scholarly journals Clinical and MRI Features of Cerebral Small-Vessel Disease in Type 1 Diabetes

Diabetes Care ◽  
2018 ◽  
Vol 42 (2) ◽  
pp. 327-330 ◽  
Author(s):  
Lena M. Thorn ◽  
Sara Shams ◽  
Daniel Gordin ◽  
Ron Liebkind ◽  
Carol Forsblom ◽  
...  
Diabetes Care ◽  
2020 ◽  
Vol 43 (8) ◽  
pp. e96-e98
Author(s):  
Marika I. Eriksson ◽  
Daniel Gordin ◽  
Sara Shams ◽  
Carol Forsblom ◽  
Paula Summanen ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
pp. e002274
Author(s):  
Marika I Eriksson ◽  
Paula Summanen ◽  
Daniel Gordin ◽  
Carol Forsblom ◽  
Sara Shams ◽  
...  

IntroductionCerebral small-vessel disease is common in neurologically asymptomatic individuals with type 1 diabetes. The retinal vasculature is thought to mirror the brain’s vasculature, but data on this association are limited in type 1 diabetes. Our aim was to study associations between diabetic retinopathy severity and cerebral small-vessel disease in type 1 diabetes.Research design and methodsFor this cross-sectional study, we enrolled 189 participants with type 1 diabetes (median age 40 (33–45) years; 53% female; diabetes duration 21.6 (18.2–30.7) years) and 29 healthy age-matched and sex-matched controls as part of the Finnish Diabetic Nephropathy Study. Participants underwent a clinical investigation, brain MRI, and fundus imaging. Signs of cerebral small-vessel disease in brain MRIs were analyzed in relation to diabetic retinopathy severity (Early Treatment Diabetic Retinopathy Study (ETDRS) score).ResultsIn type 1 diabetes, participants with cerebral small-vessel disease had higher ETDRS scores (35 (20–61) vs 20 (20–35), p=0.022) and a higher prevalence of proliferative diabetic retinopathy than those without cerebral small-vessel disease (25% vs 9%, p=0.002). In adjusted analysis, proliferative diabetic retinopathy was associated with cerebral small-vessel disease (OR 2.57 (95% CI 1.04 to 6.35)). Median ETDRS score (35 (20–65) vs 20 (20–35), p=0.024) and proliferative diabetic retinopathy prevalence were higher (29% vs 13%, p=0.002) in participants with versus without cerebral microbleeds. ETDRS scores increased by number of cerebral microbleeds (p=0.001), both ETDRS score (OR 1.05 (95% CI 1.02 to 1.09)) and proliferative diabetic retinopathy (8.52 (95% CI 1.91 to 37.94)) were associated with >2 cerebral microbleeds in separate multivariable analysis. We observed no association with white matter hyperintensities or lacunar infarcts.ConclusionsPresence of cerebral small-vessel disease on brain MRI, particularly cerebral microbleeds, is associated with the severity of diabetic retinopathy.


2021 ◽  
Vol 13 ◽  
Author(s):  
Yangyi Fan ◽  
Ming Shen ◽  
Yang Huo ◽  
Xuguang Gao ◽  
Chun Li ◽  
...  

