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PubMed1993

Effects of ethanol in traumatic brain injury.

The effects of ethanol intoxication on brain injury and cerebral blood flow (CBF) were investigated in a porcine fluid-percussion model of traumatic brain injury (TBI). Immature swine, under halothane anesthesia (1%), had a TBI delivered with a fluid-percussion device. The experimental group (n = 10) received ethanol (3.5 gm/kg) via gastric tube followed in 1 h by TBI. Two groups of control animals received normal saline and TBI (n = 10) or ethanol and no TBI (n = 5). Mean arterial blood pressure (MAP), intracranial pressure (ICP), arterial blood gases, and serum lactate were monitored for 3 h after the injury. CBF was measured with radiolabelled 15-micron diameter microspheres. Neuropathologic changes were evaluated and graded after formalin perfusion and brain removal at 3 h postinjury. The ethanol level 60 min post-head injury was 198 +/- 70 (SD) mg/dL in the ethanol+TBI group. At 90 min postinjury and thereafter, ethanol+TBI animals compared with TBI only animals had significantly lower MAP (63 +/- 26 mmHg vs 91 +/- 15 mmHg) and lower cerebral perfusion pressure (50 +/- 25 mmHg vs 78 +/- 15), and at 180 min postinjury, lower CBF (87 +/- 37% vs 62 +/- 79% of preinjury levels). Ethanol+TBI animals had higher blood lactates (28 +/- 11 mg/dL vs 13 +/- 6 mg/dL) than TBI only animals. Ethanol+TBI animals also had significantly longer postinjury apneas (11 +/- 8 min vs 0.6 +/- 0.4 min), with three of ten ethanol-treated animals never recovering spontaneous respiration. Ethanol intoxication produced hemodynamic and respiratory changes, which may have a deleterious effect on outcome and mortality after brain injury.

Alcoholic Intoxication↗
PubMed1993

Beneficial effect of the nonselective opiate antagonist naloxone hydrochloride and the thyrotropin-releasing hormone (TRH) analog YM-14673 on long-term neurobehavioral outcome following experimental brain injury in the rat.

Neurobehavioral dysfunction following traumatic brain injury results, in part, from delayed biochemical changes initiated by the traumatic insult. Endogenous opioid peptides have been implicated as one type of neurochemical factor involved in the delayed pathological sequelae of central nervous system (CNS) injury, including brain trauma. Both opiate antagonists and thyrotropin-releasing hormone (TRH) and its analogs, which antagonize the physiologic effects of endogenous opioids, have been shown to improve cardiovascular, cerebrovascular, metabolic, and neurologic status following both traumatic and ischemic CNS injury. The present study evaluated the ability of the opiate antagonist naloxone hydrochloride to improve posttraumatic neurologic motor function following experimental fluid-percussion brain injury in the rat, and compared the therapeutic effectiveness of naloxone to the long-acting, centrally active TRH analog YM-14673. Thirty minutes following fluid-percussion brain injury of moderate severity, animals received an intravenous bolus of either naloxone (2.0 mg/kg with constant infusion of 1.7 mg/kg/h, n = 8), YM-14673 (1.0 mg/kg, n = 8), or saline (n = 8). Although naloxone caused a modest and nonsignificant increase in mean arterial blood pressure (MAP); YM-14673 significantly increased MAP within 5 min of administration (p < 0.05), an effect that continued up to 4 h postinjury. Postinjury administration of both naloxone and YM-14673 caused a significant improvement in neurobehavioral outcome which persisted up to 4 weeks postinjury. These results suggest that endogenous opioid peptides may be involved in the pathologic response to traumatic CNS injury and that pharmacotherapies directed at antagonizing opioid peptides may enhance neurobehavioral recovery after brain injury.

Animals↗
PubMed1993

Behavioral protection by moderate hypothermia initiated after experimental traumatic brain injury.

