Journal of neurotrauma
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Journal of neurotrauma · Nov 2009
Therapeutic window of selective profound cerebral hypothermia for resuscitation of severe cerebral ischemia in primates.
It is well recognized that brain death starts to occur just 4-6 min after cardiac arrest, and few attempts at resuscitation succeed after 10 min of severe cerebral ischemia and anoxia. We sought to determine the therapeutic window of selective cerebral profound hypothermia of primates following severe cerebral ischemia in primates. Fourteen rhesus monkeys with severe cerebral ischemia were divided into four groups: normothermia (n = 3); profound hypothermia I (n = 4), with cooling initiated 10 min after ischemia; profound hypothermia II (n = 4), with cooling initiated 15 min after ischemia; and profound hypothermia III (n = 3), with cooling initiated 20 min after ischemia. ⋯ Neurological functions were normal in all surviving animals, and MRI scans showed no cerebral infarction in these animals. Microscopic examination showed no injured neurons in the hippocampus and cerebral cortex of the surviving animals, and showed that the heart, lung, liver, and kidneys were normal in these animals. Our data indicate that post-ischemic profound cerebral hypothermia provided significant cerebral protection with no systemic complications, and that the effective therapeutic window is more than 10 min, but less than 15 min, after severe cerebral ischemia.
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Journal of neurotrauma · Nov 2009
Metabolic response and nutritional support in traumatic brain injury: evidence for resistance to renutrition.
Abstract Traumatic brain injury (TBI) is one of the most severe injuries encountered in intensive care units. TBI patients exhibit protein wasting and gastrointestinal dysfunction, which may be risk factors for a septic state. Specific nutritional support may be required for these patients, and we hypothesize that standard nutritional support does not allow restoration of the nutritional state of TBI patients. ⋯ This work confirms that TBI is associated with profound nutritional alterations and has a major impact on nitrogen metabolism and on intestinal trophicity. It also demonstrates that using standard enteral nutrition cannot reverse this phenomenon. Thus, developing new nutritional strategies to cover TBI patients' specific nutritional requirements appears mandatory.
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Journal of neurotrauma · Nov 2009
Randomized Controlled TrialProtective effect of moderate hypothermia on severe traumatic brain injury in children.
This study investigated the safety and neuroprotective effect of moderate hypothermia in children with severe traumatic brain injury (TBI). Twenty-two children suffering from TBI were randomly divided into groups treated with moderate hypothermia (intracranial temperature of 34.5 +/- 0.2 degrees C, maintained for 72 h, n = 12) or normothermia (intracranial temperature of 38.0 +/- 0.5, n = 10). The cerebrospinal fluid levels of neuron-specific enolase (NSE), S-100, brain-specific creatine kinase (CK-BB), and intracranial pressure (ICP) levels were used to assess the protective effects. ⋯ In the moderate hypothermia group, the pH and electrolyte balance at the end of the monitoring period were normal, but the heart rates were lower (p < 0.05). There were a total of three deaths (13.6%) in this study: one in the moderate hypothermia group (8.3%) and two in the normothermia group (20%). In conclusion, moderate hypothermia provided neuronal protection for children with severe TBI, and maintaining the intracranial temperature at 34.5 degrees C for 72 h was safe in this clinical setting.
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Journal of neurotrauma · Nov 2009
A panel of neuron-enriched proteins as markers for traumatic brain injury in humans.
Surrogate markers have enormous potential for contributing to the diagnosis, prognosis, and therapeutic evaluation of acute brain damage, but extensive prior study of individual candidates has not yielded a biomarker in widespread clinical practice. We hypothesize that a panel of neuron-enriched proteins measurable in cerebrospinal fluid (CSF) and blood should vastly improve clinical evaluation and therapeutic management of acute brain injuries. Previously, we developed such a panel based initially on the study of protein release from degenerating cultured neurons, and subsequently on rodent models of traumatic brain injury (TBI) and ischemia, consisting of 14-3-3beta, 14-3-3zeta, three distinct phosphoforms of neurofilament H, ubiquitin hydrolase L1, neuron-specific enolase, alpha-spectrin, and three calpain- and caspase-derived fragments of alpha-spectrin. ⋯ Whereas different markers peaked coordinately, the time to peak varied across TBI cases from 24-96 h post-injury. In serum, TBI increased all four members of the marker panel for which sandwich immunoassays are currently available: a calpain-derived NH(2)-terminal alpha-spectrin fragment and the three neurofilament H phosphoforms. Our results identify neuron-enriched proteins that may serve as a panel of CSF and blood surrogate markers for the minimally invasive detection, management, mechanistic, and therapeutic evaluation of human TBI.
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Journal of neurotrauma · Nov 2009
Conversion in ASIA impairment scale during the first year after traumatic spinal cord injury.
The neurological severity of a spinal cord injury (SCI) is commonly classified according to the American Spinal Injury Association (ASIA) Impairment Scale (AIS). The aim of this study was to assess the course of the AIS following SCI, and to discern the nature of any changes in the classification that occur. Assessments were performed in a European cohort of SCI patients within 2 weeks and at 1, 3, 6, and 12 months after the initial injury. ⋯ When the AIS remained unchanged between successive assessment points, there was no change in the number of muscles graded three or more (NMG3(+)) in 73% of the transitions. An improvement in AIS was associated with a gain in NMG3(+) in 49% of the transitions, while an aggravation in AIS was accompanied by a loss in NMG3(+) in 10% of the transitions. These results, documenting a substantial amount of spontaneous AIS conversions, should be taken into consideration when designing clinical trials to assess the effects of potential new treatments for SCI.