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PubMed1997

Neuronal cell loss in the CA3 subfield of the hippocampus following cortical contusion utilizing the optical disector method for cell counting.

Unilateral cortical contusion in the rat results in cell loss in both the cortex and hippocampus. Pharmacological intervention with growth factors or excitatory neurotransmitter antagonists may reduce cell loss and improve neurological outcome. The window of opportunity for such intervention remains unclear because a detailed temporal analysis of neuronal loss has not been performed in the rodent cortical contusion model. To elucidate the time course of hippocampal CA3 neuronal death ensuing cortical contusion, we employed the optical disector method for assessing the total number of CA3 neurons at 1 and 6 hours, 1, 2, 10, and 30 days following injury. This stereological technique allows reporting of total cell numbers within a given region and is unaffected by change in the volume of the structure or cell size. A rapid and significant reduction in neurons/mm3 in the ipsilateral CA3 field was observed by 1 h following trauma. However, a significant increase in neurons/mm3 was seen at 30 days postinjury. This surprising finding is a result of CA3 volume shrinkage and redistribution of CA3 neurons. Utilization of the optical disector reveals that regardless of an increase in neurons/mm3 at 30 days following injury, CA3 cell loss reaches 41% of control animals by 1 day posttrauma and remains near that level at all subsequent time points examined. It is estimated that there are about 156,000 neurons in the CA3 region in control animals. By 1 h following cortical contusion the cell population decreases to 93,000 neurons indicating a very rapid cell loss. This suggests a window of less than 24 h for pharmacological intervention in order to save CA3 neurons following cortical contusion.

Animals↗
PubMed1997

GFAP and S100beta expression in the cortex and hippocampus in response to mild cortical contusion.

We studied the acute response of glial fibrillary acidic protein (GFAP) and S100beta gene expression in the cerebral cortex and hippocampus to mild unilateral cortical contusion. Our goal was to evaluate and compare the expression patterns of each gene in the early stages of the astrocytic response to brain injury. RNA was extracted from the cerebral cortex and hippocampus of male rats at 0, 3, 12, 24, or 96 h after lesion or sham-operation, then quantified using an RNase protection assay. Contusion produced a robust elevation in GFAP mRNA by 12 h in both brain regions on the ipsilateral side to the contusion. In the cortex, but not the hippocampus, this elevation was sustained at 96 h. S100beta mRNA levels were elevated bilaterally in lesioned animals at 24 h in both brain regions. However, these data are difficult to interpret because sham mRNA levels decreased with time, making it unclear whether contusion stimulates S100beta gene expression or whether it mitigates the inhibitory effect of sham. We further analyzed the effect of contusion on GFAP and S100beta immunoreactive astrocyte density at 96 h postlesion or postsham by double-label immunocytochemistry. All detectable astrocytes under all conditions were S100beta immunoreactive in both brain regions. Furthermore, all S100beta immunoreactive astrocytes in the lesioned ipsilateral cortex were also GFAP immunoreactive, whereas only about 11% of S100beta positive cells were also GFAP labeled in the contralateral lesioned or the ipsilateral sham cortex. In the hippocampus, all S100beta immunoreactive cells were also GFAP immunoreactive under all conditions. These data correlate with the gene expression data at 96 h, and suggest that, at least in the cortex, resident S100beta-expressing astrocytes produce GFAP at levels that are undetectable by immunocytochemistry until they are activated in response to injury.

Animals↗
PubMed2000

Riluzole reduces brain swelling and contusion volume in rats following controlled cortical impact injury.