The effects of postinjury hypothermia on behavioral outcome following moderate fluid percussion traumatic brain injury (TBI) were examined. In Experiment I, three groups of rats were examined. The first group was normothermic (37.5 degrees C); and hypothermia (30 degrees C) was initiated 15 min and 30 min postinjury in the second and third groups, respectively. Whole body cooling was achieved by ventral ice pack. Cooling of the brain to 30 degrees C was achieved in 25 min and maintained for 60 min. Brain temperature was measured indirectly by a probe in the temporalis muscle. Behavioral outcome was assessed by beam-balance performance, beam-walking performance, and body weight loss measured daily for 5 days after TBI. Both the normothermic group and the 30-min postinjury hypothermic group exhibited significant (p < 0.05) beam-balance and beam-walking deficits on days 1 through 5 after TBI. In contrast, the 15-min postinjury hypothermic group exhibited significant (p < 0.05) beam-walking deficits only on day 1 after TBI and significant (p < 0.05) beam-balance deficits on days 1, 3, and 4 after TBI. In Experiment II, subcortical brain temperature was compared to temporalis muscle temperature in normothermic (37.5 degrees C) and hypothermic (30 degrees C) rats subjected to TBI. In both groups brain temperature tracked within 0.4 degree C of temporalis muscle temperature. These results are similar to post-TBI excitatory receptor antagonist studies and indicate a therapeutic window for moderate hypothermia of less than 30 min after moderate fluid percussion TBI in the rat.

Animals↗
PubMed1994

Widespread metabolic depression and reduced somatosensory circuit activation following traumatic brain injury in rats.

The effects of fluid percussion brain injury on the basal metabolic state and responsiveness of a somatosensory circuit to physiologic activation were investigated with [14C]2-deoxyglucose autoradiography. Under controlled physiologic conditions and normothermic brain temperature (37 degrees C), rats were injured with a moderate fluid percussion pulse ranging from 1.7 to 2.1 atm. At 4 or 24 h after traumatic brain injury (TBI), unilateral vibrissae stimulation was carried out, resulting in the metabolic activation of the whisker-barrel circuit. In sham-operated control animals, whisker stimulation resulted in the metabolic activation of the ipsilateral trigeminal medullary complex (177% of control), contralateral ventrobasal thalamus (143% control), and primary somatosensory cortex (153% control). At 4 h after injury, local cerebral metabolic rates of glucose (ICMRglu) were significantly depressed throughout the traumatized hemisphere. Although depressed ICMRglu was most pronounced in cortical regions adjacent to the evolving contusion (53% of control), significant decreases were also seen in more remote areas, including the frontal cortex (75% of control), hippocampus (79% control), and lateral thalamus (68% of control). At 24 h following TBI, ICMRglu remained significantly reduced at the impact site, within the ipsilateral somatosensory cortex and lateral thalamus. Stimulus-evoked increases in ICMRglu were depressed within all three relay stations of the vibrissae-barrel-field circuit at 4 and 24 h after TBI. These results demonstrate both focal and diffuse metabolic depression after moderate TBI. Although the most severe and longer lasting metabolic consequences occurred in cortical and thalamic regions destined to exhibit histopathologic damage, milder abnormalities, most prominent in the early posttraumatic period, were also seen in noninjured areas. The inability to activate the somatosensory circuit metabolically indicates that circuit dysfunction is an acute consequence of TBI. Widespread circuit or synaptic dysfunction would be expected to participate in the functional and behavioral consequences of TBI.

Animals↗
PubMed1995

Superoxide dismutase improves posttraumatic cortical blood flow in rats.

Oxygen free radicals, such as the superoxide anion, are known to mediate damage to the cerebral microcirculation following traumatic brain injury. The purpose of this study was to determine if superoxide dismutase (SOD), a scavenger of superoxide anion, could alter posttraumatic cortical blood flow. Following barbiturate anesthesia, rats were surgically prepared for moderate fluid percussion brain injury. Cortical blood flow contralateral to the site of injury was measured using laser-Doppler flowmetry. Laser-Doppler flowmetry assesses flow by measuring cell volume and velocity, which are multiplied electronically to give flow. Starting 10 min before injury, animals received either superoxide dismutase (24,000 U/kg bolus, followed by continuous infusion of 1600 U/kg/min) or an equal volume of saline. Blood pressure, heart rate, and cortical blood flow were measured up to 1 h posttrauma. Rats receiving superoxide dismutase had significantly higher cortical blood flow posttrauma (F = 6.91, p < 0.02). One hour posttrauma, the blood flow in SOD-treated rats was 89 +/- 8% of preinjury baseline, whereas this value was only 66 +/- 6% of control in saline-treated rats. SOD caused not only greater blood velocity but also less reduction in cortical blood volume after injury. There were no significant differences between the groups with respect to blood pressure or heart rate. This study further supports the role of oxygen radical-mediated cerebrovascular dysfunction following traumatic brain injury and is the first to show the beneficial effect of SOD on cortical blood flow following fluid percussion brain injury.

