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PubMed2001

Uncoupling of cerebral blood flow and metabolism after cerebral contusion in the rat.

Positron emission tomography scans of patients with head injuries often show discrete areas of increased 18F-fluorodeoxyglucose uptake ("hot spots") when performed hours to days after the initial ictus. Using quantitative autoradiographic methods, the authors have investigated whether cerebral blood flow and glucose metabolism are uncoupled 2 hours after controlled head injury in an animal model, and whether any "hot spots" are accompanied by changes in cerebral glucose concentration. Experiments were performed on 18 anesthetized, ventilated (1.5% halothane in 2:1 nitrous oxide:oxygen) Sprague-Dawley rats weighing 300 to 330 g. A burr hole was made over the left parietal cortex, and all animals received a piston impact on the intact dura (2 mm in diameter, 2.0 m/sec, 2 mm in depth). All animals remained anesthetized and ventilated for a further 2 hours, after which quantitative autoradiography was used to determine either (1) local cerebral blood flow (LCBF) using 14C-iodoantipyrine, (2) local cerebral glucose utilization (LCGU) using 14C-deoxyglucose, or (3) local cerebral glucose content (LCGC) using 14C-methylglucose. Local CBF, LCGU, and LCGC were measured in five regions adjacent to the contusion, and values then were normalized on the contralateral cortex. Normalized LCBF, LCGU, or LCGC varied in parallel in ipsilateral cortex (no change) and in the ischemic core of the contusion (reduced). However, there were marked changes in the patterns observed in the boundary zone (within 1 mm of the contusion). In all six rats used for LCGU measurement, there were discrete areas of high metabolism, whereas in all six rats used for LCBF measurement, flow was universally depressed in the boundary zone. Of the six rats used for LCGC determination, there was a discrete area of high signal in only one. The authors conclude that there are discrete areas of uncoupling of cerebral blood flow and metabolism after head injury within 2 hours of cerebral contusion in the rat that cannot be explained by changes in cerebral glucose content in the majority of animals.

Animals↗
PubMed1999

Experimental investigation of cerebral contusion: histopathological and immunohistochemical evaluation of dynamic cortical deformation.

We used a new approach, termed dynamic cortical deformation (DCD), to study the neuronal, vascular, and glial responses that occur in focal cerebral contusions. DCD produces experimental contusion by rapidly deforming the cerebral cortex with a transient, nonablative vacuum pulse of short duration (25 milliseconds) to mimic the circumstances of traumatic injury. A neuropathological evaluation was performed on brain tissue from adult rats sacrificed 3 days following induction of either moderate (4 psi, n = 6) or high (8 psi, n = 6) severity DCD. In all animals, DCD produced focal hemorrhagic lesions at the vacuum site without overt damage to other regions. Examination of histological sections showed localized gross tissue and neuronal loss in the cortex at the injury site, with the volume of cell loss dependent upon the mechanical loading (p < 0.001). Axonal pathology shown with neurofilament immunostaining (SMI-31 and SMI-32) was observed in the subcortical white matter inferior to the injury site and in the ipsilateral internal capsule. No axonal injury was observed in the contralateral hemisphere or in any remote regions. Glial fibrillary acidic protein (GFAP) immunostaining revealed widespread reactive astrocytosis surrounding the necrotic region in the ipsilateral cortex. This analysis confirms that rapid mechanical deformation of the cortex induces focal contusions in the absence of primary damage to remote areas 3 days following injury. Although it is suggested that massive release of neurotoxic substances from a contusion may cause damage throughout the brain, these data emphasize the importance of combined injury mechanisms, e.g. mechanical distortion and excitatory amino acid mediated damage, that underlie the complex pathology patterns observed in traumatic brain injury.

Animals↗
PubMed1998

Intracerebral inflammation after human brain contusion.

