TY - JOUR
T1 - Impaired cerebral vasoreactivity despite symptom resolution in sports-related concussion
AU - Purkayastha, Sushmita
AU - Sorond, Farzaneh A.
AU - Lyng, Sydney
AU - Frantz, Justin
AU - Murphy, Megan N.
AU - Hynan, Linda S.
AU - Sabo, Tonia
AU - Bell, Kathleen R.
N1 - Funding Information:
This study was supported by funds from the University Research Council Grant, at SMU, Dallas, Texas (to S.P.), Pilot Grant 2016 from the Texas Institute for Brain Injury & Repair at University of Texas Southwestern Medical Center, Dallas, Texas (to K.R.B., S.P., and T.S.), and Northwestern University R01NS085002 (to F.A.S.).
Publisher Copyright:
© Copyright 2019, Mary Ann Liebert, Inc., publishers 2019.
PY - 2019/8/15
Y1 - 2019/8/15
N2 - Traumatic brain injury (TBI) is associated with increased risk of later-life neurodegeneration and dementia. However, the underpinning mechanisms are poorly understood, and secondary injury resulting from perturbed physiological processes plays a significant role. Cerebral vasoreactivity (CVR), a measure of hemodynamic reserve, is known to be impaired in TBI. However, the temporal course of this physiological perturbation is not established. We examined CVR and clinical symptoms on day 3 (T1), day 21 (T2), and day 90 (T3) after concussion in collegiate athletes and cross-sectionally in non-injured controls. Changes in middle cerebral artery blood flow velocity (MCAV; transcranial Doppler ultrasonography) were measured during changes in end-tidal CO2 (PetCO2) at normocapnia, hypercapnia (inspiring 8% CO2), and hypocapnia (hyperventilation). CVR was determined as the slope of the linear relationship and expressed as percent change in MCAV per mmHg change in PetCO2. CVR was attenuated during the acute phase T1 (1.8 ± 0.4U; p = 0.0001), subacute phases T2 (2.0 ± 0.4U; p = 0.0017), and T3 (1.9 ± 0.6U; p = 0.023) post-concussion compared to the controls (2.3 ± 0.3U). Concussed athletes exhibited higher symptom number (2.5 ± 3.0 vs. 12.1 ± 7.0; p < 0.0001) and severity (4.2 ± 6.0 vs. 29.5 ± 23.0; p < 0.0001), higher Patient Health Questionnaire-9 score (2.2 ± 2.0 vs. 9.1 ± 6.0; p = 0.0003) at T1. However, by T2, symptoms had resolved. We show that CVR is impaired as early as 4 days and remains impaired up to 3 months post-injury despite symptom resolution. Persistent perturbations in CVR may therefore be involved in secondary injury. Future studies with a larger sample size and longer follow-up period are needed to validate this finding and delineate the duration of this vulnerable period.
AB - Traumatic brain injury (TBI) is associated with increased risk of later-life neurodegeneration and dementia. However, the underpinning mechanisms are poorly understood, and secondary injury resulting from perturbed physiological processes plays a significant role. Cerebral vasoreactivity (CVR), a measure of hemodynamic reserve, is known to be impaired in TBI. However, the temporal course of this physiological perturbation is not established. We examined CVR and clinical symptoms on day 3 (T1), day 21 (T2), and day 90 (T3) after concussion in collegiate athletes and cross-sectionally in non-injured controls. Changes in middle cerebral artery blood flow velocity (MCAV; transcranial Doppler ultrasonography) were measured during changes in end-tidal CO2 (PetCO2) at normocapnia, hypercapnia (inspiring 8% CO2), and hypocapnia (hyperventilation). CVR was determined as the slope of the linear relationship and expressed as percent change in MCAV per mmHg change in PetCO2. CVR was attenuated during the acute phase T1 (1.8 ± 0.4U; p = 0.0001), subacute phases T2 (2.0 ± 0.4U; p = 0.0017), and T3 (1.9 ± 0.6U; p = 0.023) post-concussion compared to the controls (2.3 ± 0.3U). Concussed athletes exhibited higher symptom number (2.5 ± 3.0 vs. 12.1 ± 7.0; p < 0.0001) and severity (4.2 ± 6.0 vs. 29.5 ± 23.0; p < 0.0001), higher Patient Health Questionnaire-9 score (2.2 ± 2.0 vs. 9.1 ± 6.0; p = 0.0003) at T1. However, by T2, symptoms had resolved. We show that CVR is impaired as early as 4 days and remains impaired up to 3 months post-injury despite symptom resolution. Persistent perturbations in CVR may therefore be involved in secondary injury. Future studies with a larger sample size and longer follow-up period are needed to validate this finding and delineate the duration of this vulnerable period.
KW - cerebral blood flow
KW - cerebral reactivity
KW - headache
KW - return-to-play
KW - traumatic brain injury
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U2 - 10.1089/neu.2018.5861
DO - 10.1089/neu.2018.5861
M3 - Article
C2 - 30693827
AN - SCOPUS:85069725382
SN - 0897-7151
VL - 36
SP - 2385
EP - 2390
JO - Journal of neurotrauma
JF - Journal of neurotrauma
IS - 16
ER -