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PubMed2005

Chondroitinase ABCI improves locomotion and bladder function following contusion injury of the rat spinal cord.

Chondroitin sulfate proteoglycans are synthesized and deposited in the spinal cord following injury. These proteoglycans may restrict regeneration and plasticity and contribute to the limited recovery seen after an injury. Chondroitinase, a bacterial enzyme that catalyzes the hydrolysis of the chondroitin chains on proteoglycans, has been shown to improve motor and sensory function following partial transection lesions of the spinal cord. To assess the effects of chondroitinase in a clinically relevant model of spinal cord injury, 128 female Long-Evans rats received either a severe, moderate, or mild contusion injury at the vertebral level T9/T10 with a forceps model and were treated for 2 weeks with chondroitinase ABCI at 0.06 Units per dose, penicillinase, or vehicle control via an intrathecal catheter placed near the injury. Motor behavior was measured by open-field testing of locomotion and bladder function monitored by measuring daily residual urine volumes. Animals treated with chondroitinase showed significant improvements in open-field locomotor activity as measured by the Basso, Beattie and Bresnahan scoring system after both severe and moderate SCI (p<0.05 and 0.01, respectively). No significant locomotor differences were observed in the mild injury group. In the moderate injury group, residual urine volumes were reduced with chondroitinase treatment by 2 weeks after injury (p<0.05) and in the severe injury group, by 6 weeks after injury (NS). These results demonstrate that chondroitinase is effective at promoting both somatic and autonomic motor recovery following a clinically relevant contusion spinal cord injury and is a candidate as a therapeutic for human spinal cord injury.

Animals↗
PubMed2005

VEGF and VEGF receptor expression after experimental brain contusion in rat.

Angiogenesis following traumatic brain injury (TBI) may be of importance not only for post-traumatic reparative processes but also for the development of secondary injuries. Vascular endothelial growth factor (VEGF) is a major regulator of endothelial cell proliferation, angiogenesis, and vascular permeability, though its possible involvement in secondary injuries after TBI is largely unknown. This study was undertaken to analyze the expression of VEGF and the VEGF receptors in experimental brain contusion in rat. Twenty-three adult female Sprague-Dawley rats were subjected to a focal cerebral contusion injury by use of a weight-drop model. Four additional rats underwent craniotomy only. The animals were sacrificed 6 h, or 1, 2, 4, 6, 8, or 16 days post-injury. Expression of VEGF and the VEGF receptors VEGFR1 (Flt-1) and VEGFR2 (Flk-1) were studied by in situ hybridization and immunohistochemistry. VEGF messenger (m)RNA and protein expression were detected in astrocytes, neutrophils, and macrophages in or adjacent to the injury from 1 day after injury, with a peak expression after 4-6 days. Flt-1 and Flk-1 mRNA and protein were detected in vessels adjacent to the lesion from 1 day after injury throughout day 6 after injury. It was also noted that Flt-1/Flk-1 and VEGF-positive vessels often were negative for SMI-71, a marker for vessels in areas with blood-brain barrier (BBB). In conclusion, we have demonstrated that TBI leads to an upregulation of VEGF, Flt-1, and Flk-1 mRNA and protein in and around the lesion. The data provide a foundation for future pharmacological intervention studies focusing on posttraumatic angiogenesis and possible injury repair effects of the VEGF system in TBI.

Animals↗
PubMed2006

Locomotor deficits and adaptive mechanisms after thoracic spinal cord contusion in the adult rat.

The rat is widely used for modeling human spinal cord injury (SCI) and paraplegia. However, quadruped animals adapt trunk, forelimb and hindlimb movements to compensate for deficits, improving their behavioral scores and complicating the interpretation of spontaneous and treatment-induced function recovery. The kinematics of locomotion was studied in rats, both normal and after SCI (T9 contusion), and variables indicative of hindlimb function were related to brain-spinal cord connections (BSCC) spared during lesioning. Normal animals showed forward velocities characteristic of fast walking. The hind paw was placed approximately three centimeters in front of the hip at the initial contact. Hip height decreased during the first third of hindlimb stance and increased later. Mild and moderate spinal cord contusions destroyed the gray matter and adjacent axons but spared the ventrolateral tracts to various degrees. Injured animals placed the hindpaw in a more caudal position than normal and showed reduced forward velocity and hip height. Knee extension was also impaired, and both hindlimb and forelimb steps were adapted to compensate for the deficits. BSCC was estimated by averaging the transverse area of white matter at the lesion epicenter and the percentage of brain neurons labeled after peroxidase injection into L2 and L3. Recovery of hindlimb motor function was proportional to the amount of BSCC. On average, injured animals retained 18% of BSSC and recovered 23% of hindlimb function. These findings show that kinematic analysis is a reliable tool for assessing locomotor deficits and compensations and suggest limited spontaneous motor plasticity after SCI.