OBJECTIVE: This study was undertaken to analyze the inflammatory components in contused human brain tissue to compare the findings with previous experimental data regarding the pathogenesis of brain contusions. METHODS: Contused brain tissue biopsies were obtained from 12 consecutive patients undergoing surgery for brain contusions 3 hours to 5 days after trauma. Inflammatory and immunological components were analyzed by immunohistochemistry. RESULTS: In patients undergoing surgery less than 24 hours after trauma, the inflammatory response was limited to vascular margination of polymorphonuclear cells. In patients undergoing surgery 3 to 5 days after trauma, however, a massive inflammatory response consisting of monocytes/macrophages, reactive microglia, polymorphonuclear cells, and CD4- and CD8-positive T lymphocytes was detected. Human lymphocyte antigen-DQ was expressed on reactive microglia and infiltrating leukocytes in the late patient group. In addition, CD1a, which is a marker for antigen-presenting dendritic cells, was detected in a subgroup of microglial cells. CONCLUSION: The results corroborated hypotheses derived from experimental data. In the early phase after contusional trauma, inflammation is mainly intravascular and dominated by polymorphonuclear cells. The inflammation was parenchymal in patients undergoing surgery 3 to 5 days after trauma. The brain swelling seemed to be biphasic, the delayed phase correlating with a parenchymal inflammation. The inflammatory cells may produce several potentially harmful effects, such as acute cellular degeneration; they may also lead to degenerative long-term effects.

Adolescent↗
PubMed2006

Regionally distinct patterns of calpain activation and traumatic axonal injury following contusive brain injury in immature rats.

Impact-induced head injury in infants results in acute focal contusions and traumatic axonal injury (TAI) that are associated with chronic holohemispheric cortical and white matter atrophy and may contribute to poor outcome in brain-injured children less than 4 years of age. Contusive brain trauma in postnatal day (PND) 11 or PND 17 rat pups, ages neurologically equivalent to a human infant and toddler, respectively, leads to cortical tissue loss and white matter atrophy which are associated with cognitive deficits. In adult models of brain trauma and in brain-injured humans, acute and sustained activation of the calpain family of calcium-activated neutral proteases has been implicated in neuronal death and TAI. PND 11 or PND 17 rat pups were subjected to closed head injury over the left hemisphere using the controlled cortical impact device and sacrificed at 6 h, 24 h or 3 days. Hemorrhagic contusions and tissue tears in the cortex and white matter were visible at 6 h, and neuronal loss was evident by 3 days. Calpain activation was observed in cell soma and dendrites of injured neurons at 6 h, and in degenerating dendrites and atrophic neurons at 24 h after injury at both ages. Axonal accumulation of amyloid precursor protein, indicative of TAI, was observed in the corpus callosum and lateral aspects of the white matter below the site of impact, and in the thalamus in PND 11 rats only. Intra-axonal calpain activation was observed to a limited extent in the corpus callosum and subcortical white matter tracts in both brain-injured PND 11 and PND 17 rats. Collectively, these results provide evidence that calpain activation may participate in neuronal loss in the injured cortex, but may not contribute to the pathogenesis of TAI following contusive brain trauma in the immature rat.

Aging↗
PubMed1999

[Cerebral contusion in victims of fatal traffic accidents. Frequency and association with other craniocerebral lesions].

A morphological study, macro and microscopical, was made of brain lesions in 120 victims of fatal road traffic accidents. Contusions of the brain were identified in 67 (55.8%) of the patients. The contusions especially affected the orbital surfaces of the frontal lobes (27.8%) and the temporal poles (19.8%). The recent brain contusion was associated with a skull fracture in 70.1% of the cases and with a diffuse axonal injury in 89.5%. These can be explained by the association of contact and inertia from the road traffic accidents. Old contusions were identified in six patients (5.0%).

Accidents, Traffic↗
PubMed1997

Delayed cytokine expression in rat brain following experimental contusion.

