Neuroprotection and functional recovery after application of the caspase-9 inhibitor z-LEHD-fmk in a rat model of traumatic spinal cord injury

2005 ◽  
Vol 2 (3) ◽  
pp. 327-334 ◽  
Author(s):  
Ahmet Çolak ◽  
Alper Karaoǧlan ◽  
Şeref Barut ◽  
Sibel Köktürk ◽  
Aysşenur Iǧdem Akyildiz ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Rat Model ◽  
Caspase 9 ◽  
Content Type ◽  
Cord Injury ◽  
Group 3 ◽  
Group 2 ◽  
Fine Print

Object. Apoptosis is considered one of the most significant mechanisms in the pathogenesis of neuronal damage after spinal cord injury (SCI). This form of cell death occurs via mediators known as caspases. The aim of this study was to evaluate the neuroprotective effect of the caspase-9 inhibitor, z-LEHD-fmk, in a rat model of spinal cord trauma. Methods. Fifty-four Wistar albino rats were studied in the following three groups of 18 animals each: sham-operated controls (Group 1); trauma-only controls (Group 2); and trauma combined with z-LEHD-fmk—treated animals (0.8 µM/kg; Group 3). Spinal cord injury was produced at the thoracic level by using the weight-drop technique. Responses to SCI and the efficacy of z-LEHD-fmk treatment were determined on the basis of terminal deoxynucleotidyl transferase—mediated deoxyuridine triphosphate nick—end labeling staining and light and electron microscopy findings in cord tissue at 24 hours and 7 days posttrauma. Six rats from each group were also assessed for functional recovery at 3 and 7 days after SCI. This was conducted using the inclined-plane technique and a modified version of the Tarlov motor grading scale. At 24 hours postinjury, light microscopic examination of Group 2 tissue samples showed hemorrhage, edema, necrosis, polymorphonuclear leukocyte infiltration, and vascular thrombi. Those obtained in Group 3 rats at this stage showed similar features. At 24 hours postinjury, the mean apoptotic cell count in Group 2 was significantly higher than that in Group 3 (90.25 ± 2.6 and 50.5 ± 1.9, respectively; p < 0.05). At 7 days postinjury, the corresponding mean apoptotic cell counts were 49 ± 2.1 and 17.7 ± 2.6, also a significant difference (p < 0.05). Electron microscopy findings confirmed the occurrence of programmed cell death in different cell types in the spinal cord and showed that z-LEHD-fmk treatment protected neurons, glia, myelin, axons, and intracellular organelles. Conclusions. Examination of the findings in this rat model of SCI revealed that apoptosis occurs not only in neurons and astrocytes but also in oligodendrocytes and microglia. Furthermore, immediate treatment with the caspase-9 inhibitor z-LEHD-fmk blocked apoptosis effectively and was associated with better functional outcome. More in-depth research of the role of programmed cell death in spinal cord trauma and further study of the ways in which caspases are involved in this process may lead to new strategies for treating SCI.

Neuroprotective effects of GYKI 52466 on experimental spinal cord injury in rats

2003 ◽  
Vol 98 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Ahmet Çolak ◽  
Osman Soy ◽  
Hafize Uzun ◽  
Özcan Aslan ◽  
Seref Barut ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuroprotective Effects ◽  
Content Type ◽  
Gyki 52466 ◽  
Cord Injury ◽  
Group 3 ◽  
The Mean ◽  
Group 2 ◽  
Spinal Cord Injured ◽  
Fine Print

