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Traumatic brain injury-induced autoregulatory dysfunction and spreading
depression-related neurovascular uncoupling: Pathomechanisms, perspectives, and
therapeutic implications
#MMPMID27614225
Toth P
; Szarka N
; Farkas E
; Ezer E
; Czeiter E
; Amrein K
; Ungvari Z
; Hartings JA
; Buki A
; Koller A
Am J Physiol Heart Circ Physiol
2016[Nov]; 311
(5
): H1118-H1131
PMID27614225
show ga
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.
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