Vascular risk factors in older patients with depression: outcome of electroconvulsive therapy versus medication

2017 ◽  
Vol 33 (2) ◽  
pp. 371-378 ◽  
Author(s):  
Harm-Pieter Spaans ◽  
Rob M. Kok ◽  
Filip Bouckaert ◽  
Julia F. Van Den Berg ◽  
Orlaith C. Tunney ◽  
...  
L Encéphale ◽  
2019 ◽  
Vol 45 ◽  
pp. S74
Author(s):  
Lucie Jurek ◽  
Jérôme Brunelin ◽  
Jean Michel Dorey ◽  
Filipe Galvao

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Tamara Strohm ◽  
Russell Cerejo ◽  
Jason Mathew ◽  
Irene Katzan ◽  
Ken Uchino

Introduction: Intracranial atherosclerosis has been well studied in the aging population, much less is known about atherosclerotic stenosis in the young. Clinicians seek to control traditional vascular risk factors in this population, but differences in patterns of stenosis may call for varied treatment approaches. This study sought to compare age to the distribution of vessel involvement in patients with moderate-severe intracranial stenosis. Methods: This is a retrospective cohort study of patients with intracranial stenosis seen in the stroke clinic of a tertiary center from 2008-2013. Inclusion criteria were moderate-severe intracranial stenosis clinically felt to be due to atherosclerosis with ≥3 traditional vascular risk factors. Patients with other mechanisms of intracranial stenosis were excluded. Stenosis location and severity were based on cerebral angiography, CTA, or MRA. Patients were divided into young (< 50 yr), middle-age (51-64 yr), or older (≥ 65 yr). All 69 patients ≤50 yr were included; a random sample of 69 patients > 50 were selected for this analysis. Results: There were similar rates of vascular risk factors except HTN, which was less common in the young group (81.2% young, 100% middle, 96.8% older, p=0.0006). The location of stenoses varied by age category. Older patients had more posterior circulation involvement compared to the younger groups (p = 0.046), with more frequent involvement of vertebral and basilar arteries (p = 0.012) (Table). The occurrence of stenosis in the distal ICA and MCA vessels were similar among age groups. The frequency of ACA stenosis was highest in the young category (p = 0.026). Conclusion: There are differences in anatomic locations of presumed intracranial atherosclerosis across age groups with older patients (> 65 yrs) having a higher rate of posterior circulation disease. This suggests potential differences in pathophysiological mechanisms. These findings warrant further investigation.


2001 ◽  
Vol 31 (8) ◽  
pp. 1403-1412 ◽  
Author(s):  
I. HICKIE ◽  
E. SCOTT ◽  
S. NAISMITH ◽  
P. B. WARD ◽  
K. TURNER ◽  
...  

Background. Neuropsychiatric research needs to examine the relationships between aetiological, genotypic and clinical risk factors and behavioural phenotypes. These relationships can now be examined in older patients with depressive disorders.Methods. Key behavioural features, clinical and vascular risk factors and putative genotypes for late-onset neurodegenerative disorders and/or vascular disease were recorded in 78 older patients with depression (mean age = 54·9 years, S.D. = 14·1) and 22 healthy control subjects (mean age = 55·5 years, S.D. = 9·6).Results. Two or more vascular risks were more common in older patients (65% v. 26% of control subjects, P < 0·01), and in patients with late-onset disorders (82% v. 57% in patients with early-onset disorders, P < 0·05). Patients with late-onset depression had a higher prevalence of the homozygous or heterozygous forms of the C677T mutation of the methylenetetrahydrofolate reductase enzyme (MTHFR)(74% v. 48% in patients with early-onset disorders, P < 0·05). In a multivariate model, only presence of the MTHFR gene mutation predicted late-onset depression (odds ratio = 3·8, 95% CI = 1·1–12·9). Neither apolipoprotein E epsilon 4 or epsilon 2 was associated with depression, late-onset depression, cognitive impairment, or psychomotor change. Patients with apolipoprotein E epsilon 4 were less likely to have psychotic forms of depression.Conclusions. Patients with late-onset depression had an increased rate of the C677T MTHFR gene mutation and other vascular risk factors. This suggests that a proportion of these patients may have genetically-determined and/or other vascular aetiologies. Patients at risk of these disorders may be assisted by currently-available preventative strategies.


