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Mechanisms of how sarcopenia affects functional outcomes in acute ischaemic stroke
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Gwak, Dong-Seok | - |
| dc.contributor.author | Chung, Jinyong | - |
| dc.contributor.author | Schellingerhout, Dawid | - |
| dc.contributor.author | Oh, Hyerin | - |
| dc.contributor.author | Jeong, Sang-Wuk | - |
| dc.contributor.author | Lee, Ji Sung | - |
| dc.contributor.author | Kim, Dong-Eog | - |
| dc.date.accessioned | 2025-11-28T08:00:17Z | - |
| dc.date.available | 2025-11-28T08:00:17Z | - |
| dc.date.issued | 2025 | - |
| dc.identifier.issn | 2632-1297 | - |
| dc.identifier.issn | 2632-1297 | - |
| dc.identifier.uri | https://scholarworks.dongguk.edu/handle/sw.dongguk/62183 | - |
| dc.description.abstract | Sarcopenia, a common geriatric condition characterized by the loss of skeletal muscle mass and function, can negatively affect functional outcomes in acute ischaemic stroke; however, the underlying mechanisms remain unclear. We hypothesized that sarcopenia affects post-stroke outcomes, mediated through its impact on dysphagia, early neurological deterioration, or post-stroke recovery, particularly in patients with motor deficits. To explore this hypothesis, we included 600 consecutive elderly (>= 65 years) patients with acute (<1 week) ischaemic stroke and assessed: (i) the relationships sarcopenia has with dysphagia, early neurological deterioration and various phases of recovery after stroke (in-hospital, post-discharge [up to 3 months], and chronic [3 months to 1 year]) and (ii) whether either presenting symptoms or lesion locations modify the impact of sarcopenia on stroke outcomes. Temporal muscle thickness, a marker of sarcopenia, was measured by brain magnetic resonance imaging and dichotomized into low versus high temporal muscle thickness at the 25th percentile cut-off point. Logistic regression analysis, mediation analysis and statistical brain mapping were conducted. Mean age was 75.3 +/- 6.1 years and 303 (50.5%) were male. Low temporal muscle thickness (<5.1 mm) was independently associated with dysphagia (adjusted odds ratio 1.89 [95% confidence interval 1.06-3.37], P = 0.03), early neurological deterioration (adjusted odds ratio 2.75 [95% confidence interval 1.61-4.71], P < 0.001) and post-discharge recovery (adjusted odds ratio 0.56 [95% confidence interval 0.34-0.94], P = 0.03) but not with in-hospital or chronic recovery. In addition, dysphagia, early neurological deterioration and post-discharge recovery were shown to mediate the association between low temporal muscle thickness and poor functional outcome (modified Rankin scale score >= 3) at 3 months, accounting for similar to 45% of the total effect. Low temporal muscle thickness had a greater impact on stroke outcomes in patients with motor deficit, facial palsy, dysarthria, or pontine lesions. Furthermore, brain mapping revealed that low temporal muscle thickness had a stronger impact on functional outcomes in infarctions involving brain regions responsible for motor strength, planning, execution, and control: i.e. pallidum, fronto-pontine tract, parieto-occipito-temporo-pontine tract, middle cerebellar peduncle, and corticospinal tract. Sarcopenia leads to poor functional outcomes, probably due to its association with dysphagia, early neurological deterioration, and limited post-discharge recovery in elderly acute ischaemic stroke patients, particularly those with motor deficit, bulbar symptoms, or lesions involving pons and motor pathways. Understanding and identifying the mechanisms underlying sarcopenia-related effects on post-stroke outcomes may inform comprehensive, time-specific approaches to personalised management for this patient population. | - |
| dc.language | 영어 | - |
| dc.language.iso | ENG | - |
| dc.publisher | Oxford University Press | - |
| dc.title | Mechanisms of how sarcopenia affects functional outcomes in acute ischaemic stroke | - |
| dc.type | Article | - |
| dc.publisher.location | 영국 | - |
| dc.identifier.doi | 10.1093/braincomms/fcaf386 | - |
| dc.identifier.scopusid | 2-s2.0-105021428174 | - |
| dc.identifier.wosid | 001613633200001 | - |
| dc.identifier.bibliographicCitation | Brain Communications, v.7, no.6 | - |
| dc.citation.title | Brain Communications | - |
| dc.citation.volume | 7 | - |
| dc.citation.number | 6 | - |
| dc.type.docType | Article | - |
| dc.description.isOpenAccess | Y | - |
| dc.description.journalRegisteredClass | scopus | - |
| dc.description.journalRegisteredClass | esci | - |
| dc.relation.journalResearchArea | Neurosciences & Neurology | - |
| dc.relation.journalWebOfScienceCategory | Clinical Neurology | - |
| dc.relation.journalWebOfScienceCategory | Neurosciences | - |
| dc.subject.keywordPlus | SKELETAL-MUSCLE MASS | - |
| dc.subject.keywordPlus | HUMAN BRAIN | - |
| dc.subject.keywordPlus | RECOVERY | - |
| dc.subject.keywordPlus | ATLAS | - |
| dc.subject.keywordAuthor | ischaemic stroke | - |
| dc.subject.keywordAuthor | sarcopenia | - |
| dc.subject.keywordAuthor | muscle | - |
| dc.subject.keywordAuthor | prognosis | - |
| dc.subject.keywordAuthor | motor | - |
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