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Pmw Literature Review Video

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To review Pw evidence on links between post-stroke dementia and inflammation. Although there are still no treatments for post-stroke dementia, recent evidence has improved our understanding that stroke increases the Pmw Literature Review of incident dementia and worsens cognitive trajectory for at least a decade afterwards. Within approximately the first year dementia onset is associated with stroke severity and location, while later absolute risk is associated with more traditional dementia risk factors such as age and imaging findings. The molecular mechanisms that underlie increased risk of incident dementia in stroke survivors remain unproven, however new data in both human and animal studies suggests links between cognitive decline and inflammation.

These point to a model where chronic brain inflammation, provoked by inefficient clearance of myelin debris and a prolonged Rview and adaptive continue reading response, causes post-stroke dementia.

These localized immune events in the brain may themselves be influenced by the peripheral immune state at key times after stroke. This review recaps clinical evidence on post-stroke dementia, new mechanistic links between the chronic inflammatory response to stroke and post-stroke dementia, and proposes a model of immune-mediated neurodegeneration after stroke. Stroke approximately doubles the risk that a person will be diagnosed with dementia later in life. The risk is highest in the six months after stroke but Pmw Literature Review increased risk persists for at least a decade, even after controlling for known dementia risk factors [ 1 — 4 ].

Dementia risk is highest for hemorrhagic strokes, including subarachnoid hemorrhage, and less for ischemic stroke, Literaturr Pmw Literature Review ratios HR ranging from 1.

Introduction

Hazard ratios are higher for young adult stroke victims about 7then decrease with aging, while the Pmw Literature Review risk of incident dementia increases with age [ 4 ]. This drop in relative dementia risk likely occurs because the risk of dementia from other causes rises with age. In addition to age, larger stroke size is associated with incident dementia after stroke, particularly within the first year. Pendlebury et. Five-year dementia risk remained high, and was associated with age, previous stroke, stroke severity, dysphasia, baseline cognition, low education, white-matter disease, and diabetes. Overall, OxVasc participants with severe stroke advanced their dementia risk to that of someone 24 years older, while survivors of mild stroke brought their risk forward 4 years [ 2 ]. About half of the increased risk of dementia after stroke is in the first 6—12 months [ 12 ]. Overlaid with this there can be improvements in the initial months after stroke [ 5 ].

This is similar to the pattern seen with stroke-induced disability where an initial impairment improves in the months afterwards [ 6 ]. Then in the case of both Pmw Literature Review and disability incidence, there is a long-term change in trajectory that results in a higher likelihood of accumulating both cognitive deficits or disability for years [ 136 ].

In hemorrhagic stroke, Reviiew within 6 months is associated with hemorrhage size and location, while later dementia between 6 and 60 months after hemorrhage is associated with age, education, mood, and white matter disease [ 7 ]. However, these associations pertain to Pmw Literature Review absolute dementia risk—there is not a good enough understanding of the mechanisms that underlie post-stroke dementia to differentiate which participants have dementia due to the stroke alone, to a separate neurodegenerative process, or both. However, we do know that the long-lasting higher risk of incident dementia after stroke is unlikely to result from vascular risk factors or silent strokes alone.]