Impaired cerebral haemodynamic function associated with chronic traumatic brain injury in professional boxers

2012 ◽  
Vol 124 (3) ◽  
pp. 177-189 ◽  
Author(s):  
Damian M. Bailey ◽  
Daniel W. Jones ◽  
Andrew Sinnott ◽  
Julien V. Brugniaux ◽  
Karl J. New ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Function Analysis ◽  
Transcranial Doppler Ultrasound ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Mechanical Trauma ◽  
Neurocognitive Dysfunction ◽  
Arterial Blood ◽  
Transfer Function Analysis

The present study examined to what extent professional boxing compromises cerebral haemodynamic function and its association with CTBI (chronic traumatic brain injury). A total of 12 male professional boxers were compared with 12 age-, gender- and physical fitness-matched non-boxing controls. We assessed dCA (dynamic cerebral autoregulation; thigh-cuff technique and transfer function analysis), CVRCO2 (cerebrovascular reactivity to changes in CO2: 5% CO2 and controlled hyperventilation), orthostatic tolerance (supine to standing) and neurocognitive function (psychometric tests). Blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasound), mean arterial blood pressure (finger photoplethysmography), end-tidal CO2 (capnography) and cortical oxyhaemoglobin concentration (near-IR spectroscopy) were continuously measured. Boxers were characterized by fronto-temporal neurocognitive dysfunction and impaired dCA as indicated by a lower rate of regulation and autoregulatory index (P<0.05 compared with controls). Likewise, CVRCO2 was also reduced resulting in a lower CVRCO2 range (P<0.05 compared with controls). The latter was most marked in boxers with the highest CTBI scores and correlated against the volume and intensity of sparring during training (r=−0.84, P<0.05). These impairments coincided with more marked orthostatic hypotension, cerebral hypoperfusion and corresponding cortical de-oxygenation during orthostatic stress (P<0.05 compared with controls). In conclusion, these findings provide the first comprehensive evidence for chronically impaired cerebral haemodynamic function in active boxers due to the mechanical trauma incurred by repetitive, sub-concussive head impact incurred during sparring training. This may help explain why CTBI is a progressive disease that manifests beyond the active boxing career.

Artifact removal from neurophysiological signals: impact on intracranial and arterial pressure monitoring in traumatic brain injury

2020 ◽  
Vol 132 (6) ◽  
pp. 1952-1960 ◽  
Author(s):  
Seung-Bo Lee ◽  
Hakseung Kim ◽  
Young-Tak Kim ◽  
Frederick A. Zeiler ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Status ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Clinical Parameters ◽  
Artifact Removal ◽  
Clinical Events ◽  
Arterial Blood ◽  
Before And After

OBJECTIVEMonitoring intracranial and arterial blood pressure (ICP and ABP, respectively) provides crucial information regarding the neurological status of patients with traumatic brain injury (TBI). However, these signals are often heavily affected by artifacts, which may significantly reduce the reliability of the clinical determinations derived from the signals. The goal of this work was to eliminate signal artifacts from continuous ICP and ABP monitoring via deep learning techniques and to assess the changes in the prognostic capacities of clinical parameters after artifact elimination.METHODSThe first 24 hours of monitoring ICP and ABP in a total of 309 patients with TBI was retrospectively analyzed. An artifact elimination model for ICP and ABP was constructed via a stacked convolutional autoencoder (SCAE) and convolutional neural network (CNN) with 10-fold cross-validation tests. The prevalence and prognostic capacity of ICP- and ABP-related clinical events were compared before and after artifact elimination.RESULTSThe proposed SCAE-CNN model exhibited reliable accuracy in eliminating ABP and ICP artifacts (net prediction rates of 97% and 94%, respectively). The prevalence of ICP- and ABP-related clinical events (i.e., systemic hypotension, intracranial hypertension, cerebral hypoperfusion, and poor cerebrovascular reactivity) all decreased significantly after artifact removal.CONCLUSIONSThe SCAE-CNN model can be reliably used to eliminate artifacts, which significantly improves the reliability and efficacy of ICP- and ABP-derived clinical parameters for prognostic determinations after TBI.

scholarly journals Novel index for predicting mortality during the first 24 hours after traumatic brain injury

