Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Brain Concussion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources
PubMed2000

rCBF in hemorrhagic, non-hemorrhagic and mixed contusions after severe head injury and its effect on perilesional cerebral blood flow.

Intracerebral contusions can lead to regional ischemia caused by extensive release of excitotoxic aminoacids leading to increased cytotoxic brain edema and raised intracranial pressure. rCBF measurements might provide further information about the risk of ischemia within and around contusions. Therefore, the aim of the presented study was to compare the intra- and perilesional rCBF of hemorrhagic, non-hemorrhagic and mixed intracerebral contusions. In 44 patients, 60 stable Xenon-enhanced CT CBF-studies were performed (EtCO2 30 +/- 4 mmHg SD), initially 29 hours (39 studies) and subsequent 95 hours after injury (21 studies). All lesions were classified according to localization and lesion type using CT/MRI scans. The rCBF was calculated within and 1-cm adjacent to each lesion in CT-isodens brain. The rCBF within all contusions (n = 100) of 29 +/- 11 ml/100 g/min was significantly lower (p < 0.0001, Mann-Whitney U) compared to perilesional rCBF of 44 +/- 12 ml/100 g/min and intra/perilesional correlation was 0.4 (p < 0.0005). Hemorrhagic contusions showed an intra/perilesional rCBF of 31 +/- 11/44 +/- 13 ml/100 g/min (p < 0.005), non-hemorrhagic contusions 35 +/- 13/46 +/- 10 ml/100 g/min (p < 0.01). rCBF in mixed contusions (25 +/- 9/44 +/- 12 ml/100 g/min, p < 0.0001) was significantly lower compared to hemorrhagic and non-hemorrhagic contusions (p < 0.02). Intracontusional rCBF is significantly reduced to 29 +/- 11 ml/100 g/min but reduced below ischemic levels of 18 ml/100 g/min in only 16% of all contusions. Perilesional CBF in CT normal appearing brain closed to contusions is not critically reduced. Further differentiation of contusions demonstrates significantly lower rCBF in mixed contusions (defined by both hyper- and hypodense areas in the CT-scan) compared to hemorrhagic and non-hemorrhagic contusions. Mixed contusions may evolve from hemorrhagic contusions with secondary increased perilesional cytotoxic brain edema leading to reduced cerebral blood flow and altered brain metabolism. Therefore, the treatment of ICP might be individually modified by the measurement of intra- and pericontusional cerebral blood.

Adolescent↗
PubMed2000

Effect of intracerebral lesions detected in early MRI on outcome after acute brain injury.

In the present study we classified intracerebral lesions likely to influence the outcome of head injured patients according to localization, lesion type, lesion number and lesion volume. A score of intracerebral lesions based on findings in early MRI is presented. Early MRI studies were performed in 30 patients (average 5-6 days after trauma) and outcome (GOS) was determined after 3 and 12 months. Lesions were classified and lesion volume V was calculated (V = pi abc/6). The applied intracerebral lesion score included lesions in the frontal cortex, basal ganglia, corpus callosum and brainstem. Patients in a persistent vegetative state (PVS) showed a higher number (p = 0.018) and volume (p = 0.013) of frontal lesions as compared to the non-vegetative group (NPVS). Lesion volume in basal ganglia differed significantly between PVS and NPVS (p = 0.01) and correlated to outcome (r = -0.65, p < 0.005). Volume difference in the corpus callosum between PVS and NPVS was significant (p = 0.02). The number (r = -0.61, p < 0.005) and volume (r = -0.62, p < 0.005) of brainstem lesions correlated to outcome and PVS differed in number (p = 0.012) and volume (p = 0.006). The intracerebral lesion score correlated to the GOS (r = -0.57, p = 0.001) and PVS and NPVS differed significantly. A lesion volume exceeding 40 ml in the frontal cortex, 3.5 ml in the basal ganglia, 4 ml in the corpus callosum or 1.5 ml in the brainstem is likely to lead to an unfavorable outcome. More than 4 lesions in the frontal cortex or 3 lesions in the brainstem appeared more frequent in patients with unfavorable outcome. Treatment strategies in the early phase after brain injury could be modified by the knowledge of certain lesions only visible on MRI.

Brain↗
PubMed2000

Characterizing edema associated with cortical contusion and secondary insult using magnetic resonance spectroscopy.