Animals↗
PubMed1995

Posttraumatic brain hypothermia provides protection from sensorimotor and cognitive behavioral deficits.

The purpose of this study was to determine the degree of sensorimotor and cognitive protection conferred by posttraumatic brain hypothermia. Baseline measurements were taken on sensorimotor tasks involving forelimb placing and beam-walking, as well as on a spatial navigational task utilizing the water maze. Twenty-four hours after the last baseline measurements, normothermic (37 degrees C) animals were subjected to a fluid percussion pulse (1.9-2.4 atm) over the right parietal sensorimotor cortex. Following trauma, brain temperature was maintained for 3 h at either normothermic (37 degrees C, group TBI-N, n = 12) or hypothermic levels (30 degrees C, group TBI-H, n = 11). Shams (n = 10) underwent all surgical procedures including posttraumatic brain injury (TBI) temperature manipulation, but were not subjected to the fluid percussive pulse. Beam-walking and forelimb placing measures were begun 24 h post-TBI and continued for 2 weeks. Animals were tested on the water maze task for 2 days beginning 24 h post-TBI. TBI produced substantial deficits in contralateral limb placing, which recovered over approximately one week. Hypothermia provided partial protection from these deficits, with TBI-H animals exhibiting intermediate scores that differed from both sham and TBI-N animals (p < 0.03). In the water maze, there was a distinction between groups in the ability to navigate 48 h after TBI. TBI-N animals performed significantly worse than sham and TBI-H animals (both p < 0.01), whereas there was no significant difference between the scores of sham and TBI-H animals. The present data demonstrate that moderate postinjury brain hypothermia can provide protection from sensorimotor and cognitive behavioral deficits as well as neuropathology in a model of traumatic brain injury associated with early neuronal and microvascular injury.

Animals↗
PubMed1996

Working memory deficits following traumatic brain injury in the rat.

This study was designed to examine working memory following fluid-percussion traumatic brain injury (TBI) using the Morris water maze (MWM). Rats were injured (n = 9) at a moderate level of central fluid percussion injury (2.1 atm) or were prepared for injury but did not receive a fluid pulse (sham injury) (n = 10). On days 11-15 postinjury, working memory was assessed using the MWM. Each animal received 8 pairs of trials per day. For each pair of trials, animals were randomly assigned to one of four possible starting points and one of four possible escape platform positions. On the first trial of each pair, rats were placed in the maze facing the wall and were given 120 sec to locate the hidden escape platform. After remaining on the goal platform for 10 sec, they were placed back into the maze for the second trial of the pair. The platform position and the start position remained unchanged on this trial. After the second trial, the animal was given a 4 min intertrial rest. Between pairs of trials, both the start position and the goal location were changed. Analyses of the latency to reach the goal platform indicated that sham-injured animals performed significantly better on the second trial than on the first trial of each pair. However, injured animals did not significantly differ between first and second trial goal latencies on any day. These results indicate that injured animals have a profound and enduring deficit in spatial working memory function on days 11-15 after TBI.

Animals↗
PubMed1996

Regional generation of leukotriene C4 after experimental brain injury in anesthetized rats.

