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From anticipation to impulsivity in Parkinson's disease.

ABSTRACT: Anticipatory actions require to keep track of elapsed time and inhibitory control. These cognitive functions could be impacted in Parkinson's disease (iPD). To test this hypothesis, a saccadic reaction time task was used where a visual warning stimulus (WS) predicted the occurrence of an imperative one (IS) appearing after a short delay. In the implicit condition, subjects were not informed about the duration of the delay, disfavoring anticipatory behavior but leaving inhibitory control unaltered. In the explicit condition, delay duration was cued. This should favor anticipatory behavior and perhaps alter inhibitory control. This hypothesis was tested in controls (N = 18) and age-matched iPD patients (N = 20; ON and OFF L-DOPA). We found that the latency distribution of saccades before the IS was bimodal. The 1^st mode weakly depended on temporal information and was more prominent in iPD. Saccades in this mode were premature and could result of a lack of inhibition. The 2^nd mode covaried with cued duration suggesting that these movements were genuine anticipatory saccades. The explicit condition increased the probability of anticipatory saccades before the IS in controls and iPD_ON but not iPD_OFF patients. Furthermore, in iPD patients the probability of sequences of 1^st mode premature responses increased. In conclusion, the triggering of a premature saccade or the initiation of a controlled anticipatory one could be conceptualized as the output of two independent stochastic processes. Altered time perception and increased motor impulsivity could alter the balance between these two processes in favor of the latter in iPD, particularly OFF L-Dopa.

SUBMITTER: Degos B

PROVIDER: S-EPMC9527232 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

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From anticipation to impulsivity in Parkinson's disease.

Degos Bertrand B Pouget Pierre P Missal Marcus M

NPJ Parkinson's disease 20221003 1

Anticipatory actions require to keep track of elapsed time and inhibitory control. These cognitive functions could be impacted in Parkinson's disease (iPD). To test this hypothesis, a saccadic reaction time task was used where a visual warning stimulus (WS) predicted the occurrence of an imperative one (IS) appearing after a short delay. In the implicit condition, subjects were not informed about the duration of the delay, disfavoring anticipatory behavior but leaving inhibitory control unaltere ...[more]

PMID: 36184657

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Project description:Impulsive-compulsive behaviours manifest in a substantial proportion of subjects with Parkinson's disease. Reduced ventral striatum dopamine receptor availability, and increased dopamine release is noted in patients with these symptoms. Prior studies of impulsivity suggest that midbrain D2 autoreceptors regulate striatal dopamine release in a feedback inhibitory manner, and in healthy populations, greater impulsivity is linked to poor proficiency of this inhibition. This has not been assessed in a Parkinson's disease population. Here, we applied 18F-fallypride PET studies to assess striatal and extrastriatal D2-like receptor uptake in a placebo-controlled oral dextroamphetamine sequence. We hypothesized that Parkinson's disease patients with impulsive-compulsive behaviours would have greater ventral striatal dopaminergic response to dextroamphetamine, and that an inability to attenuate ventral striatal dopamine release via midbrain D2 autoreceptors would underlie this response. Twenty patients with Parkinson's disease (mean age = 64.1 ± 5.8 years) both with (n = 10) and without (n = 10) impulsive-compulsive behaviours, participated in a single-blind dextroamphetamine challenge (oral; 0.43 mg/kg) in an OFF dopamine state. All completed PET imaging with 18F-fallypride, a high-affinity D2-like receptor ligand, in the placebo and dextroamphetamine state. Both voxelwise and region of interest analyses revealed dextroamphetamine-induced endogenous dopamine release localized to the ventral striatum, and the caudal-medial orbitofrontal cortex. The endogenous dopamine release observed in the ventral striatum correlated positively with patient-reported participation in reward-based behaviours, as quantified by the self-reported Questionnaire for Impulsivity in Parkinson's disease Rating Scale. In participants without impulsive-compulsive behaviours, baseline midbrain D2 receptor availability negatively correlated with ventral striatal dopamine release; however, this relationship was absent in those with impulsive-compulsive behaviours. These findings emphasize that reward-based behaviours in Parkinson's disease are regulated by ventral striatal dopamine release, and suggest that loss of inhibitory feedback from midbrain autoreceptors may underlie the manifestation of impulsive-compulsive behaviours.

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From anticipation to impulsivity in Parkinson's disease.

Publications

From anticipation to impulsivity in Parkinson's disease.

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