It is traditionally believed that edema associated with brain contusion is vasogenic. The objective of this study was to quantify and characterize the edema in cortical contusion coupled with early hypoxia and hypotension. Sprague-Dawley rats were randomised into six groups: Sham, Trauma moderate (Tm), Trauma severe (Ts), Hypoxia and Hypotension (HH), Tm and Ts with HH (THHm; THHs). Trauma was induced with controlled cortical impact; associated secondary insults lasted 30 minutes. Water content was measured using tissue longitudinal relaxation time (T1). Apparent diffusion coefficient of water (ADC) was calculated from diffusion-weighted imaging and single voxel spectroscopy. In the trauma groups ICP increased at 30 minutes post trauma (p < 0.05) and then gradually decreased. Only in the THH groups, ICP showed a trend to continually rise. No ICP variations were seen in the others groups. The increase in water content at 4 hours post trauma was inversely related to ADC variation (p < 0.0001). A significant increase in water content with low ADC, developed in the injured region in Ts, THHm (p < 0.05) and THHs (p < 0.01) compared to Sham. Intracellular water rose in the whole brain in THH groups although more severely in the THHs (p < 0.01). Immediately after trauma ADC fell in the THH groups, but gradually increased in the THHm, whereas there was no recovery in THHs. The results indicate that the type of edema in the injured area, with and without superimposed secondary insult, is predominantly cytotoxic (cellular). Moreover, secondary insults act synergistically with focal injury to increase cellular water in both injured tissue and remote regions.

Animals↗
PubMed2000

Comparison of NAA measures by MRS and HPLC.

This work investigates the accuracy of an in vivo estimation of absolute N-acetyl aspartate (NAA) concentrations by magnetic resonance spectroscopy (MRS) using cerebral water as an internal reference standard. Single-voxel, proton spectroscopy was carried out in two groups of rats (normal and diffuse head injury), using a PRESS sequence with TR = 3 s, TE = 135 ms. Fully relaxed water spectra and water-suppressed proton spectra were obtained from a 7 x 5 x 5 mm3 volume of tissue. MRI-based brain water content measurements were also performed. Following MRS, HPLC determinations of NAA were carried out. In the normal rats the MRS yielded 10.98 +/- 0.83 mmol/kg w.w. vs 10.76 +/- 0.76 for HPLC with a mean absolute difference of 0.8. In the injured rats the corresponding results were 9.41 +/- 1.78 (MRS) and 8.16 +/- 0.77 (HPLC) with a mean absolute difference of 1.66. The in vivo absolute method accurately documented the temporal NAA changes compared to the NAA/Cr approach.

Animals↗
PubMed2000

Evidence for lactate uptake after rat fluid percussion brain injury.

UNLABELLED: Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Glucose declines and lactate increases after TBI as demonstrated in clinical and lab studies, suggesting increased glycolysis. This led us to hypothesize that high extracellular fluid (ECF) lactate may be beneficial after TBI. We measured cerebral dialysate lactate and glucose, and arterial lactate and glucose, before & after rat Fluid Percussion Injury (FPI) (2.06 +/- 0.13 atm) with and without i.v. lactate infusion (100 mM x 4.5 hours) to test the hypotheses that arterial lactate determines ECF lactate. 14C-lactate autoradiography was also performed, to demonstrate whether lactate is taken up by traumatized brain. RESULTS: Dialysate lactate was always significantly higher than arterial. After lactate infusion, both the dialysate and the arterial lactate were significantly increased (P < 0.0001). Dialysate lactate increased within 10 min. following FPI, with significantly higher values in the lactate infusion group (82% higher with lactate infusion after FPI). Dialysate glucose fell following FPI, with a more severe decline in the saline group (129% lower), suggesting lactate infusion preserves or "spares" glucose in ECF. In our autoradiographic study, i.v. 14C-lactate accumulated at the injury site, with levels 2-4 times higher than in contralateral cortex. In conclusion, arterial lactate augmentation thus increases brain dialysate lactate and results in less reduction in ECF glucose, after FPI. Infused lactate accumulates at the injury site, where metabolism is probably the greatest.

Animals↗
PubMed2000

Time profile of neuron specific enolase serum levels after experimental brain injury in rat.

The aim of this study was to investigate the time course of NSE serum levels after traumatic brain injury in rats. 65 male Wistar rats were subjected to severe cortical impact injury (100 PSI, 2 mm deformation). Blood samples were drawn directly after trauma, after 1 h, 6 h, 12 h, 24 h, and 48 h in the trauma group as well as in sham operated animals directly after craniotomy, after 6 h and after 48 h. NSE serum levels were estimated with a commercially available enzyme immuno assay (LIA-mat Sangtec). The control animals showed a NSE serum level of 8.82 micrograms/l (mean, n = 10). We demonstrated a time dependent release of NSE into the serum after trauma. The highest NSE serum values were detected six hours after trauma (31.5 micrograms/l, mean, n = 10). NSE serum level seems to reflect neuronal damage after cortical contusion in the rat in a time dependent manner.

