Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Contusions”

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 145 records · Page 8Linked to original sources
PubMed1990

Regional cerebral blood flow in the pig after a localized cerebral contusion treated with barbiturates.

Regional cerebral blood flow determined with microsphere technique in anaesthetized pigs was measured before and after a localized cerebral contusion as well as after treatment with pentobarbital. No overall reduction in intracranial pressure or perfusion pressure was observed. Flow reduction due to pentobarbital was different in different regions with a high percentage change in the highly perfused basal structures and cortical grey matter except in the centre of the contusion where the reduction was half compared to the rest of cortical grey matter. Changes in white matter were less than in cortical grey matter but more pronounced than in the very high flow areas (choroid plexus and pineal gland). The accumulated change was greatest in the damaged region. Contralateral to the contusion, where a significant increase in flow was noticed after the contusion, there was a very low accumulated change in flow. In white subcortical matter underlying the contusion a similar low flow change was observed but this was not accompanied by as large an accumulated change as in grey cortical matter. At each fraction of injected pentobarbital a short-lasting increase in intracranial pressure and a reduction in mean arterial blood pressure was observed. The amplitude and the height of the intracranial pressure change was reduced during the pentobarbital injections.

Animals↗
PubMed1998

Traumatic brain contusions: a clinical role for the kinin antagonist CP-0127.

Focal cerebral contusions can be dynamic and expansive, leading to delayed neurological deterioration. Due to the high mortality associated with such cerebral contusions, our standard practice had evolved into evacuating contusions in patients who had a deterioration in level of consciousness, lesions > 30 cc and CT suggestion of raised ICP. Experimental brain edema studies have implicated kinins in causing 2 degrees brain swelling. CP-0127 (Bradycor), a specific bradykinin antagonist, has been found to reduce cerebral edema in a cold lesion model in rats. In a randomized, single blind pilot study, a 7 day infusion of CP-0127 (3.0 micrograms/kg/min) was compared to placebo in patients with focal cerebral contusions presenting within 24-96 hours of closed head injury with an initial GCS 9-14. The ICP, GCS, and vital signs were monitored hourly. The total lesion burden (TLB) was measured on serial CT scans. There were no differences in age, baseline GCS, TLB, initial ICP, or laboratory findings between the two groups (n = 20). The mean (+/- s.d.) rise in peak ICP from baseline was greater in the placebo group than with CP-0127 (21.9 +/- 4.7 vs 9.5 +/- 2.0, P = 0.018). In addition, the mean reduction in GCS in the placebo group was significantly greater than in the CP-0127 group (4 +/- 1.0 vs 0.6 +/- 0.4, P = 0.002). Significantly raised ICP and clinically significant neurological deterioration occurred in 7/9 patients on placebo (77%) and only in 1 patient (9%; n = 11) on CP-0127, mandating surgery (P = 0.005). There were no adverse drug reactions, significant changes in vital signs or variations in the laboratory values. The cerebral perfusion pressure was adequately maintained in all patients irrespective of therapy. These preliminary results with CP-0127 provide supporting evidence that the kinin-kallikrein system could be involved in cerebral edema. In this study, treatment with CP-0127 appeared to alter the natural history of traumatic brain contusions by preventing the 2 degrees brain swelling. In addition, CP-0127 obviated the need for surgery in the majority of treated patients. CP-0127 could act on the cerebral vasculature to limit dys-autoregulation and brain swelling or on the blood brain barrier to reduce cerebral edema.

Adult↗
PubMed1981

Responses to cortical injury: I. Methodology and local effects of contusions in the rat.

In order to develop some understanding of the evolution of cortical contusions, interdisciplinary studies including behavior, morphology and histochemistry were conducted at varying intervals after standardized injuries. A method for producing graded and reproducible focal cortical contusions in the rat is described. When these impact injuries are made in the "hindpaw cortical area,' specific trauma dose dependent behavioral deficits can be readily observed in the contralateral hindlimb. While most functional recovery occurs in the first two weeks after trauma, with severe contusions, deficits persist beyond 90 days. Morphologically these injuries progress from hemorrhages in white matter directly under contused cortex during the first hours after injury to the development of a necrotic cavity by 24 hours. The cavitation appears to expand over the subsequent two weeks and by 15 days is lined with fibroblast-like elements and macrophages. Intense acid phosphatase activity is seen on the borders of the area of necrosis. This lysosomal enzyme may participate in autolysis and development of focal cavitation following cortical contusion.

