Journal of neurotrauma
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Journal of neurotrauma · Apr 2002
Attenuation of working memory and spatial acquisition deficits after a delayed and chronic bromocriptine treatment regimen in rats subjected to traumatic brain injury by controlled cortical impact.
Cognitive impairments are pervasive and persistent sequelae of human traumatic brain injury (TBI). In vivo models of TBI, such as the controlled cortical impact (CCI) and fluid percussion (FP), are utilized extensively to produce deficits reminiscent of those seen clinically with the hope that empirical study will lead to viable therapeutic interventions. Both CCI and FP produce spatial learning acquisition deficits, but only the latter has been reported to impair working memory in rats tested in the Morris water maze (MWM). ⋯ Additionally, the injured bromocriptine-treated group exhibited significantly more morphologically intact CA3 neurons than the injured vehicle-treated group (55.60 +/- 3.10% vs. 38.34 +/- 7.78% [p = 0.03]). No significant differences were observed among TBI groups in CA1 cell survival (bromocriptine, 40.26 +/- 4.74% vs. vehicle, 29.13 +/- 6.63% [p = 0.14]) or cortical lesion volume (bromocriptine, 17.78 +/- 0.62 mm3 vs. vehicle, 19.01 +/- 1.49 mm3 [p > 0.05]). These data reveal that CCI produces working memory deficits in rats that are similar to those observed following FP, and that the delayed and chronic bromocriptine treatment regimen conferred cognitive and neural protection after TBI.
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Journal of neurotrauma · Apr 2002
Fiberoptic intraparenchymal brain pressure monitoring with the Camino V420 monitor: reflections on our experience in 163 severely head-injured patients.
To assess the safety and accuracy of the Camino intraparenchymal sensor, we prospectively evaluated hemorrhagic complications, zero-drift, infection, and system malfunction in 163 patients monitored after a severe head injury. Mean duration of intracranial pressure (ICP) monitoring was 5 +/- 2.2 days (range: 12 h to 11 days). Of the 141 patients with a control CT scan, four showed a 1-2-cc collection of blood at the catheter's end. ⋯ In conclusion, continuous ICP monitoring using the Camino intraparenchymal sensor has a low complication rate. However, this sensor may underread the real ICP values in a high number of patients. The lack of correlation between duration of ICP monitoring and zero-drift suggests that, contrary to the recommendations of other reports, the intraparenchymatous Camino sensor can provide reliable readings after the fifth day of use.
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Journal of neurotrauma · Mar 2002
Craniectomy position affects morris water maze performance and hippocampal cell loss after parasagittal fluid percussion.
Valid and reliable animal models are essential for mechanistic and therapeutic studies of traumatic brain injury (TBI). Therefore, model characterization is a continual and reciprocal process between the experimental laboratory and the clinic. Several excellent experimental models of TBI, including the lateral fluid percussion rat model, are currently in wide use in many neurotrauma laboratories. ⋯ Furthermore, reactive astrocytosis was more pronounced in the medial, lateral, and caudal placements than in the rostral placement. All craniectomy position groups had similar durations of traumatic unconsciousness and similar impairment on motor tasks. We conclude that small alterations in craniectomy position produce differences in cognitive performance, hippocampal cell loss, and reactive astrocytosis but not in motor performance nor transient unconsciousness.
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Journal of neurotrauma · Mar 2002
Randomized Controlled Trial Multicenter Study Clinical TrialHypothermia on admission in patients with severe brain injury.
Data from the "National Acute Brain Injury Study: Hypothermia" were examined to identify the impact of hypothermia on admission. In all patients, temperature was measured at randomization using bladder catheters with thermistors. Patients assigned to hypothermia were cooled using fluid-circulating pads. ⋯ Patients who were hypothermic on admission, age < or = 45 years (n = 81), and assigned to hypothermia had a significantly lower percentage of poor outcomes than those assigned to normothermia (hypothermia, 52%; normothermia, 76%; p = 0.02). Factors associated with hypothermia on admission were increased age, prehospital hypotension, smaller size, positive blood alcohol, larger volume of pre-hospital fluids, slightly higher injury severity, and winter enrollment The treatment effect was found in all of the four centers, which randomized the majority (80%) of the patients. It is unclear whether the improved outcome when hypothermia is maintained is a beneficial effect of very early hypothermia induction or an adverse effect of permitting the patients to rewarm passively.
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Journal of neurotrauma · Mar 2002
Acute ethanol intake attenuates inflammatory cytokines after brain injury in rats: a possible role for corticosterone.
It has been reported that acute ethanol intoxication exerts dose-dependent effects, both beneficial and detrimental, on the outcome of traumatic brain injury (TBI), although the mechanism(s) has not been determined. Given that pro-inflammatory cytokines are either neuroprotective or neurotoxic, depending on their tissue levels, ethanol-induced alterations in brain cytokine production may be involved in determining the recovery after TBI. The present study was undertaken to examine the effect of acute ethanol pretreatments (producing blood alcohol concentrations of 100+/-16 mg/dL, and 220+/-10 mg/dL, considered low and intoxicating doses, respectively) on interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) levels in discrete brain regions. ⋯ Ethanol pretreatment lowered cytokine levels in the cortex, hippocampus and hypothalamus in a dose-dependent manner after TBI compared to the untreated injured rats. Serum corticosterone levels were markedly increased in the injured rats, and were further augmented in the ethanol-pretreated injured animals in a dose-dependent manner. Our findings suggest that ethanol-induced decrease in pro-inflammatory cytokine production may be linked to increased circulating corticosterone, both of which may contribute to the outcome of brain injury.