Modulation of the glutamatergic and excitotoxic pathway may attenuate secondary damage following traumatic brain injury by reducing presynaptic glutamate release and blocking sodium channels in their inactivated state. The aim of the present study was to investigate the neuroprotective potential of riluzole in traumatic brain-injured rats. A left temporoparietal contusion was induced in 70 male Sprague-Dawley rats (controlled cortical impact injury). Riluzole (8 mg/kg body weight) was given 30 min, and 6, 24, and 30 h after trauma, while control rats received physiological saline. Experiments were performed at two different degrees of trauma severity as defined by penetration depth of the impactor rod (1 vs. 1.5 mm) with the aim of investigating impact of severity of tissue damage on the neuroprotective potential of riluzole. At 48 h after trauma, brains were removed to determine hemispheric swelling and water content and to assess cortical contusion volume. Before brain removal cisternal cerebrospinal fluid (CSF) was collected in all rats to determine the effects of riluzole on substances associated with edema formation. For this, the excitatory transmitter glutamate, the volume-regulatory amino acid taurine, and the ATP-degradation product hypoxanthine were analyzed by high-performance liquid chromatography. Overall, the degree of tissue damage seems to influence the neuroprotective potential of riluzole. In rats with a less severe trauma (1-mm penetration depth), hemispheric swelling, cerebral water content of the traumatized hemisphere and cortical contusion volume were significantly reduced under riluzole compared to controls (p < 0.05). In rats with a more severe trauma (1.5-mm penetration depth), the neuroprotective effect of riluzole failed to reach statistical significance. Following trauma, CSF glutamate, taurine, and hypoxanthine levels were significantly increased compared to nontraumatized rats (p < 0.001). However, these neurochemical parameters as measured in cisternal CSF failed to reflect trauma-dependent increases in severity of tissue damage and did not reveal riluzole-mediated neuroprotection. Under the present study design, riluzole significantly reduced brain edema formation and contusion volume in rats subjected to a mild focal cortical contusion.

Animals↗
PubMed2005

An adult rat spinal cord contusion model of sensory axon degeneration: the estrus cycle or a preconditioning lesion do not affect outcome.

A therapeutic strategy for acute spinal cord injury would be to reduce the progressive degeneration and disconnection of axons from their targets. Here, we describe a model to evaluate degeneration of the ascending sensory projections to the nuclei in the medulla following graded spinal cord contusions in adult female Sprague-Dawley rats. Cholera toxin B (CTB) labeling from the sciatic nerve of naive rats revealed effective labeling of the terminal fibers in the gracile nucleus at 3 days post-injection and a subpopulation of rapidly transporting fibers after 1 day. Seven days after contusions using the Infinite Horizon impactor the area of CTB-labeled terminal fibers had a negative correlation with increasing impact force. Moderate spinal contusions of around 150 kilodyne (kdyn or 0.15 x 10(-3) newton) caused a reduction to 40% in the fiber area which will enable the identification of protective as well as detrimental drugs and post-injury mechanisms. A preconditioning injury of the sciatic nerve reportedly can enhance growth of sensory axons but did not affect the terminal fiber area in the gracile nucleus. Estrogen and progesterone are protective in various systems and could therefore influence experimental outcomes when using females. However, the phase of the estrus cycle at the time of contusion or during the post-injury time did not affect the outcome of the contusion, indicating that female rats may be used without consideration of the estrus cycle. This model can readily be used to evaluate pharmacological agents for protection of sensory axons and pathophysiological mechanisms of their degeneration.

Afferent Pathways↗
PubMed2005

Functional consequences of lumbar spinal cord contusion injuries in the adult rat.

Our understanding of the substrates of locomotion, and hence our understanding of the causes of deficits following spinal cord injury, is still incomplete. While severe locomotor deficits can be induced by either contusion or laceration injuries or demyelination of thoracic spinal cord ventral and ventrolateral white matter, loss of mid-thoracic gray matter (intraspinal kainic acid injection) has no impact on locomotion. In contrast, loss of gray matter from the rostral lumbar segments induces severe locomotor deficits. This study examines the histological and locomotor outcomes following contusion injuries involving the rostral segments of the lumbar enlargement in the adult rat. Adult Sprague-Dawley rats received contusion injuries centered on the T13/L1, L2, or L3/4 spinal cord segments. Moderately severe injuries centered on the T13/L1 and L2 spinal cord segments induced more severe locomotor deficits than those centered on the L3/4 segments, despite a significantly smaller total gray matter volume loss (1.7 vs. 2.7 mm3). Moderately-severe injuries at T13/L1, L2, and L3/4 showed 21%, 31%, and 39% white matter sparing, respectively, with 6-week BBB scores of 10, 10, and 15.7, respectively. These data suggest that moderately-severe contusion injuries centered on the rostral segments of the lumbar enlargement induce more severe locomotor deficits than would be predicted by the histological outcome (spared white matter), suggesting that gray matter loss may play a role in functional deficits following some lumbar contusion injuries.

