Alterations in neurovascular coupling following acute traumatic brain injury

Abstract

Following acute traumatic brain injury (TBI), timely transport to a hospital can significantly improve the prognosis for recovery. There is, however, a dearth of quantitative biomarkers for brain injury that can be rapidly acquired and interpreted in active, field environments in which TBIs are frequently incurred. We explored potential functional indicators for TBI that can be noninvasively obtained through portable detection modalities, namely optical and electrophysiological approaches. By combining diffuse correlation spectroscopy with colocalized electrophysiological measurements in a mouse model of TBI, we observed concomitant alterations in sensory-evoked cerebral blood flow (CBF) and electrical potentials following controlled cortical impact. Injury acutely reduced the peak amplitude of both electrophysiological and CBF responses, which mostly recovered to baseline values within 30 min, and intertrial variability for these parameters was also acutely altered. Notably, the postinjury dynamics of the CBF overshoot and undershoot amplitudes differed significantly; whereas the amplitude of the initial peak of stimulus-evoked CBF recovered relatively rapidly, the ensuing undershoot did not appear to recover within 30 min of injury. Additionally, acute injury induced apparent low-frequency oscillatory behavior in CBF ([Formula: see text]). Histological assessment indicated that these physiological alterations were not associated with any major, persisting anatomical changes. Several time-domain features of the blood flow and electrophysiological responses showed strong correlations in recovery kinetics. Overall, our results reveal an array of stereotyped, injury-induced alterations in electrophysiological and hemodynamic responses that can be rapidly obtained using a combination of portable detection techniques.

Cerebral Perfusion Effects of Cognitive Training and Transcranial Direct Current Stimulation in Mild-Moderate TBI

“…One of the more promising hypotheses receiving significant scientific attention is that of abnormal cerebral perfusion, in which traumatic injury causes impaired neurovascular coupling and mismatch between neuronal metabolic demand and cerebral blood flow (CBF) (13)(14)(15)(16). There is ample grounding for this pathophysiology in animal models and in severe TBI in humans (17)(18)(19), however, noninvasively detecting changes in CBF in more mild injuries has proved more challenging (20). Arterial spin-labeling (ASL) and pseudocontinuous ASL (pCASL) magnetic resonance imaging sequences are techniques for measuring cerebral perfusion that have gained traction recently.…”

Proactive inhibition deficits with normal perfusion after pediatric mild traumatic brain injury

“…Neurovascular coupling has been shown to be disrupted in animal models of trauma (Jang et al, ), and the blood oxygen‐level dependent (BOLD) response is frequently used as a proxy measure of coupling in humans (Hillman, ). BOLD activity can be quantified both during rest and during cognitive tasks, when patients are more likely to complain of increased symptom burden (Mayer et al, ).…”

Neurovascular-modulation

“…Brain hemodynamics (neurovascular coupling) and BBB transport are disrupted in brain disease, including Alzheimer's Disease and Parkinson's [89][90][91] and following brain injury [7,92,93]. Indeed, BBB dysfunction may be a link across these disorders [94,95].…”