1,720,981 research outputs found
Hyperoxia in head injury : therapeutic tool?
No full textPurpose of review: Currently, no neuroprotective therapies have been shown to reduce the secondary neuronal damage occurring after traumatic brain injury. Recent studies have addressed the potentiality of hyperoxia to ameliorate brain metabolism after traumatic brain injury. In this article, we present the principles of oxygen transport to the brain, the effects of hyperoxia on cerebral metabolism, and the role of lactate in brain metabolism after traumatic brain injury. Recent findings: It has been shown that hyperoxia obtained by increasing the inspired fraction of oxygen results in a decreased cerebral lactate concentration measured in the extracellular space using the microdialysis. However, the brain oxygen delivery is not substantially improved by eubaric hyperoxia and the ratio between lactate and pyruvate (a better indicator of the cellular redox state than lactate alone) is not changed by hyperoxia. In addition, it has been shown the lactate might be an alternative fuel for neurons during the acute postinjury phase. Summary: At present, there is no evidence supporting any clinical benefit of hyperoxia in brain-injured patients, and the meaning of posttraumatic brain extracellular lactate accumulation should be further investigated
The race for biomarkers in traumatic brain injury : what science promises and the clinicians still expect
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Cranial trauma and multiple trauma : from the street to the operating room
No full textBrain injury occurs with a range of severity: even less severe cases should be carefully observed since they may deteriorate. By definition severe head injury has a Glasgow Coma Scale score of 8 or less; comatose patients are defined as cases who do not obey commands, do not open their eyes and do not speak. Very often (50% of case in our series) brain injury is associated with relevant extracranial injuries that may add to the severity of cases and may worsen outcome. The conceptual framework for treating head injury is based on the evidence that after the impact, the initial damage may be exacerbated by insults capable of further disturbing cerebral metabolism, leading to a final damage defined as secondary damage. Secondary damage represents the final end of many pathways that can be studied at the biochemical level and are centered in a calcium influx into the neuronal cell. Most probably there is a genetic susceptibility to secondary damage leading to a range of cellular dysfunctions for any given level of insult. The management of traumatic brain injury is aimed at interrupting the chain of events leading to secondary brain damage and from this perspective the fact that damage may develop over time can be seen as a window of opportunity for timely treatment. The milestone of treatment is the removal of surgical masses. This surgical treatment can be performed only in a brain that is properly perfused and once coagulation is preserved. Therefore the organization of treatment from rescue to neuro-traumatological centers should provide appropriate restoration of the volume and a normal oxygen delivery to the brain and to the overall organism
How to quantify the severity of brain injury during intensive care after adult head trauma
No full textAdequate early assessment of brain damage is essential. Location, extension and severity of structural damage affect brain function and ultimately determine the outcome. The extent of functional impairment, and the morphology of intracranial lesions, require specific treatment, often a combination of medical and surgical interventions. Brain damage usually evolves over time, and repeated assessments are necessary. Clinical evaluation is often biased by concomitant sedation and/or anesthesia, but remains necessary. A revision of the literature is presented.
Brain damage is assessed combining clinical and instrumental data. Clinical examination is performed assessing the 3 components of the Glasgow Coma Scale. Spontaneous or stimulated (pain stimulus) eye opening, verbal and motor responses are observed after hemodynamic and respiratory stabilisation. Unfortunately a significant proportion of patients can not be properly examined for several reasons: eye opening can be altered by palpebral and facial injuries, verbal response can be impaired by maxillo-facial injuries or by endotracheal intubation, and motor response remains the most consistent parameter. Sedation, analgesia and myorelaxants, however, can profoundly diminish or abolish the motor response to maximal stimulation, so that examination should be performed after clearance of drugs. Often alcohol or other substances can further impair the neurological performances.
Pupils diameter and reactivity to light should be observed, excluding pharmacologic effects (as dilation due to catecholamines) and direct ocular or orbital damage.
The CT scan is necessary for disclosing surgical masses and for identifying the extent of diffuse damage and the location of focal lesions. These data should be combined with additional functional exploration, as provided by cerebral extraction of oxygen and electrophysiologic data.
