Effects of core body temperature on changes in spinal somatosensory-evoked potential in acute spinal cord compression injury: an experimental study in the rat.

To establish a reproducible and manipulable model of acute spinal cord compression injury in large mammals so as to provide a technical and experimental platform for the repair and reconstruction of spinal cord injury (SCI). A total of 15 adult male goats, weighting 35 - 45 kg, were selected. After intravenous anesthesia, a model of acute spinal cord compression injury was established with the balloon of kyphoplasty through mini-open laminotomy. The animals were divided into 4 groups, i.e. 3 in group A and 4 each in groups B, C and D. Goats in group A received mini-open laminotomy without insertion of balloon. In group B, balloons were surgically positioned within the T10-T11 spinal canal but not inflated. The spinal cords of goats in group C were partially compressed by inflating the balloon to approximately 30% of anterior/posterior diameter of vertebral canal. In group D, the balloon was inflated to occupy approximately 90% of canal on a lateral view. X-ray and thin-section computed tomography (CT) scans were used to determine the balloon location. CT scans were also used to calculate the magnitude of balloon inflation and the degree of spinal cord compression within vertebral canal. Improved Tarlov motor function grade test and somatosensory evoked potentials (SSEP) were employed to evaluate the goat neurofunction 24 hours before and 7 days after surgery. Dye volumes of 0, 1.26 ± 0.18 and 2.82 ± 0.20 ml were injected into the balloon to produce spinal occupancies of 0%, 33% ± 2% and 89% ± 4% on X-ray and CT scan. There was a significant dose response for the different levels of injury, with reduced conduction of somatosensory evoked potentials and impaired mobility 7 days after injury. A model of acute spinal cord injury by a tunable compression with a mini-invasive balloon in goats is a useful experiment model of spinal cord injury. It may simulate the clinical situations of acute SCI.

To establish a goat model of acute spinal cord compression injury through a modified percutaneous technique with a Foley double-lumen urine catheter and explore the method feasibility and preliminary observation. Twelve adult male Chongming goats were randomly divided into 3 groups:control (A, n = 4), 0.5 ml compression (B, n = 4) and 1 ml compression (C, n = 4). After local anesthesia, all animals received epidural balloon catheter (5Fr) insertion via a percutaneous trans-lumbosacral interlaminar space technique that mimicked the method used in vascular access for angiography. The balloon catheter was advanced under fluoroscopic guidance until its distal tip reached the middle of T6 level.One week later, for groups B and C, the balloon was inflated by half-strength contrast material, 0.5 ml and 1 ml, respectively. The balloon was left inflated for 30 min and then deflated. The images of computed tomography (CT) and magnetic resonance (MR) were taken before and after surgical procedures.Quantitative assessment of spine canal occupying rate was accomplished by an off-line software program based on CT results. Motor function was assessed by the modified Tarlov scale. Two animals of each group were sacrificed after a total observation period of 48 h and 72 h respectively.Spinal cords from the injured level were then obtained for pathologic examinations. All animals underwent successful catheterization occupying 6.8%±0.7% (Group A), 6.7%±0.7% (Group B) and 6.6%±0.6% (Group C) of spine canal respectively. After inflation, the occupying rate of groups B and C achieved 43.4%±2.5% and 88.1%±2.3% respectively.Ventral compression of spinal cord was noted on MR images.Hindlimb movement remained normal after catheter insertion in all groups. All animals in group B and C became paraplegic after inflation. And a positive correlation existed between injection volume and Tarlov score. Pathological findings confirmed neuron atrophy, increased gap around neurons, mild demyelination and vacuolar degeneration both in groups B and C at 48 h after injury. Pathological changes deteriorated at 72 h after injury. The results of behavioral evaluation, radiographic images and pathological examination reveal an evidence of acute spinal cord injury. Percutaneous epidural balloon catheter insertion differs from previous techniques by avoiding surgical exposure and associated artifacts, yet it offers injury mechanisms similar to those of human spinal cord injury. As a new means of modeling spinal cord injury in animals, this technique has many potential applications.