2019 ◽  
Vol 131 (6) ◽  
pp. 1887-1895
Author(s):  
Hakseung Kim ◽  
Hack-Jin Lee ◽  
Young-Tak Kim ◽  
Yunsik Son ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Autoregulation ◽  
Area Under The Curve ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Reactivity Index ◽  
Predictive Capacity ◽  
Arterial Blood ◽  
Prediction Of Mortality

OBJECTIVEFailure of cerebral autoregulation and subsequent hypoperfusion is common during the acute phase of traumatic brain injury (TBI). The cerebrovascular pressure-reactivity index (PRx) indirectly reflects cerebral autoregulation and has been used to derive optimal cerebral perfusion pressure (CPP). This study provides a method for the use of a combination of PRx, CPP, and intracranial pressure (ICP) to better evaluate the extent of cerebral hypoperfusion during the first 24 hours after TBI, allowing for a more accurate prediction of mortality risk.METHODSContinuous ICP and arterial blood pressure (ABP) signals acquired from 295 TBI patients during the first 24 hours after admission were retrospectively analyzed. The CPP at the lowest PRx was determined as the optimal CPP (CPPopt). The duration of a severe hypoperfusion event (dHP) was defined as the cumulative time that the PRx was > 0.2 and the CPP was < 70 mm Hg with the addition of intracranial hypertension (ICP > 20 or > 22 mm Hg). The outcome was determined as 6-month mortality.RESULTSThe cumulative duration of PRx > 0.2 and CPP < 70 mm Hg exhibited a significant association with mortality (p < 0.001). When utilized with basic clinical information available during the first 24 hours after admission (i.e., Glasgow Coma Scale score, age, and mean ICP), a dHP > 25 minutes yielded a significant predictive capacity for mortality (p < 0.05, area under the curve [AUC] = 0.75). The parameter was particularly predictive of mortality for patients with a mean ICP > 20 or > 22 mm Hg (AUC = 0.81 and 0.87, respectively).CONCLUSIONSA short duration (25 minutes) of severe hypoperfusion, evaluated as lowered CPP during worsened cerebrovascular reactivity during the 1st day after TBI, is highly indicative of mortality.

Influence of sympathoexcitation at high altitude on cerebrovascular function and ventilatory control in humans

2012 ◽  
Vol 113 (7) ◽  
pp. 1058-1067 ◽  
Author(s):  
P. N. Ainslie ◽  
S. J. E. Lucas ◽  
J.-L. Fan ◽  
K. N. Thomas ◽  
J. D. Cotter ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Function Analysis ◽  
Low Frequency ◽  
Cerebrovascular Reactivity ◽  
Adrenergic Blockade ◽  
Ventilatory Control ◽  
Phase Lead ◽  
Arterial Blood ◽  
Transfer Function Analysis

We sought to determine the influence of sympathoexcitation on dynamic cerebral autoregulation (CA), cerebrovascular reactivity, and ventilatory control in humans at high altitude (HA). At sea level (SL) and following 3–10 days at HA (5,050 m), we measured arterial blood gases, ventilation, arterial pressure, and middle cerebral blood velocity (MCAv) before and after combined α- and β-adrenergic blockade. Dynamic CA was quantified using transfer function analysis. Cerebrovascular reactivity was assessed using hypocapnia and hyperoxic hypercapnia. Ventilatory control was assessed from the hypercapnia and during isocapnic hypoxia. Arterial Pco2 and ventilation and its control were unaltered following blockade at both SL and HA. At HA, mean arterial pressure (MAP) was elevated ( P < 0.01 vs. SL), but MCAv remained unchanged. Blockade reduced MAP more at HA than at SL (26 vs. 15%, P = 0.048). At HA, gain and coherence in the very-low-frequency (VLF) range (0.02–0.07 Hz) increased, and phase lead was reduced (all P < 0.05 vs. SL). Following blockade at SL, coherence was unchanged, whereas VLF phase lead was reduced (−40 ± 23%; P < 0.01). In contrast, blockade at HA reduced low-frequency coherence (−26 ± 20%; P = 0.01 vs. baseline) and elevated VLF phase lead (by 177 ± 238%; P < 0.01 vs. baseline), fully restoring these parameters back to SL values. Irrespective of this elevation in VLF gain at HA ( P < 0.01), blockade increased it comparably at SL and HA (∼43–68%; P < 0.01). Despite elevations in MCAv reactivity to hypercapnia at HA, blockade reduced ( P < 0.05) it comparably at SL and HA, effects we attributed to the hypotension and/or abolition of the hypercapnic-induced increase in MAP. With the exception of dynamic CA, we provide evidence of a redundant role of sympathetic nerve activity as a direct mechanism underlying changes in cerebrovascular reactivity and ventilatory control following partial acclimatization to HA. These findings have implications for our understanding of CBF function in the context of pathologies associated with sympathoexcitation and hypoxemia.

