To explore the clinical significance of dynamic monitoring of cerebrospinal fluid (CSF) and serum Lactic acid（Lac), neuron-specific enolase (NSE), and the blood-brain barrier (BBB) index in ...evaluating the condition and prognosis after a severe traumatic brain injury (TBI).
A total of 52 severe TBI patients admitted to the Department of Neurosurgery within 24 hours after injury were dynamically monitored. CSF and serum samples were collected on the 1st, 3rd, and 7th day after a severe TBI to monitor the changes in Lac, NSE, and the BBB index. Intracranial pressure (ICP), Glasgow coma scale (GCS), and 6-month Glasgow outcome scale-extended (GOS-E) were tested. According to the results of GOS-E, the patients were divided into two groups (i.e. the poor prognosis group and good prognosis group). Statistical analysis was conducted to investigate the clinical significance of dynamic monitoring of CSF and serum Lac, NSE, and BBB index after a severe TBI.
After a severe TBI, the levels of Lac, NSE, and BBB in CSF and serum were significantly higher than those in the normal range. Lac, NSE, and the BBB index did not correlate with ICP (except serum Lac) but had correlations with GCS and post-injury 6 months post-injury (except serum Lac). Moreover, the correlations between Lac, NSE, and BBB index were statistically significant (p < 0.05): CSF Lac and CSF NSE; CSF Lac and serum NSE; Lac and BBB index of CSF; Lac and BBB index of CSF; NSE and CSE of serum; CSF NSE and BBB index; and serum NSE and BBB index. Additionally, serum NSE is correlated with NSE in CSF (p < 0.05).
After a severe TBI, dynamic monitoring of CSF and serum Lac, NSE, and BBB index has the potential to assess the condition, predict the prognosis, and have clinical significance.
Melatonin (MEL) is a hormone that is produced in the brain and is known to bind to MEL-specific receptors on neuronal membranes in several brain regions. MEL's documented neuroprotective properties, ...low toxicity, and ability to cross the blood-brain-barrier have led to its evaluation for patients with traumatic brain injury (TBI), a condition for which there are currently no Food and Drug Administration (FDA)-approved therapies. The purpose of this manuscript is to summarize the evidence surrounding the use of melatonin after TBI, as well as identify existing gaps and future directions. To address this aim, a search of the literature was conducted using Pubmed, Google Scholar, and the Cochrane Database. In total, 239 unique articles were screened, and the 22 preclinical studies that met the a priori inclusion/exclusion criteria were summarized, including the study aims, sample (size, groups, species, strain, sex, age/weight), TBI model, therapeutic details (preparation, dose, route, duration), key findings, and conclusions. The evidence from these 22 studies was analyzed to draw comparisons across studies, identify remaining gaps, and suggest future directions. Taken together, the published evidence suggests that MEL has neuroprotective properties via a number of mechanisms with few toxic effects reported. Notably, available evidence is largely based on data from adult male rats and, to a lesser extent, mice. Few studies collected data beyond a few days of the initial injury, necessitating additional longer-term studies. Other future directions include diversification of samples to include female animals, pediatric and geriatric animals, and transgenic strains.
This study investigates the association of nightmares beyond general sleep disturbance on neurobehavioral symptoms in adults with mild traumatic brain injury (mTBI).
Secondary analysis of a ...concussion cohort study.
One hundred and eleven adults older than 20 years with mTBI were recruited from a specialized concussion treatment center.
Behavioral Assessment Screening Tool, Pittsburgh Sleep Quality Index, and self-report of nightmare frequency in the past 2 weeks.
Among adults with mTBI, nightmares accounted for the greatest amount of variability in negative affect (β = .362, P < .001), anxiety (β = .332, P < .001), and impulsivity (β = .270, P < .001) after adjusting for age and sex. Overall sleep disturbance had the strongest association with depression (β = .493, P < .001), fatigue (β = .449, P < .001), self-reported executive dysfunction (β = .376, P < .001), and overall burden from concussive symptoms (β = .477, P < .001).
Nightmares and sleep disturbance are differentially associated with variance in neurobehavioral symptoms. Nightmares were independently associated with neurobehavioral symptoms representing an excess of normal functioning (eg, anxiety, impulsivity), while general sleep disturbance was associated with neurobehavioral symptoms representing functioning below normal levels (eg, depression, fatigue, self-reported executive dysfunction). Clinical and research implications are discussed.
Traumatic brain injury (TBI) presents in various forms ranging from mild alterations of consciousness to an unrelenting comatose state and death. In the most severe form of TBI, the entirety of the ...brain is affected by a diffuse type of injury and swelling. Treatment modalities vary extensively based on the severity of the injury and range from daily cognitive therapy sessions to radical surgery such as bilateral decompressive craniectomies. Guidelines have been set forth regarding the optimal management of TBI, but they must be taken in context of the situation and cannot be used in every individual circumstance. In this review article, we have summarized the current status of treatment for TBI in both clinical practice and basic research. We have put forth a brief overview of the various subtypes of traumatic injuries, optimal medical management, and both the noninvasive and invasive monitoring modalities, in addition to the surgical interventions necessary in particular instances. We have overviewed the main achievements in searching for therapeutic strategies of TBI in basic science. We have also discussed the future direction for developing TBI treatment from an experimental perspective.