Animals↗
PubMed2000

Isoflurane doubles plasma glutamate and increases posttraumatic brain edema.

Increased plasma and cerebral glutamate levels may contribute to posttraumatic edema formation. Since volatile anesthetics elevate plasma amino acid concentrations, the influence of isoflurane on arterial plasma glutamate levels and brain edema formation was investigated in brain-injured rats. Rats were anesthetized with chloral hydrate (380 mg/kg i.p.) or isoflurane (1.2-2.0 vol%) for four hours following controlled cortical impact injury. Isoflurane significantly increased arterial glutamate levels compared to chloral hydrate (124 +/- 12 vs. 60 +/- 5 microM; p < 0.005). At eight hours after trauma, water content was significantly increased in the traumatized hemisphere compared to the non-traumatized side (p < 0.005). In addition, four hours of isoflurane anesthesia caused a significant increase in brain water content of both hemispheres compared to chloral hydrate (80.1 +/- 0.1 vs. 79.6 +/- 0.1%; p < 0.005). Prolonged isoflurane anesthesia is associated with a significant increase in arterial plasma glutamate levels and brain water content. This increase in brain water content must be considered when performing prolonged isoflurane anesthesia.

Animals↗
PubMed2000

S-100b as a screening marker of the severity of minor head trauma (MHT)--a pilot study.

Due to its neural tissue specificity S-100b is considered as a screening marker of cerebral injury in head trauma patients. However, the occurrence and relevance of an increased S-100b serum level in minor head trauma (MHT) is still debated. Therefore, the purpose of our study was to evaluate the diagnostic utility of S-100b measurements in a level I trauma center emergency room (ER). Eighty patients presenting with clinical symptoms of MHT (GCS score of 13-15, transitory loss of consciousness, amnesia, nausea) were prospectively recruited. Blood samples were drawn at 0 h, 6 h and 24 h after admission, and a cerebral computed tomography (CT) was performed. The reference group consisted of 10 patients with severe head injury (GCS score < 8), the control group of 20 healthy volunteers. Concentrations of S-100b in serum were determined by an immunoluminometric assay. The results were compared with the plasma levels of polymorphonuclear (PMN) elastase as an established general trauma marker. In the MHT group, the S-100b serum level revealed 1.26 +/- 0.57 ng/ml at study entry (73.46 +/- 47.53 min after trauma). In comparison, the S-100b concentration was significantly elevated in patients with severe head trauma (5.26 +/- 1.65 ng/ml, p = 0.009), but no significant difference became evident in relation to the control group (0.05 +/- 0.01 ng/ml). Starting values of PMN elastase in plasma amounted to 66.40 +/- 14.92 ng/ml in severe trauma, and to 60.52 +/- 10.75 ng/ml in MHT showing significant differences only in relation to the control group (23.36 +/- 1.53 ng/ml). When correlated with the severity of the later clinical course, the first S-100b measurements exhibited steadily increasing values as demonstrated in MHT outpatients (0.29 +/- 0.11 ng/ml), MHT in-hospital patients (0.70 +/- 0.19 ng/ml) and MHT intensive care unit patients (5.03 +/- 3.18 ng/ml). PMN elastase levels revealed no significant differences concerning the three MHT subgroups. Thus, in contrast to the general trauma marker PMN elastase, assessment of the specific neuroprotein S-100b early after traumatic insult appears to be a promising laboratory marker for the prognosis of the severity of brain injury in MHT patients. Nevertheless, further investigations are required to better understand its predictive value.

Biomarkers↗
PubMed2000

Influences of secondary injury following traumatic brain injury in developing versus adult rats.

