"Punders are aware of the inapposite obtuse nature of the behaviors but even self-injury resulting from the stereotypes does not abort them (Evans et al., 2004). A positive correlation between the severities of punding and dyskinesia was found (Silveira-Moriyama et al., 2006). Moreover, a 52.8% higher prevalence of dyskinesia in punders over non-punders in Japan was reported (Miwa et al., 2004). "
[Show abstract][Hide abstract] ABSTRACT: Background: Impulsive and compulsive behaviors (ICBs) are a heterogeneous group of conditions that may be caused by long-term dopaminergic replacement therapy (DRT) of Parkinson’s disease (PD). The spectrum of ICBs includes dopamine dysregulation syndrome (DDS), punding, and impulse control disorders (ICDs).
Contents: We made a detailed review regarding the epidemiology, pathology, clinical characteristics, risk factors, diagnosis as well as treatment of ICBs.
Results: The prevalence of ICBs in PD patients is approximately 3–4% for DDS, 0.34–4.2% for punding, and 6–14% for ICDs, with higher prevalence in Western populations than in Asian. Those who take high dose of levodopa are more prone to have DDS, whereas, ICDs are markedly associated with dopamine agonists. Different subtypes of ICBs share many risk factors such as male gender, higher levodopa equivalent daily dose, younger age at PD onset, history of alcoholism, impulsive, or novelty-seeking personality. The Questionnaire for Impulsive–Compulsive Disorder in Parkinson’s Disease-Rating Scale seems to be a rather efficacious instrument to obtain relevant information from patients and caregivers. Treatment of ICBs is still a great challenge for clinicians. Readjustment of DRT remains the primary method. Atypical antipsychotics, antidepressants, amantadine, and psychosocial interventions are also prescribed in controlling episodes of psychosis caused by compulsive DRT, but attention should be drawn to balance ICBs symptoms and motor disorders. Moreover, deep brain stimulation of the subthalamic nucleus might be a potential method in controlling ICBs.
Conclusion: The exact pathophysiological mechanisms of ICBs in PD remains poorly understood. Further researches are needed not only to study the pathogenesis, prevalence, features, and risk factors of ICBs, but to find efficacious therapy for patients with these devastating consequences.
"Patients with punding received higher L-dopa and agonist-LEDD, and presented longer disease duration but not duration of treatment. Previous studies have suggested a relationship both with the dose of levodopa and the duration of treatment . Similar to previous studies the ICD-group showed clear relation to DA with a higher proportion taking DAs, and higher total and agonist-LEDD. "
[Show abstract][Hide abstract] ABSTRACT: •Compulsive eating was not related to dopaminergic replacement therapy.•Other impulse control disorders showed clear relation to dopamine agonist therapy.•Punding was associated with higher dose of both dopamine agonists and L-dopa.•Rotigotine might cause less ICRBDs than other dopamine agonists.
Journal of the Neurological Sciences 07/2014; 345(1-2). DOI:10.1016/j.jns.2014.07.004 · 2.47 Impact Factor
"Recent studies hypothesize that levodopa-induced dyskinesias (LIDs) and behavioral alterations observed in dopamine dysregulation syndrome and ICD2,18 depend on common mechanisms involving alterations of glutamate homeostasis with combined activation of sensitized dopamine and NMDA glutamatergic receptors.19 Pre- and postsynaptic mechanisms are implicated in the devolvement of LIDs and ICDs, the first based on alterations in dopamine transmission after chronic administrations and the second because of excessive expression and sensitization of D1 receptors in striatonigral neurons.2,20 "
[Show abstract][Hide abstract] ABSTRACT: Introduction
Dopamine replacement therapy for Parkinson’s disease (PD) was recently linked to the development of impulse control disorders such as pathological gambling (PG), hypersexuality, compulsive shopping, and binge or compulsive eating. Antiglutamatergic agents including amantadine (Ama) reduce these behaviors in PD and non-PD patients. The aim of our study is to evaluate the changes in executive functions, emotions, and reward/loss processing during Ama treatment in PD patients.
Thirty-three patients affected by idiopathic PD were selected from a cohort of 1,096 PD patients and categorized in three different groups: ten affected by PG (PD-PG); nine PD patients with other impulse control disorder (PD-ICD); and 14 PD patient without any psychiatric disorder (PD-CTR-controls). For the neuropsychological evaluation, the following behavioral tasks where administered: the Stroop, the emotional Stroop, and the monetary reward/loss risk-taking tasks.
During Ama treatment, PD-PGs showed a decrease in risky choices and an increase in non-risky choices (t(9)=−2.40, P<0.05 and t(9)=2,67, P<0.05 uncorrected, respectively). Between-group comparison showed a significant decrease in risky choices for PD-PG with respect to PD-CTR (t(22)=−4.16, P<0.01), and a decreased accuracy for positive words in comparison between PD-PG and PD-ICD (t(17)=−7,49, P<0.01) and PD-PG and PD-CTR (t(22)=−4.29, P<0.01). No within- and between-group differences were observed for Stroop task.
Our data showed that Ama add-on therapy reduces hypersensitivity to reward and sustains activation toward uncertainty in PD-PG patients. These finding might explain the behavioral mechanism underlying the effect of antiglutamatergic drugs.
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