Journal of neurotrauma
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Journal of neurotrauma · Mar 1999
Clinical TrialEffect of moderate hypothermia on systemic and internal jugular plasma IL-6 levels after traumatic brain injury in humans.
Moderate hypothermia may reduce subsequent neuronal damage after traumatic brain injury. Interleukin (IL)-6 may have a role in the pathogenesis of traumatic neuronal damage or repair. Using the enzyme-linked immunological sorbent assay (ELISA), we serially measured IL-6 levels in plasma obtained from the radial artery (systemic) and internal jugular vein (regional) in 13 cerebral trauma patients who underwent hypothermia of 32-33 degrees C ranged from 4-9 days postinjury and 10 head-injured patients who were maintained at normothermic levels (36-37 degrees C). ⋯ The cytokine suppression found in the hypothermic group continued even after rewarming in these patients showing an improved clinical course, but not in those whose condition worsened. In addition to these changes in cytokine levels, the Glasgow Outcome Scale at 6 months postinjury was significantly higher in the hypothermic group than in the normothermia group. Based on the above, this clinical study with its small patient sample size suggests the need for further prospective randomized studies to examine the role of cytokine suppression in the beneficial effects of moderate hypothermia in patients with traumatic brain injury.
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Journal of neurotrauma · Mar 1999
Comparative Study Clinical TrialPostpyloric enteral feeding costs for patients with severe head injury: blind placement, endoscopy, and PEG/J versus TPN.
This study describes the advantages and disadvantages of several forms of enteral nutrition for patients with severe head injury (Glasgow Coma Scale Score [GCS], <12). Included in the study are nasoenteric nutrition delivery using blind, endoscopic, percutaneous endoscopic gastrostomy (PEG) and PEG with jejeunostomy (PEG/J), and open jejeunostomy tube placement methods. These methods are compared with parenteral delivery of nutrition. ⋯ We conclude that blind transpyloric feeding tube placement is difficult to achieve in patients with severe head injury; endoscopically guided placement is a better option. Endoscopic feeding tube placement most consistently allows for early enteral nutritional support in severe head injured patients. Limitations include the inability to establish and/or maintain enteral access, increased intracranial pressure, unstable cervical spinal injuries, facial fractures, and dedication of the physician to tube placement and monitoring.
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Journal of neurotrauma · Mar 1999
Effects of six weeks of chronic ethanol administration on the behavioral outcome of rats after lateral fluid percussion brain injury.
This study examined the effects of 6 weeks of chronic ethanol administration on the behavioral outcome in rats after lateral fluid percussion (FP) brain injury. Rats were given either an ethanol liquid diet (ethanol diet-groups) or a pair-fed isocaloric sucrose control diet (control diet groups) for 6 weeks. After 6 weeks, the ethanol diet was discontinued for the ethanol diet rats and they were then given the control sucrose diet for 2 days. ⋯ Histologic analysis of both diet groups after behavioral assessment revealed comparable ipsilateral cortical damage and observable CA3 neuronal loss in the ipsilateral hippocampus. These results only suggest that chronic ethanol administration, longer than six weeks of administration, may worsen behavioral outcome following lateral FP brain injury. For more significant behavioral and/or morphological change to occur, we would suggest that the duration of chronic ethanol administration must be increased.
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Journal of neurotrauma · Mar 1999
Regional changes in cerebral extracellular glucose and lactate concentrations following severe cortical impact injury and secondary ischemia in rats.
Traumatic brain injury (TBI) causes the brain to be more susceptible to secondary insults, and the occurrence of a secondary insult after trauma increases the damage that develops in the brain. To study the synergistic effect of trauma and ischemia on brain energy metabolites, regional changes in the extracellular concentrations of glucose and lactate following a severe cortical impact injury were measured employing a microdialysis technique. Three microdialysis probes were placed in center of the impact site, in an area adjacent to the impact site, and in the contralateral parietal cortex, and perfused with artificial cerebrospinal fluid (CSF) at 2 microl/min. ⋯ The impact injury resulted in a three- to fivefold global increase in dialysate lactate concentrations, with a corresponding fall in dialysate glucose concentration by 50% compared to no change in lactate or glucose concentrations in sham-injured animals (p < .0001 for both lactate and glucose). The secondary insult resulted in a second increase in dialysate lactate and decrease in dialysate glucose concentration that was significantly greater in the animals that had suffered the impact injury than in the sham-injured animals. Ischemia and traumatic injury have synergistic effects on lactate accumulation and on glucose depletion in the brain that probably reflects persisting ischemia, but may also indicate mitochondrial abnormalities and inhibition of oxidative metabolism.
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Journal of neurotrauma · Feb 1999
One-year study of spatial memory performance, brain morphology, and cholinergic markers after moderate controlled cortical impact in rats.
Persistent cognitive deficits are one of the most important sequelae of head injury in humans. In an effort to model some of the structural and neuropharmacological changes that occur in chronic postinjury brains, we examined the longitudinal effects of moderate vertical controlled cortical impact (CCI) on place learning and memory using the Morris water maze (MWM) test, morphology, and vesicular acetylcholine (ACh) transporter (VAChT) and muscarinic receptor subtype 2 (M2) immunohistochemistry. Vertical CCI (left parietal cortex, 4 m/sec, 2.5 mm; n = 10) or craniotomy (sham) was produced in male Sprague-Dawley rats (n = 10). ⋯ This suggests a compensatory response of cholinergic neurons to increase the efficiency of ACh neurotransmission. Moderate CCI in rats produces subtle MWM performance deficits accompanied by persistent alteration in M2 and VAChT immunohistochemistry and progressive tissue atrophy. The inability of injured rats to benefit from repeated exposures to the MWM may represent a deficit in procedural memory that is independent of changes in hippocampal cholinergic systems.