Hypoxia and hypotension are both common findings following traumatic brain injury occurring with a frequency of up to 46% according to data of the Traumatic Coma Data Bank. In the present study the influence of secondary injury on intracranial pressure and the cardiovascular response is investigated in developing rats. Differences from adult rats are determined. Diffuse brain injury was produced in intubated and ventilated 17-20 days old Sprague-Dawley rats (N = 16) using a modification of the Marmarou-model. Hypoxia was induced by reducing O2-concentration to 8% lasting for 15/30 min. Mean arterial blood pressure recordings and intracranial pressure recordings were performed continuously. Animals were divided into two groups, sustaining hypoxia alone (N = 9) and trauma/hypoxia (N = 7). The results were compared to readings in adult animals subjected to hypoxia (N = 5) and trauma/hypoxia (N = 5) (450 gm/150 cm). Immediately following the onset of hypoxia in the developing rat, MABP decreased from 76.5 +/- 13 mm Hg to 35.8 +/- 7 mm Hg. In the adult rat the decrease was more marked (from 93.3 +/- 8 mm Hg to 33.5 +/- 5.7 mm Hg) (p < 0.05). Mortality rate in developing rats with trauma/hypoxia was 43% with no significant change of ICP (from 13 +/- 5.2 to 22.3 +/- 11). All adult animals recovered following trauma/hypoxia with no relevant ICP-increase within one hour post-trauma. Hypoxia induces hypotension in adult and developing rats. However, developing rats appear to be more vulnerable to hypoxia associated with trauma.

Age Factors↗
PubMed2000

The impact of acute hyponatraemia on severe traumatic brain injury in rats.

The effect of experimental acute hyponatraemia on severe traumatic brain injury (TBI) was studied in a modified impact-acceleration model. The cortical contusional volume was quantified by image analysis on serial sections, injured axons were visualized and quantified by beta-Amyloid Precursor Protein (beta-APP) immunohistochemical staining. Regional brain water content was estimated by the wet-dry weight method. The experiment was conducted in Group I (injury only) and Group II (injury followed by acute hyponatraemia). Comparison between the two groups showed that acute hyponatraemia significantly increased contusional volume (3.24 +/- 0.70 mm3 vs. 1.80 +/- 0.65 mm3, P = 0.009) and the number of injured axons (128.7 +/- 44.3 vs. 41.7 +/- 50.1, P = 0.04) in the right thalamus & basal ganglia region. Water content of the brain stem region was also significantly increased by acute hyponatraemia (73.71 +/- 0.14% vs. 72.28 +/- 0.93%, P = 0.004). These results suggest that acute hyponatraemia potentiates secondary brain damage in severe TBI by augmentation of both focal contusion and diffuse axonal injury. The injured brain stem region is more susceptible to edema formation induced by experimental acute hyponatraemia.

Amyloid beta-Protein Precursor↗
PubMed2000

Validation of a closed head injury model for use in long-term studies.

To study pharmacotherapy of traumatic brain injury in rats, a modified closed head injury model was used that expresses clinically relevant features including intracranial hypertension and morphological alterations. Long-term survival under ethically acceptable conditions would greatly improve its clinical relevance. To ensure this goal with great reproducibility, the experimental protocol was adapted, in particular the impact-acceleration kinetics. Variations in impact-acceleration conditions were obtained by modifying the stiffness of the impact site and changing the height of a 400 g weight dropped from 51.5 to 31.5 cm (51.5/400; 31.5/400). Impact and acceleration were measured with a force sensor incorporated in a rigid dummy-rat and an accelerometer mounted on the platform onto which the animals are positioned. Significant correlation was shown between impact and acceleration. Accelerations obtained in rats were significantly lower than those in the dummy. Unlike the 51.5/400 group, in the 31.5/400 group no mortality or cranial fractures were observed. In both groups intracranial pressure rose to pathological values immediately after trauma and remained elevated longer than 24 h. Diffuse axonal injury developed in all groups and remained present for at least 7 days. By reducing the impact-acceleration conditions, post-traumatic complications were diminished, while the clinically important features were maintained.

Acceleration↗
PubMed2000

Increased adrenomedullin in cerebrospinal fluid after traumatic brain injury in children: a preliminary report.

Adrenomedullin is a recently discovered 52-amino-acid peptide that is a potent vasodilator. Infusion of adrenomedullin increases regional cerebral blood flow and reduces infarct volume after vascular occlusion in rats. Adrenomedullin may represent an endogenous neuroprotectant since it is increased after focal brain ischemia. Cerebral hypoperfusion is present after traumatic brain injury (TBI) in children. We hypothesized that adrenomedullin levels would be increased in children with severe TBI. Total adrenomedullin concentrations were measured using a radioimmunometric assay. Thirty-six samples of ventricular cerebrospinal fluid (CSF) from 10 pediatric patients were collected during the first 10 days after severe TBI (GCS < 8). Control CSF was obtained from 5 children undergoing lumbar puncture, who had normal CSF parameters and no evidence of central nervous system infection. Patients underwent standard neuro-intensive care, including cerebrospinal fluid drainage. Data were analyzed using a univariate regression model. Adrenomedullin concentration was markedly elevated in CSF of children following TBI versus control (mean level 10.65 vs 1.51 fmol/ml, p = 0.006). All 36 case samples had an adrenomedullin concentration above the median value for the controls (1.52 fmol/ml). We conclude adrenomedullin is elevated in the CSF of children following severe TBI. We speculate that it participates in the endogenous response to cerebral hypoperfusion after TBI.