Early estimation of cerebral damage is complex and prone to mistakes. Accurate, repeated evaluations, based on the combination of clinical observation and imaging, are necessary
Consumo cerebrale di ossigeno e ischemia nel danno cerebrale traumatico
No full textAim. Clinical and experimental studies have shown a reduction of cerebral blood flow (CBF) and metabolic alterations following traumatic brain injury (TBI). The incidence of ischemia and the meaning of post-traumatic metabolic alterations are still unclear. Methods. Revision of CBF and metabolic changes following TBI based on the literature and on our clinical experience. Results. Cerebral ischemia and metabolic alterations are part of the secondary insults/damage leading to an increased damage following TBI. Global ischemia occurs early following TBI as shown by CBF measurements and by greater values of arterio-jugular difference of oxygen (AJDO2) during the 1st 24 hours postinjury. Post-traumatic ischemia should be defined based on the relationships between CBF and on the metabolic requirements of the brain. Regional ischemia occurs more frequently than global ischemia as shown by regional monitoring of cerebral oxygenation. Following TBI there is a transient phase of increased glycolitic activity followed by a more prolonged phase of reduced metabolic rate of glucose (CMRglc) and oxygen (CMRO2). The extent of CMRO2 reduction is a marker of injury severity and it is associated with unforavorable outcome. Conclusion. Cerebral ischemia occurs following TBI and should he defined based on CBF value and the metabolic needs of the brain. Global monitoring of cerebral oxygenation adequacy should be combined with regional monitoring. The meaning of high AJDO2 values should be reconsidered: if they can highlights potential ischemia they are also showing a still living brain with a partially preserved oxygen extraction capability
Mannose binding lectin deficiency reduces functional deficits and histological damage after experimental traumatic brain injury
No full textBackground:
Mannose binding lectin (MBL) is the activator of the lectin complement pathway. After brain ischemia MBL could be a mediator of secondary brain damage, while after brain trauma (TBI) data suggest that it could be linked to neuroprotection. In order to clarify the role of MBL after TBI we characterized its temporal activation and the effects of its inhibition in a model of cerebral contusion.
Methods:
1) Male C57/Bl6 (WT) mice received intraperitoneal anesthesia (Pentobarbital, 65 mg/kg) followed by the controlled cortical impact to model TBI (injury parameters: velocity of 5 meter/s and 1 mm depth of deformation). MBL immunostaining was evaluated at 30 min, 6, 12, 24, 48, 96 h and 1 week after TBI using anti MBL-A and MBL-C antibodies. 2) The effects of MBL inhibition were evaluated in WT and MBL double knockout (-/-) mice. Functional outcome was tested using the Neuroscore and Beam Walk test weekly for 4 weeks postinjury. Histologic outcome was evaluated by neuronal cell count in the cortex adjacent to the contusion.
Results:
We observed MBL-C positive immunostaining in the injured cortex starting at 30 minutes postinjury and up to 1 week, suggestive of an activation of this pathway. MBL-C was observed both at endothelial and tissue level. MBL-A was detected in the injured brain but its staining was much lower compared to that of MBL-C. Injured WT and MBL (-/-) mice showed motor deficits up to 4 weeks postinjury when compared to their controls. Motor deficits were reduced in MBL (-/-) compared to WT mice at 2-4 weeks postinjury (p<0.01 for Neuroscore and Beam Walk). Moreover we observed a reduced cortical cell loss at 4 weeks postinjury in MBL (-/-) mice compared to WT (p < 0.05).
Conclusions:
We observed that 1) TBI induced MBL deposition/synthesis on injured vessels and in the brain tissue; 2) MBL deficiency was associated with functional neuroprotection, suggesting that MBL modulation might be a potential therapeutic target after TBI
Motor and cognitive function evaluation following experimental traumatic brain injury
No full textTraumatic brain injury (TBI) in humans may cause extensive sensorimotor and cognitive dysfunction. As a result, many TBI researchers are beginning to assess behavioral correlates of histologically determined damage in animal models. Although this is an important step in TBI research, there is a need for standardization between laboratories. The ability to reliably test treatments across laboratories and multiple injury models will close the gap between treatment success in the lab and success in the clinic. The goal of this review is to describe and evaluate the tests employed to assess functional outcome after TBI and to overview aspects of cognitive, sensory, and motor function that may be suitable targets for therapeutic intervention
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