Proinflammatory cytokines mediate brain injury in experimental studies. This study was undertaken to analyze the production of proinflammatory cytokines in experimental contusion. A brain contusion causing delayed edema was mimicked experimentally in rats using a weight-drop model. Intracerebral expression of the cytokines interleukin (IL)-1 beta, tumor necrosis factor-alpha (TNF alpha), IL-6, and interferon-gamma (IFN gamma) was studied by in situ hybridization and immunohistochemistry. The animals were killed at 6 hours or 1, 2, 4, 6, 8, or 16 days postinjury. In the injured area, no messenger (m)RNA expression was seen during the first 2 days after the trauma. On Days 4 to 6 posttrauma, however, strong IL-1 beta, TNF alpha, and IL-6 mRNA expression was detected in mononuclear cells surrounding the contusion. Expression of IFN gamma was not detected. Immunohistochemical double labeling confirmed the in situ hybridization results and demonstrated that mononuclear phagocytes and astrocytes produced IL-1 beta and that mainly astrocytes produced TNF alpha. The findings showed, somewhat unexpectedly, a late peak of intracerebral cytokine production in the injured area and in the contralateral corpus callosum, allowing for both local and global effects on the brain. An unexpected difference in the cellular sources of TNF alpha and IL-1 beta was detected. The cytokine pattern differs from that seen in other central nervous system inflammatory diseases and trauma models, suggesting that the intracerebral immune response is not a uniform event. The dominance of late cytokine production indicates that many cytokine effects are late events in an experimental contusion: Different pathogenic mechanisms may thus be operative at different times after brain injury.

Animals↗
PubMed2002

Stilbazulenyl nitrone, a novel azulenyl nitrone antioxidant: improved neurological deficit and reduced contusion size after traumatic brain injury in rats.

OBJECT: Stilbazulenyl nitrone (STAZN) is a second-generation azulenyl nitrone that has markedly enhanced antioxidant properties compared with those of conventional alpha-phenyl nitrones. In this study, the authors assessed the potential efficacy of STAZN in a rodent model of fluid-percussion brain injury, which results in a consistent cortical contusion. METHODS: After anesthesia had been induced in normothermic Sprague-Dawley rats (brain temperature 36-36.5 degrees C) by halothane-nitrous oxide, the animals were subjected to a right parietooccipital parasagittal fluid-percussion injury (1.5-2 atm). The agent (STAZN, 30 mg/kg: eight animals) or vehicle (dimethyl sulfoxide; eight animals) was administered intraperitoneally at 5 minutes and 4 hours after trauma. The neurological status of each rat was evaluated on Days 1, 2, and 7 postinjury (normal score 0, maximum injury 12). Seven days after trauma, the rat brains were perfusion fixed, coronal sections at various levels were digitized, and areas of contusion were measured. Treatment with STAZN significantly improved neurological scores on Days 2 and 7 postinjury compared with vehicle-treated rats. Administration of STAZN also significantly reduced the total contusion area by 63% (1.8 +/- 0.5 mm2 in STAZN-treated animals compared with 4.8 +/- 2.1 mm2 in vehicle-treated animals; p = 0.04) and the deep cortical contusion area by 60% (1.2 +/- 0.2 mm2 in STAZN-treated animals compared with 2.9 +/- 1.2 mm2 in vehicle-treated animals; p = 0.03). By contrast, hippocampal cell loss in the CA3 sector was unaffected by STAZN treatment. CONCLUSIONS: Therapy with STAZN, a novel potent antioxidant, administered following traumatic brain injury, markedly improves neurological and histological outcomes. Azulenyl nitrones appear to represent a promising class of neuroprotective agents for combating this devastating condition.

Animals↗
PubMed2005

Concomitant upregulation of nuclear factor-kB activity, proinflammatory cytokines and ICAM-1 in the injured brain after cortical contusion trauma in a rat model.