2014 ◽  
Vol 5 ◽  
pp. S223-S224
Author(s):  
E.J.M. van Melick ◽  
I. Wilting ◽  
R.M. Kok ◽  
A.C.G. Egberts

2021 ◽  
Vol 279 ◽  
pp. 308-315
Author(s):  
Lucie Jurek ◽  
Jean-Michel Dorey ◽  
Mikaïl Nourredine ◽  
Filipe Galvao ◽  
Jérome Brunelin

Author(s):  
Victoria J. Williams ◽  
Steven E. Arnold ◽  
David H. Salat

Throughout the lifespan, common variations in systemic health and illness contribute to alterations in vasculature structure and function throughout the body, significantly increasing risk for cardiovascular and cerebrovascular disease (CVD). CVD is a prevalent cause of mortality in late life; it also promotes brain alterations, contributing to cognitive decline and, when severe, vascular dementia. Even prior to diseased states, individual variation in CVD risk is associated with structural and functional brain alterations. Yet, how cumulative asymptomatic alterations in vessel structure and function contribute to more subtle changes in brain tissue integrity and function that emerge in late life is unclear. Finally, vascular risk factors are associated with the clinical progression of neurodegenerative diseases such as Alzheimer’s disease (AD); however, recent theory posits that vascular degeneration may serve a contributory role in these conditions. This chapter reviews how lifespan changes in vascular health contribute to degenerative changes in neural tissue and the subsequent development of cognitive impairment and/or vascular dementia. It first discusses associations between vascular risk factors and cognition and also how declining vascular health may lead to cognitive impairment and dementia. Next, it identifies basic aspects of cerebrovascular anatomy and physiology sustaining tissue health and discusses how vulnerabilities of this system contribute to neurodegenerative changes. Finally, it reviews evidence of vascular contributions to AD and presents ideas for future research to better understand the full spectrum of cerebrovascular contributions to brain aging, cognitive decline, and dementia.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Elżbieta Krytkowska ◽  
Aleksandra Grabowicz ◽  
Katarzyna Mozolewska-Piotrowska ◽  
Zofia Ulańczyk ◽  
Krzysztof Safranow ◽  
...  

AbstractDisturbances in choroidal microcirculation may lead to the onset and progression of age-related macular degeneration (AMD). We aimed to assess changes in the choroidal volume and thickness in the macular region in AMD eyes and to investigate whether coexisting vascular risk factors alter choroidal status. We enrolled 354 AMD patients (175 dry, 179 wet AMD) and 121 healthy controls. All participants underwent a complete ophthalmologic examination and assessment of choroidal thickness and volume. A multivariate analysis adjusted for age, sex, and smoking status revealed that wet AMD was an independent factor associated with higher average thickness of the central ring area (ATC) and average volume of the central ring area (AVC) and lower choroidal vascularity index (CVI) compared to controls (β =  + 0.18, p = 0.0007, β =  + 0.18, p = 0.0008, respectively) and to dry AMD (β =  + 0.17, p = 0.00003 for both ATC and AVC and β =  − 0.30 p < 0.0001 for CVI). ATC, AVC and average volume (AV) were lower in AMD patients with hypertension and ischaemic heart disease (IHD). The duration of hypertension was inversely correlated with ATC, AVC and AV (Rs =  − 0.13, p < 0.05; Rs =  − 0.12; p < 0.05, Rs =  − 0.12; p < 0.05, respectively) while IHD duration negatively correlated with AV (Rs =  − 0.15, p < 0.05). No such associations were observed in the control group. Our findings show that the choroidal vascular system in eyes with AMD is much more susceptible to damage in the presence than in the absence of systemic vascular disease.


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