Background: Cerebral small vessel disease (cSVD) and neurodegeneration are the two main causes of dementia and are considered distinct pathological processes, while studies have shown overlaps and interactions between the two pathological pathways. Medial temporal atrophy (MTA) is considered a classic marker of neurodegeneration. We aimed to investigate the relationship of total cSVD burden and MTA on MRI using a total cSVD score and to explore the impact of the two MRI features on cognition.Methods: Patients in a memory clinic were enrolled, who underwent brain MRI scan and cognitive evaluation within 7 days after the first visit. MTA and total cSVD score were rated using validated visual scales. Cognitive function was assessed by using Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scales. Spearman's correlation and regression models were used to test (i) the association between MTA and total cSVD score as well as each cSVD marker and (ii) the correlation of the MRI features and cognitive status.Results: A total of 312 patients were finally enrolled, with a median age of 75.0 (66.0–80.0) years and 40.7% (127/312) males. All of them finished MRI and MMSE, and 293 subjects finished MoCA. Of note, 71.8% (224/312) of the patients had at least one of the cSVD markers, and 48.7% (152/312) of them had moderate–severe MTA. The total cSVD score was independently associated with MTA levels, after adjusting for age, gender, years of education, and other vascular risk factors (OR 1.191, 95% CI 1.071–1.324, P = 0.001). In regard to individual markers, a significant association existed only between white matter hyperintensities and MTA after adjusting for the factors mentioned above (OR 1.338, 95% CI 1.050–1.704, P = 0.018). Both MTA and total cSVD score were independent risk factors for MMSE ≤ 26 (MTA: OR 1.877, 95% CI 1.407–2.503, P < 0.001; total cSVD score: OR 1.474, 95% CI 1.132–1.921, P = 0.004), and MoCA < 26 (MTA: OR 1.629, 95% CI 1.112–2.388, P = 0.012; total cSVD score: OR 1.520, 95% CI 1.068–2.162, P = 0.020). Among all the cSVD markers, microbleed was found significantly associated with MMSE ≤ 26, while no marker was demonstrated a relationship with MoCA < 26.Conclusion: Cerebral small vessel disease was related to MTA in patients of a memory clinic, and both the MRI features had a significant association with cognitive impairment.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Ilse M. J. Kant ◽  
◽  
Henri J. M. M. Mutsaerts ◽  
Simone J. T. van Montfort ◽  
Myriam G. Jaarsma-Coes ◽  
...  

2021 ◽  
Author(s):  
Wei-Ju Lee ◽  
Kun-Hsien Chou ◽  
Pei-Lin Lee ◽  
Li-Ning Peng ◽  
Pei-Ning Wang ◽  
...  

Abstract The present study aimed to determine whether a recently proposed cerebral small vessel disease (CSVD) classification scheme could differentiate the 5-year all-cause mortality in middle-to-old aged asymptomatic CSVD. Stroke-free and non-demented participants recruited from the community-based I-Lan Longitudinal Aging Study underwent baseline brain magnetic resonance imaging (MRI) between 2011 and 2014 and were followed-up between 2018 and 2019. The study population was classified into control (non-CSVD) and CSVD type 1–4 groups based on MRI markers. We determined the association with mortality using Cox regression models, adjusting for the age, sex, and vascular risk factors. A total of 735 participants were included. During a mean follow-up of 5.7 years, 62 (8.4%) died. There were 335 CSVD type 1 (57.9 ± 5.9 years), 249 type 2 (65.6 ± 8.1 years), 52 type 3 (67.8 ± 9.2 years), and 38 type 4 (64.3 ± 9.0 years). Among the four CSVD types, CSVD type 4 individuals had significantly higher all-cause mortality (adjusted hazard ratio = 3.7, 95% confidence interval = 1.3−10.8) compared to controls. This novel MRI-based CSVD classification scheme was able to identify individuals at risk of mortality at an asymptomatic, early stage of disease and might be applied for future community-based health research and policy.


Author(s):  
Jussi Inkeri ◽  
◽  
Anniina Tynjälä ◽  
Carol Forsblom ◽  
Ron Liebkind ◽  
...  