Animals↗
PubMed2005

Motoneuron loss associated with chronic locomotion impairments after spinal cord contusion in the rat.

Information on the nature of deficits and adaptive mechanisms occurring after spinal cord injury is essential to the design of strategies for promoting functional recovery. Motor impairments and compensations were quantified by three-dimensional kinematic analysis in freely walking rats, 6 months after mild cervical (C7) or moderate lumbar (L2) spinal cord contusion. After C7 contusion, the animals showed reduced elbow extension and wrist movement, whereas reduced knee extension was the main impairment after L2 contusion. In both cases, the duration of the walking cycle increased and forward velocity was reduced due to a longer stance phase. Histology revealed reproducible lesions extending approximately to one spinal cord segment. In the transverse plane, the lesion involved the central gray matter and adjacent axons, including the dorsal corticospinal tract, but partially spared the ventrolateral tracts. Retrograde motoneuron tracing by nerve exposure to HRP or intramuscular injection of aminostilbamidine demonstrated that C7 contusion caused the loss of approximately 40% of triceps brachii motoneurons, whereas approximately 30% of quadriceps femoris motoneurons were lost after L2 contusion. These results demonstrate permanent deficits after incomplete lesions at the spinal cord enlargements and suggest that motoneuron loss contributes to their production.

Animals↗
PubMed1996

Effect of lung contusion on surfactant composition in multiple-trauma patients.

OBJECTIVE: The aim of this study was to investigate alterations of the surfactant system in multiple-trauma patients (MTP) with lung contusion and the influence of single- or multiple-organ dysfunction syndrome (OF/MOF) on the surfactant system. SETTING: University hospital, trauma-intensive care unit. DESIGN: Prospective, nonrandomized study. METHODS: MTP with an Injury Severity Score > 19 points have been recorded prospectively since 1992. Bronchoalveolar lavages were obtained daily either until day 14 or extubation. Three groups of MTP were compared: noL: MTP, no lung contusion (n = 14); LuCo-: MTP, lung contusion, no OF/MOF (n = 17); LuCo+: MTP, lung contusion, with OF/MOF (n = 10). Also, surfactant samples of 11 healthy volunteers (Con) were investigated and compared with MTP. All data were presented as mean +/- SEM. Statistical analysis were performed using programs of SPSS 6.0.1. (univariate ANOVA, Fisher's Exact Test, p < = 0.05). RESULTS: There were no differences in sex and age. Injury Severity Score was significantly impaired in group LuCo+ (44 +/- 4), compared with groups noL (31 +/- 3) and LuCo- (34 +/- 3). Group noL showed no statistical differences for lung function, total protein, and total phospholipid content of the bronchoalveolar lavage compared with group LuCo-. Furthermore, the relative content of phosphatidylcholine and phosphatidylglycerol in total phospholipids and surfactant-associated protein A were not significantly altered compared with group LuCo-. Lung function in group LuCo+ was significantly impaired and led to hypoxemia on the day of trauma. Total protein content and total phospholipids were significantly elevated in group LuCo+ compared with groups noL and LuCo- on the first day. Also, the relative content of phosphatidylcholine was significantly increased in group LuCo+ up to day 4, compared with groups noL and LuCo-. In comparison with groups noL and LuCo-, a significant decrease of the relative content of phosphatidylglycerol was obtained in group LuCo+ up to day 7. The surfactant-associated protein A was increased in group LuCo+ during the whole observation time, compared with the other groups. CONCLUSIONS: Multiple trauma leads to alterations in the surfactant system. The composition of surfactant was not further influenced by lung contusion alone. Only MTP with OF/MOF during the intensive care unit treatment showed significant alterations in surfactant composition and a decrease in lung function.

