Persistent alterations in cerebrovascular reactivity in response to hypercapnia following pediatric mild traumatic brain injury

Author:

Dodd Andrew B1,Lu Hanzhang2,Wertz Christopher J1,Ling Josef M1,Shaff Nicholas A1,Wasserott Benjamin C1,Meier Timothy B345,Park Grace6,Oglesbee Scott J6,Phillips John P17,Campbell Richard A8,Liu Peiying2,Mayer Andrew R1789

Affiliation:

1. The Mind Research Network/Lovelace Biomedical and Environmental Research Institute, Albuquerque, NM, USA

2. Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA

3. Department of Neurosurgery, Medical College of Wisconsin, Milwaukee, WI, USA

4. Departments of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, Milwaukee, WI, USA

5. Department of Biomedical Engineering, Medical College of Wisconsin, Milwaukee, WI, USA

6. Department of Pediatric Emergency Medicine, University of New Mexico, Albuquerque, NM, USA

7. Department of Neurology, University of New Mexico, Albuquerque, NM, USA

8. Department of Psychiatry, University of New Mexico, Albuquerque, NM, USA

9. Department of Psychology, University of New Mexico, Albuquerque, NM, USA

Abstract

Much attention has been paid to the effects of mild traumatic brain injury (mTBI) on cerebrovascular reactivity in adult populations, yet it remains understudied in pediatric injury. In this study, 30 adolescents (12–18 years old) with pediatric mTBI (pmTBI) and 35 age- and sex-matched healthy controls (HC) underwent clinical and neuroimaging assessments during sub-acute (6.9 ± 2.2 days) and early chronic (120.4 ± 11.7 days) phases of injury. Relative to controls, pmTBI reported greater initial post-concussion symptoms, headache, pain, and anxiety, resolving by four months post-injury. Patients reported increased sleep issues and exhibited deficits in processing speed and attention across both visits. In grey-white matter interface areas throughout the brain, pmTBI displayed increased maximal fit/amplitude of a time-shifted end-tidal CO2 regressor to blood oxygen-level dependent response relative to HC, as well as increased latency to maximal fit. The alterations persisted through the early chronic phase of injury, with maximal fit being associated with complaints of ongoing sleep disturbances during post hoc analyses but not cognitive measures of processing speed or attention. Collectively, these findings suggest that deficits in the speed and degree of cerebrovascular reactivity may persist longer than current conceptualizations about clinical recovery within 30 days.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Neurology (clinical),Neurology

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