Abstract
Hemiparkinsonism duration in patients with Parkinson's disease (PD) is a key time window to study early pathology of PD. We aimed to comprehensively explore the alterations of deformation and structural network in PD patients with hemiparkinsonism, which could potentially disclose the early biomarker for PD. Thirty-one PD patients with hemiparkinsonism and 37 age- and gender- matched normal controls were included in the present study. First of all, we normalized the left hemisphere of structural images as the contralateral side to the affected limbs. Deformation-based morphometry (DBM) was conducted to evaluate the brain atrophy and/or enlargement. structural networks were constructed by thresholding gray matter volume correlation matrices of 116 regions and analyzed using graph theoretical approaches (e.g., small-worldness, global, and nodal measures). Significantly decreased deformation values were observed in the temporoparietal regions like bilateral middle temporal gyri, ipsilateral precuneus and contralateral Rolandic operculum extending to supramarginal and postcentral gyri. Lower deformation values in contralateral middle temporal gyrus were negatively correlated with higher motor impairment which was dominated by akinesia/rigidity. Moreover, nodal reorganization of structural network mainly located in frontal, temporal, subcortex and cerebellum was bilaterally explored in PD patients with hemiparkinsonism. Increased nodal properties could be commonly observed in frontal lobes. Disruption of subcortex including basal ganglia and amygdala was detected by nodal local efficiency and nodal clustering coefficient. Twelve hubs, mainly from paralimbic-limbic and heteromodal networks, were disrupted and, alternatively, 14 hubs, most of which were located in frontal lobes, were additionally detected in PD patients with hemiparkinsonism. In conclusion, during hemiparkinsonism period, mild brain atrophy in the temporoparietal regions and widespread reorganization of structural network, e.g., enhanced frontal function and disruption of basal ganglia nodes, occurred in both hemispheres. With our data, we can also argue that MTG contralateral to the affected limbs (expressing clinically verified brain atrophy) might be a potential living biomarker to monitor disease progression. Therefore, the combination of DBM and structural network analyses can provide a comprehensive and sensitive evaluation for potential pathogenesis of early PD patients with hemiparkinsonism.
Highlights
Parkinson’s disease (PD) is becoming acknowledged as a multisystem disease gradually involving the whole brain following an ascending pattern from the lower brainstem to cortical areas (Braak et al, 2003; Braak and Del, 2008)
Though early PD patients including those who suffered from hemiparkinsonism were investigated (Borghammer et al, 2010; Agosta et al, 2013; Luo et al, 2015), studies have rarely tried to customize experimental protocols focusing on hemiparkinsonism except for a recent study showing bilaterally widespread functional alterations of the cortico-striatal-thalamic network (Agosta et al, 2014)
Through analyzing nodal measures in structural correlation network (SCN), we found that, (1) bilaterally nodal reorganization of SCN mainly composed of frontal, temporal, subcortex and cerebellum was explored in PD patients with hemiparkinsonism; (2) increased nodal properties could be commonly observed in frontal lobes, which was consistently seen in the hub analysis; (3) disruption of subcortex including basal ganglia and amygdala was detected by nodal local efficiency and clustering coefficient but not centralities, which indicated that the dysfunction in these regions was more likely localized in certain subgraph
Summary
Parkinson’s disease (PD) is becoming acknowledged as a multisystem disease gradually involving the whole brain following an ascending pattern from the lower brainstem to cortical areas (Braak et al, 2003; Braak and Del, 2008). Though early PD patients including those who suffered from hemiparkinsonism were investigated (Borghammer et al, 2010; Agosta et al, 2013; Luo et al, 2015), studies have rarely tried to customize experimental protocols focusing on hemiparkinsonism except for a recent study showing bilaterally widespread functional alterations of the cortico-striatal-thalamic network (Agosta et al, 2014) While such evidence is far from explaining the disease substrates of PD hemiparkinsonism, the exploration of the structural basis for disease unilaterality in hemiparkinsonism might lead to an improved understanding of the underlying pathogenesis of early PD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