Object. The toxic effects of glutamate in the central nervous system are well known. This neurotoxicity occurs through metabotropic and ionotropic receptors, the latter group composed of N-methyl-d-aspartate, α-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA), and kainate receptors. The authors investigated the neuroprotective effects of GYKI 52466, a 2,3-benzodiazepine that is a selective and potent AMPA receptor antagonist, in a rat spinal cord trauma model. Methods. Sixty Wistar albino rats were studied in three groups of 20 animals each: sham-operated controls (Group 1); spinal cord—injured rats (Group 2); and spinal cord—injured plus GYKI 52466—treated rats (Group 3). In Groups 2 and 3, spinal cord injury (SCI) was induced at the thoracic level by applying an aneurysm clip to the cord for 1 minute. One minute after the clip was removed, the rats in Group 3 received an intraperitoneal injection of 15 mg/kg GYKI 52466. Responses to injury and treatment were evaluated based on biochemical parameters (lipid peroxidation and adenosine 5′-triphosphate [ATP] levels in tissue), and on light and transmission electron microscopy findings in cord tissue collected at different times post-SCI. Five rats from each group underwent assessment of functional recovery at 1, 3, and 5 days after SCI; evaluation was performed using the inclined-plane technique and Tarlov motor grading scale. The mean lipid peroxidation levels in Groups 1 and 2 were 21.73 ± 4.35 and 35.53 ± 2.99 nmol/g of wet tissue, respectively. The level in Group 3 was 27.98 ± 3.93 nmol/g of wet tissue, which was significantly lower than that in Group 2 (p < 0.01). The mean ATP levels in Groups 1 and 2 were 166.21 ± 25.57 and 41.72 ± 12.28 nmol/g of wet tissue, respectively. The ATP level in Group 3 was 85.82 ± 13.92 nmol/g of wet tissue, which was significantly higher than that in Group 2 (p < 0.01). Light microscopic examination of Group 2 tissues showed hemorrhage, necrosis, polymorphonuclear leukocyte infiltration, and vascular thrombi. In contrast, the examination of Group 3 tissues showed limited hemorrhage and no necrosis or vascular thrombi. The most prominent findings in Group 2 were hemorrhage and necrosis, whereas the most prominent findings in Group 3 were focal hemorrhage and leukocyte infiltration. Electron microscopy demonstrated that GYKI 52466 protected the neurons, myelin, axons, and intracellular organelles. The mean inclined-plane angles in Groups 1, 2, and 3 were 65°, 40 to 45°, and 55°, respectively. Motor scale results in all groups showed a similar trend. Conclusions. The findings in this rat model suggest that GYKI 52466 may provide significant therapeutic protection from secondary damage after acute SCI. This agent may be a viable alternative treatment for SCI.

Dural closure, cord approximation, and clot removal: enhancement of tissue sparing in a novel laceration spinal cord injury model

2004 ◽  
Vol 100 (4) ◽  
pp. 343-352 ◽  
Author(s):  
Yi Ping Zhang ◽  
Christopher Iannotti ◽  
Lisa B. E. Shields ◽  
Yingchun Han ◽  
Darlene A. Burke ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Connective Tissue ◽  
Scar Formation ◽  
Content Type ◽  
Dural Closure ◽  
Cord Injury ◽  
Group 2 ◽  
Fine Print ◽  
Group 1

Object. Laceration-induced spinal cord injury (SCI) results in the invasion of a connective tissue scar, progressive damage to the spinal cord due to complex secondary injury mechanisms, and axonal dieback of descending motor pathways. The authors propose that preparation of the spinal cord for repair strategies should include hematoma removal and dural closure, resulting in apposition of the severed ends of the spinal cord. Such procedures may reduce the size of the postinjury spinal cord cyst as well as limit scar formation. Methods. Using a novel device, the Vibraknife, the authors created a dorsal hemisection of the spinal cord at C-6 in the adult rat. In Group 1 (eight rats), the dura mater was repaired with apposition of the two stumps of the spinal cord to reduce the lesion gap. In Group 2 (10 rats), the dura was not closed and the two cord stumps were not approximated. All rats were killed at 4 weeks postinjury, and the spinal cords from each group were removed and examined using histological, stereological, and immunohistochemical methods. In Group 1 rats a significant reduction of the total lesion volume and connective tissue scar was observed compared with those in Group 2 (Student t-test, p < 0.05). Approximation of the stumps did not promote the regeneration of corticospinal tract fibers or sensory axons through the lesion site. Conclusions. Apposition of the severed ends of the spinal cord by dural closure reduces the lesion gap, cystic cavitation, and connective tissue scar formation. These outcomes may collectively reduce secondary tissue damage at the injury site and shorten the length of the lesion gap, which will facilitate transplantation-mediated axonal regeneration after laceration-induced SCI.

