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Traumatic brain injury is a multifaceted condition that encompasses a spectrum of injuries: contusions, axonal injuries in specific brain regions, edema, and hemorrhage. Brain injury determines a broad clinical and disability spectrum due to the implication of various cellular pathways, genetic phenotypes, and environmental factors. It is challenging to predict patient outcomes, to appropriately evaluate the patients, to determine a suitable treatment strategy and rehabilitation program, and to communicate with patient relatives. Biomarkers detected from body fluids are potential evaluation tools for traumatic brain injury patients. These may serve as internal indicators of cerebral damage, delivering valuable information about the dynamic cellular, biochemical, and molecular environments. The diagnostic and prognostic value of biomarkers tested both in animal models of traumatic brain injury is still under question, despite a considerable scientific literature. Recent publications emphasize that a more realistic approach involves combining multiple types of biomarkers with other investigative tools (imaging, outcome scales, and genetic polymorphisms). Additionally, there is increasing interest in the use of biomarkers as tools for treatment monitoring and as surrogate outcome variables to facilitate the design of distinct randomized controlled trials. This review highlights the latest available evidence regarding biomarkers in adults after traumatic brain injury and discusses new approaches in the evaluation of this patient group.

Traumatic brain injury (TBI) is one of the leading causes of injury-related death. In the United States alone, an estimated 1.7 million people sustain a TBI each year, and approximately 5.3 million people live with a TBI-related disability. The direct medical costs and indirect costs such as lost productivity of TBIs totaled an estimated $76.5 billion in the U.S. in the year 2000. Improving the limited treatment options for this condition remains challenging. However, recent reports from interdisciplinary working groups (consisting primarily of neurologists, neurosurgeons, neuropsychologists, and biostatisticians) have stated that to improve TBI treatment, important methodological lessons from the past must be taken into account in future clinical research. An evaluation of the neuroprotection intervention studies conducted over the last 30 years has indicated that a limited understanding of the underlying biological concepts and methodological design flaws are the major reasons for the failure of pharmacological agents to demonstrate efficacy. Cerebrolysin is a parenterally-administered neuro-peptide preparation that acts in a manner similar to endogenous neurotrophic factors. Cerebrolysin has a favorable adverse effect profile, and several meta-analyses have suggested that Cerebrolysin is beneficial as a dementia treatment. CAPTAIN is a randomized, double-blind, placebo-controlled, multi-center, multinational trial of the effects of Cerebrolysin on neuroprotection and neurorecovery after TBI using a multidimensional ensemble of outcome scales. The CAPTAIN trial will be the first TBI trial with a 'true' multidimensional approach based on full outcome scales, while avoiding prior weaknesses, such as loss of information through "dichotomization," or unrealistic assumptions such as "normal distribution."

Traumatic Brain Injury (TBI) is among the most frequent neurological disorders. Of all TBIs 90% are considered mild with an annual incidence of 100–300/100.000. Intracranial complications of Mild Traumatic Brain Injury (MTBI) are infrequent (10%), requiring neurosurgical intervention in a minority of cases (1%), but potentially life-threatening (case fatality rate 0,1%). Hence, a true health management problem exists because of the need to exclude the small chance of a life threatening complication in large numbers of individual patients. The 2002 EFNS guidelines used a best evidence approach based on the literature until 2001 to guide initial management with respect to indications for CT, hospital admission, observation and follow up of MTBI patients. This updated EFNS guideline version for initial management inMTBI proposes a more selectively strategy for CT when major (dangerous mechanism, GCS<15, 2 points deterioration on the GCS, clinical signs of (basal) skull fracture, vomiting, anticoagulation therapy, post traumatic seizure) or minor (age, loss of consciousness, persistent anterograde amnesia, focal deficit, skull contusion, deterioration on the GCS) risk factors are present based on published decision rules with a high level of evidence. In addition clinical decision rules for CT now exist for children as well. Since 2001 recommendations, although with a lower level of evidence, have been published for clinical in hospital observation to prevent and treat other potential threads to the patient including behavioral disturbances (amnesia, confusion and agitation) and infection.

Changes in quantitative EEG (qEEG) recordings over a 1-year period and the effects of Cerebrolysin (Cere) on qEEG slowing and cognitive performance were investigated in postacute moderate-severe traumatic brain injury (TBI) patients. Time-related changes in qEEG activity frequency bands (increases of alpha and beta, and reductions of theta and delta relative power) and in qEEG slowing (reduction of EEG power ratio) were statistically significant in patients with a disease progress of less than 2 years at baseline, but not in those patients having a longer disease progress time. Slowing of qEEG activity was also found to be significantly reduced in TBI patients after 1 month of treatment with Cere and 3 months later. Therefore, Cere seems to accelerate the time-related reduction of qEEG slowing occurring in untreated patients. The decrease of qEEG slowing induced by Cere correlated with the improvement of attention and working memory. Results of this exploratory study suggest that Cere might improve the functional recovery after brain injury and encourage the conduction of further controlled clinical trials.