Regional concentrations of leukotriene C4 and extravasation of Evans blue were measured after lateral fluid-percussion brain injury in rats. Tissue levels of LTC4 were elevated in the injured cortex at 10 min, 30 min, and 1 h after injury; these levels returned to normal by 2 h after injury. Increases in the levels of LTC4 were also observed in the ipsilateral hippocampus after brain injury, and these elevations persisted for 2 h after injury. No significant increase in levels of LTC4 was observed in the contralateral cortex at any time after injury. A substantial extravasation of Evans blue was observed only in the ipsilateral cortex and hippocampus at 3 h and 6 h after brain injury. Although a temporal association between LTC4 and blood-brain barrier (BBB) breakdown is suggested by these data, no cause-and-effect relationship has been addressed in this study. However, it is possible that, as is true for cerebral ischemia, LTC4 may play a role as a mediator in the BBB breakdown associated with fluid-percussion brain injury in rats.

Animals↗
PubMed2000

Cognitive impairment and synaptosomal choline uptake in rats following impact acceleration injury.

Traumatic brain injury is well known to cause deficits in learning and memory, which typically improve with time. Animal studies with fluid percussion or controlled cortical impact injury have identified transient disturbances in forebrain cholinergic innervation which may contribute to such cognitive problems. This study examines the extent to which water maze performance and forebrain synaptosomal choline uptake are affected one week after injury using the newly developed impact acceleration injury model. Injury or sham injury was delivered to adult male Sprague-Dawley rats under halothane anesthesia using a 500-g 2.1-m weight drop. Based on righting reflex, injured rats were divided into moderate (< or = 12 min) or severe (>12 min) groups. Water maze testing was performed on days 5-7 postinjury. On day 7, choline uptake was determined in synaptosomes from hippocampus, a parietal cortex, and entorhinal cortex. Maze learning was severely impaired in the severe injury group but not in the moderate injury group. Learning retention was slightly impaired in the moderate injury group and severely affected in the severe injury group. There was a very strong correlation between the severity of injury as determined by prolongation of righting times and disruption of maze learning at 1 week postinjury. There was no change in synaptosomal choline uptake in any of the forebrain regions in the severe injury group, but a slight (14%) decrease in the hippocampus and parietal cortex of the moderate injury group. Correlation analysis showed no relationship between synaptosomal choline uptake in any brain region and performance in either water maze learning or retention. This study shows that the impact acceleration model produces cognitive impairments equivalent to those seen with fluid percussion injury and controlled cortical impact. Compared with those models, the impact acceleration model does not produce a similar disruption of forebrain cholinergic nerve terminals.

Acceleration↗
PubMed2000

Altered expression of amyloid precursors proteins after traumatic brain injury in rats: in situ hybridization and immunohistochemical study.

The expression of alternatively spliced mRNAs for amyloid precursor protein (APP) isoforms and their translation products were examined in the rat cerebral cortex 1, 3, 6, and 12 h and 1, 3, and 7 days (n = 4-5 in each group) after fluid-percussion brain injury. In situ hybridization studies demonstrated that the expression of APP695 mRNA decreased in and around the damaged area of the cerebral cortex exposed to fluid-percussion injury 1 h after the insult. On the other hand, APP751/770 mRNAs were increased in the regions surrounding the damaged cortical areas 1 day after the injury. An increase of immunoreactive APP was detected in the regions around the damaged cortical areas 3 h after traumatic injury and maintained for the following 3 days. The APP immunoreactivity in the damaged cortices declined to the level of sham-operated animals by post-experimental day 7. Using an anti-amyloid beta (Abeta) protein (17-24) antibody, no deposits of immunoreactive Abeta (17-24) were observed in any of the samples examined in these experiments. These results suggest that the induction of Kunitz-type protease inhibitor (KPI) domain-containing APP mRNAs and the increased accumulation of APP are involved in the physiological and neuropathological responses of brains under various neurodegenerative conditions, including head trauma.

Alternative Splicing↗
PubMed2004

The effects of traumatic brain injury on cerebral blood flow and brain tissue nitric oxide levels and cytokine expression.

