The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Pathophysiology and treatment of cerebral edema in traumatic brain injury
Open accessAbstract
Cerebral edema (CE) and resultant intracranial hypertension are associated with unfavorable prognosis in traumatic brain injury (TBI). CE is a leading cause of in-hospital mortality, occurring in >60% of patients with mass lesions, and ∼15% of those with normal initial computed tomography scans. After treatment of mass lesions in severe TBI, an important focus of acute neurocritical care is evaluating and managing the secondary injury process of CE and resultant intracranial hypertension. This review focuses on a contemporary understanding of various pathophysiologic pathways contributing to CE, with a subsequent description of potential targeted therapies. There is a discussion of identified cellular/cytotoxic contributors to CE, as well as mechanisms that influence blood-brain-barrier (BBB) disruption/vasogenic edema, with the caveat that this distinction may be somewhat artificial since molecular processes contributing to these pathways are interrelated. While an exhaustive discussion of all pathways with putative contributions to CE is beyond the scope of this review, the roles of some key contributors are highlighted, and references are provided for further details. Potential future molecular targets for treating CE are presented based on pathophysiologic mechanisms. We thus aim to provide a translational synopsis of present and future strategies targeting CE after TBI in the context of a paradigm shift towards precision medicine. This article is part of the Special Issue entitled "Novel Treatments for Traumatic Brain Injury".
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Cites
The far-reaching scope of neuroinflammation after traumatic brain injury
Simon, D. W., McGeachy, M. J., Bayır, H., Clark, R. S. B., Loane, D. J., & Kochanek, P. M. (2017) · Nature Reviews Neurology · doi:10.1038/nrneurol.2017.13 · Cited by 1,190 · cited 3×
“In animal models, cerebrovascular endothelium in the injured hemisphere increases expression of neutrophilic vascular adhesion molecules (E-selectin, ICAM1) within 4 h, thus facilitating migration of these peripheral immune cells beyond the BBB (Simon et al., 2017).”
Impairment of Glymphatic Pathway Function Promotes Tau Pathology after Traumatic Brain Injury
Iliff, J. J., Chen, M. J., Plog, B. A., Zeppenfeld, D. M., Soltero, M., Yang, L., Singh, I., Deane, R., & Nedergaard, M. (2014) · The Journal of Neuroscience · doi:10.1523/jneurosci.3020-14.2014 · Cited by 1,159
Neuroimmunology of Traumatic Brain Injury: Time for a Paradigm Shift
Jassam, Y. N., Izzy, S., Whalen, M., McGavern, D. B., & El Khoury, J. (2017) · Neuron · doi:10.1016/j.neuron.2017.07.010 · Cited by 799
The impact of microglial activation on blood-brain barrier in brain diseases
da Fonseca, A. C. C., Matias, D., Garcia, C., Amaral, R., Geraldo, L. H., Freitas, C., & Lima, F. R. S. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00362 · Cited by 572
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Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer’s Disease
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Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries
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Targeting Aquaporin-4 Subcellular Localization to Treat Central Nervous System Edema
Kitchen, P., Salman, M. M., Halsey, A. M., Clarke-Bland, C., MacDonald, J. A., Ishida, H., Vogel, H. J., Almutiri, S., Logan, A., Kreida, S., et al. (2020) · Cell · doi:10.1016/j.cell.2020.03.037 · Cited by 452
Emerging roles for dynamic aquaporin-4 subcellular relocalization in CNS water homeostasis
Salman, M. M., Kitchen, P., Halsey, A., Wang, M. X., Törnroth-Horsefield, S., Conner, A. C., Badaut, J., Iliff, J. J., & Bill, R. M. (2022) · Brain · doi:10.1093/brain/awab311 · Cited by 303
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Recent Developments in Mouse Trauma Research Models: A Mini-Review
Gihring, A., Gärtner, F., Schirmer, M., Wabitsch, M., & Knippschild, U. (2022) · Frontiers in Physiology · doi:10.3389/fphys.2022.866617 · Cited by 6
Metadata
- Authors
- Jha, R. M., Kochanek, P. M., & Simard, J. M.
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2019-02
- Volume
- 145
- Issue
- Pt B
- Pages
- 230-246
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W2886166995
- Cited by
- 481
- References
- 7
- FWCI
- 19.56
- Type
- journal article
- Language
- en
- Open access
- hybrid
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