White matter hyperintensities

Background: White matter hyperintensities are an important marker of cerebral small vessel disease.

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. White matter hyperintensities WMHs are commonly seen on brain MRI in older people, and result from chronic ischaemia associated with cerebral small vessel disease.

White matter hyperintensities

White matter hyperintensities WMHs are lesions in the brain that show up as areas of increased brightness when visualised by T2-weighted magnetic resonance imaging MRI. The prevailing view is that these intensities are a marker of small-vessel vascular disease and in clinical practice, are indicative of cognitive and emotional dysfunction, particularly in the ageing population. This is clearly not true. Although WMH do become more common with advancing age, their prevalence is highly variable. There is strong evidence that WMH are clinically important markers of increased risk of stroke, dementia, death, depression, impaired gait, and mobility, in cross-sectional and in longitudinal studies. They associate with brain damage such as global atrophy and other features of small vessel brain damage, with focal progressive visible brain damage, are markers of underlying subvisible diffuse brain damage, and predict infarct growth and worse outcome after large artery stroke. They could be considered as the neuroimaging marker of brain frailty. Wardlaw et al. A review by Debette and Markus sought to review the evidence of the association between WMHs and the risk of cognitive impairment, dementia, death and stroke. White matter hyperintensities are a predictor for vascular disease for which age and high blood pressure are the main risk factors. The review showed that WMHs are significantly associated with an increased risk of stroke.

Griffanti, L.

As such, white matter hyperintensities have been targeted as a surrogate biomarker in intervention trials with older adults. However, it is unclear at what stage of aging white matter hyperintensities begin to relate to cognition and if they may be a viable target for early prevention. In the Dunedin Study, a population-representative cohort followed since birth, we measured white matter hyperintensities in year-old participants using T 2 -weighted magnetic resonance imaging and we assessed cognitive decline from childhood to midlife. Our results demonstrate that a link between white matter hyperintensities and early signs of cognitive decline is detectable decades before clinical symptoms of dementia emerge. Thus, white matter hyperintensities may be a useful surrogate biomarker for identifying individuals in midlife at risk for future accelerated cognitive decline and selecting participants for dementia prevention trials.

A hyperintensity or T2 hyperintensity is an area of high intensity on types of magnetic resonance imaging MRI scans of the brain of a human or of another mammal that reflect lesions produced largely by demyelination and axonal loss. The volume and frequency is strongly associated with increasing age. For example, deep white matter hyperintensities are 2. Hyperintensities are commonly divided into 3 types depending on the region of the brain where they are found. Deep white matter hyperintensities occur deep within white matter, periventricular white matter hyperintensities occur adjacent to the lateral ventricles and subcortical hyperintensities occur in the basal ganglia. Hyperintensities are often seen in auto immune diseases that have effects on the brain. Postmortem studies combined with MRI suggest that hyperintensities are dilated perivascular spaces , or demyelination caused by reduced local blood flow.

White matter hyperintensities

However, the relationship between WMH volumes and cross-sectional cognitive measures has been inconsistent. We hypothesize that this inconsistency may arise from 1 the presence of AD-specific neuropathology that may obscure any WMH effects on cognition, and 2 varying criteria for creating a WMH segmentation. Manual and automated programs are typically used to determine segmentation boundaries, but criteria for those boundaries can differ. It remains unclear whether WMH volumes are associated with cognitive deficits, and which segmentation criteria influence the relationships between WMH volumes and clinical outcomes. In a sample of non-demented participants ages , males, females from the Alzheimer's Disease Neuroimaging Initiative ADNI , we compared the performance of five WMH segmentation methods, by relating the WMH volumes derived using each method to both clinical diagnosis and composite measures of executive function and memory. To separate WMH effects on cognition from effects related to AD-specific processes, we performed analyses separately in people with and without abnormal cerebrospinal fluid amyloid levels. WMH volume estimates that excluded more diffuse, lower-intensity lesions were more strongly correlated with clinical diagnosis and cognitive performance, and only in those without abnormal amyloid levels. These findings may inform best practices for WMH segmentation, and suggest that AD neuropathology may mask WMH effects on clinical diagnosis and cognition. Publication types Research Support, N. Gov't Research Support, U.

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O'Brien, J. Neurology 95, e79—e Vascular risk factors and neurodegeneration in ageing related dementias: Alzheimer's disease and vascular dementia. Diffuse brain oedema in idiopathic intracranial hypertension: a quantitative MR imaging study. Historical Perspective Worldwide, about 15 million people have a stroke, from which 6 million die and 5 million are left permanently disabled each year 1 ; Knowledge of their pathology derives mostly from post mortem studies, many from some years ago. Periventricular venous collagenosis: association with leukoaraiosis. Chao, L. Neurology 64 , — Both studies suggest, however, that this spatial distinction might be an early marker for cognitive impairment in younger people, where the overall WMH burden in the brain is still relatively low. Intra- and interscanner variability of automated voxel-based volumetry based on a 3D probabilistic atlas of human cerebral structures.

White matter provides connections between the different parts of the brain.

Roseborough, A. Hypertension and cerebral white matter lesions in a prospective cohort study. Neuroimage ; 38 : 95 — Periventricular cerebral white matter lesions predict rate of cognitive decline. Effects of dexamethasone on cerebral perfusion and water diffusion in patients with high-grade glioma. Demographic characteristics for the participants from the Dunedin Study included in the current analyses. We cover melancholic and psychotic depression along with a case of vascular depression here. In dynamic contrast-enhanced MRI a series of T1-weighted images are acquired dynamically after injection, enabling the measurement of BBB permeability. Thus, our findings suggest that WMHs may be a surrogate biomarker for identifying individuals in midlife who are at risk for future clinically significant cognitive decline or ADRD. The aim of this systematic review is to give an overview of the evidence demonstrating pathological, clinical, and cerebrovascular risk factor effects on spatial patterns of WMHs in adult populations and clinical cohorts, by summarizing the increasing evidence of spatial specificity with respect to WMH burden. Dynamic temporal change of cerebral microbleeds: long-term follow-up MRI study. MS: supervision. Tabara, Y. Results: A total of studies were identified by the initial literature search, of which 41 studies satisfied the inclusion criteria.