Adaptation, Physiological↗
PubMed2006

Neuroprotection by selective inhibition of inducible nitric oxide synthase after experimental brain contusion.

The inflammatory response is thought to be important for secondary damage following traumatic brain injury (TBI). The inducible nitric oxide synthase (iNOS) isoform is a mediator in inflammatory reactions and may catalyze substantial synthesis of NO in the injured brain. This study was undertaken to analyze neuronal degeneration and survival, cellular apoptosis and formation of nitrotyrosine following treatment with the iNOS-inhibitor L-N-iminoethyl-lysine (L-NIL) in a model of brain contusion. A brain contusion was produced using a weight-drop device in 30 rats. The animals received treatment with L-NIL or NaCl at 15 min and 12 h after the injury and were sacrificed at 24 h or 6 days after trauma. iNOS activity was measured at 24 h post-trauma by the conversion of L-[U- ( 14 )C]arginine to L-[U-( 14 )C]citrulline and immunohistochemistry for iNOS. Peroxynitrite formation was indirectly assessed by nitrotyrosine (NT) immunohistochemistry. Neuronal degeneration and survival were assessed by Fluoro-Jade (FJ) and NeuN stainings, and cellular death by TUNEL staining. iNOS activity but not iNOS immunoreactivity was significantly reduced in animals that received L-NIL. Neuronal degeneration (FJ) and NT immunoreactivity were significantly reduced at 24 h. Neuronal survival was unchanged at 24 h but increased at 6 days in L-NIL-treated animals. Cellular apoptosis of ED-1 and NeuN positive cells was significantly reduced following L-NIL treatment at 6 days after trauma. We demonstrated neuroprotection by selective inhibition of iNOS after trauma. L-NIL appeared to protect the injured brain by limiting peroxynitrite formation. Our findings support a putative harmful role of iNOS induction early after TBI.

Animals↗
PubMed2006

Changes in soleus muscle function and fiber morphology with one week of locomotor training in spinal cord contusion injured rats.

The purpose of this study is two-fold: (1) to examine skeletal muscle function in a rat model of midthoracic contusion spinal cord injury (SCI) and (2) to evaluate the therapeutic influence of a short bout (1 week) of treadmill locomotor training on soleus muscle function (peak force, fatigability, contractile properties, fiber types), size (fiber area), and motor deficit and recovery (BBB scores) after SCI. The rats were injured with a moderate T8 spinal cord contusion and were assigned to either receive treadmill locomotor training (TM), starting 1 week after SCI for 5 consecutive days (20 min/trial, 2 trials/day) or not to receive any exercise intervention (no TM). Locomotor training resulted in a significant improvement in overall locomotor function (32% improvement in BBB scores) when compared to no TM. Also, the injured animals that trained for 1 week had 38% greater peak soleus tetanic forces (p < 0.05), a 9% decrease in muscle fatigue (p < 0.05), 23% larger muscle fiber CSA (p < 0.05), and decreased immunoexpression of fast heavy chain fiber types than did rats receiving no TM. In addition, there was a good correlation (0.704) between the BBB scores of injured animals and peak soleus muscle force regardless of group assignment. No significant differences were seen in twitch or time to peak tension values across groups. Collectively, these results indicate that 1 week of treadmill locomotor training, initiated early after SCI, can significantly improve motor recovery following SCI. The magnitude of these changes is remarkable considering the relatively short training interval and clearly illustrates the potential that initiating treadmill locomotor training shortly after injury may have on countering some of the functional deficits resulting from SCI.

Animals↗
PubMed2006

Behavioral and histological characterization of unilateral cervical spinal cord contusion injury in rats.

