{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362825894601871872.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1111/j.1582-4934.2010.01164.x"}},{"identifier":{"@type":"URI","@value":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1582-4934.2010.01164.x"}},{"identifier":{"@type":"URI","@value":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1582-4934.2010.01164.x"}}],"dc:title":[{"@value":"Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title><jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Introduction</jats:p></jats:list-item>\n<jats:list-item><jats:p>Classifying TBI</jats:p></jats:list-item>\n<jats:list-item><jats:p>Clinical characteristics</jats:p></jats:list-item>\n<jats:list-item><jats:p>Pathophysiological mechanisms of focal injury</jats:p></jats:list-item>\n<jats:list-item><jats:p>Pathophysiological mechanisms of diffuse injury</jats:p></jats:list-item>\n<jats:list-item><jats:p>Conclusions</jats:p></jats:list-item>\n</jats:list>\n</jats:p><jats:p>Traumatic brain injury (TBI) is a frequent and clinically highly heterogeneous neurological disorder with large socioeconomic consequences. TBI severity classification, based on the hospital admission Glasgow Coma Scale (GCS) score, ranges from mild (GCS 13–15) and moderate (GCS 9–12) to severe (GCS ≤ 8). The GCS reflects the risk of dying from TBI, which is low after mild (∼1%), intermediate after moderate (up to 15%) and high (up to 40%) after severe TBI. Intracranial damage can be focal, such as epidural and subdural haematomas and parenchymal contusions, or diffuse, for example traumatic axonal injury and diffuse cerebral oedema, although this distinction is somewhat arbitrary. Study of the cellular and molecular post‐traumatic processes is essential for the understanding of TBI pathophysiology but even more to find therapeutic targets for the development of neuroprotective drugs to be eventually used in human beings. To date, studies <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo</jats:italic>, mainly in animals but also in human beings, are unravelling the pathological TBI mechanisms at high pace. Nevertheless, TBI pathophysiology is all but completely elucidated. Neuroprotective treatment studies in human beings have been disappointing thus far and have not resulted in commonly accepted drugs. This review presents an overview on the clinical aspects and the pathophysiology of focal and diffuse TBI, and it highlights several acknowledged important events that occur on molecular and cellular level after TBI.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382825894601871873","@type":"Researcher","foaf:name":[{"@value":"Teuntje M. J. C. Andriessen"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894601871744","@type":"Researcher","foaf:name":[{"@value":"Bram Jacobs"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894601871872","@type":"Researcher","foaf:name":[{"@value":"Pieter E. Vos"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"15821838"},{"@type":"EISSN","@value":"15824934"}],"prism:publicationName":[{"@value":"Journal of Cellular and Molecular Medicine"}],"dc:publisher":[{"@value":"Wiley"}],"prism:publicationDate":"2010-10","prism:volume":"14","prism:number":"10","prism:startingPage":"2381","prism:endingPage":"2392"},"reviewed":"false","dc:rights":["http://onlinelibrary.wiley.com/termsAndConditions#vor"],"url":[{"@id":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1582-4934.2010.01164.x"},{"@id":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1582-4934.2010.01164.x"}],"createdAt":"2010-08-29","modifiedAt":"2023-10-14","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360004233586336640","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Potential protective effect of highly bioavailable curcumin on an oxidative stress model induced by microinjection of sodium nitroprusside in mice brain"}]},{"@id":"https://cir.nii.ac.jp/crid/1360005520785633024","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Neuronal Ca<sup>2+</sup>‐dependent activator protein 1 (NCDAP1) induces neuronal cell death by activating p53 pathway following traumatic brain injury"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285709097025664","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Facial emotion recognition in patients with focal and diffuse axonal injury"}]},{"@id":"https://cir.nii.ac.jp/crid/1361975841735516288","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Prevention of head trauma and death in patients with head injuries: A forensic autopsy study"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1111/j.1582-4934.2010.01164.x"},{"@type":"CROSSREF","@value":"10.1039/c4fo00009a_references_DOI_OmQopz5ojvedr8taU0mVaiAy8hK"},{"@type":"CROSSREF","@value":"10.1111/jnc.14803_references_DOI_OmQopz5ojvedr8taU0mVaiAy8hK"},{"@type":"CROSSREF","@value":"10.1080/02699052.2017.1285052_references_DOI_OmQopz5ojvedr8taU0mVaiAy8hK"},{"@type":"CROSSREF","@value":"10.1016/j.iatssr.2019.06.004_references_DOI_OmQopz5ojvedr8taU0mVaiAy8hK"}]}