White matter hyperintensities

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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. However, the success of this investment hinges on developing surrogate biomarkers—biological measures that are part of the putative disease pathway and are measurable before the onset of clinical symptoms—so that prevention can target at-risk individuals before cerebral decline has taken hold.

White matter hyperintensities

Background: White matter hyperintensities are an important marker of cerebral small vessel disease. This disease burden is commonly described as hyperintense areas in the cerebral white matter, as seen on T2-weighted fluid attenuated inversion recovery magnetic resonance imaging data. Studies have demonstrated associations with various cognitive impairments, neurological diseases, and neuropathologies, as well as clinical and risk factors, such as age, sex, and hypertension. Due to their heterogeneous appearance in location and size, studies have started to investigate spatial distributions and patterns, beyond summarizing this cerebrovascular disease burden in a single metric—its volume. Here, we review the evidence of association of white matter hyperintensity spatial patterns with its risk factors and clinical diagnoses. We used the standards for reporting vascular changes on neuroimaging criteria to construct a search string for literature search on PubMed. Studies written in English from the earliest records available until January 31st, , were eligible for inclusion if they reported on spatial patterns of white matter hyperintensities of presumed vascular origin. Results: A total of studies were identified by the initial literature search, of which 41 studies satisfied the inclusion criteria. Additionally, 6 of 41 studies investigated cognitively normal, older cohorts, two of which were population-based, or other clinical findings such as acute ischemic stroke or reduced cardiac output. The studies included in this review have identified spatial heterogeneity of WMHs with various impairments, diseases, and pathologies as well as with sex and cerebro vascular risk factors. Conclusion: The results show that studying white matter hyperintensities on a more granular level might give a deeper understanding of the underlying neuropathology and their effects.

Research should target the enormous unfinished agenda that constitutes brain damage represented by WMH and diffuse small vessel disease. Fourth, white matter hyperintensities association between volume and change in IQ was tested using ordinary least squares multiple regression.

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.

Leukoaraiosis is a particular abnormal change in appearance of white matter near the lateral ventricles. It is often seen in aged individuals, but sometimes in young adults. These white matter changes are also commonly referred to as periventricular white matter disease, or white matter hyperintensities WMH , due to their bright white appearance on T2 MRI scans. Many patients can have leukoaraiosis without any associated clinical abnormality. However, underlying vascular mechanisms are suspected to be the cause of the imaging findings. Hypertension , smoking, diabetes , [3] hyperhomocysteinemia , and heart diseases are all risk factors for leukoaraiosis. Leukoaraiosis has been reported to be an initial stage of Binswanger's disease but this evolution does not always happen. White matter hyperintensities can be caused by a variety of factors, including ischemia , micro- hemorrhages , gliosis , damage to small blood vessel walls, breaches of the barrier between the cerebrospinal fluid and the brain, or loss and deformation of the myelin sheath.

White matter hyperintensities

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. However, the success of this investment hinges on developing surrogate biomarkers—biological measures that are part of the putative disease pathway and are measurable before the onset of clinical symptoms—so that prevention can target at-risk individuals before cerebral decline has taken hold. Successful surrogate biomarkers would allow clinicians to assess risk, monitor sub-clinical disease progression and intervene before clinically significant dementia symptoms manifest.

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Debette, S. Postmortem examination of vascular lesions in cognitive impairment: a survey among neuropathological services. Results A total of studies were identified by the initial literature search, of which 41 studies satisfied the inclusion criteria see Figure 1 for a detailed description of the selection phase Auer et al. While research into spatial patterns of WMH is a rapidly developing field that first emerged around 20 years ago with most publications in the last decade, a commonly agreed terminology does not yet exist, which hinders the identification of related literature. Donepezil in vascular dementia: combined analysis of two large-scale clinical trials. Efficacy and safety of memantine in patients with mild to moderate vascular dementia: a randomized, placebo-controlled trial MMM AJNR Am. Attenuation of brain white matter hyperintensities after cerebral infarction. You can also search for this author in PubMed Google Scholar. Better methods to measure WMH are needed that are reliable and efficient, with minimal human input, for large population studies. Page, M. More from Oxford Academic. Ahmad R. Chao, L.

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

Neuroimage ; 38 : 95 — Cerebral white matter lesions in the elderly: vascular risk factors and cognitive consequences [Dutch]. A limitation of existing trials is that they have targeted older adults in their 60s, 70s and 80s. Large, longitudinal population-based and hospital-based studies have confirmed a dose-dependent relationship between WMHs and clinical outcome, and have demonstrated a causal link between large confluent WMHs and dementia and disability. Cigarette smoking is associated with reduced microstructural integrity of cerebral white matter. Yoshida, T. The effects of small vessel disease and amyloid burden on neuropsychiatric symptoms: a study among patients with subcortical vascular cognitive impairments. Cerebral white matter lesions and cognitive function: the Rotterdam scan study. Longitudinal studies in older adults have reported that the spread of WMHs contributes to elevated risk for ADRD and coincides with age-related cognitive decline Debette and Markus, Neurocognitive functions and everyday functions change together in old age. De Groot, J.