RECENT RESEARCH INVOLVING THE SATA:
Len TK, Neary JP. (2011). Cerebrovascular pathophysiology following mild traumatic brain injury. Clinical Physiology and Functional Imaging 31(2): 85 - 93.
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.
Len TK, Neary JP, Asmundson GJG, Goodman DG, Bjornson B, Bhambhani YN. (2011). Cerebrovascular reactivity impairment following sport-induced concussion. Medicine & Science in Sports & Exercise 43(12): 2241-48..
PURPOSE: This study evaluated cerebrovascular reactivity (CVR) following a sport-induced concussion, also referred to as mild traumatic brain injury (mTBI), by monitoring middle cerebral artery blood velocity (vMCA) with transcranial Doppler ultrasonography (TCD) and simultaneous end-tidal carbon dioxide (PETCO2) measurements. METHODS: Thirty-one athletes (16 - 25 years old) participated in this study. The participants were divided into two groups - healthy (n = 21) and mTBI (n = 10). Participants in the mTBI group suffered a mTBI within the last seven days (x = 4.5 ± 1.1 days). Outcome measures included vMCA and PETCO2 in response to breath-holding (5 × 20 seconds, 40 seconds rest) and hyperventilation (5 × 20 seconds, 40 seconds rest). RESULTS: Resting vMCA values between groups were not significantly different. Percentage change of vMCA was significantly different following the recovery period of the second hyperventilation (P = 0.034). mTBI subjects failed to return to resting levels following each breath-hold. End-tidal CO2 changes mirrored the vMCA changes. CONCLUSION: These data suggest that normal CVR responses may be disrupted in the days immediately following occurrence of mTBI. Transcranial Doppler ultrasonography combined with expired gas measurements provides a useful method for assessing CVR impairment following mTBI. Further research, including serial monitoring following mTBI and analysis of CVR response to exercise, is warranted before any firm conclusions can be drawn.