Avoiding brain hypoxia in severe traumatic brain injury in settings with limited resources - A pathophysiological guide. Journal of critical care Cerebral oxygenation represents the balance between oxygen delivery, consumption and utilization by the brain, and therefore reflects the adequacy of cerebral perfusion. Different factors can influence the amount of oxygen to the brain including arterial blood pressure, hemoglobin levels, systemic oxygenation, and transfer of oxygen from blood to the cerebral microcirculation. A mismatch between cerebral oxygen supply and demand results in cerebral hypoxia/ischemia, and is associated with secondary brain damage and worsened outcome after acute brain injury. Therefore, monitoring and prompt treatment of cerebral oxygenation compromise is warranted in both neuro and general intensive care unit populations. Several tools have been proposed for the assessment of cerebral oxygenation, including non-invasive/invasive or indirect/direct methods, including Jugular Venous Oxygen Saturation (SjO2), Partial Brain Tissue Oxygen Tension (PtiO2), Near infrared spectroscopy (NIRS), Transcranial Doppler, electroencephalography and Computed Tomography. In this manuscript, we aim to review the pathophysiology of cerebral oxygenation, describe monitoring technics, and generate recommendations for avoiding brain hypoxia in settings with low availability of resources for direct brain oxygen monitoring. 10.1016/j.jcrc.2023.154260

Cerebral vasospasm after traumatic brain injury: an update. Perrein A,Petry L,Reis A,Baumann A,Mertes P,Audibert G Minerva anestesiologica BACKGROUND:Post-traumatic vasospasm (PTV) remains a poorly understood entity. Using a systematic review approach, we examined the incidence, mechanisms, risk factors, impact on outcome and potential therapies of PTV. METHODS:A search on Medline database up to 2015 performed with "traumatic brain injury" and "vasospasm" key-words retrieved 429 references. This systematic review was reported and analysed following the PRISMA criteria and according to the relevance in human clinical practice. RESULTS:The research retrieved 429 references of which 226 were excluded from analysis because of their irrelevance and 87 finally included in the review. CONCLUSION:Mechanical stretching, inflammation, calcium dysregulation, endotelin, contractile proteins, products of cerebral metabolism and cortical spreading depolarization have been involved in PTV pathophysiology. PTV occurs in up to 30-40% of the patients after severe traumatic brain injury. Usually, PTV starts within the first 3 days following head trauma and may last 5 to 10 days. Young age, low Glasgow Coma Score at admission and subarachnoid hemorrhage have been identified as risk factors of PTV. Suspected on transcranial Doppler, PTV diagnosis is best confirmed by angiography, CT angiography or MR angiography, and perfusion and ischaemic consequences by perfusion CT or MRI. Early PTV is associated with poor outcome. No PTV prevention strategy has proved efficient up to now. Regarding PTV treatment, only nimodipine and intra-arterial papaverine have been studied up to now. Treatment with milrinone has been described in a few cases reports and may represent a new therapeutic option.

Oxidative Stress: Major Threat in Traumatic Brain Injury. Khatri Nidhi,Thakur Manisha,Pareek Vikas,Kumar Sandeep,Sharma Sunil,Datusalia Ashok Kumar CNS & neurological disorders drug targets BACKGROUND & OBJECTIVE:Traumatic Brain Injury (TBI) is one of the major causes of mortality and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed by secondary injury which leads to biochemical, cellular, and physiological changes like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately people start facing some serious disabilies. CONCLUSION:In the present review we provide extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI. 10.2174/1871527317666180627120501

Protein biomarkers of epileptogenicity after traumatic brain injury. Neurobiology of disease Traumatic brain injury (TBI) is a major risk factor for acquired epilepsy. Post-traumatic epilepsy (PTE) develops over time in up to 50% of patients with severe TBI. PTE is mostly unresponsive to traditional anti-seizure treatments suggesting distinct, injury-induced pathomechanisms in the development of this condition. Moderate and severe TBIs cause significant tissue damage, bleeding, neuron and glia death, as well as axonal, vascular, and metabolic abnormalities. These changes trigger a complex biological response aimed at curtailing the physical damage and restoring homeostasis and functionality. Although a positive correlation exists between the type and severity of TBI and PTE, there is only an incomplete understanding of the time-dependent sequelae of TBI pathobiologies and their role in epileptogenesis. Determining the temporal profile of protein biomarkers in the blood (serum or plasma) and cerebrospinal fluid (CSF) can help to identify pathobiologies underlying the development of PTE, high-risk individuals, and disease modifying therapies. Here we review the pathobiological sequelae of TBI in the context of blood- and CSF-based protein biomarkers, their potential role in epileptogenesis, and discuss future directions aimed at improving the diagnosis and treatment of PTE. 10.1016/j.nbd.2018.07.017