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Am J Physiol Heart Circ Physiol. 2016 Nov 1;311(5):H1118-H1131. doi: 10.1152/ajpheart.00267.2016. Epub 2016 Sep 9.

Traumatic brain injury-induced autoregulatory dysfunction and spreading depression-related neurovascular uncoupling: Pathomechanisms, perspectives, and therapeutic implications.

Toth P1,2,3, Szarka N4,5, Farkas E6, Ezer E4, Czeiter E4,2,7, Amrein K4,2,7, Ungvari Z3, Hartings JA8, Buki A4,2,7, Koller A4,2,9,10.

Author information

1
Department of Neurosurgery, University of Pecs, Pecs, Hungary; peter-toth@ouhsc.edu.
2
Janos Szentagothai Research Centre, University of Pecs, Pecs, Hungary.
3
Department of Geriatric Medicine, Reynolds Oklahoma Center on Aging, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
4
Department of Neurosurgery, University of Pecs, Pecs, Hungary.
5
Department of Translational Medicine, University of Pecs, Pecs, Hungary.
6
Faculty of Medicine and Faculty of Science and Informatics, Department of Medical Physics and Informatics, University of Szeged, Szeged, Hungary.
7
MTA-PTE Clinical Neuroscience MR Research Group, Pecs, Hungary.
8
Department of Neurosurgery, University of Cincinnati College of Medicine, Cincinnati, Ohio.
9
Institute of Natural Sciences, University of Physical Education, Budapest, Hungary; and.
10
Department of Physiology, New York Medical College, Valhalla, New York.

Abstract

Traumatic brain injury (TBI) is a major health problem worldwide. In addition to its high mortality (35-40%), survivors are left with cognitive, behavioral, and communicative disabilities. While little can be done to reverse initial primary brain damage caused by trauma, the secondary injury of cerebral tissue due to cerebromicrovascular alterations and dysregulation of cerebral blood flow (CBF) is potentially preventable. This review focuses on functional, cellular, and molecular changes of autoregulatory function of CBF (with special focus on cerebrovascular myogenic response) that occur in cerebral circulation after TBI and explores the links between autoregulatory dysfunction, impaired myogenic response, microvascular impairment, and the development of secondary brain damage. We further provide a synthesized translational view of molecular and cellular mechanisms involved in cortical spreading depolarization-related neurovascular dysfunction, which could be targeted for the prevention or amelioration of TBI-induced secondary brain damage.

KEYWORDS:

autoregulation; brain damage; cerebral blood flow; myogenic; neurovascular coupling

PMID:
27614225
PMCID:
PMC5504422
DOI:
10.1152/ajpheart.00267.2016
[Indexed for MEDLINE]
Free PMC Article

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