To evaluate the effects of 4-aminopyridine-3-methyl hydroxide (4-AP-3-MeOH) in rat's acute spinal cord injury. A total of 12 adult male SD rats (250-300 g) were randomly divided into treatment (n = 6) and control (n = 6) groups. After compressing segment T11 of spinal cord for 30 min, the injured segment received 1 ml 4-AP-3-MeOH (100 µmol/ml) by topically application in treatment group while the control group received 1 ml saline.Somatosensory evoked potential (SSEP) was detected in both groups at pre-injury, 30 min post-injury and post-dosing. Then Luxol fast blue (LFB) staining of target spinal segment was performed. In treatment group, the values of SSEP at pre-injury, 30 min post-injury and post-dosing were 1.26 ± 0.35, 0.03 ± 0.05 and 0.45 ± 0.19 µv respectively. Comparing SSEP of 30 min post-injury with post-dosing, the difference was statistically significant (P < 0.01).While in control group, the values of SSEP at pre-injury, 30 min post-injury and post-dosing were 1.05 ± 0.39, 0.01 ± 0.02 and 0.02 ± 0.02 µv respectively. Comparing SSEP of 30 min post-injury with post-dosing, there was no statistical difference (P > 0.05). After 30 min injury, there were swelling and bleeding of spinal cord.LFB staining showed that both gray and white matter had swelling and bleeding and central canal was destroyed with varying degrees of demyelination. After 30 min of acute spinal cord injury, there are bleeding of gray and white matter with varying degrees of demyelination. Topical usage of K(+) blocker 4-AP-3-MeOH can effectively improve the conduction of SSEP after acute spinal cord injury in rats.

A clip compression method was used to produce acute spinal cord compression injury in rats. The force and duration of the spinal cord compression were independently varied, and functional recovery of the cord was assessed using the inclined plane technique. Mathematical modeling produced a curve defining the relationship between force, duration, and functional recovery for each week after injury. The study clearly showed the beneficial effect of decompression and that increasing either the force or duration of compression, or both, caused a reduction in recovery.

Objective To investigate the relationship of nuclear factor kappa B(NF-κB),Bcl-2 and Bax with limb function after acute spinal cord injury in rats. Methods Forty-eight rats were divided at random into a control group and an experimental group with 24 rats in each.The spinal cords of the rats in the experimental group were injured at the T8,9,10 level through moderate compression.Four hours,8 h,and 1,3,7 and 14 days after the injury,4 rats were selected randomly from each group and graded with a BBB score.They were then sacrificed and their spinal cords were collected.Immunohistochemical measurements were used to observe the expression of NF-κB, Bcl-2 and Bax. Results NF-κB,Bcl-2 and Bax were observed in the injured spinal nerve cells of rats in the exper imental group but were absent in the control group.After injury,the expression of these factors increased at first and then decreased.BBB scores for limb function increased gradually.No correlation was found between the changes in NF-κB and Bcl-2,but the expression of NF-κB was positively correlated with that of Bax.There was negative correla tion between NF-kB levels and BBB scores,and between NF-kB levels and the ratio of Bcl-2 to Bax. Conclusion In rats,there is a close negative correlation between NF-kappa B levels,the ratio of Bcl-2/Bax and limb function after acute spinaI cord iujury. Key words: Spinal cord injury; Nuclear factor kappa B; Apoptosis; Bcl-2; Bax; Limb function

The effect of acute spinal cord compression injury on thyroid function in the rat

