Abstract
BackgroundPunding, one of dopamine replacement treatment related complications, refers to aimless and stereotyped behaviors. To identify possible neural correlates of punding behavior in patients with Parkinson’s disease (PD), we investigated the patterns of cognitive profiles and cortical thinning.MethodsOf the 186 subjects with PD screened during the study period, we prospectively enrolled 10 PD patients with punding and 43 without punding on the basis of a structured interview. We performed comprehensive neuropsychological tests and voxel-based and regions-of-interest (ROIs)-based cortical thickness analysis between PD patients with and without punding.ResultsThe prevalence of punding in patients with PD was 5.4%. Punding behaviors were closely related to previous occupations or hobbies and showed a temporal relationship to changes of levodopa-equivalent dose (LED). Significant predisposing factors were a long duration of PD and intake of medications of PD, high total daily LED, dyskinesia, and impulse control disorder. Punding severity was correlated with LED (p = 0.029). The neurocognitive assessment revealed that PD patients with punding showed more severe cognitive deficits in the color Stroop task than did those without punding (p = 0.022). Voxel-based analysis showed that PD-punders had significant cortical thinning in the dorsolateral prefrontal area relative to controls. Additionally, ROI-based analysis revealed that cortical thinning in PD-punders relative to PD-nonpunders was localized in the prefrontal cortices, extending into orbitofrontal area.ConclusionsWe demonstrated that PD patients with punding performed poorly on cognitive tasks in frontal executive functions and showed severe cortical thinning in the dorsolateral prefrontal and orbitofrontal areas. These findings suggest that prefrontal modulation may be an essential component in the development of punding behavior in patients with PD.
Highlights
Parkinson’s disease (PD), a chronic neurodegenerative disease caused by a loss of nigral dopaminergic neurons, is characterized clinically by cardinal motor symptoms, such as bradykinesia, tremor, rigidity, and postural instability
Significant predisposing factors were a long duration of PD and intake of medications of PD, high total daily levodopa-equivalent dose (LED), dyskinesia, and impulse control disorder
ROI-based analysis revealed that cortical thinning in PD-punders relative to PD-nonpunders was localized in the prefrontal cortices, extending into orbitofrontal area
Summary
Parkinson’s disease (PD), a chronic neurodegenerative disease caused by a loss of nigral dopaminergic neurons, is characterized clinically by cardinal motor symptoms, such as bradykinesia, tremor, rigidity, and postural instability. Non-motor symptoms, including psychiatric and behavioral disorders have become the focus of active concern because these symptoms can lead to a greater level of incapacity than do motor complications.[1] Today, dopamine replacement treatment (DRT)-related complications are attracting more attention. Punding refers to aimless and stereotyped behaviors and encompasses complex, non-productive, and repetitive activities such as manipulations of technical equipment, cleaning or tidying, sorting of common objects, and hoarding. In the present study, we investigated the patterns of cognitive profiles and regional cortical thinning to identify possible neural correlates of punding behavior in patients with PD using comprehensive neuropsychological tests and voxel-based cortical thickness analysis. One of dopamine replacement treatment related complications, refers to aimless and stereotyped behaviors. To identify possible neural correlates of punding behavior in patients with Parkinson’s disease (PD), we investigated the patterns of cognitive profiles and cortical thinning
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