Apoptosis following spinal cord injury in rats and preventative effect of N-methyl-d-aspartate receptor antagonist

1999 ◽  
Vol 91 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Shoichi Wada ◽  
Kazunori Yone ◽  
Yasuhiro Ishidou ◽  
Tomonori Nagamine ◽  
Shinji Nakahara ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Nmda Receptor ◽  
Content Type ◽  
Mk 801 ◽  
Cord Injury ◽  
Number Of Cells ◽  
Fine Print

Object. The aims of this study were to clarify the histological and histochemical changes associated with cell death in the spinal cord after acute traumatic injury and to examine the role of excitatory amino acid release mediated by N-methyl-d- aspartate (NMDA) receptors. Methods. Following laminectomy, the spinal cord in 70 rats was injured at the T-9 level by applying extradural static weight—compression, in which a cylindrical compressor was used to induce complete and irreversible transverse spinal cord injury (SCI) with paralysis of the lower extremities. The injured rats were killed between 30 minutes and 14 days after injury, and the injured cord was removed en bloc. Rats that received NMDA receptor antagonist (MK-801) were killed at the same time points as those that received saline. The specimens were stained with hematoxylin and eosin, Nissl, and Klüver—Barrera Luxol fast blue and subjected to in situ nick-end labeling, a specific in situ method used to allow visualization of apoptosis. Thirty minutes post-SCI, a large hematoma was observed at the compressed segment. Six hours after injury, large numbers of dead cells that were not stained by in situ nick-end labeling were observed. Between 12 hours and 14 days postinjury, nuclei stained by using the in situ nick-end labeling technique were observed not only at the injury site but also in adjoining segments that had not undergone mechanical compression, suggesting that the delayed cell death was due to apoptosis. The number of cells stained by in situ nick-end labeling was maximum at 3 days postinjury. The results of electron microscopic examination were also consistent with apoptosis. In the MK-801—treated rats, the number of cells stained by in situ nick-end labeling was smaller than in nontreated rats at both 24 hours and 7 days after injury. Conclusions. These findings suggest that NMDA-receptor activation promotes delayed neuronal and glial cell death due to apoptosis.

Effect of mexiletine on lipid peroxidation and early ultrastructural findings in experimental spinal cord injury

1999 ◽  
Vol 91 (2) ◽  
pp. 200-204 ◽  
Author(s):  
Erkan Kaptanoglu ◽  
Hakan H. Caner ◽  
H. Selçuk Sürücü ◽  
Filiz Akbiyik
Keyword(s):  
Spinal Cord ◽  
Lipid Peroxidation ◽  
Spinal Cord Injury ◽  
Sodium Succinate ◽  
Content Type ◽  
Methylprednisolone Sodium Succinate ◽  
Cord Injury ◽  
Group 3 ◽  
Ultrastructural Findings ◽  
Fine Print

Object. The purpose of this study was to investigate the effect of mexiletine on lipid peroxidation and on ultrastructural findings after induced spinal cord injury (SCI). The authors also compared the activity of mexiletine to that of the well-known antioxidant, methylprednisolone sodium succinate (MPSS). Methods. Wistar rats were divided into seven groups, (Groups 1–7). Those in Groups 1 and 2 were control animals that underwent laminectomy only, after which nontraumatized spinal cord samples were obtained immediately (Group 1) and 2 hours postsurgery (Group 2). Spinal cord injury was induced in all other groups, and cord samples were obtained at 2 hours postsurgery. The rats in Group 3 underwent SCI alone; those in Group 4 received 30 mg/kg of MPSS intraperitoneally immediately after trauma was induced; and those in Groups 5, 6, and 7 received 1, 10, and 50 mg/kg of mexiletine, respectively, by intraperitoneal injection immediately after trauma was induced. Compared with the levels in control animals, lipid peroxidation was significantly elevated in rats in Groups 3 and 5, but there were no statistical differences among those in Groups 1, 2, 4, 6 and 7 in this regard. Compared with the findings in rats in Group 3, ultrastructural damage post-SCI was minor in rats in Groups 4 and 5, and there was even less damage evident in rats in Group 7. Conclusions. Analysis of these findings showed that administration of 50 mg/kg mexiletine significantly decreased the level of lipid peroxidation and protected spinal cord ultrastructure following SCI.