Most experimental studies of spinal cord injury (SCI) in rats damage the thoracic cord, with the consequent functional loss being due to interruption of long tracts connecting the caudal spinal cord to the rostral nervous system. Less work has been done evaluating injury to the cervical cord, even though it is the most common level of human SCI. In addition to the long tracts, the cervical spinal cord contains the sensory and motor neurons responsible for upper extremity function. The purpose of this study was to further develop a rat model of cervical spinal cord contusion injury using a modified NYU/MASCIS weight drop device. Mild (6.25 mm) and moderate (12.5 mm) C5 unilateral injuries were produced. Behavioral recovery was examined using a grooming test, a paw preference test, a walkway test (The Catwalk), and a horizontal ladder test. Histological outcome measures included sparing at the lesion epicenter, sparing throughout the extent of the lesion, quantification of myelin loss rostral and caudal to the lesion, and motor neuron counts. Compared to controls, animals receiving SCI exhibited injury severity-specific deficits in forelimb, locomotor, and hindlimb function persisting for 6-weeks post-SCI. Histological analysis revealed ipsilateral containment of the injury, and differentiation between groups on all measures except motor neuron counts. This model has many advantages: (1) minimal animal care requirements post-SCI, (2) within subject controls, (3) functional loss involves primarily the ipsilateral forelimb, and (4) it is a behavioral and histological model for both gray and white matter damage caused by contusive SCI.

Animals↗
PubMed2002

Lung contusion: pathophysiology and management.

Management of severe pulmonary contusion is a challenge for clinicians. The incidence of adult respiratory distress syndrome (5-20%), pneumonia (5-50%), and mortality (5-10%) associated with traumatic lung injury has changed little in the past three decades. Therapeutic options are limited to basic supportive measures such as mechanical ventilation, positive end expiratory pressure, invasive cardiopulmonary monitoring, analgesics and aggressive pulmonary hygiene. Presently, no pharmacological agents can prevent the progressive respiratory embarrassment that is associated with the natural history of the disease, but several drugs have been tested in the laboratory. The purpose of this brief review is to summarize information published since January 2000 related to the clinical management and pathophysiology of lung contusion.

Journal Article↗
PubMed2004

MHC expression after human neural stem cell transplantation to brain contused rats.

Human neural stem cells survive and improve motor function after transplantation to the contused brain. However, the transplants might be rejected and that depends on the graft immunogenicity, the host immunological status and the immunosuppression strategy. We transplanted human neural stem cells to rats with brain contusion and analyzed the donor and host MHC antigen expression and the effect of a short-term immunosuppression with cyclosporine. In vitro human neural stem cells expressed only MHC-II antigens. This expression was down-regulated 6 weeks after transplantation. The host response was characterized by an increased MHC-II expression which was down-regulated by a longer term of immunosuppression. These findings are novel and necessary in order to understand the immunogenicity of human neural stem cell grafts.

Animals↗
PubMed1982

Delayed deterioration in the syndrome of temporal lobe contusion: evaluation by computed tomography (CT).

The clinical and computed tomographic (CT) features of three consecutive cases of temporal lobe contusion emphasize the presentation and frequent subsequent progressive neurological deterioration. The initial presentation was one of lethargy and combativeness with little or no focal neurological deficits. Thereafter all patients developed progressive neurological deterioration with decreasing levels of consciousness and lateralizing signs. Computed tomography (CT) which aided in making the initial diagnosis was repeated following clinical deterioration. Worsening in the patient's clinical condition correlated positively with changes within the contusion as visualized by CT.

Adult↗
PubMed1988

Myocardial contusion in blunt trauma: clinical characteristics, means of diagnosis, and implications for patient management.

The incidence, diagnosis, and impact on surgical management of myocardial contusion (MC) are incompletely defined. During a 12-month period, all patients admitted to a Level I trauma center with blunt trauma were prospectively evaluated for MC (n = 1,110). Those with anterior chest wall contusions, sternal or anterior rib fractures, or pain/tenderness of the anterior chest (n = 140, 13%) underwent immediate and daily ECG, and CPK isoenzymes were measured at admission and every 6 hours in the first 24 hours. Eighty-nine of these patients underwent gated ventricular angiography (GVA) and 66 underwent two-dimensional echocardiography (2D ECHO). MC was considered present if either: 1) CPK-MB was greater than or equal to 5% of total CPK, or 2) an abnormal admission ECG reverted to normal before patient discharge. Fifty-six patients (5% of admissions, 40% of those with apparent chest trauma) were positive by one or both criteria. Thirty patients (54%) were positive by CPK alone, 23 (41%) by both CPK and ECG, and three (5%) by ECG alone. Of the 53 with elevated CPK-MB, 14 (26%) were normal on admission with the remainder becoming elevated in the first 24 hours. 2D ECHO was abnormal in only three of 21 positive patients (14%), and GVA was abnormal in only three of 40 positive patients (7%). Surgical procedures requiring general anesthesia were performed in 37 (66%) of the positive patients. No significant arrhythmias developed under general anesthesia.

Adult↗
PubMed1991

Pulmonary contusion causes long-term respiratory dysfunction with decreased functional residual capacity.

