Cerebrovascular Risk-Factors of Prevalent and Incident Brain Infarcts in the General Population: The AGES-Reykjavik Study

Stroke ◽  
2021 ◽  
Author(s):  
Sigurdur Sigurdsson ◽  
Thor Aspelund ◽  
Olafur Kjartansson ◽  
Elias Gudmundsson ◽  
Palmi V. Jonsson ◽  
...  

Background and Purpose: Studies on the association of cerebrovascular risk factors to magnetic resonance imaging detected brain infarcts have been inconsistent, partly reflecting limits of assessment to infarcts anywhere in the brain, as opposed to specific brain regions. We hypothesized that risk-factors may differ depending on where the infarct is located in subcortical-, cortical-, and cerebellar regions. Methods: Participants (n=2662, mean age 74.6±4.8) from the longitudinal population-based AGES (Age, Gene/Environment Susceptibility)-Reykjavik Study underwent brain magnetic resonance imaging at baseline and on average 5.2 years later. We assessed the number and location of brain infarcts (prevalent versus incident). We estimated the risk-ratios of prevalent (PRR) and incident (IRR) infarcts by baseline cerebrovascular risk-factors using Poisson regression. Results: Thirty-one percent of the study participants had prevalent brain infarcts and 21% developed new infarcts over 5 years. Prevalent subcortical infarcts were associated with hypertension (PRR, 2.7 [95% CI, 1.1–6.8]), systolic blood pressure (PRR, 1.2 [95% CI, 1.1–1.4]), and diabetes (PRR, 2.8 [95% CI, 1.9–4.1]); incident subcortical infarcts were associated with systolic (IRR, 1.2 [95% CI, 1.0–1.4]) and diastolic (IRR, 1.3 [95% CI, 1.0–1.6]) blood pressure. Prevalent and incident cortical infarcts were associated with carotid plaques (PRR, 1.8 [95% CI, 1.3–2.5] and IRR, 1.9 [95% CI, 1.3–2.9], respectively), and atrial fibrillation was significantly associated with prevalent cortical infarcts (PRR, 1.8 [95% CI, 1.2–2.7]). Risk-factors for prevalent cerebellar infarcts included hypertension (PRR, 2.45 [95% CI, 1.5–4.0]), carotid plaques (PRR, 1.45 [95% CI, 1.2–1.8]), and migraine with aura (PRR, 1.6 [95% CI, 1.1–2.2]). Incident cerebellar infarcts were only associated with any migraine (IRR, 1.4 [95% CI, 1.0–2.0]). Conclusions: The risk for subcortical infarcts tends to increase with small vessel disease risk-factors such as hypertension and diabetes. Risk for cortical infarcts tends to increase with atherosclerotic/coronary processes and risk for cerebellar infarcts with a more mixed profile of factors. Assessment of risk-factors by location of asymptomatic infarcts found on magnetic resonance imaging may improve the ability to target and optimize preventive therapeutic approaches to prevent stroke.

1997 ◽  
Vol 27 (2) ◽  
pp. 421-431 ◽  
Author(s):  
B. S. GREENWALD ◽  
E. KRAMER-GINSBERG ◽  
B. BOGERTS ◽  
M. ASHTARI ◽  
P. AUPPERLE ◽  
...  

Background. Several clinical and neuroimaging investigations support the notion that underlying brain changes may relate to depression in older patients, especially those with a later-age initial episode. However uncertainty still exists about diagnostic and pathogenic significance of structural brain abnormalities in aged depressives, in part because many studies lack all-elderly and age-similar normal comparison populations.Methods. Brain morphology of elderly depressives (N = 30) and normal controls (N = 36) was compared by assessing magnetic resonance imaging (MRI) brain scans with qualitative criteria-based scales. Ratings included lateral and third ventricle enlargement, and cortical, medial temporal, and caudate atrophy.Results. Significant differences between depressed and control groups were not demonstrated. Later-onset depressives had significantly more left medial temporal and left caudate atrophy than early-onset counterparts of similar age. Medial temporal atrophy significantly correlated with cognitive impairment and was not related to physical illness. Depressives with medial temporal atrophy (N = 7) were older and had later age at onset of depression than those without such changes. Cerebrovascular disease risk factors did not predict MRI abnormalities.Conclusions. Results indicate non-specificity and lack of homogeneity of qualitatively measured structural brain changes in geriatric depression, but suggest that pathology of specific, lateralized brain regions may be implicated in some later-onset patients. The relationship between medial temporal atrophy and late-onset depression raises the possibility that such patients may suffer from as-yet undeclared Alzheimer's disease. Lack of association between cerebrovascular disease risk factors and brain changes suggests other pathophysiological contributions.