Apoptosis after traumatic human spinal cord injury

1998 ◽  
Vol 89 (6) ◽  
pp. 911-920 ◽  
Author(s):  
Evelyne Emery ◽  
Philipp Aldana ◽  
Mary Bartlett Bunge ◽  
William Puckett ◽  
Anu Srinivasan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Caspase 3 ◽  
Apoptotic Cells ◽  
Content Type ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Fine Print

Object. Apoptosis is a form of programmed cell death seen in a variety of developmental and disease states, including traumatic injuries. The main objective of this study was to determine whether apoptosis is observed after human spinal cord injury (SCI). The spatial and temporal expression of apoptotic cells as well as the nature of the cells involved in programmed cell death were also investigated. Methods. The authors examined the spinal cords of 15 patients who died between 3 hours and 2 months after a traumatic SCI. Apoptotic cells were found at the edges of the lesion epicenter and in the adjacent white matter, particularly in the ascending tracts, by using histological (cresyl violet, hematoxylin and eosin) and nuclear staining (Hoechst 33342). The presence of apoptotic cells was supported by staining with the terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick-end labeling technique and confirmed by immunostaining for the processed form of caspase-3 (CPP-32), a member of the interleukin-1β-converting enzyme/Caenorhabditis elegans D 3 (ICE/CED-3) family of proteases that plays an essential role in programmed cell death. Apoptosis in this series of human SCIs was a prominent pathological finding in 14 of the 15 spinal cords examined when compared with five uninjured control spinal cords. To determine the type of cells undergoing apoptosis, the authors immunostained specimens with a variety of antibodies, including glial fibrillary acidic protein, 2′,3′-cyclic nucleotide 3′-phosphohydrolase (CNPase), and CD45/68. Oligodendrocytes stained with CNPase and a number of apoptotic nuclei colocalized with positive staining for this antibody. Conclusions. These results support the hypothesis that apoptosis occurs in human SCIs and is accompanied by the activation of caspase-3 of the cysteine protease family. This mechanism of cell death contributes to the secondary injury processes seen after human SCI and may have important clinical implications for the further development of protease inhibitors to prevent programmed cell death.

A Phase I trial of naloxone treatment in acute spinal cord injury

1985 ◽  
Vol 63 (3) ◽  
pp. 390-397 ◽  
Author(s):  
Eugene S. Flamm ◽  
Wise Young ◽  
William F. Collins ◽  
Joseph Piepmeier ◽  
Guy L. Clifton ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Phase I ◽  
Phase I Trial ◽  
Loading Dose ◽  
Content Type ◽  
Cord Injury ◽  
Group 2 ◽  
Time Of Admission ◽  
Fine Print

