Effects of decompression combined with electro-acupuncture on rat with acute severe upper cervical spinal cord compression injury

Acute spinal cord injury was induced by a clip compression model in rats to approximate spinal cord injury encountered in spinal surgery. Spinal somatosensory-evoked potential neuromonitoring was used to study the electrophysiologic change. To compare and correlate changes in evoked potential after acute compression at different core temperatures with postoperative neurologic function and histologic change, to evaluate current intraoperative neuromonitoring warning criteria for neural damage, and to confirm the protective effect of hypothermia in acute spinal cord compression injury by electrophysiologic, histologic, and clinical observation. With the increase in aggressive correction of spinal deformities, and the invasiveness of surgical instruments, the incidence of neurologic complication appears to have increased despite the availability of sensitive intraoperative neuromonitoring techniques designed to alert surgeons to impending neural damage. Many reasons have been given for the frequent failures of neuromonitoring, but the influence of temperature-a very important and frequently encountered factor-on evoked potential has not been well documented. Specifically, decrease in amplitude and elongation of latency seem not to have been sufficiently taken into account when intraoperative neuromonitoring levels were interpreted and when acceptable intraoperative warning criteria were determined. Experimental acute spinal cord injury was induced in rats by clip compression for two different intervals and at three different core temperatures. Spinal somatosensory-evoked potential, elicited by stimulating the median nerve and recorded from the cervical interspinous C2-C3, was monitored immediately before and after compression, and at 15-minute intervals for 1 hour. Spinal somatosensory-evoked potential change is almost parallel to temperature-based amplitude reduction and latency elongation. Significant neurologic damage induced by acute compression of the cervical spinal cord produced a degree of effect on the amplitude of spinal somatosensory-evoked potential in normothermic conditions that differed from the effect in moderately hypothermic conditions. Using the same electromonitoring criteria,moderately hypothermic groups showed a significantly higher false-negative rate statistically (35%) than normothermic groups (10%). Systemic cooling may protect against the detrimental effects of aggressive spinal surgical procedures. There is still not enough published information available to establish statistically and ethically acceptable intraoperative neuromonitoring warning and intervention criteria conclusively. Therefore, an urgent need exists for further investigation. Although a reduction of more than 50% in evoked potential still seems acceptable as an indicator of impending neural function loss, maintenance of more than 50% of baseline evoked potential is no guarantee of normal postoperative neural function, especially at lower than normal temperatures.

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.

All patients were acute, multi-segment cervical spinal cord compression injury secondary to subaxial cervical spine fracture. These patients underwent emergency posterior cervical pedicle screw-rod/plate instrumentation combined with unilateral open-door laminoplasty. Well-placed pedicle screws and good cervical canal dilation were achieved in all patients, as assessed by radiography. Patients were followed up for 6-10 months and showed at least one class improvement in spinal impairment. These cases suggest that simple posterior cervical pedicle screw-rod/plate instrumentation combined with extensive unilateral open-door laminoplasty could repair acute, multi-segment cervical spinal cord compression injury secondary to subaxial cervical spine fracture if the cervical spine sequence is well preserved and does not require restoration.

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

The objective of this study is to investigate whether preexisting severe cervical spinal cord compression affects the severity of paralysis once patients develop traumatic cervical spinal cord injury (CSCI) without bone injury. We retrospectively investigated 122 consecutive patients with traumatic CSCI without bone injury. The severity of paralysis on admission was assessed by the American Spinal Injury Association impairment scale (AIS). The degree of preexisting cervical spinal cord compression was evaluated by the maximum spinal cord compression (MSCC) and was divided into three categories: minor compression (MSCC ≤ 20 %), moderate compression (20 % < MSCC ≤ 40 %), and severe compression (40 % < MSCC). We investigated soft-tissue damage on magnetic resonance imaging to estimate the external force applied. Other potential risk factors, including age, sex, fused vertebra, and ossification of longitudinal ligament, were also reviewed. A multivariate logistic regression analysis was performed to investigate the risk factors for developing severe paralysis (AIS A-C) on admission. Our study included 103 males and 19 females with mean age of 65 years. Sixty-one patients showed severe paralysis (AIS A-C) on admission. The average MSCC was 22 %. Moderate compression was observed in 41, and severe in 20. Soft-tissue damage was observed in 91. A multivariate analysis showed that severe cervical spinal cord compression significantly affected the severity of paralysis at the time of injury, whereas both mild and moderate compression did not affect it. Soft-tissue damage was also significantly associated with severe paralysis on admission. Preexisting severe cervical cord compression is an independent risk factor for severe paralysis once patients develop traumatic CSCI without bone injury.

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.

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.

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.

Experiments were conducted to determine the therapeutic value of subarachnoid perfusion of the traumatized dog spinal cord with the fluorocarbon, Fluosol-DA (20%). Control dogs without lesions, but which had durotomy, subarachnoid catheter placement, and saline irrigation for 4 hours, did not have any residual neurological deficit. A series of 41 dogs underwent an acute spinal cord compression using an epidural balloon inflated to a pressure of 160 mm Hg and maintained for 1 hour. Treatment included durotomy only (11 dogs), durotomy with saline perfusion at room temperature (15 dogs), and durotomy with oxygenated Fluosol-DA perfusion at room temperature (15 dogs). The dogs underwent daily grading of neurological status for a 60-day period. Dogs undergoing perfusion of the spinal cord with either saline or oxygenated Fluosol-DA had significantly improved motor recovery (p less than 0.004) compared with dogs undergoing durotomy only. Perfusion with oxygenated Fluosol-DA resulted in significantly better motor recovery (p less than 0.05) than did perfusion with normal saline. Microscopic examination of the traumatized spinal cords failed to reveal a substantial difference between the three groups. However, dogs with better functional results tended to have less destruction of the white matter. Hemorrhagic necrosis of the central gray matter was consistently observed in all traumatized spinal cords.

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.

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

Brachytelephalangic chondrodysplasia punctata (CDPX1, OMIM: #302950) is a rare congenital skeletal dysplasia caused by arylsulfatase E deficiency (OMIM: #300180). Although the symptoms are usually mild, severe spinal cord compression by dysplastic vertebras may develop. We report four new cases with severe cervical spinal canal narrowing documented by radiography, magnetic resonance imaging (MRI), and autopsy. In all, nine cases of CDPX1 with severe cervical spinal cord compression have now been described. Because these cases account for a large proportion of all reported CDPX1 cases, we believe that an antenatal suspicion of CDPX1 should lead to genetic counseling and to investigations for spinal cord compression. After birth, this complication must be routinely anticipated, and we suggest spinal MRI in all CDPX1 infants. Unless spinal cord compression is confidently ruled out, we recommend that these newborns receive the same care as trauma patients suspected of craniocervical junction disruption.

SummaryThe objective of the study was to compare platelet activating factor (PAF) concentrations in pre-eclamptic and healthy normotensive pregnant women. Blood samples for measurement of platelet count, urea and creatinine, and of PAF by thin layer chromatography and high performance liquid chromatography were obtained from seven pre-eclamptic and seven healthy primigravidae. The main outcomes were PAF concentrations in the pre-eclampsia and control groups and correlation of PAF concentrations with gestational age. PAF concentration in the pre-eclamptic group was lower than that of the controls (18˙8 versus 36˙0, P = 0˙001). Both groups exhibited a correlation between plasma PAF levels and gestational age (study group, r =-0˙84; control group, r=-0˙79). Decreased circulating PAF levels in the pre-eclamptic group may represent loss of physiological control of vascular reactivity and platelet function by PAF.