White matter hyperintensities

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

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.

White matter hyperintensities

Federal government websites often end in. The site is secure. White matter hyperintensities WMH of presumed vascular origin, also referred to as leukoaraiosis, are a very common finding on brain magnetic resonance imaging MRI or computed tomography CT in older subjects and in patients with stroke and dementia. They are associated with cognitive impairment, triple the risk of stroke and double the risk of dementia. Knowledge of their pathology derives mostly from post mortem studies, many from some years ago. These, by their nature, were generally small, sampled from selected brain regions and probably reflect late-stage disease. They focus on features of demyelination and axonal degeneration, which may be easier to detect histopathologically than changes in extracellular fluid. Here we review advances in brain magnetic resonance imaging MRI that are revealing white matter hyperintensities at earlier stages, and changes in normal-appearing white matter that indicate tissue pathology, less marked than those found in WMH. Neuroimaging is also revealing the dynamic nature of WMH, their interactions with other pathological features such as secondary cortical and long tract damage, and contribution to accumulating brain damage. These insights provide opportunities to improve understanding the etiology and pathogenesis of small vessel disease, and represents an enormous unfinished agenda for preventing accumulation of brain damage, and its associated cognitive and physical problems, from mid to later life. Recognizing the earliest stages leading to WMH development will provide important opportunities to prevent or even reverse brain damage due to small vessel disease at the earliest stages, and ameliorate its cognitive, physical, stroke and dementia consequences.

There seems to be a significant association between WMHs and mortality in both the general population and in high-risk populations such as those with a history of stroke and depression. Descriptive studies without the aim white matter hyperintensities describe the association of the observed patterns were excluded for the purpose of this review.

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.

Federal government websites often end in. The site is secure. White matter hyperintensities WMH of presumed vascular origin, also referred to as leukoaraiosis, are a very common finding on brain magnetic resonance imaging MRI or computed tomography CT in older subjects and in patients with stroke and dementia. They are associated with cognitive impairment, triple the risk of stroke and double the risk of dementia. Knowledge of their pathology derives mostly from post mortem studies, many from some years ago.

White matter hyperintensities

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.

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Protocol for a randomized controlled trial evaluating the effect of physical activity on delaying the progression of white matter changes on MRI in older adults with memory complaints and mild cognitive impairment: the AIBL Active trial. Heterogeneity of small vessel disease: a systematic review of MRI and histopathology correlations. Microstructural white matter changes in normal aging: a diffusion tensor imaging study with higher-order polynomial regression models. Stroke 43 , — White matter lesion progression, brain atrophy, and cognitive decline: the Austrian stroke prevention study. Studies including MCI patients were most prevalent. Microstructural white matter changes in cognitively normal individuals at risk of amnestic MCI. Enlarged perivascular spaces are associated with cognitive function in healthy elderly men. Neuroimage 47, — Figure 2: Axial fluid-attenuated inversion recovery images illustrating the Fazekas scores. Standardized assessment of automatic segmentation of white matter hyperintensities and results of the WMH segmentation challenge. Richardson, K. Moreover, studies using MTR show that MTR differs between frontal and occipital WMH, either indicating different stages of tissue damage or possibly different underlying tissue constructs. Development of a semi-automated method for quantification of MRI gray and white matter lesions in geriatric subjects.

If you've had a brain magnetic resonance imaging MRI , you may be alarmed to hear that it shows small white spots. These white spots may indicate a cause for concern, including strokes or multiple sclerosis MS.

White matter hyperintensity accumulation during treatment of late-life depression. The association between blood pressure, hypertension, and cerebral white matter lesions: cardiovascular determinants of dementia study. More metrics information. DeCarli, C. Here, we focused on adults, but WMH can emerge earlier in life and is often linked with disease state. Standardized assessment of automatic segmentation of white matter hyperintensities and results of the WMH segmentation challenge. Bink, D. The appearance of a new white matter lesion adjacent to the old infarct in first-ever lacunar stroke patients: a two-year follow-up study with MRI. Studies in humans have shown that MD and T1 increase while FA and MTR decrease significantly in areas of WMH when compared to normal appearing white matter, 98 , — indicating pathological processes involving increased water content and mobility, demyelination, and axonal loss. The genetics of small-vessel disease. Thank you for visiting nature. Learn more.