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Non-invasive measurement of cerebrovascular reactivity after traumatic brain injury using functional near-infrared spectroscopy
Abstract   Open access

Non-invasive measurement of cerebrovascular reactivity after traumatic brain injury using functional near-infrared spectroscopy

Michael Sangobowale, Franck Amyot, Hasan Ayaz, Pratusha Reddy, Nimay Kulkarni and Ramon Diaz-Arrastia
Frontiers in human neuroscience, v 12
2018
DOI: https://doi.org/10.3389/conf.fnhum.2018.227.00049
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https://doi.org/10.3389/conf.fnhum.2018.227.00049View
Published, Version of Record (VoR) Open CC BY V4.0

Abstract

Traumatic cerebrovascular injury (TCVI) is common after TBI and is responsible for a significant portion of TBI-related disability. Development of therapies targeting TCVI will require reliable and inexpensive biomarkers to measure vascular dysfunction and document target engagement. Cerebrovascular reactivity (CVR) is impaired following TBI and methods which reliably and non-invasively measure CVR are available, making CVR an attractive candidate predictive and pharmacodynamic biomarker for TCVI-directed therapies. Changes in the concentrations of oxy- and deoxy- hemoglobin in response to a dynamic challenges measured by functional Near Infrared Spectroscopy (fNIRS) indicate local perfusion changes. This study was designed to assess CVR longitudinally after TBI in humans using fNIRS from the acute to the subacute and chronic stages. We also studied the effect of treatment with a phosphodiesterase 5 inhibitor, sildenafil citrate, in order to assess the utility of fNIRS as a pharmacodynamic biomarker in future clinical trials. 15 participants with complicated mild TBI were studied in the acute (within 72 after injury), subacute (14 days after injury), and chronic (6 months after injury) stages in addition to 11 age- matched healthy controls (HC), who were studied once. CVR was assessed by measuring the changes in oxygenated hemoglobin (ΔHbO) and deoxygenated hemoglobin (ΔHbR) concentration produced by mild hypercapnia (5% CO2). The change in CVR before and one hour after the administration of single dose of sildenafil citrate (60 mg orally) was also assessed. Mean (+ SEM) CVR was lower in TBI patients compared to HC (HC: 0.100 ± 0.028%/mmHg; and TBI: CVR 0.057 ± 0.011%/mmHg, p=0.22). Sildenafil administration did not result in an increase in CVR in HC (t=2.052 df=6, p=.08) whereas TBI patients show a significant increase in CVR at 72hrs (t=3.179 df=13, p=.007), 2 weeks (t=2.391 df=10, p=0.03), 3 months (t=2.518 df=6, p=0.04), and 6 months (t=4.218 df=3, p=0.02) after injury. These findings support the hypothesis that vascular injury represents a distinct endophenotype following TBI and PDE5 inhibition as a potential therapy for TCVI.

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