Abstract Details

Title Non-invasive Longitudinal Assessment of Cerebrovascular Reactivity after TBI using functional Near Infrared Spectroscopy

Topic Cerebrovascular Disease and Interventional Neurology

Presentation(s) P5 - Poster Session 5 (5:30 PM-6:30 PM)

Poster/Presentation
Number 3-069

Objective NA

Background Traumatic cerebrovascular injury (TCVI) is common after TBI and is responsible for a significant portion of TBI-related disability. 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.

Design/Methods 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. Participants with complicated mild TBI were longitudinally studied in the acute (within 72 after injury, n = 17), subacute (14 days after injury, n = 15), and chronic (6 months after injury, n = 6) 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) before and after the administration of a single dose of sildenafil citrate (60 mg orally).

Results Mean (+ SD) CVR was comparable in TBI patients and HC at 72 hours (HC: 0.176 ± 0.028%/mmHg; and TBI: CVR 0.161 ± 0.011%/mmHg, p=0.23). Sildenafil administration did not result in an increase in CVR in HC (t=1.62 df=8, p=.14) whereas TBI patients showed a significant increase in CVR at 72hrs (t=3.882 df=16, p=.001), 2 weeks (t=2.5951 df=13, 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.

Conclusions

These findings support the hypothesis that vascular injury represents a distinct and persistent endophenotype following TBI and PDE5 inhibition as a potential therapy for TCVI.

Authors/Disclosures
PRESENTER	No disclosure on file
Justin A. Morrison (Penn Presbyterian Medical Center)	Mr. Morrison has nothing to disclose.
Franck G. Amyot, PhD (HJF)	Dr. Amyot has nothing to disclose.
	No disclosure on file
	No disclosure on file
	No disclosure on file
Erika Silverman (University of Pennsylvania)	Ms. Silverman has nothing to disclose.
	No disclosure on file
Megan T. Moyer, NP	No disclosure on file
Danielle Sandsmark, MD	The institution of Dr. Sandsmark has received research support from NINDS. The institution of Dr. Sandsmark has received research support from BrainBox Solutions Inc. The institution of Dr. Sandsmark has received research support from Department of Defense.
Ramon R. Diaz-Arrastia, MD, PhD, FAAN (University of Pennsylvania)	Dr. Diaz-Arrastia has stock in BrainBox, LLC. Dr. Diaz-Arrastia has stock in Nia Therpeutics. The institution of Dr. Diaz-Arrastia has received research support from National Institutes of Health. The institution of Dr. Diaz-Arrastia has received research support from Department of Defense.

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