To elucidate the mechanism of persistent dyspnea after blunt chest trauma, we prospectively studied the pulmonary function of 18 patients with blunt chest trauma for 6 months. Nine of the patients had flail chest and 12 had pulmonary contusion (PC). Pulmonary function was evaluated using spirometry, arterial blood gas analysis, chest x-ray studies and CT scans. Functional residual capacity (FRC) remained significantly reduced throughout the 6 months in patients with PC. Such patients experienced a fall in Pao2 when changed from a sitting position to a supine position and they had fibrous changes in the contused lung as demonstrated by CT scans at 6 months after injury. These findings were supported in an additional study of another 20 patients who had suffered PC 1 to 4 years previously. This study demonstrated that pulmonary function recovered within 6 months in patients without PC even with a residual deformity of the thoracic wall caused by flail chest, while patients with PC had decreased FRC and a fall in Pao2 when moved to the supine position even several years after injury. This might be related to the persistent dyspnea seen after blunt chest trauma.

Adult↗
PubMed2000

Apoptosis occurs after cerebral contusions in humans.

OBJECTIVE: Animal model systems have shown that head trauma can induce cell death in regions of the brain away from the site of the impact via a process of apoptosis. We sought to determine whether there was evidence of cellular apoptosis in clinically collected materials from human head trauma patients, as well as to attempt to determine the pathway by which it may occur. METHODS: Thirty-one sequential specimens of brain tissue excised during emergency craniotomy for evacuation of cerebral contusions with mass effect were examined. Non-necrotic pericontusional tissues were detected in 11 samples. These were examined for the presence of apoptotic cells by the terminal deoxynucleotide transferase-mediated nick end labeling method as well as by immunohistochemistry to detect possible expression of the apoptosis-related genes p53, bcl-2, and bax. RESULTS: Bax expression was detected in all patients, whereas bcl-2 expression was noted in six patients. Terminal deoxynucleotide transferase-mediated nick end labeling-positive cells were noted in eight patients. One instance of p53-positive immunostaining was observed. Patients with bcl-2 expression had a better survival rate than patients in whom no bcl-2 expression was noted (P = 0.01). CONCLUSION: Although necrosis seemed to be the main finding in cerebral contusions, these results support the hypothesis that apoptosis does occur in patients after traumatic brain injury, and this may contribute to the secondary injury processes that are seen with head injury. Patients in whom anti-apoptotic bcl-2 is induced seem to have a better prognosis. This may have important clinical significance in the development of bcl-2 homologs or bax inhibitors to prevent apoptosis.

Adult↗
PubMed2002

Nitric oxide synthase expression after human brain contusion.

OBJECTIVE: Nitric oxide is a universal mediator of biological effects in the brain, and it has been implicated in the pathophysiological processes of traumatic brain injury. Experimental studies have indicated posttraumatic up-regulation of the three different isoforms of nitric oxide synthase (NOS) (i.e., inducible NOS [iNOS], endothelial NOS, and neuronal NOS) after brain trauma. This study was undertaken to investigate the cellular sources and tissue compartments of nitric oxide produced by human patients undergoing surgical treatment for contusional brain injuries. METHODS: Contused brain tissue specimens from eight consecutive patients who underwent surgical treatment for brain contusions 3 hours to 5 days after trauma were evaluated in immunohistochemical analyses. Double-staining assays were used to define which cells produced the different isoforms. RESULTS: Increases in iNOS-positive cells were detectable within 6 hours after trauma, with a peak at 8 to 23 hours. Expression of iNOS after trauma was detected in neurons, macrophages, neutrophils, astrocytes, and oligodendrocytes. The cellular sources of iNOS differed at different times after trauma. No detectable difference in the expression of the neuronal or endothelial isoforms was observed for trauma patients, compared with control subjects. CONCLUSION: iNOS expression was up-regulated in a time-dependent manner in human brain tissue obtained from patients undergoing surgical treatment for contusional trauma. Our human data largely parallel experimental findings in rats, indicating that such trauma models are relevant for experimental studies and treatment trials.

Adolescent↗
PubMed2003

Differential effects of atrial natriuretic peptide on the brain water and sodium after experimental cortical contusion in the rat.

