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 ◽  
...  

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.

2012 ◽  
Vol 124 (3) ◽  
pp. 177-189 ◽  
Author(s):  
Damian M. Bailey ◽  
Daniel W. Jones ◽  
Andrew Sinnott ◽  
Julien V. Brugniaux ◽  
Karl J. New ◽  
...  

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.


2019 ◽  
Vol 131 (6) ◽  
pp. 1887-1895
Author(s):  
Hakseung Kim ◽  
Hack-Jin Lee ◽  
Young-Tak Kim ◽  
Yunsik Son ◽  
Peter Smielewski ◽  
...  

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.


10.2196/18740 ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. e18740
Author(s):  
Alwyn Gomez ◽  
Joshua Dian ◽  
Logan Froese ◽  
Frederick Adam Zeiler

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


2020 ◽  
Author(s):  
Alwyn Gomez ◽  
Joshua Dian ◽  
Logan Froese ◽  
Frederick Adam Zeiler

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


2021 ◽  
Vol 92 (5) ◽  
pp. 519-527
Author(s):  
Yasmina Molero ◽  
David James Sharp ◽  
Brian Matthew D'Onofrio ◽  
Henrik Larsson ◽  
Seena Fazel

ObjectiveTo examine psychotropic and pain medication use in a population-based cohort of individuals with traumatic brain injury (TBI), and compare them with controls from similar backgrounds.MethodsWe assessed Swedish nationwide registers to include all individuals diagnosed with incident TBI between 2006 and 2012 in hospitals or specialist outpatient care. Full siblings never diagnosed with TBI acted as controls. We examined dispensed prescriptions for psychotropic and pain medications for the 12 months before and after the TBI.ResultsWe identified 239 425 individuals with incident TBI, and 199 658 unaffected sibling controls. In the TBI cohort, 36.6% had collected at least one prescription for a psychotropic or pain medication in the 12 months before the TBI. In the 12 months after, medication use increased to 45.0%, an absolute rate increase of 8.4% (p<0.001). The largest post-TBI increases were found for opioids (from 16.3% to 21.6%, p<0.001), and non-opioid pain medications (from 20.3% to 26.6%, p<0.001). The majority of prescriptions were short-term; 20.6% of those prescribed opioids and 37.3% of those with benzodiazepines collected prescriptions for more than 6 months. Increased odds of any psychotropic or pain medication were associated with individuals before (OR: 1.62, 95% CI: 1.59 to 1.65), and after the TBI (OR: 2.30, 95% CI: 2.26 to 2.34) as compared with sibling controls, and ORs were consistently increased for all medication classes.ConclusionHigh rates of psychotropic and pain medications after a TBI suggest that medical follow-up should be routine and review medication use.


2020 ◽  
Vol 37 (12) ◽  
pp. 847.1-847
Author(s):  
James Price ◽  
Daniel Sandbach ◽  
Ari Ercole ◽  
Alastair Wilson ◽  
Ed Barnard

Aims/Objectives/BackgroundIn the United Kingdom (UK), 20% of patients with severe traumatic brain injury (TBI) receive pre-hospital emergency anaesthesia (PHEA). Current guidance recommends an end-tidal carbon dioxide (ETCO2) of 4.0–4.5kPa to achieve a low-normal arterial partial pressure of CO2 (PaCO2), and reduce secondary brain injury. This recommendation assumes a 0.5kPa ETCO2-PaCO2 gradient. However, the gradient in the acute phase of TBI is unknown. Our primary aim was to report the ETCO2-PaCO2 gradient of TBI patients at hospital arrival.Methods/DesignA retrospective cohort study of adult patients with serious TBI, who received a PHEA by a pre-hospital critical care team in the East of England between 1st April 2015 to 31st December 2017. Linear regression was performed to test for correlation and reported as R-squared (R2). A Bland-Altman plot was used to test for paired ETCO2 and PaCO2 agreement and reported with 95% confidence intervals (95%CI). ETCO2-PaCO2 gradient data were compared with a two-tailed, unpaired, t-test.Results/Conclusions107 patients were eligible for inclusion. Sixty-seven patients did not receive a PaCO2 sample within 30 minutes of hospital arrival and were therefore excluded. Forty patients had complete data and were included in the final analysis; per protocol.The mean ETCO2-PaCO2 gradient was 1.7 (±1.0) kPa, with only moderate correlation of ETCO2 and PaCO2 at hospital arrival (R2=0.23, p=0.002). The Bland-Altman bias was 1.7 (95%CI 1.4–2.0) kPa with upper and lower limits of agreement of 3.6 (95%CI 3.0–4.1) kPa and -0.2 (95%CI -0.8–0.3) kPa respectively. There was no significant gradient correlation in patients with a co-existing serious thoracic injury (R2=0.13, p=0.10), and this cohort had a larger ETCO2-PaCO2 gradient, 2.0 (±1.1) kPa, p=0.01. Patients who underwent pre-hospital arterial blood sampling had an arrival PaCO2 of 4.7 (±0.2) kPa.Lower ETCO2 targets than previously recommended may be safe and appropriate. The use of pre-hospital PaCO2 measurement is advocated.


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