Abstract Aims To determine if arterial functional and structural changes are associated with underlying cerebral small vessel disease in neurologically asymptomatic individuals with type 1 diabetes. Methods We enrolled 186 individuals (47.8% men; median age 40.0, IQR 33.0—45.0 years) with type 1 diabetes (median diabetes duration of 21.6, IQR 18.2—30.3 years), and 30 age- and sex-matched healthy controls, as part of the Finnish Diabetic Nephropathy (FinnDiane) Study. All individuals underwent a biochemical work-up, brain magnetic resonance imaging (MRI), ultrasound of the common carotid arteries and arterial tonometry. Arterial structural and functional parameters were assessed by carotid intima-media thickness (CIMT), pulse wave velocity and augmentation index. Results Cerebral microbleeds (CMBs) were present in 23.7% and white matter hyperintensities (WMHs) in 16.7% of individuals with type 1 diabetes. Those with type 1 diabetes and CMBs had higher median (IQR) CIMT 583 (525 – 663) μm than those without 556 (502 – 607) μm, p = 0.016). Higher CIMT was associated with the presence of CMBs (p = 0.046) independent of age, eGFR, ApoB, systolic blood pressure, albuminuria, history of retinal photocoagulation and HbA1c. Arterial stiffness and CIMT were increased in individuals with type 1 diabetes and WMHs compared to those without; however, these results were not independent of cardiovascular risk factors. Conclusions Structural, but not functional, arterial changes are associated with underlying CMBs in asymptomatic individuals with type 1 diabetes.


2020 ◽  
pp. 0271678X2095851
Author(s):  
Maarten HT Zwartbol ◽  
Anja G van der Kolk ◽  
Hugo J Kuijf ◽  
Theo D Witkamp ◽  
Rashid Ghaznawi ◽  
...  

The etiology of cerebral small vessel disease (CSVD) is the subject of ongoing research. Although intracranial atherosclerosis (ICAS) has been proposed as a possible cause, studies on their relationship remain sparse. We used 7 T vessel wall magnetic resonance imaging (MRI) to study the association between intracranial vessel wall lesions—a neuroimaging marker of ICAS—and MRI features of CSVD. Within the SMART-MR study, cross-sectional analyses were performed in 130 patients (68 ± 9 years; 88% male). ICAS burden—defined as the number of vessel wall lesions—was determined on 7 T vessel wall MRI. CSVD features were determined on 1.5 T and 7 T MRI. Associations between ICAS burden and CSVD features were estimated with linear or modified Poisson regression, adjusted for age, sex, vascular risk factors, and medication use. In 125 patients, ≥1 vessel wall lesions were found (mean 8.5 ± 5.7 lesions). ICAS burden (per + 1 SD) was associated with presence of large subcortical and/or cortical infarcts (RR = 1.65; 95%CI: 1.12–2.43), lacunes (RR = 1.45; 95% CI: 1.14–1.86), cortical microinfarcts (RR = 1.48; 95%CI: 1.13–1.94), and total white matter hyperintensity volume ( b = 0.24; 95%CI: 0.02–0.46). Concluding, patients with a higher ICAS burden had more CSVD features, although no evidence of co-location was observed. Further longitudinal studies are required to determine if ICAS precedes development of CSVD.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Misun Hwang ◽  
Dana L. Tudorascu ◽  
Karen Nunley ◽  
Helmet Karim ◽  
Howard J. Aizenstein ◽  
...  

Slower psychomotor speed is very common in patients with type 1 diabetes mellitus (T1D), but the underlying mechanisms are not clear. We propose that hyperglycemia is associated with slower psychomotor speed via disruption of brain activation. Eighty-five adults (48% women, mean age: 49.0 years, mean duration: 40.8) with childhood onset T1D were recruited for this cross-sectional study. Median response time in seconds (longer = worse performance) and brain activation were measured while performing a psychomotor speed task. Exposure to hyperglycemia, measured as glycosylated hemoglobin A1c, was associated with longer response time and with higher activation in the inferior frontal gyrus and primary sensorimotor and dorsal cingulate cortex. Higher activation in inferior frontal gyrus, primary sensorimotor cortex, thalamus, and cuneus was related to longer response times; in contrast, higher activation in the superior parietal lobe was associated with shorter response times. Associations were independent of small vessel disease in the brain or other organs. In this group of middle-aged adults with T1D, the pathway linking chronic hyperglycemia with slower processing speed appears to include increased brain activation, but not small vessel disease. Activation in the superior parietal lobe may compensate for dysregulation in brain activation in the presence of hyperglycemia.


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