Atrial natriuretic peptide (ANP) plays an important role in the regulation of water and sodium in the body via cyclic GMP (cGMP) pathway. Although ANP has been shown to be protective in cerebral ischemia or intracerebral hemorrhage, its role in traumatic brain injury (TBI) has yet to be elucidated. We herein assessed ANP effects on brain water and sodium in TBI. Controlled cortical impact (3 mm depth, 6 m/sec) was used to induce an experimental cortical contusion in rats. Continuous administration of ANP 0.2 (n = 6) or 0.7 microg/kg/24 h (n = 6), cGMP analogue (8-Bromo-cGMP) 0.1 (n = 5) or 0.3 mg/kg/24 h (n = 5), or vehicle (n = 6) was begun 15 minutes after injury, using a mini-osmotic pump implanted into the peritoneal cavity. At 24 hours after injury, ANP significantly exacerbated brain edema in the injured hemisphere in a dose-dependent manner while it reduced brain sodium concentrations in both hemispheres. These ANP effects could be mimicked by a cGMP analogue. In the second series (n = 20), BBB integrity was assessed by evaluating the extravasation of Evans blue dye. ANP or cGMP analogue significantly worsened BBB disruption in the injured hemisphere at 24 hours after injury. These findings suggest that ANP administration exacerbates brain edema after the experimental cortical contusion in rats, possibly because of an increase in the BBB permeability via cGMP pathway, whereas it reduces brain sodium levels.

Animals↗
PubMedDate not supplied

Contusion injuries and their ocular effects.

A 22-year-old female optometry student presented with a one-day history of a contusion injury to the right eye with blurred vision inferiorly. Slitlamp examination showed mild anterior chamber reaction. Angle recession was visible by gonioscopy and dilated fundus examination revealed commotio retinae with macular involvement and vitreal haemorrhages. Peripheral retinal tears were later detected. The management of a patient with a history of a contusion injury is discussed.

Journal Article↗
PubMed2005

Real-time quantitative PCR analysis of temporal-spatial alterations in gene expression after spinal cord contusion.

Rat spinal cord contusion injury models the histopathology associated with much clinical spinal cord injury (SCI). Studies on altered gene expression after SCI in these models may identify therapeutic targets for reducing secondary injury after the initial trauma and/or enhancing recovery processes. However, complex spatial and temporal alterations after injury could complicate interpretation of changes in gene expression. To test this hypothesis, we selected six genes and studied their temporal and spatial patterns of expression at 1 h, 1, 3 and 7 days after a standardized spinal cord contusion produced by a weight drop device (10 g x 25 mm at T8). Real-time RT-PCR using TaqMan probes was employed to quantify mRNA for proteolipid protein, glyceraldehyde-3-phosphate dehydrogenase, glial fibrillary acidic protein, nestin, and the GluR2 and NR1 subunits of glutamate receptors. We found widely different temporal and spatial patterns of altered gene expression after SCI, including instances of opposing up- and down-regulation at different locations in tissue immediately adjacent to the injury site. We conclude that greater use of the reliable and extremely sensitive technique of quantitative real-time PCR for regional tissue analysis is important for understanding the altered gene expression that occurs after CNS trauma.

Animals↗
PubMed1989

Brain contusions: the time sequence of the histological changes.

Microscopical sections from 65 cases with brain contusions of known age were studied in order to obtain histological data for age determination of the lesions. The earliest histological alterations were observed within one hour after the lesion and they changed in an orderly fashion over the following hours, days and weeks. It is concluded that the age of brain contusions can be determined with reasonable accuracy from routinely stained histological sections.

Adolescent↗
PubMedDate not supplied

A muscle contusion injury model. Biomechanics, physiology, and histology.

We developed a reproducible muscle contusion injury and studied its effect on contractile function, histology, and passive failure. An instrumented drop-mass technique (mass, 171 g; height, 102 cm; spherical radius, 6.4 mm) delivered a single impact to the posterior surface of the gastrocnemius muscle in one limb of 40 male Wistar rats. On Day 0, the impact significantly (N = 12, P < 0.01) decreased maximum tetanic tension to 63% of the contralateral control value. Histologic examination demonstrated extravasation of erythrocytes, edema, myofiber disruption, and vacuolation of myofibers. Passive failure initiated at the site of injury. At 2 days, tetanic tension was 75% of controls (N = 11, P < 0.01). Histologically, acute inflammation and phagocytosis were noted. Tetanic tension at 7 days was 81% of controls (N = 8, P < 0.01). Vimentin staining indicated a dramatic increase in myoblast activity. Contractile strength was near normal at 24 days. Histologic examination showed complete regeneration of normal striated muscle fibers. No vimentin activity was found. No passive failures initiated at the injury site. Contusion injury produced a significant deficit in contractile function that continually diminished with gross histologic evidence of degeneration, regeneration, and normalization at the injured muscle fibers.

Animals↗