✓ Results of a Phase I trial of the opiate antagonist naloxone for treatment of patients with acute spinal cord injury are reported. Naloxone was administered in doses ranging from 5 to 200 mg/sq m (0.14 to 5.4 mg/kg) for up to 48 hours. The patients ranged in age from 16 to 79 years (mean 37 years). Twenty patients received naloxone as a loading dose of 5 to 50 mg/sq m (0.14 to 1.43 mg/kg), followed by a maintenance dose of 20% of the loading dose given as a continuous infusion hourly for 47 hours (Group 1). Nine patients received a loading dose of 100 to 200 mg/sq m (2.7 to 5.4 mg/kg) and a maintenance dose of 75% of the initial dose hourly for 23 hours (Group 2). These higher doses (2.7 to 5.4 mg/kg) have been found to be effective in experimental spinal cord injury. Neurological examinations were performed and somatosensory evoked potentials (SEP's) were obtained as soon after admission as possible and again 1, 2, 3, and 7 days, 3 weeks, and 6 weeks to 6 months after admission. The 20 Group 1 patients who received 1.43 mg/kg or less of naloxone showed no improvement in neurological status or SEP's. All but three (15%) of these patients had a complete neurological deficit at the time of admission. Treatment was begun an average of 12.9 hours after injury. Among the nine Group 2 patients treated with 2.7 mg/kg or more, there were five patients (56%) with incomplete deficits. This group received naloxone an average of 6.6 hours after admission. Two of the five Group 2 patients with incomplete lesions showed improvement in their neurological condition and/or SEP's within 36 hours of receiving the drug. One of the four Group 2 patients with a complete lesion at the time of admission was able to localize pressure sensation in his legs 36 hours after completion of the drug infusion. Four Group 2 patients (two with complete and two with incomplete lesions) have shown improvement in their SEP's, suggesting recovery of SEP's in a dose-related fashion. Four patients experienced increased pain after administration of the loading dose and during the maintenance infusion; in only one patient was this severe enough to require discontinuation of the drug. Of the 29 patients treated with naloxone, four died within 6 weeks of admission, for a mortality rate of 13.8%. This study demonstrates that, in spinal cord-injured patients, naloxone given as an intravenous loading dose of 200 mg/sq m, followed by a continuous infusion of up to 150 mg/sq m/hr for 23 hours, has minimal side effects. The observed improvement in the clinical examination and SEP's at the higher doses, while not statistically verified in this Phase I trial, is encouraging.

Effects of dexamethasone on apoptosis-related cell death after spinal cord injury

2002 ◽  
Vol 96 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Mercedes Zurita ◽  
Jesús Vaquero ◽  
Santiago Oya ◽  
Carmen Morales
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Glial Cells ◽  
Spinal Cord Tissue ◽  
Injured Spinal Cord ◽  
Content Type ◽  
Related Cell ◽  
Cord Injury ◽  
Fine Print

Object. The purpose of this study was to analyze the expression of F7–26 (Apostain) in injured spinal cord tissue, and the modifying effects of dexamethasone administration. Methods. A total of 56 adult female Wistar rats were subjected to traumatic spinal cord injury (SCI) to induce complete paraplegia. These rats were divided into two groups according to whether they received dexamethasone (doses of 1 mg/kg daily) post-SCI. Injured spinal cord tissue was studied by means of conventional histological techniques, and Apostain expression was determined by immunohistochemical analysis at 1, 4, 8, 24, and 72 hours, and at 1 and 2 weeks after SCI in all the animals. Apostain-positive cells, mainly neurons and glial cells, were detected 1 hour after injury, peaking at 8 hours, after which the number decreased. One week after injury, apoptosis was limited to a few glial cells, mainly oligodendrocytes, and 2 weeks after injury there was no evidence of Apostain-positive cells. In the group of paraplegic rats receiving post-SCI intraperitoneal dexamethasone, there was a significant decrease in the number of Apostain-positive cells. Conclusions. Analysis of the results indicated that apoptosis plays a role in the early period after SCI and that administration of dexamethasone decreases apoptosis-related cell death in the injured spinal cord tissue.

The effects of methylprednisolone and the ganglioside GM1 on acute spinal cord injury in rats

1994 ◽  
Vol 80 (1) ◽  
pp. 97-111 ◽  
Author(s):  
Shlomo Constantini ◽  
Wise Young
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Body Weight Loss ◽  
Ganglioside Gm1 ◽  
Rat Spinal Cord ◽  
Neuroprotective Effects ◽  
Content Type ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Fine Print