scholarly journals Near-Infrared Cerebrovascular Reactivity for Monitoring Cerebral Autoregulation and Predicting Outcomes in Moderate to Severe Traumatic Brain Injury: Proposal for a Pilot Observational Study

10.2196/18740 ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. e18740
Author(s):  
Alwyn Gomez ◽  
Joshua Dian ◽  
Logan Froese ◽  
Frederick Adam Zeiler
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Data Collection ◽  
Near Infrared ◽  
Short Form ◽  
Cerebrovascular Reactivity ◽  
Biomedical Signal Processing ◽  
Post Injury ◽  
Arterial Blood

Background Impaired cerebrovascular reactivity after traumatic brain injury (TBI) in adults is emerging as an important prognostic factor, with strong independent association with 6-month outcomes. To date, it is unknown if impaired cerebrovascular reactivity during the acute phase is associated with ongoing impaired continuously measured cerebrovascular reactivity in the long-term, and if such measures are associated with clinical phenotype at those points in time. Objective We describe a prospective pilot study to assess the use of near-infrared spectroscopy (NIRS) to derive continuous measures of cerebrovascular reactivity during the acute and long-term phases of TBI in adults. Methods Over 2 years, we will recruit up to 80 adults with moderate/severe TBI admitted to the intensive care unit (ICU) with invasive intracranial pressure (ICP) monitoring. These patients will undergo high-frequency data capture of ICP, arterial blood pressure (ABP), and NIRS for the first 5 days of care. Patients will then have 30 minutes of noninvasive NIRS and ABP monitoring in the clinic at 3, 6, and 12 months post-injury. Outcomes will be assessed via the Glasgow Outcome Scale and Short Form-12 questionnaires. Various relationships between NIRS and ICP-derived cerebrovascular reactivity metrics and associated outcomes will be assessed using biomedical signal processing techniques and both multivariate and time-series statistical methodologies. Results Study recruitment began at the end of February 2020, with data collection ongoing and three patients enrolled at the time of writing. The expected duration of data collection will be from February 2020 to January 2022, as per our local research ethics board approval (B2018:103). Support for this work has been obtained through the National Institutes of Health (NIH) through the National Institute of Neurological Disorders and Stroke (NINDS) (R03NS114335), funded in January 2020. Conclusions With the application of NIRS technology for monitoring of patients with TBI, we expect to be able to outline core relationships between noninvasively measured aspects of cerebral physiology and invasive measures, as well as patient outcomes. Documenting these relationships carries the potential to revolutionize the way we monitor patients with TBI, moving to more noninvasive techniques. International Registered Report Identifier (IRRID) DERR1-10.2196/18740

scholarly journals Near-Infrared Cerebrovascular Reactivity for Monitoring Cerebral Autoregulation and Predicting Outcomes in Moderate to Severe Traumatic Brain Injury: Proposal for a Pilot Observational Study (Preprint)

2020 ◽  
Author(s):  
Alwyn Gomez ◽  
Joshua Dian ◽  
Logan Froese ◽  
Frederick Adam Zeiler
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Data Collection ◽  
Near Infrared ◽  
Short Form ◽  
Cerebrovascular Reactivity ◽  
Biomedical Signal Processing ◽  
Post Injury ◽  
Arterial Blood