Acid Phosphatase↗
PubMed1990

CT evidence of intracranial contusion and haematoma in relation to the presence, site and type of skull fracture.

The skull films and CT scans of 1383 patients with acute head injury transferred to a regional neurosurgical unit were reviewed. Of the 850 patients with a skull fracture, contusion and/or haematoma was found in 71%, compared with 46% of the 533 patients with no fracture. Thirty-nine per cent of patients had neither contusion nor haematoma, and 21% had neither skull fracture nor contusion/haematoma. Haematomas occurred more frequently in association with lateral and occipital fracture than with frontal fracture, but the incidence of contusion was similar for all fracture sites. Linear fractures were more often associated with extra- and subdural haematomas than were depressed fractures. Intracranial damage associated with depressed fractures was localized more frequently than with linear fractures. Frontal fractures were rarely associated with posterior damage alone, but with occipital fractures anterior contusion was more frequent than posterior. Damage associated with lateral fracture was solely contralateral in 26%. Skull fracture was present in 77% of patients with contusion, 87% of those with an extradural, 72% with a subdural, and 66% with an intracerebral haematoma (70% of all those with an intracranial haematoma).

Brain Concussion↗
PubMed1997

Orbital-frontal delayed hemorrhagic contusions: clinical course and neurosurgical treatment protocol.

BACKGROUND: Delayed posttraumatic hemorrhage into the underlying contusion could cause significant elevation of intracranial pressure (ICP) and dramatic clinical and radiographic deterioration. The authors identified a subgroup of young patients with initial mild/moderate head injury, who presented with orbito-frontal and temporal tip minimal punctate contusions, which within 24 hours, expanded into dramatically larger noncoalesced hemorrhagic contusions. METHODS: Four consecutive patients within a 13-month period admitted to our institution with the above radiographic picture are presented and their clinical and treatment courses compared. RESULTS: After observing the relentless downhill course of two earlier patients treated for the control of ICP, our treatment protocol changed to early prophylactic intubation and moderate hyperventilation, insertion of an intraventricular catheter for ICP monitoring, hyperosmolar therapy with mannitol, sedation, chemical paralytics, and eventually pentobarbital for control of increased ICP. These interventions were mostly taken before the radiographic evidence of contusion blossoming and dramatic clinical deterioration. These two subsequent patients had a prolonged course of intubation and ICP problems requiring tracheostomy placement. The clinical outcome was excellent, however, with both patients decanulated from the tracheostomy within 6 weeks, and both returned to relatively normal premorbid functions. CONCLUSION: Although the series consists only of four consecutive patients with similar radiographic appearances, the authors advocate ultra-early aggressive medical treatment for this subgroup of patients with orbito-frontal contusion, prior to dramatic clinical and radiographic deterioration, as the outcome difference could be great.

Adult↗
PubMed2004

Cathepsin B mRNA and protein expression following contusion spinal cord injury in rats.

We provide the first data that cathepsin B (Cath B), a lysosomal cysteine protease, is up-regulated following contusion-spinal cord injury (SCI). Following T12 laminectomy and moderate contusion, Cath B mRNA and protein expression profiles were examined from 2 to 168 h post-injury in rats using real-time PCR and immunoblots, respectively. Contusion injury significantly increased [mRNA]Cath B in the injury site and adjacent segments over sham injury levels. While the largest [mRNA]Cath B induction (20-fold over naive) was seen in the injury site, the caudal segment routinely yielded [mRNA]Cath B levels greater than 10-fold over naive. Interestingly, sham injury animals also experienced mRNA induction at several time points at the injury site and in segments rostral and caudal to the injury site. Contusion injury also significantly elevated levels of Cath B proenzyme protein (37 kDa) over sham injury in the injury site (48, 72 and 168 h post-injury). Furthermore, significant protein increases of single and double chain Cath B (both active forms) occurred at the injury site at 72 and 168 h post-injury. Similar significant increases in Cath B protein levels were seen in areas adjacent to the injury site. The induction of Cath B mRNA and protein expression following contusion injury is previously undescribed and suggests that Cath B may potentially be involved in the secondary injury cascade, perhaps for as long as 1 week post-injury.