✓ Recent clinical trials have reported that methylprednisolone sodium succinate (MP) or the monosialic ganglioside GM1 improves neurological recovery in human spinal cord injury. Because GM1 may have additive or synergistic effects when used with MP, the authors compared MP, GM1, and MP+GM1 treatments in a graded rat spinal cord contusion model. Spinal cord injury was caused by dropping a rod weighing 10 gm from a height of 1.25, 2.5, or 5.0 cm onto the rat spinal cord at T-10, which had been exposed via laminectomy. The lesion volumes were quantified from spinal cord Na and K shifts at 24 hours after injury and the results were verified histologically in separate experiments. A single dose of MP (30 mg/kg), given 5 minutes after injury, reduced 24-hour spinal cord lesion volumes by 56% (p = 0.0052), 28% (p = 0.0065), and 13% (p > 0.05) in the three injury-severity groups, respectively, compared to similarly injured control groups treated with vehicle only. Methylprednisolone also prevented injury-induced hyponatremia and increased body weight loss in the spine-injured rats. When used alone, GM1 (10 to 30 mg/kg) had little or no effect on any measured variable compared to vehicle controls; when given concomitantly with MP, GM1 blocked the neuroprotective effects of MP. At a dose of 3 mg/kg, GM1 partially prevented MP-induced reductions in lesion volumes, while 10 to 30 mg/kg of GM1 completely blocked these effects of MP. The effects of MP on injury-induced hyponatremia and body weight loss were also blocked by GM1. Thus, GM1 antagonized both central and peripheral effects of MP in spine-injured rats. Until this interaction is clarified, the authors recommend that MP and GM1 not be used concomitantly to treat acute human spinal cord injury. Because GM1 modulates protein kinase activity, protein kinases inhibit lipocortins, and lipocortins mediate anti-inflammatory effects of glucocorticoids, it is proposed that the neuroprotective effects of MP are partially due to anti-inflammatory effects and that GM1 antagonizes the effects of MP by inhibiting lipocortin. Possible beneficial effects of GM1 reported in central nervous system injury may be related to the effects on neural recovery rather than acute injury processes.

Therapeutic trial of hypercarbia and hypocarbia in acute experimental spinal cord injury

1984 ◽  
Vol 61 (5) ◽  
pp. 925-930 ◽  
Author(s):  
Ronald W. J. Ford ◽  
David N. Malm
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Mortality Rates ◽  
Therapeutic Trial ◽  
Tissue Preservation ◽  
Content Type ◽  
Experimental Spinal Cord Injury ◽  
Cord Injury ◽  
Fine Print

✓ Hypocarbia, normocarbia, or hypercarbia was maintained for an 8-hour period beginning 30 minutes after acute threshold spinal cord injuries in cats. No statistically significant differences in neurological recovery or histologically assessed tissue preservation were found among the three groups of animals 6 weeks after injury. No animal recovered the ability to walk. It is concluded that maintenance of hypercarbia or hypocarbia during the early postinjury period is no more therapeutic than maintenance of normocarbia. Mortality rates and tissue preservation data suggest, however, that postinjury hypocarbia may be less damaging than hypercarbia.

Ultrastructural scoring of graded acute spinal cord injury in the rat

2002 ◽  
Vol 97 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Erkan Kaptanoglu ◽  
Selcuk Palaoglu ◽  
H. Selcuk Surucu ◽  
Mutlu Hayran ◽  
Etem Beskonakli
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Behavioral Assessment ◽  
Traumatic Injury ◽  
Significant Negative Correlation ◽  
Content Type ◽  
Cord Injury ◽  
Contusion Injury ◽  
Weight Drop ◽  
Fine Print

Object. There is a need for an accurate quantitative histological technique that also provides information on neurons, axons, vascular endothelium, and subcellular organelles after spinal cord injury (SCI). In this paper the authors describe an objective, quantifiable technique for determining the severity of SCI. The usefulness of ultrastructural scoring of acute SCI was assessed in a rat model of contusion injury. Methods. Spinal cords underwent acute contusion injury by using varying weights to produce graded SCI. Adult Wistar rats were divided into five groups. In the first group control animals underwent laminectomy only, after which nontraumatized spinal cord samples were obtained 8 hours postsurgery. The weight-drop technique was used to produce 10-, 25-, 50-, and 100-g/cm injuries. Spinal cord samples were also obtained in the different trauma groups 8 hours after injury. Behavioral assessment and ultrastructural evaluation were performed in all groups. When the intensity of the traumatic injury was increased, behavioral responses showed a decreasing trend. A similar significant negative correlation was observed between trauma-related intensity and ultrastructural scores. Conclusions. In the present study the authors characterize quantitative ultrastructural scoring of SCI in the acute, early postinjury period. Analysis of these results suggests that this method is useful in evaluating the degree of trauma and the effectiveness of pharmacotherapy in neuroprotection studies.

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