To explore the effect and underlying mechanism of decompression(DE)combined with Governor Vessel(GV)electro-acupuncture(EA) on rats with acute severe upper cervical spinal cord compression injury. Thirty SPF rats were randomly divided into 5 groups(control group A, B and experiment group C, D, E), 6 rats in each group. The model of acute severe upper cervical spinal cord compression injury were made by forcing a balloon catheter put in atlas pillow clearance. The group A was blank one, the group B put balloon catheter in atlas pillow clearance without forcing, and the group C, D, E sustained compressed for 48 h. The group C received electric acupuncture intervention, selecting the Baihui and Dazhui point, having the continuous wave and frequency of 2 Hz, with the treatment time of 15 min and continuous treatment for 14 d; the group D received methylprednisolone intervention, injected by caudal vein; the group E did not received any intervention again. The arterial blood and injured spinal cord tissue of all the rats were obtained after 14 days' treatment, and BBB score was used to evaluate the change of each group hind limbs motor function, the contents of platelet activating factor(PAF) in injured spinal cord tissue and blood serum were assess by ELISA method; the Caspase-9 expression for each group after 14 days' treatment was assess by Western blot method. BBB scores were(21.000±0.000) points at the 6 time points, that was, 1 h, 48 h after forcing in control group, 24 h, 3 d, 7 d, 14 d after treating in experiment group; the score of experimental groups (group C, D, E) were always lower than control groups(group A, B); compared with group E, group C and D were significantly higher(P<0.05); and there was no significant difference between group C and group D(P>0.05). The results of PAF by ELISA method to measure:the concentration of serum PAF, there was no statistical difference among group A, B, D, E (P>0.05), group C was lower than the other groups (P<0.05); the concentration of tissue PAF, there was no significant difference between group A and group B(P>0.05), group D was significantly higher than that of group A, B, and C(P<0.05), group E was the highest one than that of the other groups(P<0.05). Western blot med tests showed that the Caspase-9 protein expression in group A and B was similar (P>0.05), group C was higher than that of group A and B(P<0.05), group D was higher than group A, B and C(P<0.05), group E was the highest than that of group A, B, C and D (P<0.05). Decompression and Governor Vessel electro-acupuncture on acute severe upper cervical spinal cord compression injury had a better effect compare with decompression and methylprednisolone or simple decompression only, its mechanism may be related to lower the PAF levels and downregulating Caspase-9 protein expression in spinal injury tissue.

To evaluate the sensitivity of an electro-monitoring method in acute nerve root injury, and to determine a proposed criterion for irreversible electrophysiologic degradation. Acute nerve root injury was induced by a clip compression model in rabbits, mimicking nerve root injury by a transpedicular screw. A common neuromonitoring technique, spinal somatosensory-evoked potential, was used to study the electrophysiologic change during the procedure. With the advent of the transpedicular screw system, increased risk of injury to the spinal root because of the passage of screws is not unexpected. Although both an experimental model and a clinical application in intraoperative neuromonitoring of spinal cord function have been established, the value of neuromonitoring of an acute spinal root injury remains obscure. Several neurophysiologic surveillance techniques have been used successfully to monitor the potential injury to the spinal cord during orthopedic procedures around the spinal cord and spinal column. Spinal somatosensory-evoked potential, which has the advantages of high amplitude and quick recording time, is used to detect nerve root impairment during the insertion of transpedicular screws. Experimental acute nerve root injury was induced in rabbits by direct hemostatic clip compression on the nerve root (S1) during different time intervals. Spinal somatosensory-evoked potential elicited by stimulating the sciatic nerve and recorded from a needle electrode at the L6-L7 interspinous ligament was monitored immediately before and after compression. Spinal somatosensory-evoked potential is sensitive enough to detect the compromise of a single nerve root and that a decrease in the amplitude is the most reliable and sensitive sign. With this model, there was a statistically significant correlation between the compression time and reduction of amplitude and delay of latency. The criterion for irreversible electrophysiologic change was an amplitude loss of more than 20% and a delay in latency immediately after nerve root compression. It was concluded that spinal somatosensory-evoked potential can provide immediate feedback of nerve root injury and should be considered for use during the dynamic phase of transpedicular screw insertion.