Author(s):  
Marta Bianciardi ◽  
Nicola Toschi ◽  
Jonathan R. Polimeni ◽  
Karleyton C. Evans ◽  
Himanshu Bhat ◽  
...  

The influence of cardiac activity on the viscoelastic properties of intracranial tissue is one of the mechanisms through which brain–heart interactions take place, and is implicated in cerebrovascular disease. Cerebrovascular disease risk is not fully explained by current risk factors, including arterial compliance. Cerebrovascular compliance is currently estimated indirectly through Doppler sonography and magnetic resonance imaging (MRI) measures of blood velocity changes. In order to meet the need for novel cerebrovascular disease risk factors, we aimed to design and validate an MRI indicator of cerebrovascular compliance based on direct endogenous measures of blood volume changes. We implemented a fast non-gated two-dimensional MRI pulse sequence based on echo-planar imaging (EPI) with ultra-short repetition time (approx. 30–50 ms), which stepped through slices every approximately 20 s. We constrained the solution of the Bloch equations for spins moving faster than a critical speed to produce an endogenous contrast primarily dependent on spin volume changes, and an approximately sixfold signal gain compared with Ernst angle acquisitions achieved by the use of a 90° flip angle. Using cardiac and respiratory peaks detected on physiological recordings, average cardiac and respiratory MRI pulse waveforms in several brain compartments were obtained at 7 Tesla, and used to derive a compliance indicator, the pulsatility volume index (pVI). The pVI, evaluated in larger cerebral arteries, displayed significant variation within and across vessels. Multi-echo EPI showed the presence of significant pulsatility effects in both S 0 and signals, compatible with blood volume changes. Lastly, the pVI dynamically varied during breath-holding compared with normal breathing, as expected for a compliance indicator. In summary, we characterized and performed an initial validation of a novel MRI indicator of cerebrovascular compliance, which might prove useful to investigate brain–heart interactions in cerebrovascular disease and other disorders.


2021 ◽  
Vol 10 (2) ◽  
pp. 225
Author(s):  
Łukasz Zwarzany ◽  
Ernest Tyburski ◽  
Wojciech Poncyljusz

Background: We decided to investigate whether aneurysm wall enhancement (AWE) on high-resolution vessel wall magnetic resonance imaging (HR VW-MRI) coexists with the conventional risk factors for aneurysm rupture. Methods: We performed HR VW-MRI in 46 patients with 64 unruptured small intracranial aneurysms. Patient demographics and clinical characteristics were recorded. The PHASES score was calculated for each aneurysm. Results: Of the 64 aneurysms, 15 (23.4%) showed wall enhancement on post-contrast HR VW-MRI. Aneurysms with wall enhancement had significantly larger size (p = 0.001), higher dome-to-neck ratio (p = 0.024), and a more irregular shape (p = 0.003) than aneurysms without wall enhancement. The proportion of aneurysms with wall enhancement was significantly higher in older patients (p = 0.011), and those with a history of prior aneurysmal SAH. The mean PHASES score was significantly higher in aneurysms with wall enhancement (p < 0.000). The multivariate logistic regression analysis revealed that aneurysm irregularity and the PHASES score are independently associated with the presence of AWE. Conclusions: Aneurysm wall enhancement on HR VW-MRI coexists with the conventional risk factors for aneurysm rupture.


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