Objective: To evaluate the safety and efficacy of Cerebrolysin as an add-on therapy to local standard treatment protocol in patients after moderate-to-severe traumatic brain injury. Methods: The patients received the study medication in addition to standard care (50 mL of Cerebrolysin or physiological saline solution daily for 10 days, followed by two additional treatment cycles with 10 mL daily for 10 days) in a prospective, randomized, double-blind, placebo-controlled, parallel-group, multi-centre phase IIIb/IV trial. The primary endpoint was a multidimensional ensemble of 14 outcome scales pooled to be analyzed by means of the multivariate, correlation-sensitive Wei-Lachin procedure. Results: In 46 enrolled TBI patients (Cerebrolysin 22, placebo 24), three single outcomes showed stand-alone statistically significant superiority of Cerebrolysin [Stroop Word/Dots Interference (p = 0.0415, Mann–Whitney(MW) = 0.6816, 95% CI 0.51–0.86); Color Trails Tests 1 and 2 (p = 0.0223/0.0170, MW = 0.72/0.73, 95% CI 0.53–0.90/0.54–0.91), both effect sizes lying above the benchmark for "large" superiority (MW > 0.71)]. While for the primary multivariate ensemble, statistical significance was just missed in the intention-to-treat population (pWei-Lachin < 0.1, MWcombined = 0.63, 95% CI 0.48–0.77, derived standardized mean difference (SMD) 0.45, 95% CI −0.07 to 1.04, derived OR 2.1, 95% CI 0.89–5.95), the per-protocol analysis showed a statistical significant superiority of Cerebrolysin (pWei-Lachin = 0.0240, MWcombined = 0.69, 95% CI 0.53 to 0.85, derived SMD 0.69, 95% CI 0.09 to 1.47, derived OR 3.2, 95% CI 1.16 to 12.8), with effect sizes of six single outcomes lying above the benchmark for "large" superiority. Safety aspects were comparable to placebo. Conclusion: Our trial suggests beneficial effects of Cerebrolysin on outcome after TBI. Results should be confirmed by a larger RCT with a comparable multidimensional approach. [ABSTRACT FROM AUTHOR]

The above article was published online with incorrect abbreviations in Figures 2 and 3 last sentence of the legend. HDA should be corrected to HADS. [ABSTRACT FROM AUTHOR]

Galvos smegenųtrauma (GST) yra vienas dažniausių neurologiniųsutrikimų. Iš visųGST 90 % yra lengvos, jųdažnis siekia 100-300/100 000 kasmet. Intrakranijinės lengvos galvos smegenųtraumos (LGST) komplikacijos nėra dažnos (10 %). Labai retai prireikia neurochirurginės intervencijos (1 %), tačiau tai gali būti pavojinga gyvybei (mirtingumas -0,1 %). Taigi, tikroji gydymo problema kyla dėl poreikio išsiaiškinti nedidelę gyvybei grėsmingos komplikacijos galimybę dideliam pacientųskaičiui. 2002 m. EFNS nuorodose taikytas geriausio ąrodymo požiūris, remiantis literatūra iki 2001 m. nurodant pradiną gydymą, KT indikacijas, hospitalizavimą ir pacientų, patyrusių LGST, stebėjimą. šios atnaujintos EFNS nuorodos siūlo selektyvesnę KT atlikimo taktiką, esant didiesiems (pavojingas traumos mechanizmas, GKS < 15 balų, GKS vertės sumažėjimas 2 balais, klinikiniai kaukolės (pamato) l ūžio požymiai, vėmimas, gydymas antikoaguliantais, potrauminiai traukuliai) ar mažiesiems (amžius, sąmonės netekimas, išliekanti anterogradinė amnezija, židininiai simptomai, galvos sumušimas, GKS balųblogėjimas) rizikos veiksniams. Nuorodos paremtos publikuotais sprendimais, esant aukštam ąrodymųlygiui. Be to, dabar egzistuoja rekomendacijos dėl KT atlikimo vaikams. Nors ir su žemesniu ąrodymųlygiu, pateikiamos nuorodos dėl klinikinio stebėjimo ligoninėje, siekiant išvengti galimųpavojingųkomplikacijų, ąskaitant elgesio sutrikimus (amnezija, sumišimas ir neramumas) ir infekciją. [ABSTRACT FROM AUTHOR]