BACKGROUND: Nuclear factor kappa B (NF-kB), proinflammatory cytokines and intercellular adhesion molecule 1 (ICAM-1) are frequently upregulated in the injured brain after traumatic brain injury (TBI). However, the temporal pattern of upregulation is not well defined. AIMS: The current study was undertaken to investigate the temporal profile of the expression of NF-kB, proinflammatory cytokines and ICAM-1 in the injured brain after cortical contusion trauma of the rat brain. SETTINGS AND DESIGN: A rat model of cortical contusion was produced by a free-falling weight on the exposed dura of right parietal lobe. The rats were randomly divided into control group and TBI groups at hours 3, 12, 24 and 72, and on day 7. MATERIAL AND METHODS: NF-kB binding activity in the surrounding brain of injured area was studied by electrophoretic mobility shift assay (EMSA). The levels of TNF-alpha and IL-6 were detected using ELISA and ICAM-1 expression studied by immunohistochemistry. STATISTICAL ANALYSIS: The data were analyzed by one-way ANOVA followed by Student-Newman-Keuls post hoc test. Relation between variables was analyzed using bivariate correlation with two-tailed test. RESULTS: Compared with that of control group, NF-kB binding activity in the injured brain was significantly increased through 12 h and 7 days postinjury, with the maximum at 72 h. The concentrations of TNF-alpha and IL-6 in the injured brain were significantly increased from 3 h to 7 days and maximal at 24 h postinjury. The number of ICAM-1 immunostained microvessels was significantly increased in the injured brain from 24 h to 7 days postinjury, with its peak at 72 h. Concomitant upregulation of TNF-alpha, IL-6, ICAM-1 and the cytokine mediators NF-kB in the injured brain was observed in the injured brain after cortical contusion, and there was a highly positive relation among these variables. CONCLUSIONS: Cortical contusion trauma could induce a concomitant and persistent upregulation of NF-kB binding activity, TNF-alpha, IL-6 and ICAM-1 in the injured rat brain which might play a central role in the injury-induced immune response of brain.

Animals↗
PubMedDate not supplied

[Early changes in the bioelectrical activity of retina after eyeball contusion].

Characteristic signs of changes in the bioelectrical activity of the retina soon after contusion of the eyeball supplement the functional criteria used for accurate diagnosis of the severity of contusion (classification of the injury). The most sensitive indicator of electroretinography is the amplitude of the electroretinogram (ERG) a-wave, which is sharply suppressed during the first three days in injury of any severity. Recovery of the bioelectrical activity of photoreceptors is delayed in comparison with the time course of the function of the second-order neurons (more rapid recovery of the b-wave in comparison with the a-wave). The reactivity of Müller cells increases in severe contusion, which is shown by a more pronounced decrease in the ERG b-wave amplitude and less expressed changes in low-frequency ERG. Analysis of the time course of biopotentials during repeated examinations of the patients helps control the efficacy of treatment. The results indicate that electroretinographic examinations are the most desirable 5-7 days after the contusion, because at this period the differences in the bioelectrical activity of the retina are the most expressed. The most informative parameters of electroretinography are the time course of total ERG a- and b-waves and the low-frequency rhythmic ERG.

Action Potentials↗
PubMed2000

Effects of hyperbaric oxygen on focal brain contusions.

The effect of hyperbaric oxygen (HBO) on focal brain contusion was examined for possible prevention of neural degeneration in the central nervous system following blunt trauma. All animals were tested for memory and balance/motor skills, prior to and after injury, using the Morris water maze and beam walk test. Experimental and control groups, each containing 12 juvenile male hooded Wistar rats (Rattus norviegicus), were contused using a 20 g weight dropped from 20 cm onto the dura mater over the somatosensory cortex. The experimental group underwent 45 minute HBO dives at 2.5 atmospheres absolute (ATA) four times a day for 10 days. Memory and motor skills were tested on both groups at 3, 6 and 9 days after injury. Animals were sacrificed and their brains were sectioned and analyzed histologically for neural damage. Examination of the damage to the surface of the brain showed hole sizes in the experimental group were smaller than those in the control group (p = 0.0475). Initial examination of behavioral testing showed mixed results. Beam walk scores 3 days post contusion were significantly better for experimental vs control groups (p = 0.0442) suggesting initial benefits of HBO treatment. However, preliminary analysis of cells in the CA3 region of the hippocampus showed no significant difference between pyramidal cell counts 10 days post-contusion in the ipsilateral sides of either group.

Animals↗
PubMed2001

[A study of the relation between interval of the injury and the reaction of neurons, glial cells after experimental brain contusion].