Machine learning head models (MLHMs) are developed to estimate brain deformation from sensor-based kinematics for early detection of traumatic brain injury (TBI). However, the overfitting to ...simulated impacts and the decreasing accuracy caused by distributional shift of different head impact datasets hinder the broad clinical applications of current MLHMs. We propose a new MLHM configuration that integrates unsupervised domain adaptation with a deep neural network (DNN) to predict whole-brain maximum principal strain (MPS) and MPS rate (MPSR). With 12780 simulated head impacts, we performed unsupervised domain adaptation on target head impacts from 302 college football (CF) impacts and 457 mixed martial arts (MMA) impacts using domain regularized component analysis (DRCA) and cycle-generative adversarial network (GAN)-based methods. The new model improved the MPS/MPSR estimation accuracy, with the DRCA method outperforming other domain adaptation methods in prediction accuracy: MPS mean absolute error (MAE): 0.017 (CF) and 0.020 (MMA); MPSR MAE: <inline-formula> <tex-math notation="LaTeX">4.09\,\,\text {s}^{-{1}} </tex-math></inline-formula> (CF) and <inline-formula> <tex-math notation="LaTeX">6.61\,\,\text {s}^{-{1}} </tex-math></inline-formula> (MMA). On another two hold-out test sets with 195 CF impacts and 260 boxing impacts, the DRCA model outperformed the baseline model without domain adaptation in MPS and MPSR estimation MAE. The DRCA domain adaptation approach reduces the error of MPS/MPSR estimation to be well below previously reported TBI thresholds, enabling accurate brain deformation estimation to detect TBI in future clinical applications.
Traumatic brain injury (TBI) is a leading cause of death and disability in young adults worldwide. TBI survival is associated with persistent neuropsychiatric and neurological impairments, including ...posttraumatic epilepsy (PTE). To date, no pharmaceutical treatment has been found to prevent PTE or ameliorate neurological/neuropsychiatric deficits after TBI. Brain trauma results in immediate mechanical damage to brain cells and blood vessels that may never be fully restored given the limited regenerative capacity of brain tissue. This primary insult unleashes cascades of events, prominently including neuroinflammation and massive oxidative stress that evolve over time, expanding the brain injury, but also clearing cellular debris and establishing homeostasis in the region of damage. Accumulating evidence suggests that oxidative stress and neuroinflammatory sequelae of TBI contribute to posttraumatic epileptogenesis. This review will focus on possible roles of reactive oxygen species (ROS), their interactions with neuroinflammation in posttraumatic epileptogenesis, and emerging therapeutic strategies after TBI. We propose that inhibitors of the professional ROS-generating enzymes, the NADPH oxygenases and myeloperoxidase alone, or combined with selective inhibition of cyclooxygenase mediated signaling may have promise for the treatment or prevention of PTE and other sequelae of TBI.
This article is part of the special issue entitled ‘New Epilepsy Therapies for the 21st Century – From Antiseizure Drugs to Prevention, Modification and Cure of Epilepsy’.
•Reactive oxygen species (ROS) and neuroinflammation contribute to the secondary injury after traumatic brain injury (TBI).•ROS-induced cytotoxicity and dysregulation of redox-regulated processes both contribute to secondary injury after TBI.•Oxidative stress / ROS generation and inflammation are highly interdependent and mutually reinforcing after TBI.•Targeting both ROS generation and inflammation may synergize to reduce secondary injury and prevent epilepsy after TBI.
•Modulating the gut-brain-axis has the potential to improve traumatic brain injury outcomes.•Sub-symptom threshold aerobic exercise may improve post-traumatic brain injury outcomes.•While a valuable ...tool, cerebral micro-dialysis is not without risks or complications.
The aggregation of amyloid-beta peptide and tau protein dysregulation are implicated to play key roles in Alzheimer's disease pathogenesis and are considered the main pathological hallmarks of this ...devastating disease. Physiologically, these two proteins are produced and expressed within the normal human body. However, under pathological conditions, abnormal expression, post-translational modifications, conformational changes, and truncation can make these proteins prone to aggregation, triggering specific disease-related cascades. Recent studies have indicated associations between aberrant behavior of amyloid-beta and tau proteins and various neurological diseases, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, as well as retinal neurodegenerative diseases like Glaucoma and age-related macular degeneration. Additionally, these proteins have been linked to cardiovascular disease, cancer, traumatic brain injury, and diabetes, which are all leading causes of morbidity and mortality. In this comprehensive review, we provide an overview of the connections between amyloid-beta and tau proteins and a spectrum of disorders.
Abstract The role and timing of percutaneous mechanical circulatory support (MCS) devices in the treatment of acute myocardial infarction complicated by cardiogenic shock (AMICS) is not well ...understood. We sought to evaluate patient characteristics and predictors of outcomes in patients presenting with AMICS supported with an axial flow percutaneous MCS device. 287 consecutive unselected patients enrolled in the cVAD Registry presenting with AMICS who underwent percutaneous coronary intervention (PCI) were included in this analysis. All patients were supported with either the Impella 2.5 or Impella CP. Mean patient age was 66±12.5 years, 76% were male, mean left ventricular ejection fraction was 25 ±12 %. Prior to receiving MCS, 80% of patients required inotropes or vasopressors and 40% were supported with intra-aortic balloon pump. 9% of patients were under active cardiopulmonary resuscitation at the time of MCS implantation. Survival to discharge was 44%. In a multivariate analysis early implantation of a MCS device prior to PCI (p=0.04) and prior to requiring inotropes and vasopressors (p=0.05) was associated with increased survival. Survival was 66% when MCS was initiated <1.25 hours from shock onset, 37% when initiated within 1.25-4.25 hours, and 26% when initiated after 4.25 hours (p=0.017). Survival was 68%, 46%, 35%, 35%, 26% for patients requiring 0, 1, 2, 3, ≥4 inotropes prior to MCS support respectively (P<0.001). In conclusion, MCS implantation early after shock onset, before initiation of inotropes or vasopressors and prior to PCI, is independently associated with improved survival in patients presenting with AMICS.
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