White matter hyperintensities

Background: White matter hyperintensities are an important white matter hyperintensities 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.

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.

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. Research shows that white matter hyperintensities WMHs are one such surrogate biomarker of cognitive decline and ADRD that can be measured in the brains of older adults Cees De Groot et al. While WMHs are uncommon in adults before age 30 Habes et al. In older adults, WMHs are associated with multiple dementia risk factors, including increasing age, hypertension, stroke, brain atrophy and cognitive ability Prins and Scheltens, 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,

First, descriptive statistics was generated for the sample as a whole Table 1, white matter hyperintensities. 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.

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.

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.

White matter hyperintensities

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.

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Sensitivity encoding for fast MR imaging of the brain in patients with stroke. Figure 3. Associations between T1 white matter lesion volume and regional white matter microstructure in aging. Psychiatry Res. More from Oxford Academic. The genetics of small-vessel disease. Ahmad R Hariri. Wechsler D. Nat Rev Neurol ; 11 : — Radiology , — In a population-representative birth cohort of individuals now in midlife, we found that WMHs are i common, ii associated with cognitive abilities in childhood and midlife and iii associated with cognitive decline from childhood to midlife. The clinical importance of white matter hyperintensities on brain magnetic resonance imaging: systematic review and meta-analysis. Histopathologic correlate of hypointense lesions on T1-weighted spin-echo MRI in multiple sclerosis. White matter hyperintensities are associated with amyloid burden in APOE4 non-carriers. See J Am Heart Assoc.

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.

Given that prevention of damage is often more efficacious than reversal of damage Sperling et al. How much do focal infarcts distort white matter lesions and global cerebral atrophy measures? 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. Progression of cerebral small vessel disease in relation to risk factors and cognitive consequences: Rotterdam Scan study. Better methods to measure WMH are needed that are reliable and efficient, with minimal human input, for large population studies. Fundamental concepts. Yoshita, M. Therefore, regardless of where the albumin or other plasma proteins came from, or how they got into the interstitial tissues, there does appear to be a role for loss of normal BBB function and fluid shifts into the brain leading to secondary brain damage 91 , 92 ; if arrested or reversed early, the interstitial fluid shifts may be more reversible than demyelination and axonal loss. Show results from All journals This journal. Neuroinformatics 13, — White matter hyperintensities are a predictor for vascular disease for which age and high blood pressure are the main risk factors. Assessment of blood—brain barrier disruption using dynamic contrast-enhanced MRI. Studies have been identified by an advanced search on PubMed.