A concerted effort to tackle the global health problem posed by traumatic brain injury (TBI) is long overdue. TBI is a public health challenge of vast, but insufficiently recognised, proportions. Worldwide, more than 50 million people have a TBI each year, and it is estimated that about half the world's population will have one or more TBIs over their lifetime. TBI is the leading cause of mortality in young adults and a major cause of death and disability across all ages in all countries, with a disproportionate burden of disability and death occurring in low-income and middle-income countries (LMICs). It has been estimated that TBI costs the global economy approximately $US400 billion annually. Deficiencies in prevention, care, and research urgently need to be addressed to reduce the huge burden and societal costs of TBI. This Commission highlights priorities and provides expert recommendations for all stakeholders—policy makers, funders, health-care professionals, researchers, and patient representatives—on clinical and research strategies to reduce this growing public health problem and improve the lives of people with TBI.Additional co-authors: Endre Czeiter, Marek Czosnyka, Ramon Diaz-Arrastia, Jens P Dreier, Ann-Christine Duhaime, Ari Ercole, Thomas A van Essen, Valery L Feigin, Guoyi Gao, Joseph Giacino, Laura E Gonzalez-Lara, Russell L Gruen, Deepak Gupta, Jed A Hartings, Sean Hill, Ji-yao Jiang, Naomi Ketharanathan, Erwin J O Kompanje, Linda Lanyon, Steven Laureys, Fiona Lecky, Harvey Levin, Hester F Lingsma, Marc Maegele, Marek Majdan, Geoffrey Manley, Jill Marsteller, Luciana Mascia, Charles McFadyen, Stefania Mondello, Virginia Newcombe, Aarno Palotie, Paul M Parizel, Wilco Peul, James Piercy, Suzanne Polinder, Louis Puybasset, Todd E Rasmussen, Rolf Rossaint, Peter Smielewski, Jeannette Söderberg, Simon J Stanworth, Murray B Stein, Nicole von Steinbüchel, William Stewart, Ewout W Steyerberg, Nino Stocchetti, Anneliese Synnot, Braden Te Ao, Olli Tenovuo, Alice Theadom, Dick Tibboel, Walter Videtta, Kevin K W Wang, W Huw Williams, Kristine Yaffe for the InTBIR Participants and Investigator

In November 2017, the Lancet Neurology Commission on Traumatic Brain Injury (TBI) highlighted existing deficiencies in epidemiology, patient characterization, identifying best practice, outcome assessment, and evidence generation. The Commission concluded that C needed to address deficiencies in prevention , and made a recommendation for large collaborative studies which could provide the framework for precision medicine and comparative effectiveness research (CER).

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Background and Purpose-The clinical application of intracranial near-infrared spectroscopy in adults has been hampered by concerns over contamination from extracranial tissues. The NIRO 300 (Hamamatsu Photonics) provides continuous online measurements of hemoglobin and cytochrome oxidase concentrations and a calculated tissue oxygen index (TOI). The present study seeks confirmation of the anatomic source of TOI in the adult cranium. Methods-Sixty patients undergoing carotid endarterectomy were studied. The NIRO 300 was incorporated into an established multimodal monitoring system. TOI, oxyhemoglobin, and deoxyhemoglobin changes were assessed and compared with (1) frontal cutaneous laser-Doppler flowmetry and (2) transcranial Doppler measurement of the ipsilateral middle cerebral artery flow velocity. Results-Changes in TOI were seen during cross-clamping of the carotid vessels in 49 patients (mean ⌬TOIϭϪ9.4%, SDϭ7.1). Significant correlation was seen between TOI and flow velocity (rϭ0.56) but not with laser-Doppler flowmetry (rϭ0.13). In 31 patients, oxyhemoglobin and deoxyhemoglobin concentrations were recorded, showing significant changes during both external carotid artery and internal carotid artery clamping. A change in TOI was predominantly associated with internal carotid artery clamping (nϭ41). When TOI changed during external carotid artery clamping (nϭ8), significant blood pressure changes occurred, or extracranial-to-intracranial anastomosis was evident. In the absence of such variables, the sensitivity of TOI to intracranial and extracranial changes was 87.5% and 0%, respectively, and specificity was 100% and 0%, respectively. Conclusions-The NIRO 300 reflects changes in cerebral tissue oxygenation when TOI is calculated, with a high degree of sensitivity and specificity. (Stroke. 2001;32:2492-2500.)

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NIRS signal changes in HbO2, Hb, and total hemoglobin concentration are very sensitive to alterations in EtCO2, which are largely independent of extracranial tissue perfusion. NIRS may be developed as an alternative method for testing cerebrovascular reactivity and may be of particular clinical importance when the ultrasound window is poor.

Hyperventilation increases the volume of severely hypoperfused tissue within the injured brain, despite improvements in cerebral perfusion pressure and intracranial pressure. Significant hyperperfusion is uncommon, even at a time when conventional clinical management includes a role for modest hyperventilation. These reductions in regional cerebral perfusion are not associated with ischemia, as defined by global monitors of oxygenation, but may represent regions of potentially ischemic brain tissue.

Objectives: In patients at risk of hypoxic ischemic brain injury following cardiac arrest, we sought to (i) characterize brain oxygenation and determine the prevalence of brain hypoxia, (ii) characterize autoregulation using the pressure reactivity index (PRx) and identify the optimal mean arterial pressure (MAPOPT), and (iii) assess the relationship between MAPOPT and brain tissue oxygenation (PbtO2). Design: Prospective interventional study. Setting: Quaternary intensive care unit. Patients: Adult patients with return to spontaneous circulation (ROSC) greater than 10 minutes and a post-resuscitation Glasgow Coma Score under 9 within 72 hours of cardiac arrest. Interventions: All patients underwent multimodal neuromonitoring which included: (i) PbtO2, (ii) intracranial pressure; (iii) jugular venous continuous oximetry (SjvO2); (iv) regional saturation of oxygen (rSO2) using near-infrared spectroscopy, and (iv) PRx based determination of MAPOPT, lower and upper limit of autoregulation. We additionally collected MAP, end tidal carbon dioxide (ETCO2) and temperature. All data were captured at 300 Hz using ICM+® brain monitoring software. Measurements and Main Results: Ten patients (7 males) were included with a median age 47 (range 20-71) and ROSC 22 minutes (12-36). The median duration of monitoring was 47 hours (15-88) and median duration from cardiac arrest to inclusion was 15 hours (6-44). The mean PbtO2 was 23 mmHg (SD 8) and the mean percentage of time with a PbtO2 below 20 mmHg was 38% (6-100). The mean PRx was 0.23 (0.27) and the percentage of time with a PRx greater than 0.3 was 50% (12-91). The mean MAPOPT, lower and upper of autoregulation were 89 mmHg (11), 82mmHg (8) and 96 mmHg (9), respectively. There was marked betweenpatient variability in the relationship between MAP and indices of brain oxygenation. As the patients' actual MAP approached MAPOPT, PbtO2 increased (p<0.001). This positive relationship did not persist when the actual MAP was above MAPOPT. Conclusions: Episodes of brain hypoxia in HIBI are frequent and perfusion within proximity of MAPOPT is associated with increased PbtO2. PRx can yield MAPOPT, lower and upper limit of autoregulation in patients following cardiac arrest.