Abstract
Neurodegenerative change in the central nervous system has been suggested as one of the pathophysiological mechanisms of autonomic nervous system dysfunction in Parkinson’s disease (PD). We analyzed gray matter (GM) volume changes and clinical parameters in patients with PD to investigate any involvement in the brain structures responsible for autonomic control in patients with PD having orthostatic hypotension (OH). Voxel-based morphometry was applied to compare regional GM volumes between PD patients with and without OH. Multivariate logistic regression analysis using a hierarchical model was carried out to identify clinical factors independently contributing to the regional GM volume changes in PD patients with OH. The Sobel test was used to analyze mediation effects between the independent contributing factors to the GM volume changes. PD patients with OH had more severe autonomic dysfunction and reduction in volume in the right inferior temporal cortex than those without OH. The right inferior temporal volume was positively correlated with the Qualitative Scoring MMSE Pentagon Test (QSPT) score, reflecting visuospatial/visuoperceptual function, and negatively correlated with the Composite Autonomic Severity Score (CASS). The CASS and QSPT scores were found to be factors independently contributing to regional volume changes in the right inferior temporal cortex. The QSPT score was identified as a mediator in which regional GM volume predicts the CASS. Our findings suggest that a decrease in the visuospatial/visuoperceptual process may be involved in the presentation of autonomic nervous system dysfunction in PD patients.
Highlights
Orthostatic hypotension (OH) is a common and debilitating manifestation of autonomic dysfunction in patients with Parkinson’s disease (PD) [1,2]
Our findings suggest that a decrease in the visuospatial/visuoperceptual process may be involved in the presentation of autonomic nervous system dysfunction in PD patients
Pathological studies have demonstrated that neurodegenerative processes associated with α-synucleinopathies in PD occur along the central autonomic network, including the hypothalamus, dorsal motor nucleus of the vagus, and insular cortex [4,5,6]; this suggests that selective involvement of neurodegeneration in the brain structures responsible for autonomic control might be implicated in the pathophysiological mechanism underlying OH in PD patients
Summary
Orthostatic hypotension (OH) is a common and debilitating manifestation of autonomic dysfunction in patients with Parkinson’s disease (PD) [1,2]. Pathological studies have demonstrated that neurodegenerative processes associated with α-synucleinopathies in PD occur along the central autonomic network, including the hypothalamus, dorsal motor nucleus of the vagus, and insular cortex [4,5,6]; this suggests that selective involvement of neurodegeneration in the brain structures responsible for autonomic control might be implicated in the pathophysiological mechanism underlying OH in PD patients. In addition to the direct involvement of neurodegeneration in the central autonomic network, the relationship is causative or associative is unclear, increasing evidence suggests that cognitive impairment could be associated with OH in patients with PD [7,8,9,10,11]. Understanding the mechanisms of the link between OH and cognitive function in PD may provide insight into the management strategy that could ameliorate subsequent cognitive decline in PD patients [13]
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