Adult, male, Sprague-Dawley rats were anesthetized, intubated, and mechanically ventilated with 1.5-2.0% isoflurane in oxygen (30%) and air. Rats were prepared for fluid percussion traumatic brain injury (TBI), laser Doppler flowmetry, and measurement of brain tissue nitric oxide (NO) levels using an ISO-NO electrode system. After preparation, isoflurane was reduced to 1.5%, and the rats were randomly assigned to receive sham (n = 6), moderate (1.9 atm, n = 6), or severe (2.8 atm, n = 6) parasagittal fluid percussion TBI. CBF and brain tissue NO levels were measured for 4 h, and then isoflurane levels were increased to 4.0% and the rats were decapitated and the brains were removed. Total RNA was isolated from rat brains and cytokine expression was determined. Laser Doppler flow velocity remained constant in the sham-injured rats but decreased significantly in rats subjected to moderate (p < 0.05) or severe (p < 0.05) TBI. Brain tissue NO levels remained constant in the sham-injured rats but decreased significantly (p < 0.01) after moderate TBI. Severe TBI produced slight, insignificant reductions in NO levels. Cytokine expression was very low in the shaminjured rats. TBI-induced expression of mRNAs for interleukin-1 alpha (IL-1alpha), IL-1beta, IL-6, and tumor necrosis factor-alpha (TNFa). IL-1alpha and IL-1beta mRNA expression increased significantly (p < 0.05 vs. sham-injury) after severe TBI and IL-6 and TNFa mRNA expression increased significant (p < 0.05 vs. sham-injury) after both moderate and severe TBI. Other cytokine mRNA expression was unchanged after TBI.

Animals↗
PubMed2003

Selective blockade of AT1 receptor attenuates impairment of hypotensive autoregulation and improves cerebral blood flow after brain injury in the newborn pig.

BACKGROUND: Fluid percussion injury (FPI) in piglets produces vasoconstriction of pial arteries (PAs), decreases in cerebral blood flow (CBF), and impairment of hypotensive autoregulation. Two types of angiotensin II receptors, AT1 and AT2, have been identified in the brain. This study characterized the effect of pretreatment with AT1- and AT2-selective antagonists on CBF and hypotensive autoregulation after FPI. METHODS: Fluid percussion injury was induced in chloralose-anesthetized newborn pigs equipped with closed cranial windows. CBF was determined by the radiolabeled microsphere technique. RESULTS: Moderate and severe hypotension (71 +/- 3, 53 +/- 2, and 40 +/- 1 mmHg for normotension, moderate hypotension, and severe hypotension, respectively) elicited PA dilation without changes in CBF in sham control piglets. The AT1 antagonist ZD 7155 partially restored impaired hypotension-induced PA dilation after FPI (19 +/- 1 and 34 +/- 1 vs. 5 +/- 1 and 7 +/- 1 vs. 12 +/- 1 and 20 +/- 3% for PA dilation during moderate and severe hypotension in sham control, FPI, and FPI + ZD 7155 animals, respectively). ZD 7155 also blunted the reductions in CBF during normotension and hypotension observed in untreated animals (43 +/- 4, 38 +/- 5, and 55 +/- 3 vs. 32 +/- 4, 19 +/- 2, and 27 +/- 5% CBF reductions during normotension, moderate hypotension, and severe hypotension in untreated and pretreated animals, respectively). The AT2 selective antagonist PD 123,319 did not restore hypotension-induced PA dilation and did not prevent decreases in CBF observed during normotension and moderate and severe hypotension after FPI. CONCLUSION: These data indicate that blockade of the AT1 and not the AT2 receptor diminished the reduction in hypotensive PA dilation after FPI. AT1 blockade also blunted the decrease in CBF during normotension as well as the further decrease in CBF observed during hypotension after FPI. These data suggest that AT1 receptor activation by angiotensin II contributes to cerebrovascular dysregulation during hypotension after FPI.

Angiotensin II Type 1 Receptor Blockers↗
PubMed1999

Induction of tolerance against traumatic brain injury by ischemic preconditioning.

We tested the hypothesis that a transient non-lethal ischemic insult lasting 2 min would protect against subsequent moderate traumatic brain injury. Sprague-Dawley rats were randomized into three experimental groups, including sham ischemia procedures and ischemic preconditioning (IPC) followed 48 h later by moderate traumatic brain injury (TBI) provoked by parasagittal fluid percussion injury (1.8-2.1 atm) and IPC followed by 48 h sham TBI. Seven days after the secondary insult, animals were perfusion-fixed for quantitative histopathological analysis. The CA3 necrotic cell count was decreased by 63% in TBI animals that had undergone IPC as compared to TBI animals that underwent sham IPC. TBI animals that had undergone IPC demonstrated significantly smaller contusion volumes than the TBI alone group (6.44 +/- 1.51 vs 1.37 +/- 0.63 mm3, mean +/- s.e.m.) These data indicate that IPC applied 2 days before moderate fluid percussion brain injury increases the brain resistance to traumatic brain damage.