Adolescent↗
PubMed1990

Positron emission tomographic studies on cerebral hemodynamics in patients with cerebral contusion.

Positron emission tomography is currently one of the most useful methods for measurements of cerebral hemodynamics and oxygen metabolism, because it facilitates accurate analysis of the local cerebral circulation in three-dimensional quantitative images. In this study, we performed positron emission tomography studies to measure cerebral circulation in a total of 11 patients who sustained head injuries with contusion. Several parameters were measured including regional cerebral blood flow, regional cerebral blood volume, permeability, and regional cerebral metabolic rate for oxygen. Data from brains both with and without contusion were analyzed for chronological changes, in the subacute stage from the 8th to 29th day and in the chronic stage until 360 days after the injury and compared with similar data in a group of normal subjects. It was concluded that in the subacute stage, regional cerebral blood flow decreased (26 +/- 7 and 39 +/- 10 ml/100 g/min) and regional cerebral blood volume increased (5.6 +/- 1.8 and 5.4 +/- 0.9 ml/100 g) both in areas of cerebral contusion and in areas remote from cerebral contusion and that permeability increased in areas of contusion but not in remote brain areas. In the chronic stage, these parameters showed a tendency for recovery.

Adolescent↗
PubMed1989

Delayed deterioration in patients with traumatic frontal contusions.

The clinical course of 18 head injured patients in whom CT had shown frontal contusions without diffuse brain injury or intracranial haematoma was reviewed. All 10 patients with unilateral frontal contusion made a good recovery. Only two of five patients with limited bilateral frontal contusions made a good recovery. Two of three patients with extensive bilateral frontal contusions deteriorated more than 24 hours after injury, and one died. Delayed deterioration is an important complication of extensive traumatic bifrontal contusions.

Adolescent↗
PubMed2000

Effects of the novel NMDA receptor antagonist gacyclidine on recovery from medial frontal cortex contusion injury in rats.

Gacyclidine, a novel, noncompetitive NMDA receptor antagonist, was injected (i.v.) into rats at three different doses to determine if the drug could promote behavioral recovery and reduce the behavioral and anatomical impairments that occur after bilateral contusions of the medial frontal cortex (MFC). In the Morris water maze, contused rats treated with gacyclidine at a dosage of 0.1 mg/kg performed better than their vehicle-treated conspecifics. Rats given gacyclidine at either 0.3 or 0.03 mg/kg performed better than brain-injured controls, but not as well as those treated with 0.1 mg/kg. Counts of surviving neurons in the nucleus basalis magnocellularis (NBM) and the medial dorsal nucleus (MDN) of the thalamus were used to determine whether gacyclidine treatment attenuated secondary cell death. In both the NBM and the MDN, the counts revealed fewer surviving neurons in untreated contused rats than in gacyclidine-treated rats. Increases in the size and number of microglia and astrocytes were observed in the striatum of gacyclidine-treated contused brains. Although most consequences of MFC contusions were attenuated, we still observed increases in ventricle dilation and thinning of the cortex. In fact, the ventricles of rats treated with 0.1 mg/kg of gacyclidine were larger than those of their vehicle treated counterparts, although we observed no behavioral impairment.

Animals↗
PubMedDate not supplied

The effect of seizures on recovery of function following cortical contusion in the rat.

The effect of seizures on recovery of motor function was studied in rats following unilateral contusion of the sensorimotor cortex. Animals receiving two electroconvulsive seizures (ECSs) within the first 24 hours postcontusion showed accelerated recovery of beam-walking ability, reduced volume of necrosis and less spontaneous activity compared to animals receiving only contusions. Animals receiving seven ECSs after contusion had an even smaller volume of necrosis and also reduced spontaneous activity compared to the two ECS group and to controls receiving contusions alone. However, for recovery of beam-walking ability, the seven ECS group did not differ from control rats receiving only contusions. The results are discussed in terms of the effects of seizures on catcholamines, gamma-amino butyric acid, cerebral blood flow and possible effects on remote functional depression after brain injury.

Animals↗
PubMed2000

Passive or active immunization with myelin basic protein promotes recovery from spinal cord contusion.

