Moderate and severe traumatic brain injury in adults.

Department of Neurosurgery, University Hospital Antwerp, Antwerp, Belgium.
The Lancet Neurology (Impact Factor: 21.82). 08/2008; 7(8):728-41. DOI: 10.1016/S1474-4422(08)70164-9
Source: PubMed

ABSTRACT Traumatic brain injury (TBI) is a major health and socioeconomic problem that affects all societies. In recent years, patterns of injury have been changing, with more injuries, particularly contusions, occurring in older patients. Blast injuries have been identified as a novel entity with specific characteristics. Traditional approaches to the classification of clinical severity are the subject of debate owing to the widespread policy of early sedation and ventilation in more severely injured patients, and are being supplemented with structural and functional neuroimaging. Basic science research has greatly advanced our knowledge of the mechanisms involved in secondary damage, creating opportunities for medical intervention and targeted therapies; however, translating this research into patient benefit remains a challenge. Clinical management has become much more structured and evidence based since the publication of guidelines covering many aspects of care. In this Review, we summarise new developments and current knowledge and controversies, focusing on moderate and severe TBI in adults. Suggestions are provided for the way forward, with an emphasis on epidemiological monitoring, trauma organisation, and approaches to management.

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    ABSTRACT: Management of traumatic brain injury (TBI) is focused on preventing secondary brain injury. Remote ischemic conditioning (RIC) is an established treatment modality that has been shown to improve patient outcomes secondary to inflammatory insults. The aim of our study was to assess whether RIC in trauma patients with severe TBI could reduce secondary brain injury. This prospective consented interventional trial included all TBI patients admitted to our Level 1 trauma center with an intracranial hemorrhage and a Glasgow Coma Scale (GCS) score of 8 or lower on admission. In each patient, four cycles of RIC were performed within 1 hour of admission. Each cycle consisted of 5 minutes of controlled upper limb (arm) ischemia followed by 5 minutes of reperfusion using a blood pressure cuff. Serum biomarkers of acute brain injury, S-100B, and neuron-specific enolase (NSE) were measured at 0, 6, and 24 hours. Outcome measure was reduction in the level of serum biomarkers after RIC. A total of 40 patients (RIC, 20; control, 20) were enrolled. The mean (SD) age was 46.15 (18.64) years, the median GCS score was 8 (interquartile range, 3-8), and the median head Abbreviated Injury Scale (AIS) score was 3 (interquartile range, 3-5), and there was no difference between the RIC and control groups in any of the baseline demographics or injury characteristics including the type and size of intracranial bleed or skull fracture patterns. There was no difference in the 0-hour S-100B (p = 0.9) and NSE (p = 0.72) level between the RIC and the control group. There was a significant reduction in the mean levels of S-100B (p = 0.01) and NSE (p = 0.04) at 6 hours and 24 hours in comparison with the 0-hour level in the RIC group. This study showed that RIC significantly decreased the standard biomarkers of acute brain injury in patients with severe TBI. Our study highlights the novel therapeutic role of RIC for preventing secondary brain insults in TBI patients. Prospective interventional study, level II.
    Journal of Trauma and Acute Care Surgery 03/2015; DOI:10.1097/TA.0000000000000584 · 1.97 Impact Factor
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    ABSTRACT: Much progress has been made over the past two decades in the treatment of severe acute brain injury, including traumatic brain injury and subarachnoid hemorrhage, resulting in a higher proportion of patients surviving with better outcomes. This has arisen from a combination of factors. These include improvements in procedures at the scene (pre-hospital) and in the hospital emergency department, advances in neuromonitoring in the intensive care unit, both continuously at the bedside and intermittently in scans, evolution and refinement of protocol-driven therapy for better management of patients, and advances in surgical procedures and rehabilitation. Nevertheless, many patients still experience varying degrees of long-term disabilities post-injury with consequent demands on carers and resources, and there is room for improvement. Biomarkers are a key aspect of neuromonitoring. A broad definition of a biomarker is any observable feature that can be used to inform on the state of the patient, e.g., a molecular species, a feature on a scan, or a monitoring characteristic, e.g., cerebrovascular pressure reactivity index. Biomarkers are usually quantitative measures, which can be utilized in diagnosis and monitoring of response to treatment. They are thus crucial to the development of therapies and may be utilized as surrogate endpoints in Phase II clinical trials. To date, there is no specific drug treatment for acute brain injury, and many seemingly promising agents emerging from pre-clinical animal models have failed in clinical trials. Large Phase III studies of clinical outcomes are costly, consuming time and resources. It is therefore important that adequate Phase II clinical studies with informative surrogate endpoints are performed employing appropriate biomarkers. In this article, we review some of the available systemic, local, and imaging biomarkers and technologies relevant in acute brain injury patients, and highlight gaps in the current state of knowledge.
    Frontiers in Neurology 02/2015; 6:26. DOI:10.3389/fneur.2015.00026
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    ABSTRACT: BACKGROUND In this study we aimed to explore the effects of pregabalin on a traumatic brain injury model in rats. MATERIAL AND METHODS This study included 40 adult male Sprague-Dawley rats randomized into 4 groups, each of which contained equal numbers of animals. The control group had no head trauma and thus was not treated. The trauma group had head trauma but was not treated. The pregabalin group had no head trauma but was treated by pregabalin. The trauma + pregabalin group had head trauma treated with pregabalin. The biopsy samples taken from the study animals were histopathologically examined for the presence of edema, inflammation, and neuronal damage. RESULTS All animals in the trauma group had edema, inflammation, and neuronal damage. Four subjects in the control group, 6 in the pregabalin group, and 4 in the trauma + pregabalin group had edema; inflammation was present in 1 subject in the control group, 3 subjects in the pregabalin group, and 3 subjects in the trauma + pregabalin group; neuronal damage existed in 1 subject in the control group, 1 subject in the pregabalin group, and 6 subjects in the trauma+pregabalin group. The trauma group had significantly higher edema and neuronal damage scores than the other groups. Similarly, inflammation was significantly more prevalent in the trauma group than the control and trauma+pregabalin groups. CONCLUSIONS The results of the present study indicated anti-edema, anti-inflammatory, and neuroprotective effects of pregabalin in an experimental head trauma model in rats. Pregabalin may thus be beneficial in humans with acute TBI by relieving concomitant edema and inflammation.
    Medical science monitor: international medical journal of experimental and clinical research 01/2015; 21:813-20. DOI:10.12659/MSM.893887 · 1.22 Impact Factor

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