Abstract
Impulse control disorders (ICDs) are relatively frequent in patients with Parkinson’s disease (PD), although it is still unclear whether an underlying pathological process plays a significant role in the development of ICD in PD apart from dopaminergic replacement therapy. In this study, we have investigated alterations of white matter tract in drug-naïve PD patients with ICDs via diffusion MRI connectometry. Our results showed that disrupted connectivity in the complex network of dynamic connections between cerebellum, basal ganglia, cortex, and its spinal projections serves as the underlying neuropathology of ICD in PD not interfered with the contribution of dopaminergic replacement therapy. These findings provide the first evidence on involved white matter tracts in the neuropathogenesis of ICD in drug-naïve PD population, supporting the hypothesis that neural disturbances intrinsic to PD may confer an increased risk for ICDs. Future studies are needed to validate the attribution of the impaired corticocerebellar network to impulsivity in PD.
Highlights
Impulse control disorders (ICDs) are repetitive, excessive, and compulsive behaviors, disrupting a person’s function in major areas of life [1]
In order to examine whether an underlying neuropathological process apart from medication-related effects plays a remarkable role in the establishment of ICD in Parkinson’s disease (PD), we investigated alterations of white matter tract in drug-naïve early PD patients with ICDs (PD-ICD) compared to PD patients without ICD (PD-nICD) and healthy controls (HC) via diffusion MRI connectometry
The differences were that connectivity in HC was higher than that in PD-ICD patients in the left and right inferior longitudinal fasciculus (ILF), genu and body of the corpus callosum (CC), the left and right corticospinal tract (CST), the left superior cerebellar peduncle (SCP), and the left and right cingulum (FDR = 0.002)
Summary
Impulse control disorders (ICDs) are repetitive, excessive, and compulsive behaviors, disrupting a person’s function in major areas of life [1]. It is suggested that ICD should be considered as a distinct endophenotype in PD, resulting from neuroanatomical abnormalities in impulse control regions of the brain, which would be provoked mainly by dopaminergic replacement therapy [24]. All these studies have been conducted on PD patients already on dopaminergic treatment, so it is impossible to distinguish these findings as a reflection of treatment [25] or potential biomarkers of ICD in PD. In order to examine whether an underlying neuropathological process apart from medication-related effects plays a remarkable role in the establishment of ICD in PD, we investigated alterations of white matter tract in drug-naïve early PD patients with ICDs (PD-ICD) compared to PD patients without ICD (PD-nICD) and healthy controls (HC) via diffusion MRI connectometry
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