BACKGROUND Impaired cerebrovascular reactivity after traumatic brain injury (TBI) in adults is emerging as an important prognostic factor, with strong independent association with 6-month outcomes. To date, it is unknown if impaired cerebrovascular reactivity during the acute phase is associated with ongoing impaired continuously measured cerebrovascular reactivity in the long-term, and if such measures are associated with clinical phenotype at those points in time. OBJECTIVE We describe a prospective pilot study to assess the use of near-infrared spectroscopy (NIRS) to derive continuous measures of cerebrovascular reactivity during the acute and long-term phases of TBI in adults. METHODS Over 2 years, we will recruit up to 80 adults with moderate/severe TBI admitted to the intensive care unit (ICU) with invasive intracranial pressure (ICP) monitoring. These patients will undergo high-frequency data capture of ICP, arterial blood pressure (ABP), and NIRS for the first 5 days of care. Patients will then have 30 minutes of noninvasive NIRS and ABP monitoring in the clinic at 3, 6, and 12 months post-injury. Outcomes will be assessed via the Glasgow Outcome Scale and Short Form-12 questionnaires. Various relationships between NIRS and ICP-derived cerebrovascular reactivity metrics and associated outcomes will be assessed using biomedical signal processing techniques and both multivariate and time-series statistical methodologies. RESULTS Study recruitment began at the end of February 2020, with data collection ongoing and three patients enrolled at the time of writing. The expected duration of data collection will be from February 2020 to January 2022, as per our local research ethics board approval (B2018:103). Support for this work has been obtained through the National Institutes of Health (NIH) through the National Institute of Neurological Disorders and Stroke (NINDS) (R03NS114335), funded in January 2020. CONCLUSIONS With the application of NIRS technology for monitoring of patients with TBI, we expect to be able to outline core relationships between noninvasively measured aspects of cerebral physiology and invasive measures, as well as patient outcomes. Documenting these relationships carries the potential to revolutionize the way we monitor patients with TBI, moving to more noninvasive techniques. INTERNATIONAL REGISTERED REPORT DERR1-10.2196/18740

Cerebral hypoperfusion during hypoxic exercise following two different hypoxic exposures: independence from changes in dynamic autoregulation and reactivity

2008 ◽  
Vol 295 (5) ◽  
pp. R1613-R1622 ◽  
Author(s):  
Philip N. Ainslie ◽  
Michael Hamlin ◽  
John Hellemans ◽  
Peter Rasmussen ◽  
Shigehiko Ogoh
Keyword(s):  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Function Analysis ◽  
Low Frequency ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Cerebrovascular Function ◽  
Transfer Function Analysis ◽  
End Tidal ◽  
Hypoxic Exercise

We examined the effects of exposure to 10–12 days intermittent hypercapnia [IHC: 5:5-min hypercapnia (inspired fraction of CO2 0.05)-to-normoxia for 90 min ( n = 10)], intermittent hypoxia [IH: 5:5-min hypoxia-to-normoxia for 90 min ( n = 11)] or 12 days of continuous hypoxia [CH: 1,560 m ( n = 7)], or both IH followed by CH on cardiorespiratory and cerebrovascular function during steady-state cycling exercise with and without hypoxia (inspired fraction of oxygen, 0.14). Cerebrovascular reactivity to CO2 was also monitored. During all procedures, ventilation, end-tidal gases, blood pressure, muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAv) were measured continuously. Dynamic cerebral autoregulation (CA) was assessed using transfer-function analysis. Hypoxic exercise resulted in increases in ventilation, hypocapnia, heart rate, and cardiac output when compared with normoxic exercise ( P < 0.05); these responses were unchanged following IHC but were elevated following the IH and CH exposure ( P < 0.05) with no between-intervention differences. Following IH and/or CH exposure, the greater hypocapnia during hypoxic exercise provoked a decrease in MCAv ( P < 0.05 vs. preexposure) that was related to lowered cerebral oxygenation ( r = 0.54; P < 0.05). Following any intervention, during hypoxic exercise, the apparent impairment in CA, reflected in lowered low-frequency phase between MCAv and BP, and MCAv-CO2 reactivity, were unaltered. Conversely, during hypoxic exercise following both IH and/or CH, there was less of a decrease in muscle oxygenation ( P < 0.05 vs. preexposure). Thus IH or CH induces some adaptation at the muscle level and lowers MCAv and cerebral oxygenation during hypoxic exercise, potentially mediated by the greater hypocapnia, rather than a compromise in CA or MCAv reactivity.

