White matter alterations in early Parkinson’s disease: role of motor symptom lateralization

2019 ◽  
Vol 41 (2) ◽  
pp. 357-364 ◽  
Author(s):  
Laura Pelizzari ◽  
Sonia Di Tella ◽  
Maria M. Laganà ◽  
Niels Bergsland ◽  
Federica Rossetto ◽  
...  
2017 ◽  
Author(s):  
Mahsa Dadar ◽  
Yashar Zeighami ◽  
Yvonne Yau ◽  
Seyed-Mohammad Fereshtehnejad ◽  
Josefina Maranzano ◽  
...  

AbstractObjectiveWhite Matter Hyperintensities (WMHs) are associated with cognitive decline in normative aging and Alzheimer’s disease. However, the pathogenesis of cognitive decline in Parkinson’s disease (PD) is not directly related to vascular causes, and therefore the role of WMHs in PD remains unclear. If WMH has a higher impact on cognitive decline in PD, vascular pathology should be assessed and treated with a higher priority in this population. Here we investigate whether WMH leads to increased cognitive decline in PD, and if these effects relate to cortical thinningMethodsTo investigate the role of WMHs in PD, it is essential to study recently-diagnosed/non-treated patients.De novoPD patients and age-matched controls (NPD=365,NControl=174) with FLAIR/T2-weighted scans at baseline were selected from Parkinson’s Progression Markers Initiative (PPMI). WMHs and cortical thickness were measured to analyse the relationship between baseline WMHs and future cognitive decline (follow-up:4.09±1.14 years) and cortical thinning (follow-up:1.05±0.10 years).ResultsHigh WMH load (WMHL) at baseline in PD was associated with increased cognitive decline, significantly more than i) PDs with low WMHL and ii) controls with high WMHL. Furthermore, PD patients with higher baseline WMHL showed more cortical thinning in right frontal lobe than subjects with low WMHL. Cortical thinning of this region also predicted decline in performance on a cognitive test.InterpretationPresence of WMHs inde novoPD patients predicts greater future cognitive decline and cortical thinning than in normal aging. Recognizing WMHs as a potential predictor of cognitive deficit in PD provides an opportunity for timely interventions.


2017 ◽  
Vol 4 (4) ◽  
pp. 552-558 ◽  
Author(s):  
Abhishek Lenka ◽  
Shaik Afsar Pasha ◽  
Sandhya Mangalore ◽  
Lija George ◽  
Ketan Ramakant Jhunjhunwala ◽  
...  

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ting Shen ◽  
Yumei Yue ◽  
Shuai Zhao ◽  
Juanjuan Xie ◽  
Yanxing Chen ◽  
...  

AbstractPerivascular space (PVS) is associated with neurodegenerative diseases, while its effect on Parkinson’s disease (PD) remains unclear. We aimed to investigate the clinical and neuroimaging significance of PVS in basal ganglia (BG) and midbrain in early-stage PD. We recruited 40 early-stage PD patients and 41 healthy controls (HCs). Both PVS number and volume were calculated to evaluate PVS burden on 7 T magnetic resonance imaging images. We compared PVS burden between PD and HC, and conducted partial correlation analysis between PVS burden and clinical and imaging features. PD patients had a significantly more serious PVS burden in BG and midbrain, and the PVS number in BG was significantly correlated to the PD disease severity and L-dopa equivalent dosage. The fractional anisotropy and mean diffusivity values of certain subcortical nuclei and white matter fibers within or nearby the BG and midbrain were significantly correlated with the ipsilateral PVS burden indexes. Regarding to the midbrain, the difference between bilateral PVS burden was, respectively, correlated to the difference between fiber counts of white fiber tract passing through bilateral substantia nigra in PD. Our study suggests that PVS burden indexes in BG are candidate biomarkers to evaluate PD motor symptom severity and aid in predicting medication dosage. And our findings also highlight the potential correlations between PVS burden and both grey and white matter microstructures.


2020 ◽  
Vol 35 (6) ◽  
pp. 882-882
Author(s):  
Lee G ◽  
Suhr J ◽  
Boxley L ◽  
Nguyen C

Abstract Objective Parkinson’s disease (PD) is a neurodegenerative disorder characterized by motor and nonmotor symptoms. While much of the extant literature on neuropsychiatric symptoms and cognitive deficits have focused on depression, comparatively less have examined the role of anxiety among patients with PD. Here, we examined levels of anxiety severity (i.e., minimal, mild, moderate–severe) and cognition in this population. Method Fifty-six PD patients (M age = 60.8 ± 9.3; 69.6% male) being considered for surgical intervention were evaluated at an outpatient clinic. Inclusion criteria included no history of neurosurgical procedure and no other diagnosis of a neurodegenerative disorder. Participants completed a battery of neuropsychological tests and reported mood symptoms (Geriatric Depression Scale-15, Beck Anxiety Inventory). Those who scored above clinical cutoffs for depressive symptoms were excluded due to high comorbidity with anxiety. Motor symptom severity was rated by neurologists using the Unified Parkinson’s Disease Rating Scale. Results Analysis of covariance revealed significant group differences on tests of working memory (p = .03), set-shifting (p = .04), problem-solving (p = .05), and phonemic fluency (p = .03) when controlling for motor symptom severity. PD patients with moderate–severe levels of anxiety performed significantly lower than those with minimal or mild anxiety (p’s < .05). There were no other significant group differences in neuropsychological test performance. Conclusions These findings suggest measurable differences in neurocognitive functions associated with frontostriatal circuits among PD patients with varying levels of overall anxiety. Future work should consider the potential overlap between anxiety and PD symptoms as they relate to cognition.


Sign in / Sign up

Export Citation Format

Share Document