Adrenomedullin↗
PubMed1998

Morphological and hemodynamic evaluations by means of transcranial power Doppler imaging in patients with severe head injury.

The following conditions of 17 patients with severe head injury (ages 9-76; mean 37:12 focal and 5 diffuse injuries) were evaluated during acute phase (1-14 days after injury, mean 5) by transcranial power Doppler imaging (PDI), a new color Doppler ultrasound technique: a) morphological changes via temporal window, b) hemodynamic changes in major intracranial/cervical arteries based on measured angle-corrected time-averaged mean (TAM)/ peak velocities and vessel diameter (Va), and calculated pulsatility indices (PI), vessel area (Va), and flow volume (Vf = TAM x Va). a) 1) Major trunks of intracranial vessels and circle of Willis and pathological changes in frontal/temporal lobes and midbrain were finely visualized. 2) Contusional hemorrhage and cerebral contusion demonstrated irregular hyper- and hypo-echoic lesions, respectively. 3) Delayed epidural hematoma showed a hyper-echoic band. b) 1) Decreased velocities, significant PI increase, and Va increase tendency were observed in intracranial arteries. 2) Increased velocities with Vf increase but no Va decrease indicated hyperemia rather than vasospasm. 3) Va in the intracranial vessels, however, tended to increase PDI appears useful in evaluating real-time and simultaneous morphological and hemodynamic information in pathogenesis and neurointensive care of patients with severe head injury.

Adolescent↗
PubMed1998

Blood brain barrier permeability and acute inflammation in two models of traumatic brain injury in the immature rat: a preliminary report.

We sought to investigate the course and magnitude of blood brain barrier (BBB) permeability following focal and diffuse traumatic brain injury (TBI) in immature rats and examine the time course of markers of acute inflammation (neutrophil accumulation and E-selectin [E-sel] expression) following these two types of injury. We measured BBB permeability using i.v. injection Evans Blue (EB) and the extent of inflammation using immunohistochemical techniques identifying neutrophils (monoclonal antibody RP-3) and the endothelial adhesion molecule, E-selectin. Male Sprague-Dawley immature (17 day-old) rats (30-45 g, n = 80) were subjected to a controlled cortical impact (CCI: 2 mm, 4 m/s), a closed head diffuse injury (DI: 150 g/2m) or a corresponding sham procedure (with or without craniotomy). EB was injected i.v. at 30 min before sacrifice, which occurred at 1 h, 4 h, or 24 h after injury. BBB permeability was observed in both the CCI and DI rats at 1 h after injury which largely resolved by 24 h. In the CCI, EB extravasation was seen within and around the contusion. In DI, diffuse BBB permeability was seen. DI was not associated with acute inflammation since there was neither neutrophil accumulation nor E-selectin expression. The CCI rats though had 5.1 +/- 2.2 neutrophils/hpf and 3.0 +/- 0.4 endothelial cells/hpf expressing E-selectin (mean +/- SEM) (both p < 0.05 vs sham and DI). These data suggest that BBB breakdown occurs in the immature rat after both focal and diffuse TBI. This early BBB permeability was not associated with acute inflammation in DI but was in CCI. These data also suggest that contusion is a key factor in the development of a traditional acute inflammatory response after TBI in the immature rat.

Animals↗
PubMed1998

Effects of cerebral perfusion pressure on brain tissue PO2 in patients with severe head injury.

Ischemia causes secondary brain damage after severe head injury (SHI). Cerebral perfusion is commonly estimated by monitoring CPP, but the adequacy of cerebral oxygenation requires further measurements, such as jugular oxygen saturation or, more recently, PtiO2 monitoring. In 7 patients with severe head injury, ICP, MAP, CPP, SjO2 and PtiO2 were monitored for a mean time of 9.0 +/- 2.2 days. Most of the data were in a "normal" range. Focusing on values under the thresholds of 60 mm Hg for CPP and 20 mm Hg for PtiO2, we found a relationship between CPP and PtiO2. Looking at the PtiO2 time-course, we observed a quite constant increasing trend during the first 48 hours of monitoring, then the values remained relatively constant within a normal range. Our data show that decreases of PtiO2 are not uncommon after severe head injury and therefore it seems that monitoring of PtiO2 in SHI may be useful in order to minimize secondary insults.

