Rapid triage and decision-making in the treatment of traumatic brain injury (TBI) present challenging dilemma in "resource poor" environments such as the battlefield and developing areas of the world. There is an urgent need for additional tools to guide treatment of TBI. The aim of this review is to establish the possible use of diagnostic TBI biomarkers in (1) identifying diffuse and focal brain injury and (2) assess their potential for determining outcome, intracranial pressure (ICP), and responses to therapy. At present, there is insufficient literature to support a role for diagnostic biomarkers in distinguishing focal and diffuse injury or for accurate determination of raised ICP. Presently, neurofilament (NF), S100β, glial fibrillary acidic protein (GFAP), and ubiquitin carboxyl terminal hydrolase-L1 (UCH-L1) seemed to have the best potential as diagnostic biomarkers for distinguishing focal and diffuse injury, whereas C-tau, neuron-specific enolase (NSE), S100β, GFAP, and spectrin breakdown products (SBDPs) appear to be candidates for ICP reflective biomarkers. With the combinations of different pathophysiology related to each biomarker, a multibiomarker analysis seems to be effective and would likely increase diagnostic accuracy. There is limited research focusing on the differential diagnostic properties of biomarkers in TBI. This fact warrants the need for greater efforts to innovate sensitive and reliable biomarkers. We advocate awareness and inclusion of the differentiation of injury type and ICP elevation in further studies with brain injury biomarkers.

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Stroke is the most prevalent cardiovascular disease worldwide, and is still one of the leading causes of death and disability. Stem cell-based therapy is actively being investigated as a new potential treatment for certain neurological disorders, including stroke. Various types of cells, including bone marrow mononuclear cells, bone marrow mesenchymal stem cells, dental pulp stem cells, neural stem cells, inducible pluripotent stem cells, and genetically modified stem cells have been found to improve neurological outcomes in animal models of stroke, and there are some ongoing clinical trials assessing their efficacy in humans. In this review, we aim to summarize the recent advances in cell-based therapies to treat stroke.

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Our findings suggest that global end-diastolic volume index impacts both delayed cerebral ischemia and pulmonary edema after subarachnoid hemorrhage. Maintaining global end-diastolic volume index slightly above normal levels has promise as a fluid management goal during the treatment of subarachnoid hemorrhage.

Physician-directed prophylactic triple-H administration was not associated with improved clinical outcomes or quantitative hemodynamic indicators for intravascular volume. Further, GEDI-directed intervention studies are warranted to better define management algorithms for SAH patients with the aim of preventing DCI.

Background The exacerbation of intracranial bleeding is critical in traumatic brain injury (TBI) patients. Tranexamic acid (TXA) has been used to improve outcomes in TBI patient. However, the effectiveness of TXA treatment remains unclear. This study aimed to assess the effect of administration of TXA on clinical outcomes in patients with TBI by systematically reviewing the literature and synthesizing evidence of randomized controlled trials (RCTs). Methods MEDLINE, the Cochrane Central Register of Controlled Trials, and Igaku Chuo Zasshi (ICHUSHI) Web were searched. Selection criteria included randomized controlled trials with clinical outcomes of adult TBI patients administered TXA or placebo within 24 h after admission. Two investigators independently screened citations and conducted data extraction. The primary “critical” outcome was all-cause mortality. The secondary “important” outcomes were good neurological outcome rates, enlargement of bleeding, incidence of ischemia, and hemorrhagic intracranial complications. Random effect estimators with weights calculated by the inverse variance method were used to report risk ratios (RRs). Results A total of 640 records were screened. Seven studies were included for quantitative analysis. Of 10,044 patients from seven of the included studies, 5076 were randomly assigned to the TXA treatment group, and 4968 were assigned to placebo. In the TXA treatment group, 914 patients (18.0%) died, while 961 patients (19.3%) died in the placebo group. There was no significant difference between groups (RR, 0.93; 95% confidence interval, 0.86–1.01). No significant differences between the groups in other important outcomes were also observed. Conclusions TXA treatment demonstrated a tendency to reduce head trauma-related deaths in the TBI population, with no significant incidence of thromboembolic events. TXA treatment may therefore be suggested in the initial TBI care.