Cerebrovascular pathophysiology following mild traumatic brain injury

Abstract

Mild traumatic brain injury (mTBI) or sport-induced concussion has recently become a prominent concern not only in the athletic setting (i.e. sports venue) but also in the general population. The majority of research to date has aimed at understanding the neurological and neuropsychological outcomes of injury as well as return-to-play guidelines. Remaining relatively unexamined has been the pathophysiological aspect of mTBI. Recent technological advances including transcranial Doppler ultrasound and near infrared spectroscopy have allowed researchers to examine the systemic effects of mTBI from rest to exercise, and during both asymptomatic and symptomatic conditions. In this review, we focus on the current research available from both human and experimental (animal) studies surrounding the pathophysiology of mTBI. First, the quest for a unified definition of mTBI, its historical development and implications for future research is discussed. Finally, the impact of mTBI on the control and regulation of cerebral blood flow, cerebrovascular reactivity, cerebral oxygenation and neuroautonomic cardiovascular regulation, all of which may be compromised with mTBI, is discussed.

Cerebral Blood Flow Alterations in Acute Sport-Related Concussion

“…3,6,8,9,[11][12][13][14][15] However, studies of the biological substrates of SRC have been limited in scope, and knowledge regarding the functional physiological deficits following mTBI remains relatively unknown. 11,13,[16][17][18][19][20][21][22] Although the pathogenesis of concussion has yet to be fully elucidated, it is becoming increasingly clear that cerebrovascular alterations play a significant role in the evolution of injury sequelae, as well as in the process of post-traumatic brain repair. 4,11,[22][23][24] Reduced cerebral blood flow (CBF) signifies one of the most lasting markers of concussion in animal models of traumatic brain injury (TBI), 14,25,26 while CBF has been shown to be decreased immediately after injury in an animal model 27,28 and decreased regional CBF persisted after injury.…”

“…11,13,[16][17][18][19][20][21][22] Although the pathogenesis of concussion has yet to be fully elucidated, it is becoming increasingly clear that cerebrovascular alterations play a significant role in the evolution of injury sequelae, as well as in the process of post-traumatic brain repair. 4,11,[22][23][24] Reduced cerebral blood flow (CBF) signifies one of the most lasting markers of concussion in animal models of traumatic brain injury (TBI), 14,25,26 while CBF has been shown to be decreased immediately after injury in an animal model 27,28 and decreased regional CBF persisted after injury. 29 Reduced CBF during the acute and subacute phases of mTBI has been detected using imaging methods such as single-photon emission computed tomography 30,31 and perfusion computed tomography, 32 which have several disadvantages, including financial cost, ionizing radiation, and limited repetition of acquisitions.…”

Early Cortical Thickness Change after Mild Traumatic Brain Injury following Motor Vehicle Collision

“…Other pathological mechanisms to consider for explaining cortical thinning at an early stage after mTBI would include vascular changes, 65 and acute (less than 72 h) hypoperfusion, as has been reported in the cortex of concussed survivors with persistence in several survivors over the following months. 58,[66][67][68] Acute hypoperfusions are attributed to reversible microvasoconstriction in a rat model of mTBI, 69 and acute vasoconstriction has been reported within an hour after TBI in human survivors with subarachnoid hemorrhage. 70,71 Further, even transient hypoperfusion may produce prolonged changes in cortical thickness as evidenced by decreased cortical thickness and less fMRI activation in rats at 4 months after a single episode of hypoxia-ischemia.…”

Pediatric Sports-Related Concussion Produces Cerebral Blood Flow Alterations

“…Possibilities include alterations in cerebral autoregulation, reductionoflargearterycaliber(ie,vasospasm), or extensive regional perfusion perturbations. 72,75,81,[86][87][88][89][90] Although loss of autoregulation (during which reduced CBF becomes dependent on mean blood pressure) was observed in 2 of 10 patients with mild TBI in a previous investigation, 91 we did not observe altered mean blood pressure in any of our patients. Based on the methodology we employed for determining CBF by using phase contrast angiography data, the calibers of the internal carotid and basilar vessels were influential.…”