Animals↗
PubMed2002

Effects of fluoxetine on the 5-HT1A receptor and recovery of cognitive function after traumatic brain injury in rats.

OBJECTIVE: This study examined the effects of chronic administration of fluoxetine, a selective serotonin reuptake inhibitor, on cognitive performance and 5-HT1A receptor immunoreactivity following traumatic brain injury. DESIGN: Rats received a moderate severity of lateral fluid percussive injury or sham injury 24 hr after surgical preparation. Fluoxetine or vehicle was administered chronically on postinjury days 1-15. Motor performance and Morris water maze performance were assessed on postinjury days 1-5 and 11-15, respectively. RESULTS: Results indicated that chronic fluoxetine treatment did not affect motor or maze performance. Injured groups showed significantly higher 5-HT1A receptor immunoreactivity on postinjury day 15 than sham-injured rats, and fluoxetine treatment did not alter 5-HT1A receptor immunoreactivity. CONCLUSIONS: These results indicate that chronic postinjury fluoxetine administration did not influence the recovery of motor or Morris water maze performance following lateral fluid percussive injury. They also indicate that injury-induced changes in the 5-HT1A receptor may contribute to traumatic brain injury-induced cognitive deficits.

Animals↗
PubMed2000

Chest physiotherapy in mechanically ventilated children: a review.

OBJECTIVE: Many physicians, nurses, and respiratory care practitioners consider chest physiotherapy (CP) a standard therapy in mechanically ventilated children beyond the newborn period. CP includes percussion, vibration, postural drainage, assisted coughing, and suctioning via the endotracheal tube. DATA SOURCES: We searched the medical literature by using the key words "chest physiotherapy" and "chest physical therapy" (among others) by means of the MEDLINE and Current Contents databases. STUDY SELECTION: Because of the paucity of objective data, we examined all reports dealing with this topic, including studies on adult patients. For data extraction, not enough material existed to perform a meta-analysis. DATA SYNTHESIS: Despite its widespread use, almost no literature dealing with this treatment modality in pediatric patients exists. Studies with mechanically ventilated pediatric and adult patients have shown that CP is the most irritating routine intensive care procedure to patients. An increase in oxygen consumption often occurs when a patient receives CP accompanied by an elevation in heart rate, blood pressure, and intracranial pressure. CP leads to short-term decreases in oxygen, partial pressure in the blood, and major fluctuations in cardiac output. Changes in these vital signs and other variables may be even more pronounced in pediatric patients because the lung of a child is characterized by a higher closing capacity and the chest walls are characterized by a much higher compliance, thus predisposing the child to the development of atelectasis secondary to percussion and vibration. CONCLUSION: CP in mechanically ventilated children may not be considered a standard therapy. Controlled studies examining the impact of CP on the duration of mechanical ventilatory support, critical illness, and hospital stay are needed.

Adult↗
PubMed1997

Early white blood cell dynamics after traumatic brain injury: effects on the cerebral microcirculation.

