scholarly journals Adverse effects of hypertension, supine hypertension, and perivascular space on cognition and motor function in PD

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Na-Young Shin ◽  
Yae Won Park ◽  
Sang-Won Yoo ◽  
Ji-Yeon Yoo ◽  
Yangsean Choi ◽  
...  

AbstractDilated perivascular space (dPVS) has recently been reported as a biomarker for cognitive impairment in Parkinson’s disease (PD). However, comprehensive interrelationships between various clinical risk factors, dPVS, white-matter hyperintensities (WMH), cognition, and motor function in PD have not been studied yet. The purpose of this study was to test whether dPVS might mediate the effect of clinical risk factors on WMH, cognition, and motor symptoms in PD patients. A total of 154 PD patients were assessed for vascular risk factors (hypertension, diabetes mellitus, and dyslipidemia), autonomic dysfunction (orthostatic hypotension and supine hypertension [SH]), APOE ε4 genotype, rapid eye movement sleep-behavior disorder, motor symptoms, and cognition status. The degree of dPVS was evaluated in the basal ganglia (BG) and white matter using a 5-point visual scale. Periventricular, deep, and total WMH severity was also assessed. Path analysis was performed to evaluate the associations of these clinical factors and imaging markers with cognitive status and motor symptoms. Hypertension and SH were significantly associated with more severe BGdPVS, which was further associated with higher total WMH, consequently leading to lower cognitive status. More severe BGdPVS was also associated with worse motor symptoms, but without mediation of total WMH. Similar associations were seen when using periventricular WMH as a variable, but not when using deep WMH as a variable. In conclusion, BGdPVS mediates the effect of hypertension and SH on cognitive impairment via total and periventricular WMH, while being directly associated with more severe motor symptoms.

2013 ◽  
Vol 146 (3) ◽  
pp. 543-549.e1 ◽  
Author(s):  
Michael J. Rivkin ◽  
Christopher G. Watson ◽  
Lisa A. Scoppettuolo ◽  
David Wypij ◽  
Sridhar Vajapeyam ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Joëlle Bagautdinova ◽  
Maria C. Padula ◽  
Daniela Zöller ◽  
Corrado Sandini ◽  
Maude Schneider ◽  
...  

AbstractDisruptions of white matter microstructure have been widely reported in schizophrenia. However, the emergence of these alterations during preclinical stages remains poorly understood. 22q11.2 Deletion Syndrome (22q11.2DS) represents a unique model to study the interplay of different risk factors that may impact neurodevelopment in premorbid psychosis. To identify the impact of genetic predisposition for psychosis on white matter development, we acquired longitudinal MRI data in 201 individuals (22q11.2DS = 101; controls = 100) aged 5–35 years with 1–3 time points and reconstructed 18 white matter tracts using TRACULA. Mixed model regression was used to characterize developmental trajectories of four diffusion measures—fractional anisotropy (FA), axial (AD), radial (RD), and mean diffusivity (MD) in each tract. To disentangle the impact of additional environmental and developmental risk factors on white matter maturation, we used a multivariate approach (partial least squares (PLS) correlation) in a subset of 39 individuals with 22q11.2DS. Results revealed no divergent white matter developmental trajectories in patients with 22q11.2DS compared to controls. However, 22q11.2DS showed consistently increased FA and reduced AD, RD, and MD in most white matter tracts. PLS correlation further revealed a significant white matter-clinical risk factors relationship. These results indicate that while age-related changes are preserved in 22q11.2DS, white matter microstructure is widely disrupted, suggesting that genetic high risk for psychosis involves early occurring neurodevelopmental insults. In addition, multivariate modeling showed that clinical risk factors further impact white matter development. Together, these findings suggest that genetic, developmental, and environmental risk factors may play a cumulative role in altering normative white matter development during premorbid stages of psychosis.


2018 ◽  
Vol 6 (3) ◽  
pp. 133-140
Author(s):  
Dr Anil Sejwar ◽  
◽  
Dr Gopal Krishna ◽  
Dr Arpit Dhiran ◽  
Dr T.N. Dubey ◽  
...  

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Wenjun Deng ◽  
David McMullin ◽  
Ferdinando Buonanno ◽  
Eng Lo ◽  
MingMing Ning

Background: Right-to-left interatrial shunting through a patent foramen ovale (PFO) has been associated with white matter lesions in literature and in our data. Since white matter lesions, particularly those in the periventricular and subcortical regions, increase the risk of cognitive impairment, we investigate the relationship between PFO shunting and dementia. Method: 1078 consecutive PFO stroke patients were prospectively recruited in accordance with IRB protocol. No patient had diagnosis of dementia prior to initial stroke. PFO shunt size was evaluated by echocardiography with saline contrast. Cognitive status and recurrent events were followed for up to 11 years. Result: 27 patients (2.50%) developed vascular cognitive impairment and dementia over 11 years. As expected, dementia patients were older (p<0.001) and were more likely to have hypertension (p<0.001) and hyperlipidemia (p=0.001) (Table 1). Notably, the dementia patients were also more likely to have a large PFO shunt (22.2% vs 8.3%, p=0.023). The association of PFO shunt and dementia remained robust (Odds ratio: 3.07; 95% CI: 1.11~8.55; p=0.031) after adjusting for important traditional risk factors (age, hypertension, hyperlipidemia, diabetes). But PFO risk factors (hypermobile septum, atrial septal aneurysm) that enhance PFO shunting remain significant (Table 2). Conclusion: Our study provides support for the hypothesis that the presence of large PFO right-to-left shunting is associated with increased risk of later dementia. We previously reported that PFO shunting enables vasoactive factors to stay elevated in circulation and to contribute to cerebrovascular dysfunction. We hypothesize here that prolonged exposure to PFO shunting may lead to cognitive decline. Further studies assessing PFO shunt size, dementia severity, and other confounders in a non-stroke PFO cohort are ongoing to validate these findings.


2019 ◽  
Vol 23 ◽  
pp. 101820 ◽  
Author(s):  
Diliana Pecheva ◽  
J-Donald Tournier ◽  
Maximilian Pietsch ◽  
Daan Christiaens ◽  
Dafnis Batalle ◽  
...  

2020 ◽  
Vol 16 (S5) ◽  
Author(s):  
Lei Zhao ◽  
Brian Yiu ◽  
Bonnie Y.K. Lam ◽  
J. Matthijs Biesbroek ◽  
Yishan Luo ◽  
...  

2017 ◽  
Vol 182 ◽  
pp. 34-40.e1 ◽  
Author(s):  
Nienke Wagenaar ◽  
Vann Chau ◽  
Floris Groenendaal ◽  
Karina J. Kersbergen ◽  
Kenneth J. Poskitt ◽  
...  

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