Partial injury to the spinal cord can propagate itself, sometimes leading to paralysis attributable to degeneration of initially undamaged neurons. We demonstrated recently that autoimmune T cells directed against the CNS antigen myelin basic protein (MBP) reduce degeneration after optic nerve crush injury in rats. Here we show that not only transfer of T cells but also active immunization with MBP promotes recovery from spinal cord injury. Anesthetized adult Lewis rats subjected to spinal cord contusion at T7 or T9, using the New York University impactor, were injected systemically with anti-MBP T cells at the time of contusion or 1 week later. Another group of rats was immunized, 1 week before contusion, with MBP emulsified in incomplete Freund's adjuvant (IFA). Functional recovery was assessed in a randomized, double-blinded manner, using the open-field behavioral test of Basso, Beattie, and Bresnahan. The functional outcome of contusion at T7 differed from that at T9 (2.9+/-0.4, n = 25, compared with 8.3+/-0.4, n = 12; p<0.003). In both cases, a single T cell treatment resulted in significantly better recovery than that observed in control rats treated with T cells directed against the nonself antigen ovalbumin. Delayed treatment with T cells (1 week after contusion) resulted in significantly better recovery (7.0+/-1; n = 6) than that observed in control rats treated with PBS (2.0+/-0.8; n = 6; p<0.01; nonparametric ANOVA). Rats immunized with MBP obtained a recovery score of 6.1+/-0.8 (n = 6) compared with a score of 3.0+/-0.8 (n = 5; p<0.05) in control rats injected with PBS in IFA. Morphometric analysis, immunohistochemical staining, and diffusion anisotropy magnetic resonance imaging showed that the behavioral outcome was correlated with tissue preservation. The results suggest that T cell-mediated immune activity, achieved by either adoptive transfer or active immunization, enhances recovery from spinal cord injury by conferring effective neuroprotection. The autoimmune T cells, once reactivated at the lesion site through recognition of their specific antigen, are a potential source of various protective factors whose production is locally regulated.

Animals↗
PubMed2001

Cardiac contusion in blunt chest trauma: a combined study of transesophageal echocardiography and cardiac troponin I determination.

BACKGROUND: The role of cardiac troponin I (cTnI) is well established in acute myocardial ischemia. However, its role in myocardial contusion remains to be clarified. Since transesophageal echocardiography (TEE) appears, at present, to be the best method for the diagnosis of myocardial contusion, the aim of this study was to measure the concentration of cTnI in patients with blunt chest trauma studied using TEE. METHODS: Thirty-two patients (27 males, 5 females, mean age 44+/-20 years), admitted to the Trauma Center of our Institution with clinical and/or radiological signs of acute blunt chest trauma, underwent biplane TEE within 24 hours of injury; serial blood samples were taken to measure cTnI levels (normal values < 0.4 ng/ml), using fluorimetric enzyme immunoassay. RESULTS: Abnormal levels of cTnI were found in 17 patients (53%): 7 patients had levels of cTnI between 0.4 and 1 ng/ml, whereas 10 patients had levels > 1 ng/ml. Segmental wall motion abnormalities consistent with myocardial contusion could be identified by echocardiography in 6/10 patients with cTnI levels > 1 ng/ml (60%) but in no patients with normal cTnI levels or with titers between 0.4 and 1 ng/ml; mean cTnI levels showed a significant difference between the two groups of patients with and without echocardiographic signs of myocardial contusion (2.6+/-1.6 vs 0.6+/-1.4 ng/ml, p < 0.001). CONCLUSIONS: Abnormal titers of cTnI suggesting myocardial contusion may be found in more than half of patients with blunt chest trauma; however, myocardial injury can be detected by TEE only for cTnI levels > 1 ng/ml; cTnI concentrations ranging between 0.4 and 1 ng/ml might be indicative of myocardial microlesions, not detectable by echocardiography, even if TEE is used; cTnI assay could therefore be suggested as a screening test before performing TEE after blunt chest trauma.

Adult↗
PubMed1976

The edema of cerebral contusion.