Studies were performed on the effect of triiodo-L-thyronine (T3) on clinical recovery and axonal counts in the pyramidal tract of 56 rats subjected to an acute spinal cord compression injury at T-7. The T3 was given at a daily dose of 5 micrograms/kg for 4 weeks to 28 rats in the treatment group. The treatment and control animals were tested weekly for clinical recovery, and cord function as determined by the inclined-plane technique. Groups of animals were killed at 4 weeks and 12 weeks, and the axons in the pyramidal tract cephalad and caudad to the injury site were counted in sections prepared with Holmes' silver stain. There was no difference in clinical recovery between the treatment and control groups. This negative result contrasts with other studies which showed improved recovery of cord-injured animals treated with thyroid hormones. The possible explanations for this discrepancy are discussed. Similarly, there was no difference in the axon counts between the treated and control groups. Thus, T3 did not improve recovery or axonal regeneration in the pyramidal tract of rats after acute spinal cord compression injury. Between 4 and 12 weeks, there was a marked reduction in the cephalad axon counts in the pyramidal tract in both groups, indicating that approximately 50% of the axons in the pyramidal tract had undergone retrograde degeneration or dying back by 12 weeks after this degree of injury. The T3 did not affect the degree of retrograde degeneration.

Agmatine inhibits nuclear factor-κB nuclear translocation in acute spinal cord compression injury rat model

The effect of triiodothyronine (T3) or thyroxine (T4) on functional recovery after acute spinal cord compression injury in the rat was assessed. Rats treated with T3 for 14 consecutive days after injury showed significantly improved recovery at 12 and 16 weeks, and rats treated with T4 for 4 days after injury showed significantly improved recovery at 12 weeks as compared with control animals. The possible modes of action of these two hormones on the injured spinal cord are briefly discussed.

Experimental investigation of an acute thoracic spinal cord injury model in rats involving acute clip compression that simulates human injury. To assess the dose-response of this model for the relationship between the force of injury on the rat thoracic spinal cord and histological and functional outcome measures. Acute extradural clip compression injury has been a reliable model for producing acute experimental cervical spinal cord injury; however, this model has not been formally evaluated with dose-response curves for acute injury of the thoracic spinal cord. After laminectomy at T2 in Sprague-Dawley rats, a modified aneurysm clip exerting a closing force of 20, 26, or 35 g was applied extradurally around the spinal cord at T2, and then rapidly released with cord compression persisting for 1 minute. These forces were selected to simulate acute compression injuries of mild to moderate, moderate, and moderate to severe degrees, respectively (n = 8/group). Motor activity was assessed weekly for 4 weeks with the Basso, Beattie, and Bresnahan (BBB) open field locomotor test. The injured spinal cord was then examined histologically including quantification of cavitation. A significant main effect was observed for clip force and BBB score (F(2,20) = 5.42, P = 0.013). For 4 weeks after injury, the BBB scores for the 20 g and 35 g clip injury groups were significantly different (P < 0.05). The cavitation volume at 4 weeks was directly proportional to the severity of injury: the 20 g group had significantly smaller cavities than the 35 g group (P < 0.05), and the cavitation volume correlated with the BBB scores. The rat thoracic cord clip compression model is a reproducible, clinically relevant spinal cord injury model. This is the first time that the force of clip compression injury in the rat thoracic cord has been correlated with both functional and histologic outcome measures.

