Chronic cerebrovascular dysfunction after traumatic brain injury

Amandine Jullienne, Andre Obenaus, Aleksandra Ichkova, Catherine Savona-Baron, William J. Pearce, Jerome Badaut
Journal of Neuroscience Research. 2016-04-27; 94(7): 609-622
DOI: 10.1002/jnr.23732

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Jullienne A(1), Obenaus A(1)(2)(3), Ichkova A(4), Savona-Baron C(4), Pearce WJ(5), Badaut J(2)(4).

Author information:
(1)Department of Pediatrics, Loma Linda University School of Medicine, Loma Linda, California.
(2)Department of Physiology, Loma Linda University School of Medicine, Loma Linda, California.
(3)Center for Glial-Neuronal Interactions, Division of Biomedical Sciences, University of California Riverside, Riverside, California.
(4)CNRS UMR5287, University of Bordeaux, Bordeaux, France.
(5)Center for Perinatal Biology, Loma Linda University School of Medicine, Loma Linda, California.

Traumatic brain injuries (TBI) often involve vascular dysfunction that leads to
long-term alterations in physiological and cognitive functions of the brain.
Indeed, all the cells that form blood vessels and that are involved in
maintaining their proper function can be altered by TBI. This Review focuses on
the different types of cerebrovascular dysfunction that occur after TBI,
including cerebral blood flow alterations, autoregulation impairments,
subarachnoid hemorrhage, vasospasms, blood-brain barrier disruption, and edema
formation. We also discuss the mechanisms that mediate these dysfunctions,
focusing on the cellular components of cerebral blood vessels (endothelial cells,
smooth muscle cells, astrocytes, pericytes, perivascular nerves) and their known
and potential roles in the secondary injury cascade. © 2016 Wiley Periodicals,
Inc.

© 2016 Wiley Periodicals, Inc.

 

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