A model is described for study of the cerebral edema associated with the contusion of closed head injury. A Remington Humane Stunner was used to deliver blows to the skulls of anesthetized cats. Forty-eight hours after impact, those cats demonstrating a one-sided contusion were tested for cerebral edema by measurement of the decrease in density (specific gravity) of white matter from normal values. Significant change in tissue density was seen in the white matter of contused hemispheres. Hemispheres with contusion limited to the cortex (gray matter) showed a change in tissue density which was considerably less than that seen in hemispheres with contusion involving both gray and white matter.

Animals↗
PubMed2002

[Cell apoptosis in closed cerebellar contusion in rat].

OBJECTIVE: To observe the cell apoptosis explore closed cerebellar contusion in rat. METHODS: SD rats model of contusion was established and apototic cells were detected by TUNEL method at 5, 10, 30, 45, 60 min and 2, 4, 6, 8, 12 h, after injury. RESULTS: Apototic cells in contusion area appeared at 1 h after closed cerebellar contusion, reached the peak at 4-6 h, then decreased and so as marginal area where the peak was in 6-8 h. CONCLUSION: The apoptotic index of closed contusion of cerebellum in different injury time may provide a new sensitive and objective method for the forensic early injury time estimation.

Animals↗
PubMed2004

[A primary study on the gene expression profiling of human brain contusion by cDNA microarray].

OBJECTIVE: To screen the differential expression of oncogenes and tumors suppressed genes(OTS genes) after human brain contusion by cDNA microrarray. METHODS: The total RNAs isolated from normal and contusion human brain tissues were purified by Oligotex to obtain mRNAs. Both sources of mRNAs were reversely transcribed to cDNAs with the incorporation of fluorescent dUTP to prepare the hybridization probes. The probe from normal tissue and the contusion brain tissue were labeled with Cy3-dUTP and Cy5-dUTP respectively. The mixed probes were hybridized to the BioDoor Chip OTS-2.2S, a cDNA microarray which contains 227 oncogenes and tumors suppressed genes. After high-stringent washing, the cDNA microarray was scanned for the fluorescent signals and showed differences between two tissues. RESULTS: Among the 227 target genes, 3 genes including Human carcinoma associated HOJ-1 (HoJ-1), Human KIAAOO65 gene,Human retinoblastoma related protein (p107) gene, showed distinct deference in expression level between the human brain contusion tissue and normal tissue. CONCLUSION: The 3 genes in the brain contusion was significantly the differential expression by OTS 2.2S cDNA microarray. Further analysis of these genes will be helpful to understand the molecular mechanism of brain injury and utilization in forensic medicine.

Brain Injuries↗
PubMedDate not supplied

[Surgical treatment of contusion foci in different age groups].

The specific features of surgical treatment of contusion foci in patients of various age groups were studied basing on analysis of 606 cases. Two groups of cases were analysed: those with an isolated brain contusion and cases with contusion and compression of the brain by hematoma and bone fragments. It is shown that removal of the contusion foci in patients of various age groups improves the results of treatment. The patient's age has an essential influence on the choice of surgical tactics in brain contusion.

Adolescent↗
PubMed1981

[Clinico-anatomic variants of the course of cerebral hemisphere contusions].

An analysis of 237 cases of brain hemisphere contusions verified at operation or on autopsy has made if possible to distinguish between three variants of the traumatic disease which corresponded to the three pathoanatomical forms of the contusion. Convexital contusions (pathoanatomically-chiefly cortical or cortico-subcortical) ran the most favourable course and were characterized by distinct focal symptoms prevailing over slight, in most cases, general cerebral disturbances. Polarobasal contusions (anatomically - extensive or massive, i.e. penetrating down to subcortical ganglia or the lateral ventricles) ran a grave course and were characterized by progressing focal hemispheric symptoms in the presence of undulating development of general cerebral disturbances. Diffuse contusions of the brain hemispheres (anatomically small foci of destruction and hemorrhages in the cortex and the paraventricular divisions of the white matter) were characterized by prevalence of marked general cerebral disturbances over slight scattered focal symptoms.

Adult↗