives are discussed in the light of the non-dopaminergic basis of this function.

scholarly journals Abnormal interhemispheric resting state functional connectivity in Parkinson’s disease patients with impulse control disorders

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Caiting Gan ◽  
Lina Wang ◽  
Min Ji ◽  
Kewei Ma ◽  
Huimin Sun ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Functional Connectivity ◽  
Resting State ◽  
Impulse Control ◽  
Diffusion Tensor ◽  
Inferior Frontal Gyrus ◽  
Impulse Control Disorders ◽  
Reward Processing ◽  
The Mean

AbstractImpulse control disorders (ICD) in Parkinson’s disease (PD) might be attributed to misestimate of rewards or the failure to curb inappropriate choices. The mechanisms underlying ICD were reported to involve the lateralization of monoamine network. Our objective was to probe the significant role of lateralization in the pathogenesis of ICD. Twenty-one PD patients with ICD (PD-ICD), thirty-three without ICD (PD-no ICD), and thirty-seven healthy controls (HCs) were recruited and performed T1-weighted, diffusion tensor imaging (DTI) scans and resting state functional magnetic resonance imaging (rs-fMRI). By applying the Voxel-mirrored Homotopic Connectivity (VMHC) and Freesurfer, we evaluated participants’ synchronicity of functional connectivity and structural changes between hemispheres. Also, tract-based spatial statistics (TBSS) was applied to compare fiber tracts differences. Relative to PD-no ICD group, PD-ICD group demonstrated reduced VMHC values in middle frontal gyrus (MFG). Compared to HCs, PD-ICD group mainly showed decreased VMHC values in MFG, middle and superior orbital frontal gyrus (OFG), inferior frontal gyrus (IFG) and caudate, which were related to reward processing and inhibitory control. The severity of impulsivity was negatively correlated with the mean VMHC values of MFG in PD-ICD group. Receiver operating characteristic (ROC) curves analyses uncovered that the mean VMHC values of MFG might be a potential marker identifying PD-ICD patients. However, we found no corresponding asymmetrical alteration in cortical thickness and no significant differences in fractional anisotropy (FA) and mean diffusivity (MD). Our results provided further evidence for asymmetry of functional connectivity in mesolimbic reward and response inhibition network in ICD.

Current Classification of Impulse Control Disorders: Neurocognitive and Behavioral Models of Impulsivity and the Role of Personality

2012 ◽  
Author(s):  
Ashwini K. Padhi ◽  
Ali M. Mehdi ◽  
Kevin J. Craig ◽  
Naomi A. Fineberg
Keyword(s):  
Impulse Control ◽  
Impulse Control Disorders ◽  
Reward Processing ◽  
Impulsive Behavior ◽  
Behavioral Models ◽  
Current Classification ◽  
Motor Impulsivity ◽  
Compulsive Disorders

Impulse control disorders (ICDs) are common disabling disorders that have impulsive behavior as a core feature. They emerge early in life and run a chronic lifelong course. They are assumed to lie at the severest end of a continuum of impulsivity that connects normal with pathological states. People with ICDs experience a drive to undertake repetitive acts. Although the consequences are damaging, performance of the impulsive act may be experienced as rewarding, or alternatively may relieve distress, implicating dysfunction of the neural circuitry involved in reward processing and/or behavioral inhibition. Clinical data are increasingly pointing toward an etiological association between some ICDs, such as pathological gambling and addiction, and others, such as trichotillomania and compulsive disorders. Comorbidity with other psychiatric disorders is also common, and hints at overlapping psychobiological processes across several diagnostic groups. The results of neurocognitive studies suggest that impulsivity is multidimensional and comprises dissociable cognitive and behavioral indices governed by separate underlying neural mechanisms. For example, trichotillomania may primarily involve motor impulsivity, whereas problem gambling may involve reward impulsivity and reflection impulsivity. Exploring neurocognitive changes in individuals with ICDs and other mental disorders characterized by poor impulse control, and among their family members, may help to elucidate the underpinning neurocircuitry and clarify their nosological status.

scholarly journals Unlucky punches: the vulnerability-stress model for the development of impulse control disorders in Parkinson’s disease

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Hendrik Theis ◽  
Catharina Probst ◽  
Pierre-Olivier Fernagut ◽  
Thilo van Eimeren
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Replacement Therapy ◽  
Impulse Control ◽  
Ventral Striatum ◽  
Impulse Control Disorders ◽  
Current Evidence ◽  
Relative Reduction ◽  
Stress Model ◽  
Dopamine Replacement Therapy

AbstractImpulse-control disorders are commonly observed during dopamine-replacement therapy in Parkinson’s disease, but the majority of patients seems “immune” to this side effect. Epidemiological evidence suggests that a major risk factor may be a specific difference in the layout of the dopaminergic-reinforcement system, of which the ventral striatum is a central player. A series of imaging studies of the dopaminergic system point toward a presynaptic reduction of dopamine-reuptake transporter density and dopamine synthesis capacity. Here, we review current evidence for a vulnerability-stress model in which a relative reduction of dopaminergic projections to the ventral striatum and concomitant sensitization of postsynaptic neurons represent a predisposing (hypodopaminergic) vulnerability. Stress (hyperdopaminergic) is delivered when dopamine replacement therapy leads to a relative overdosing of the already-sensitized ventral striatum. These alterations are consistent with consecutive changes in reinforcement mechanisms, which stimulate learning from reward and impede learning from punishment, thereby fostering the development of impulse-control disorders. This vulnerability-stress model might also provide important insights into the development of addictions in the non-Parkinsonian population.

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