Asymptomatic Cerebral Small Vessel Disease: Insights from Population-Based Studies

Abstract

Cerebral small vessel disease (CSVD) is a common group of neurological conditions that confer a significant burden of morbidity and mortality worldwide. In most cases, CSVD is only recognized in its advanced stages once its symptomatic sequelae develop. However, its significance in asymptomatic healthy populations remains poorly defined. In population-based studies of presumed healthy elderly individuals, CSVD neuroimaging markers including white matter hyperintensities, lacunes, cerebral microbleeds, enlarged perivascular spaces, cortical superficial siderosis, and cerebral microinfarcts are frequently detected. While the presence of these imaging markers may reflect unique mechanisms at play, there are likely shared pathways underlying CSVD. Herein, we aim to assess the etiology and significance of these individual biomarkers by focusing in asymptomatic populations at an epidemiological level. By primarily examining population-based studies, we explore the risk factors that are involved in the formation and progression of these biomarkers. Through a critical semi-systematic review, we aim to characterize "asymptomatic" CSVD, review screening modalities, and draw associations from observational studies in clinical populations. Lastly, we highlight areas of research (including therapeutic approaches) in which further investigation is needed to better understand asymptomatic CSVD.

The ability to understand emotions is associated with interoception‐related insular activation and white matter integrity during aging

“…The subjects with and without this diagnosis did not differ in IAc, MSCEIT scores, right aIns activation, and the mean ADC value. The latter unexpected lack of association (mean ADC 747 ± 38 vs. 734 ± 17, p = .6) may be explained by the use of antihypertensive drugs, which were received by 8 of the 10 hypertensive participants: lowering arterial blood pressure, this therapy alleviates the risk of vascular diseases (Das et al, ). Analyzing the role of the blood pressure level as measured by the 24‐hr ambulatory blood pressure monitoring, we found a tendency toward correlation of the mean night diastolic pressure with the mean ADC ( R = .365, p = .087).…”

“…During the time course of SVD, abnormalities of the smaller cerebral vessels (i.e., perforating arteries, arterioles, and capillaries) lead to progressive vascular brain damage with predominant involvement of the white matter, which, in turn, results in cognitive impairment (Pantoni, ). Several vascular risk factors are linked to the pathogenesis of SVD, including arterial hypertension and smoking (Das et al, ). However, the prophylaxis of SVD targeted at correcting these “traditional” factors is of limited efficacy (SPRINT MIND Investigators for the SPRINT Research Group et al, ) and, thus, the investigation of “nontraditional” vascular risk factors is appropriate (Bairey Merz et al, ).…”

Correlation Between Internal Carotid Artery Tortuosity and Imaging of Cerebral Small Vessel Disease

“…The definition of SVD neuroimaging markers were as follows. Periventricular and deep WMHs were both coded on the basis of the Fazekas scale (grades 0-3), by using FLAIR and T2WI (12,13). The definition of CMBs was homogeneous, small (<5 mm), round foci in the basal ganglia, white matter, corticosubcortical junction, brainstem, or cerebellum, differentiated from mineral depositions in the globi pallidi and vessel flow voids, with hypointensity on gradient-echo images (12,13).…”

“…Periventricular and deep WMHs were both coded on the basis of the Fazekas scale (grades 0-3), by using FLAIR and T2WI (12,13). The definition of CMBs was homogeneous, small (<5 mm), round foci in the basal ganglia, white matter, corticosubcortical junction, brainstem, or cerebellum, differentiated from mineral depositions in the globi pallidi and vessel flow voids, with hypointensity on gradient-echo images (12,13). Lacunes were defined as round or ovoid lesions with a small (3-20 mm) diameter in the basal ganglia, internal capsule, centrum semiovale, or brainstem, with cerebrospinal fluid intensity on T2WI and FLAIR, generally with a high signal intense rim on FLAIR and no hyperintensity on DWI (12,13).…”

Calgary Normative Study: Study Design of a Prospective Longitudinal Study to Characterize Potential Quantitative MR Biomarkers Over the Adult Lifespan

“…Similar prevalence of covert lacunar infarcts of presumed vascular origin, white matter hyperintensities and cerebral microbleeds in older community-dwelling populations have been reported previously. 24 We may need to consider increasing our recruitment numbers in the older age categories to maintain a balanced design of healthy individuals over the adult lifespan. The decision on whether to oversample the older participants is dependent on the definition of what is "normal" aging.…”