1. [Pathophysiology of intracranial injuries].
- Author
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Lahner D and Fritsch G
- Subjects
- Biomarkers metabolism, Brain physiopathology, Brain Damage, Chronic physiopathology, Brain Edema classification, Brain Edema physiopathology, Brain Injuries, Diffuse physiopathology, Brain Injuries, Traumatic classification, Glial Fibrillary Acidic Protein metabolism, Hematoma, Epidural, Cranial classification, Hematoma, Epidural, Cranial physiopathology, Hematoma, Subdural classification, Hematoma, Subdural physiopathology, Humans, Intracranial Pressure physiology, Neurofilament Proteins metabolism, Phosphopyruvate Hydratase metabolism, S100 Calcium Binding Protein beta Subunit metabolism, Synapses physiology, Tauopathies physiopathology, Brain Injuries, Traumatic physiopathology
- Abstract
Traumatic brain injury (TBI) constitutes a heterogeneous condition that affects the most complex organ of the human body. It is commonly classified by its location as focal injury (e.g. epidural hematoma) and diffuse injury (e.g. diffuse axonal shearing injury) as well as by primary and secondary tissue injury. Accordingly, direct mechanical force causes the primary insult. The tissue damage occurring afterwards is subsumed under the term secondary brain damage. Some of these processes are overlapping and include in the early phase local cerebral ischemia resulting in excitotoxicity, which together with the triggered neuroinflammatory cascade causes the formation of cerebral edema and ultimately increased intracranial pressure once the intracranial compliance is exhausted. In survivors the long-term sequelae of the late stage include seizures caused by synaptic reorganization (incidence depending on the severity of TBI), persistent neuroinflammation promoting further neurodegeneration and increased risk for Alzheimer's disease probably because of TBI-related protein misfolding (tauopathy). Acute phase biomarkers of TBI should ideally originate from the injured brain. They should help distinguish disease severity and predict morbidity and mortality; however, the most commonly used biomarkers (S-100β and neurone-specific enolase) show a low specificity. In theory their successors (i. e. GFAP, pNF-H) seem more specific; however, these "new kids on the block" still need to be thoroughly investigated in large scale studies.
- Published
- 2017
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