Adolescent↗
PubMed1998

Neuroprotective properties of aptiganel HCL (Cerestat) following controlled cortical impact injury.

Recent studies revealed a neuroprotective effect of the non-competitive NMDA receptor antagonist Aptiganel HCL (Cerestat CNS 1102) in focal cerebral ischemia. This study investigates the influence of Cerestat on contusion volume, post-traumatic brain edema and intracranial pressure (ICP) following Controlled Cortical Impact Injury (CCII). In rats (n = 54) CCII was applied to the left hemisphere using a pneumatic impactor. Cerestat (2 mg/kg i.v.) or vehicle was injected 15 min after injury animals were sacrificed 24 hours later. Contusion volume was measured planimetrically (n = 18). Hemispheric swelling and water content were determined gravimetrically (n = 20). ICP, mean arterial blood pressure (MABP) and cerebral perfusion pressure (CPP) were monitored for 30 min before sacrifice (n = 16). Cerestat reduced contusion volume from 77.3 +/- 5.8 mm3 to 66.8 +/- 3.9 mm3 (p < 0.05). Hemispheric swelling was also diminished from 11.1 +/- 0.8% to 8.2 +/- 1.4% as soon was water content (Cerestat 82.30 +/- 0.18% vs. control: 82.78 +/- 0.12%, p < 0.05). ICP was decreased by treatment from 31.7 +/- 3.5 mm Hg to 26.3 +/- 2.2 mm Hg and CPP was significantly improved (82.1 +/- 4.4 mm Hg vs 57.7 +/- 4.8 mm Hg; p < 0.05) 24 hours after injury. Cerestat administration was associated with decrease contusion volume, less hemispheric swelling, a lower ICP and increased CPP.

Animals↗
PubMed1998

Antioxidant, OPC-14117, attenuates edema formation, and subsequent tissue damage following cortical contusion in rats.

Oxygen free radicals contribute to various kinds of tissue injury processes within the central nervous system. It has been suggested that inhibition of free radical formation has the potential to attenuate secondary neural tissue damage involving ischemia or trauma, and antioxidant therapy may offer a promising approach. In the present study, employing a cortical contusion model in the rat, contusion-induced neural damage, was evaluated by investigating edema formation, behavioral activities and histological changes. The effects of the superoxide radical scavenger, OPC-14117, were also tested to determine how free radicals may contribute to such neural damage. The results demonstrated that cerebral contusion induces a progressive decrease in tissue specific gravity representing edema formation, and behavioral deficits in the Morris water maze test and habituation of exploratory activity. Histological examinations revealed necrotic cavity formation in the cortex and selective neuronal death of the hippocampal CA3 region. These changes were significantly attenuated by OPC-14117, which was administered as a single dose immediately following trauma induction. The above results indicate that oxygen free radicals are involved in contusion-induced edema formation, subsequent tissue damage and cognitive deficits. The superoxide radical scavenger, OPC-14117, has a powerful therapeutic potential for preventing secondary cell damage following traumatic brain injury.

Animals↗
PubMed1998

Effects of lecithinized SOD on sequential change in SOD activity after cerebral contusion in rats.

To analyze the effect of lecithinized superoxide dismutase (SOD) on superoxide accumulation after traumatic brain injury (TBI) in rats, we studied the SOD activity by NBT-reducing method and the expression of Cu,Zn-SOD mRNA by Northern blot analysis. As determined by the specific gravity method, the administration of lecithinized SOD decreased brain edema in the periphery of the lesion at 6 hr after contusion. SOD activity, without lecithinized SOD administration, increased at the peripheral portion at 30 min after contusion, but decreased to normal level at 6 hr after TBI. By administration of lecithinized SOD, the increase of SOD activity was preserved until 6 hr after TBI. The expression of Cu,Zn-SOD mRNA increased in the core lesion, peripheral portion, and contralateral hemisphere until 6 hr after TBI, then was suppressed in all three areas by lecithinized SOD. These results support the hypothesis that superoxide anions may play an important role in the development of brain edema after TBI, and that leciyhinized SOD appears to prevent brain edema through a protective effect against superoxide anions.

Animals↗