Acute acalculous cholecystitis (AAC) is a very serious complication which can be found in patients with multiple serious traumatic lesions ('polytrauma'). Very few patients have been reported in the literature with an acute spinal injury and associated AAC. We report seven patients with polytrauma and acute spinal cord injury who developed AAC. All had no complaint of the principal warning symptom: right upper quadrant abdominal pain. All presented with a palpable mass in this site and the laboratory results were compatible with cholestasis. The diagnosis of AAC was confirmed both by ultra sound and CT scanning. We discuss the possible precipitating factors and the treatment. One hundred and ninety one patients were admitted to the Intensive Care Unit in our Hospital with SCI over a period of 2 years, all of these in the acute stage. AAC was diagnosed in seven patients among them. Our purpose is to call attention to this clinical condition which can complicate the outcome of patients with multiple trauma and acute spinal cord injury. To date AAC in this group of patients has been infrequently described in the available literature.

Intestinal dysfunction plays a crucial role in the developing of early and late complications in patients with spinal injury. Intestinal dysfunction can lead to metabolic imbalances like maldigestion, malabsorption, and intestinal dyskinesia. The study of metabolic processes in the tissues of the intestinal tube against the spinal cord injury can help to treat enteral and colonic insufficiency and reduce the number of surgical complications. The objective of the study is to examine the dynamics of metabolic processes in the tissues of the small and large intestines in acute spinal cord injury. Materials and Methods. The experiment was performed on laboratory animals, Wistar rats (n=22). Spinal cord injury was reproduced by complete transection of the spinal cord at the level of the Th5-Th6 vertebrae. The dynamics of cellular metabolism were assessed at different time intervals during the development of post-traumatic disease in vivo using fluorescence lifetime imaging microscopy (FLIM) based on autofluorescence in the spectral channel of the metabolic cofactor NAD(P)H. Results. The acute spinal cord injury is accompanied by changes in endogenous autofluorescence of the serous membrane tissues in the small and large intestines. A decrease in the activity of metabolic processes and their catabolic orientation are noted in the small intestine. On the contrary, metabolic processes intensify over time in the large intestine Conclusion. For the first time an in vivo experiment showed that the acute spinal injury was accompanied by a disruption of metabolic processes in the intestinal tissues. Fundamental multidirectionality was observed. Thus, a more balanced approach is necessary to combat intestinal failure in patients with acute traumatic spinal cord disease.

Objective To evaluate the effect of recombinant human erythropoietin (rhEPO) combined with methylprednisolone sodium succinate (MPSS), compared to MPSS alone, in the treatment of neurological function of patients with acute spinal cord injury (SCI). Methods Twenty-one patients presenting in hospital within less than 8 hours after acute SCI were randomly divided into two groups, the control group (10 cases) and the intervention group (11 cases). The control group was treated by MPSS combined with placebo, while the intervention group received MPSS with rhEPO.Both groups received MPSS 30 mg/kg within the first hour, and if the patient was admitted within 4 hours, MPSS would be applied in the treatment with 5.4 mg/kg per hour in the subsequent 23 hours and till 47 hours if the patient was admitted within 4-8 hours after injury.The intervention group received 500 U/kg rhEPO on admission and another 500 U/kg in the next 24 hours, compared with the control group where placebo was used.The evaluation on neurologic function recovery was made on admission, 24 h, 72 h, one week, 2 months and 6 months later, and statistical analysis was performed. Results The change in ASIA score: in the control group, the increase was seen from admission to 6 months after injury in terms of exercise, algesia and tactile sensation ( (31.2±6.6) points vs.(57.8±9.8) points, (41.4±9.5) points vs.(64.3±10.6) points, (39.2±6.8) points vs, (61.5±11.3) points), the increase also took place in the intervention group ( (29.5±7.2) points vs.(77.4±10.3) points, (39.7±7.2) points vs.(82.3±12.1) points, (37.4±6.2) points vs.(78.6±12.4) points). As time went on, the increase range in the intervention group became larger, compared with the control group.The difference between the two groups in ASLA score was statistically significant (P 0.05). Conclusion The application of MPSS combined with rhEPO within 8 hours after acute spinal injury may be more effective than MPSS with placebo in the neurologic dysfunction recovery. Key words: Recombinant human erythropoietin; Methylprednisolone sodium succinate; Spinal cord injury