Brain Atrophy and Reorganization of Structural Network in Parkinson's Disease With Hemiparkinsonism

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.

Alterations of Brain Structural Network in Parkinson’s Disease With and Without Rapid Eye Movement Sleep Behavior Disorder

“…Nodal properties could be divided to two field, nodal centralities (e.g., nodal degree and nodal betweenness) and nodal cliquishness properties (e.g., nodal local efficiency and nodal clustering coefficient) ( 35 , 36 , 57 ). In our study, we showed a shift between nodal centralities and nodal cliquishness properties in PD-pRBD.…”

Neural correlates of distinct cognitive phenotypes in early Parkinson's disease

“…The only differences between Weak-Visuospatial class and the Typical class were weakness in visuospatial functioning, and atrophy in left rolandic operculum including the precentral gyrus and the insula. In PD, atrophy of the Rolandic operculum has been seen in patients with mild to moderate diseases [33]. In particular, left insular atrophy has been shown to correlate with visuospatial performance in PD-MCI [34].…”

Asymmetrical nigral iron accumulation in Parkinson’s disease with motor asymmetry: an explorative, longitudinal and test-retest study

“…As numerously documented, along the disease trajectory, most PD patients would experience a special stage (Hoehn-Yahr stage = 1 and 1.5), hemiparkinsonism [ 6 , 21 , 46 ], when motor symptoms only occur in the unilateral side of limbs while the other side of limbs is possibly unaffected. In this section, we aimed to extend previous findings to the patients in this special stage.…”

“…Second, the sample sizes included in these studies were relatively small. Last but not least, none of them tested the hypothesis in both PD patients with bilaterally asymmetrically affected limbs, and with unilaterally affected limbs (known as hemiparkinsonism [ 6 , 21 ]).…”