Animals↗
PubMed1981

[Computerized tomographic findings in brain contusions (author's transl)].

Over a 1 1/2 year period computerized tomographical examinations were performed on 104 patients suffering from brain concussions. The evaluation of findings resulted in the following classification: Type 1: severe generalized brain oedema without visible contusional foci, Type IIa: typical contusion with solitary or multiple contusional foci, Type IIb: typical contusion with severe, locally pronounced oedema, Type IIIa: contusion with flat subdural contusional bleeding, Type IIIb: contusion with minor intracerebral contusional bleeding, Type IIIc: contusion with intraventricular bleeding. Space-occupying haemorrhages were excluded. The comparison of computerized tomographic findings with the clinical course justifies such a classification. There are significant correlation between CT findings and the clinical picture, especially with the degree of clouding of consciousness as well as with further prognosis.

Brain↗
PubMed2002

Effect of posttraumatic hyperglycemia on contusion volume and neutrophil accumulation after moderate fluid-percussion brain injury in rats.

The purpose of this study was to evaluate the effects of posttraumatic hyperglycemia on contusion volume and neutrophil accumulation following moderate traumatic brain injury (TBI) in rats. A parasagittal fluid-percussion (F-P) brain injury (1.8-2.1 atm) was induced in male Sprague-Dawley rats. Rats were then randomized into four trauma groups (n = 7/group) by the timing of dextrose injection (2.0 gm/kg/ip), which included (1) early (E) group: 5 min after TBI; (2) delayed (D) group: 4 h after TBI; (3) 24-h group: 24 h after TBI; or (4) control (C) group: no dextrose injection. A sham operated control group also received dextrose to document physiological parameters (n = 4). Rats were perfusion fixed 3 days following TBI, and the brains were processed for routine histopathological and immunocytochemical analysis. Contusion areas and volumes, as well as the frequency of myeloperoxidase immunoreactive polymorphonuclear leukocytes (PMNLs) were determined. Dextrose injections significantly increased blood glucose levels (p < 0.005) in all treated groups. Although acute hyperglycemia following TBI did not significantly affect total contusion volume, contusion area was significantly elevated in the early treatment group. In addition, early posttraumatic hyperglycemia enhanced neutrophil accumulation in the area of the cortical contusion (p < 0.005). In contrast, delayed induced hyperglycemia (i.e., 4 h, 24 h) did not significantly affect histopathological outcome or neutrophil accumulation. Taken together, these findings indicate that acute but not delayed hyperglycemia aggravates histopathological outcome and increased accumulation of PMNLs. Posttraumatic hyperglycemia in the acute phase may worsen traumatic outcome by enhancing secondary injury processes, including inflammation.

Animals↗
PubMed2004

Combined demyelination plus Schwann cell transplantation therapy increases spread of cells and axonal regeneration following contusion injury.

Several cell populations have been shown to provide a permissive environment for axonal extension following transplantation to injury sites. The limited spread of transplanted cells from implantation sites in the mature CNS, and the superior substrate and trophic environment that they provide, likely contribute to the fact that few transplantation-based therapies have elicited axonal extension beyond the transplant. The aim of this study was to determine whether (1) regions of demyelination cranial and caudal to a spinal cord injury site would improve the spread of Schwann cells transplanted into the site of injury, and (2) whether this combination therapy was associated with improved anatomical regeneration. Three days following contusion injury, anti-galactocerebroside antibodies plus complement proteins were injected into the dorsal column cranial and caudal to the injury site, resulting in complete and well defined regions of demyelination that extended 8 mm either side of the injury site. One day later, naïve Schwann cells in suspension were injected into the contusion site. Transplanted Schwann cells homogeneously redistributed throughout the contusion site and the adjacent regions of demyelination cranial and caudal to the contusion site, providing a long-distance prospective path for repair that was free of myelin and contained transplanted cells. Animals that received demyelination plus transplantation therapy, but not untreated or single-treatment groups, exhibited robust axonal regeneration beyond the contusion site within the treated dorsal column. Axonal regeneration in these animals was not associated with an improvement in locomotor ability. These findings suggest that this combination therapy may overcome a central limitation of transplant strategies in which the permissive environment provided remains at the implantation site.

Animals↗
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↗
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↗