OBJECTIVE: To observe the change of c-fos protein(Fos) and nerve growth factor receptor (NGFR) staining in the brain of rat after experimental brain contusion. METHODS: Immunohistochemistry of c-fos and NGFR were applied to investigate the brain contusion. RESULTS: (1) The expression of Fos protein could be observed at 0.5 h after injury and then increased with the prolonging of time. By 3 h after injury, the positive staining cells could be detected massively not only in and round the wound site but also in other areas of the whole ipsilateral cortex. The stains decreased 6-12 h later and could hardly be detected 1 d after the brain contusion. The control-experiment is negative. (2) NGFR positive staining cells could be found round the wound area 1 d postlesion. At 3 d following injury, a peak of massive positively stained cells appeared both in number and in intensity, showing significant differences compare with that of 1 d after damage (P < 0.01). 5 d later the positive express declined slowly. The express in the control-rat is negative. CONCLUSION: There is a rule that the expression of Fos and NGFR positive staining changes with time going after brain contusion, which will be of great value in estimation of brain injury time. Detection of Fos can be used for time deduction in earlier period after injury, while NGFR in later period. They are also very important for distinguishing between antemortem or postmortem injury.

Animals↗
PubMed2005

[A study on the expression of HSP70 and iNOS after human brain contusion].

OBJECTIVE: To study the relationship between expression of HSP70, iNOS and traumatic brain contusion (TBI) in different posttraumatic intervals. METHODS: 35 samples of brain contusion were examined using immunohistochemecal staining to evaluate the expression of HSP70 and iNOS. RESULTS: Maximal HSP70 expression was found at 0h after brain contusion. The intensity of HSP70 staining decreased remarkably to the minimum at 24h after TBI, then increased gradually. Expression of iNOS positive cells increased significantly and reached the maximum level 48h after TBI, then the expression decreased gradually from the 2nd day to the 11th day. CONCLUSION: The changes of HSP70 and iNOS immunohistochemical staining can be used as a referential data for estimating time interval after human brain contusion.

Adult↗
PubMed2006

Lung contusion from focal low-moderate chest trauma.

Apparently minor chest trauma may result in localized pulmonary contusion. Complications of the contusion, particularly infection, may be delayed. The association between the infection and initial injury may not be appreciated due to the time frame between the injury and clinical presentation. We report two cases of low-moderate impact pulmonary trauma resulting in focal pulmonary contusion, complicated by infection.

Adolescent↗
PubMed1994

Progesterone facilitates cognitive recovery and reduces secondary neuronal loss caused by cortical contusion injury in male rats.

The ability of progesterone to reduce the cerebral edema associated with traumatic brain damage first became apparent when we observed that males had significantly more edema than females after cortical contusion. In addition, edema was almost absent in pseudopregnant female rats, a condition in which progesterone levels are high relative to estrogen. Progesterone injections given after injury also reduced edema and were equally effective in both males and females. The present experiment was done to determine if the progesterone-induced reduction in edema could also prevent secondary neuronal degeneration and reduce the behavioral impairments that accompany contusion of the medial frontal cortex. Progesterone-treated rats were less impaired on a Morris water maze spatial navigation task than rats treated with the oil vehicle. Progesterone-treated rats also showed less neuronal degeneration 21 days after injury in the medial dorsal thalamic nucleus, a structure that has reciprocal connections with the contused area.

Analysis of Variance↗
PubMed1999

Clenbuterol, a beta(2)-adrenoceptor agonist, improves locomotor and histological outcomes after spinal cord contusion in rats.

An important goal of rehabilitation following spinal cord injury is recovery of locomotor function and muscular strength. In the present studies, we determined whether the beta(2)-agonist, clenbuterol, can improve recovery of locomotor function following spinal cord injury. A model of spinal cord injury was examined in which four graded levels of contusion injury were produced in rats at the level of T10 with a weight-drop device. Locomotor recovery was determined with the Basso, Beattie, and Bresnahan (BBB) scale, which distinguishes between 22 progressive levels of recovery. As observed previously, recovery during the 6 weeks following injury was inversely related to the severity of injury. However, clenbuterol caused substantial enhancement of recovery of locomotor function at the two most severe levels of injury (BBB scores 10-12 vs 2-4). In addition, the extent of recovery was directly related to sparing of spinal cord tissue at the contusion center in both untreated and clenbuterol-treated spinal cords. Optimization of beta(2)-agonist treatment may lead to a useful therapeutic modality for treatment of spinal cord contusion injury.

