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. 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

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. This motivates further studies examining the spatial patterns of white matter hyperintensities. Moreover, it has been demonstrated that this cerebrovascular disease burden is associated with various impairments, diseases, and pathologies, such as motor Smith et al. Additionally, the presentation of WMHs in the brain are associated with sex Lohner et al. Due to its high prevalence, multiple studies have reviewed the evidence on its prevalence and modifying factors over the years Herrmann et al.

Ambulatory blood pressure and the brain: a 5-year follow-up.

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.

But in recent years, it has become clear that the monkey is just as important as its master. Our exquisitely folded gray matter has long been the show pony of the brain; it deals with the heavy number-crunching we all rely on to make sense of the world. The white matter, it was thought, simply carries out the task of relaying messages back and forth, as little more than a collection of passive wires. Although there is some truth to this division of labor, it does white matter a huge disservice. As scientific knowledge grows, the importance of white matter comes into sharp focus.

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.

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Ylikoski, A. White matter hyperintensities on MRI in the neurologically nondiseased elderly. Avshalom Caspi. WMH accumulation occurs over significantly shorter intervals ie 12 weeks than has been previously shown. 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. Midlife vascular risk factor exposure accelerates structural brain aging and cognitive decline. Email alerts Article activity alert. 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. Murray, M. Ethics declarations Competing interests The authors declare no competing financial interests. Association of data-driven white matter hyperintensity spatial signatures with distinct cerebral small vessel disease etiologies. MR signal abnormalities at 1. Spatial signature of white matter hyperintensities in stroke patients.

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.

Required augmentation strategies to achieve remission. How much do focal infarcts distort white matter lesions and global cerebral atrophy measures? Maillard, P. Ann Neurol ; 47 : — Fourth ventricle, aqueduct, cistern ventral to mesencephalon. 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 hyperintensity progression and late-life depression outcomes. However, there is as yet no automated approach that can identify WMH accurately without any human input — all require visual assessment and manual correction, particularly in populations with advanced age or stroke where the brains are more likely to be abnormal Figure 8 and features of similar signal characteristics like stroke lesions, if not excluded, will distort the WMH volume measurements with subsequent alterations on the outcome of the study. Future research and meta-analyses would also significantly benefit from a consensus for standard terminology and of image analysis methodology for spatial patterns analyses of WMH. In this particular study population, spatial patterns of WMH appear across the entire brain. Stroke 32 , — 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.