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Introduction: Dopaminergic medications can trigger impulsive-compulsive behaviors (ICBs) in pre-disposed patients with Parkinson's disease (PD), but what this implies on a neurocognitive level is unclear. Previous findings highlighted potentially exacerbated incentive motivation (willingness to work for rewards) and choice impulsivity (preferring smaller, immediate rewards over larger, delayed rewards) in PD patients with ICBs (PD + ICBs)., Methods: To deeply understand this evidence, we studied 24 PD + ICBs and 28 PD patients without ICBs (PD-ICBs). First of all, patients underwent the assessment of impulsivity traits, mood, anxiety, and addiction condition. We further administered robust objective and subjective measures of specific aspects of motivation. Finally, we explored whether these processes might link to any heightened antisocial behavior (aggression and risky driving) in PD + ICBs., Results: High levels of positive urgency trait characterized PD + ICBs. They choose to exert more effort for rewards under the conditions of low and medium reward probability and as reward magnitude increases. Findings on choice impulsivity show a great tendency to delay discounting in PD + ICBs, other than a high correlation between delay and probability discounting. In addition, we found what appears to be the first evidence of heightened reactive aggression in PD patients with ICBs. Exacerbated incentive motivation and delay discounting trended toward positively predicting reactive aggression in PD + ICBs., Discussion: Our promising results suggest that there might be immense value in future large-scale studies adopting a transdiagnostic neurocognitive endophenotype approach to understanding and predicting the addictive and aggressive behaviors that can arise from dopaminergic medication in PD., Competing Interests: AC has provided paid expert testimony in a civil litigation case involving patients with PD and a manufacturer of DAs. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Dawson, Ortelli, Carter, Ferrazzoli, Dissanayaka, Evans, Chye, Lorenzetti, Frazzitta and Yücel.)

Patients with severe mental illnesses may present extrapyramidal symptoms as part of a concomitant neurological disorder or secondary to medications. Extrapyramidal symptoms are frequently unrecognized, have negative consequences for adherence to treatment, negatively affect quality of life and can induce stigma. We estimated and correlated with demographic and clinical variables prevalence of extrapyramidal symptoms in in-patients with severe mental illnesses. Additionally we evaluated 123 I-FP-CIT SPECT binding to striatal dopamine transporter in subjects with clinical manifestations suggestive of Parkinson's Disease and recorded therapeutic management and clinical evolution for 6-months. Extrapyramidal symptoms were present in 144 out of 285 patients (50.5%), mainly tremor (94 patients, 33%). There were 38 patients (13.3%) with parkinsonism and they had older age, more medical comorbidities and medical treatments. In 15/38 patients striatal dopamine transporter binding was abnormal resulting in dose reduction or change of psychotropic drugs as well as combination with antiparkinson therapy. Our study confirmed the clinical and epidemiological relevance of extrapyramidal symptoms among inpatients with severe mental illnesses. A small percentage of patients with extrapyramidal symptoms had features compatible with possible diagnosis of Parkinson's Disease. 123 I-FP-CIT SPECT was useful to identify dopaminergic dysfunction and initiate dopamine replacement therapy., (Copyright © 2020 Roiter, Pigato and Antonini.)

The principal feature of Parkinson's disease (PD) is the impaired ability to acquire and express habitual-automatic actions due to the loss of dopamine in the dorsolateral striatum, the region of the basal ganglia associated with the control of habitual behavior. Dopamine replacement therapy (DRT) compensates for the lack of dopamine, representing the standard treatment for different motor symptoms of PD (such as rigidity, bradykinesia and resting tremor). On the other hand, rehabilitation treatments, exploiting the use of cognitive strategies, feedbacks and external cues, permit to "learn to bypass" the defective basal ganglia (using the dorsolateral area of the prefrontal cortex) allowing the patients to perform correct movements under executive-volitional control. Therefore, DRT and rehabilitation seem to be two complementary and synergistic approaches. Learning and reward are central in rehabilitation: both of these mechanisms are the basis for the success of any rehabilitative treatment. Anyway, it is known that "learning resources" and reward could be negatively influenced from dopaminergic drugs. Furthermore, DRT causes different well-known complications: among these, dyskinesias, motor fluctuations, and dopamine dysregulation syndrome (DDS) are intimately linked with the alteration in the learning and reward mechanisms and could impact seriously on the rehabilitative outcomes. These considerations highlight the need for careful titration of DRT to produce the desired improvement in motor symptoms while minimizing the associated detrimental effects. This is important in order to maximize the motor re-learning based on repetition, reward and practice during rehabilitation. In this scenario, we review the knowledge concerning the interactions between DRT, learning and reward, examine the most impactful DRT side effects and provide suggestions for optimizing rehabilitation in PD.