Adrenergic beta-Agonists↗
PubMed1984

Crystalloid resuscitation of patients with pulmonary contusion.

One hundred nine patients with the diagnosis of pulmonary contusion were studied retrospectively. Thirteen deaths were respiratory related (12 percent of patients). All of the patients were quickly resuscitated with crystalloid solutions as necessary to restore perfusion to normal. Twenty-eight of the most severely injured patients, all of whom were intubated and ventilated and in whom serial PaO2 and total protein determinations were available, were examined for the relationship between crystalloid induced hemodilution as measured by the plasma colloid oncotic pressure and oxygenation as measured by the PaO2/FiO2 ratio. When survivors and nonsurvivors were analyzed by group, both individually and collectively, no correlation was found between oxygenation and oncotic pressure. Survivors and nonsurvivors exhibited similar post-traumatic courses in the PaO2/FiO2 ratios with differences not becoming significant until the eleventh day after injury. We conclude that contusion is not a progressive lesion unless pneumonia supervenes and that pulmonary dysfunction after contusion is unrelated to hemodilution.

Adult↗
PubMed1994

Cardiac contusion and creatine kinase-MB: a pertinent case history and brief review of the utility of CK-MB.

Cardiac contusion is defined as the myocardial cellular damage that can result from nonpenetrating chest trauma. However the noninvasive diagnosis of this lesion is problematic. Among the criteria suggested for the diagnosis of cardiac contusion is an elevation of serum levels of the heart-specific isoform of the enzyme creatine kinase (CK-MB). We present here the case of a patient who, on the basis of an initial elevation of CK-MB, was suspected of having cardiac contusion as a result of a motor vehicle accident. The patient was clinically stable and there were no other signs to support this diagnosis. Serial analyses showed a fall in total CK to below the upper limit of the reference interval but, as a percent of total activity, CK-MB was constantly slightly elevated (values 5.1-6.5%, upper limit of normal = 4%). At the same time the patient appeared to be improving clinically. The patient's status deteriorated suddenly and he eventually went to surgery where a large intramural haematoma and a left ventricular aneurysm were discovered. The significance of the elevations of serum CK-MB is discussed and a brief review of the literature is presented.

Biomarkers↗
PubMed1989

Correlative analyses of lesion development and functional status after graded spinal cord contusive injuries in the rat.

The development of both histopathological changes and functional deficits was quantitatively assessed after mild, moderate, and severe spinal cord contusive injuries. The cross-sectional area of the spinal cord at the epicenter (region of maximal damage) and the areas of hemorrhage, lesion, and remaining gray and white matter were determined from 15 min to 8 weeks after injury. From 24 h to 8 weeks after injury, functional deficits were quantified using a combined behavioral score (CBS) based on the results from a number of behavioral tests of function. Regression analysis was used to examine the correlations between the amount of residual white matter and both the severity of contusive impact and the functional deficit over time after injury. The area of hemorrhage at 15 min and 24 h was greater in the mild and moderate injury groups than after the severe contusive injury. Significant loss of gray and white matter occurred primarily between 24 h and 1 week after injury along with concomitant increases in the area of lesion. In the mild injury group the rate of lesion development appeared slower than that in the moderate and severe injury groups and significant white matter loss continued to occur between 1 and 4 weeks after injury. Behavioral tests of functional deficit were performed at 24 h and weekly thereafter. The development of stable functional deficits was observed beginning at 3 weeks after injury. There was a significant correlation between residual white matter and the degree of initial injury at 24 h after injury and all subsequent time points. However, a significant correlation between residual white matter and functional deficit, as measured by the CBS, was not observed at 24 h or 1 week but did develop by 4 weeks after injury.

Animals↗