Cerebrovascular reactivity and dynamic autoregulation in tetraplegia

2010 ◽  
Vol 298 (4) ◽  
pp. R1035-R1042 ◽  
Author(s):  
Luke C. Wilson ◽  
James D. Cotter ◽  
Jui-Lin Fan ◽  
Rebekah A. I. Lucas ◽  
Kate N. Thomas ◽  
...  
Keyword(s):  
Transfer Function ◽  
Cerebral Oxygenation ◽  
Function Analysis ◽  
Plasma Catecholamines ◽  
Peripheral Resistance ◽  
Cardiovascular Function ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Cord Injury

Humans with spinal cord injury have impaired cardiovascular function proportional to the level and completeness of the lesion. The effect on cerebrovascular function is unclear, especially for high-level lesions. The purpose of this study was to evaluate the integrity of dynamic cerebral autoregulation (CA) and the cerebrovascular reactivity in chronic tetraplegia (Tetra). After baseline, steady-state hypercapnia (5% CO2) and hypocapnia (controlled hyperventilation) were used to assess cerebrovascular reactivity in 6 men with Tetra (C5–C7 lesion) and 14 men without [able-bodied (AB)]. Middle cerebral artery blood flow velocity (MCAv), cerebral oxygenation, arterial blood pressure (BP), heart rate (HR), cardiac output (Q̇; model flow), partial pressure of end-tidal CO2 (PetCO2), and plasma catecholamines were measured. Dynamic CA was assessed by transfer function analysis of spontaneous fluctuations in BP and MCAv. MCAv pulsatility index (MCAv PI) was calculated as (MCAvsystolic − MCAvdiastolic)/MCAvmean and standardized by dividing by mean arterial pressure (MAP). Resting BP, total peripheral resistance, and catecholamines were lower in Tetra ( P < 0.05), and standardized MCAv PI was ∼36% higher in Tetra ( P = 0.003). Resting MCAv, cerebral oxygenation, HR, and PetCO2 were similar between groups ( P > 0.05). Although phase and transfer function gain relationships in dynamic CA were maintained with Tetra ( P > 0.05), coherence in the very low-frequency range (0.02–0.07 Hz) was ∼21% lower in Tetra ( P = 0.006). Full (hypo- and hypercapnic) cerebrovascular reactivity to CO2 was unchanged with Tetra ( P > 0.05). During hypercapnia, standardized MCAv PI reactivity was enhanced by ∼78% in Tetra ( P = 0.016). Despite impaired cardiovascular function, chronic Tetra involves subtle changes in dynamic CA and cerebrovascular reactivity to CO2. Changes are evident in coherence at baseline and MCAv PI during baseline and hypercapnic states in chronic Tetra, which may be indicative of cerebrovascular adaptation.

scholarly journals Longitudinal assessment of hemodynamic alterations after mild traumatic brain injury in adolescents: Selected case study review

2022 ◽  
Vol 6 ◽  
pp. 205970022110658
Author(s):  
Corey M. Thibeault ◽  
Amber Y. Dorn ◽  
Shankar Radhakrishnan ◽  
Robert B. Hamilton
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Injuries ◽  
Population Level ◽  
Transcranial Doppler Ultrasound ◽  
Cerebrovascular Reactivity ◽  
Breath Hold ◽  
Longitudinal Assessment ◽  
Post Injury ◽  
Cross Sectional

Alterations in the neurovasculature after traumatic brain injury (TBI) represents a significant sequelae. However, despite theoretical and empirical evidence supporting the near-ubiquity of vascular injury, its pathophysiology remains elusive. Although this has been shown for all grades of TBI, the vascular changes after injuries with the broad mild traumatic brain injuries (mTBI) classification, remain particularly difficult to describe. Our group has previously demonstrated hemodynamic alterations in mTBI by utilizing transcranial Doppler ultrasound and cerebrovascular reactivity in a cross-sectional study. That work identified a phasic progression of deviations over varying days post-injury. These phases were then characterized by a set of inverse models that provided a hypothetical process of hemodynamic dysfunction after mTBI. This model set provides a framework with the potential for guiding clinical treatment over the course of recovery. However, it is still unclear if individual patients will progress through the phases of dysfunction similar to that found at the population level. The work presented here explores six individual patients with high-density data collected during their post-injury recovery. Breath-hold index (BHI) was found to be the most robust feature related to mTBI longitudinally. All six subjects exhibited BHI recovery curves that followed the population model's progression. The changes in pulsatile features lacked the universality of BHI, but were present in subjects with higher self-reported symptom scores and longer periods of recovery. This work suggests neurovascular dysfunction after an mTBI may be a robust phenomenon. Additionally, the capabilities of TCD in capturing these changes highlights its potential for aiding clinicians in monitoring patient's recovery post mTBI.

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