Increasing clinical and experimental evidence suggests that traumatic brain injury (TBI) elicits an acute inflammatory response. In the present study we investigated whether white blood cells (WBC) are activated in the cerebral microcirculation early after TBI and whether WBC accumulation affects the posttraumatic cerebrovascular response. Twenty-four anesthetized rabbits had chronic cranial windows implanted 3 weeks before experimentation. Animals were divided into four experimental groups and were studied for 7 hours (groups I, IIa, and III) or 2 hours (group IIb). Intravital fluorescence videomicroscopy was used to visualize WBC (rhodamine 6G, intravenously), pial vessel diameters, and blood-brain barrier (BBB) integrity (Na+-fluorescein) at 6 hours (groups I, IIa, and III) or 1 hour (group IIb) after TBI. Group I (n = 5) consisted of sham-operated animals. Groups IIa (n = 7) and IIb (n = 5) received fluid-percussion injury at 1 hour. Group III (n = 7) received fluid-percussion injury and 1 mg/kg anti-adhesion monoclonal antibody (MoAb) "IB4" 5 minutes before injury. Venular WBC sticking, intracranial pressure (ICP), and arterial vessel diameters increased significantly for 6 hours after trauma. IB4 reduced WBC margination and prevented vasodilation. Intracranial pressure was not reduced by treatment with IB4. Blood-brain barrier damage occurred at 1 hour but not at 6 hours after TBI and was independent of WBC activation. This first report using intravital videomicroscopy to study the inflammatory response after TBI reveals upregulated interaction between WBC and cerebral endothelium that can be manipulated pharmacologically. White blood cell activation is associated with pial arteriolar vasodilation. White blood cells do not induce BBB breakdown less than 6 hours after TBI and do not contribute to posttraumatic ICP elevation. The role of WBC more than 6 hours after TBI should be investigated further.

Animals↗
PubMed1999

Interleukin-1 receptor antagonist attenuates regional neuronal cell death and cognitive dysfunction after experimental brain injury.

The effect of systemic administration of human recombinant interleukin-1 receptor antagonist (rhIL-1ra) on behavioral outcome and histopathologic damage after lateral fluid-percussion brain injury of moderate severity was evaluated. In study 1, brain-injured Sprague Dawley rats received timed subcutaneous injections beginning 15 minutes after injury of either 100 mg/kg rhIL-1ra (high dose, total dose = 1900 mg/kg), 10 mg/kg rhIL-1ra (low dose, total dose = 190 mg/kg), or vehicle over 7 days. No effect of low-dose rhIL-1ra was observed in study 1. High-dose rhIL-1ra significantly attenuated posttraumatic neuronal loss in the injured hippocampal CA3 region (P < 0.05), dentate hilus (P < 0.05), and cortex (P < 0.05) but impaired recovery of motor function at 7 days after trauma (P < 0.05). In study 2, rats were pretrained to learn a visuospatial task in a Morris water maze, subjected to fluid-percussion brain injury or sham treatment, and randomly assigned to receive multiple subcutaneous injections at timed intervals of 100 mg/kg rhIL-1ra (total dose = 900 mg/kg) or vehicle over 42 hours, followed by continuous infusion of a lower concentration of rhIL-1ra (20 mg/kg/day, total dose = 100 mg/kg), or vehicle for 5 days using subcutaneously implanted osmotic minipumps. Postinjury administration of rhIL-1ra significantly attenuated cognitive deficits compared with vehicle-treated animals at 42 hours (P < 0.05) but did not affect motor function at 48 hours, 1 week, and 2 weeks. These results suggest that inhibitors of cytokine pathways may be therapeutically useful for the treatment of brain trauma.

Animals↗
PubMed2000

Pain reduction in untreated irreversible pulpitis using an intraosseous injection of Depo-Medrol.

The purpose of this prospective, double-blind, randomized study was to evaluate pain reduction using an intraosseous injection of slow-releasing methylprednisolone in teeth with irreversible pulpitis. Forty subjects presenting for emergency treatment completed the study. Each subject had a tooth with a clinical diagnosis of irreversible pulpitis with actively associated moderate to severe pain. After local anesthesia was attained, the subjects were randomly assigned to receive an intraosseous injection of either 1.0 ml of Depo-Medrol (40 mg) or 1.0 ml of sterile saline (control). No endodontic therapy was begun at the initial appointment. The subjects received ibuprofen and Tylenol #3 and completed a 7-day questionnaire on pain, percussion pain, and analgesic medications taken each day. Over the 7-day observation period, the subjects who received the intraosseous injection of Depo-Medrol reported significantly (p < 0.05) less pain and percussion pain while taking significantly (p < 0.05) fewer pain medications. Clinically the intraosseous injection of Depo-Medrol could be used to temporarily alleviate the symptoms of irreversible pulpitis until definitive treatment can be rendered.

Acetaminophen↗