Traumatic Brain Injury

Ouellet, Marie‐Christine; Beaulieu‐Bonneau, Simon; Morin, Charles M.

doi:10.1016/b978-0-12-813014-8.00010-x

Cited by 2 publications

(2 citation statements)

References 159 publications

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“…Traumatic brain injury (TBI) represents a significant clinical burden 1,2 . Beyond local brain injury and neuroinflammatory activations, 3 TBI could associate with peripheral organ adaptations, with proposed implications of systemic inflammation and autonomic dysregulation 4 .…”

Section: Introductionmentioning

confidence: 99%

“…Traumatic brain injury (TBI) represents a significant clinical burden. 1,2 Beyond local brain injury and neuroinflammatory activations, 3 TBI could associate with peripheral organ adaptations, with proposed implications of systemic inflammation and autonomic dysregulation. 4 The effects of TBI on the cardiovascular system are emerging in clinical studies employing echocardiographic examination; 5 TBI has been associated with a higher risk of chronic cardiovascular comorbidities in adult patients.…”

Section: Introductionmentioning

confidence: 99%

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Neurovascular hypoxia after mild traumatic brain injury in juvenile mice correlates with heart–brain dysfunctions in adulthood

et al. 2023

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Aim Retrospective studies suggest that mild traumatic brain injury (mTBI) in pediatric patients may lead to an increased risk of cardiac events. However, the exact functional and temporal dynamics and the associations between heart and brain pathophysiological trajectories are not understood. Methods A single impact to the left somatosensory cortical area of the intact skull was performed on juvenile mice (17 days postnatal). Cerebral 3D photoacoustic imaging was used to measure the oxygen saturation (sO2) in the impacted area 4 h after mTBI followed by 2D and 4D echocardiography at days 7, 30, 90, and 190 post‐impact. At 8 months, we performed a dobutamine stress test to evaluate cardiac function. Lastly, behavioral analyses were conducted 1 year after initial injury. Results We report a rapid and transient decrease in cerebrovascular sO2 and increased hemoglobin in the impacted left brain cortex. Cardiac analyses showed long‐term diastolic dysfunction and a diminished systolic strain response under stress in the mTBI group. At the molecular level, cardiac T‐p38MAPK and troponin I expression was pathologic modified post‐mTBI. We found linear correlations between brain sO2 measured immediately post‐mTBI and long‐term cardiac strain after 8 months. We report that initial cerebrovascular hypoxia and chronic cardiac dysfunction correlated with long‐term behavioral changes hinting at anxiety‐like and memory maladaptation. Conclusion Experimental juvenile mTBI induces time‐dependent cardiac dysfunction that corresponds to the initial neurovascular sO2 dip and is associated with long‐term behavioral modifications. These imaging biomarkers of the heart–brain axis could be applied to improve clinical pediatric mTBI management.

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Section: Introductionmentioning

confidence: 99%