Civilian Gunshot Injuries of the Spinal Cord: A Systematic Review of the Current Literature

Background

The principles that guide management of spinal cord injury (SCI) derive from injury resulting from blunt trauma, not gunshot wounds. Civilian gunshot-induced spinal cord injury (CGSWSCI) is a common, potentially serious cause of neurological deficit; there is disagreement about whether the same approaches used for SCI caused by blunt-force trauma should apply to gunshot-induced SCI.

Questions/purposes

We reviewed the literature to answer the following questions regarding presentation and outcome of gunshot wound-induced SCI: (1) Are there differences in recovery prognosis between complete SCI and other patterns of SCI in CGSWSCI. (2) Does the use of steroids improve neurological recovery? (3) Does surgery to remove the bullet affect neurological recovery in CGSWSCI? (4) Does surgery result in an increased risk of complications of treatment?

Methods

We performed a systematic literature review of articles related to civilian gunshot injuries to the spine. Information relating to incidence, pattern of neurological injury, associated injuries, treatment, neurological outcome, and associated complications was extracted. Three independent reviewers assessed the strength of evidence present in the literature by examining quality, quantity, and consistency of results.

Results

A total of 15 articles met the predetermined inclusion criteria. Complete SCIs are associated with the worst functional recovery regardless of treatment. Steroids do not appear to have any added benefit in terms of restoring sensory and motor function. There appears to be some neurologic benefit to surgical decompression with intracanalicular bullet retrieval in patients with an incomplete lesion and a cauda equina syndrome. Complication rates are greater in operated patients.

Conclusions

These findings should be interpreted with caution because of considerable heterogeneity among the studies in the literature on gunshot-induced SCI and because of generally poor-quality study design and a high associated risk of selection bias. Supportive management should be the primary method of care, whereas surgery should be an option in case of radiographic evidence of a static compression on the spinal cord. Future studies are necessary to develop better treatment guidelines for patients with gunshot wound-associated SCI.     

Spinal cord injury in the pediatric population: a systematic review of the literature

Spinal Cord Injury (SCI) in the pediatric population is relatively rare but carries significant psychological and physiological consequences. An interdisciplinary group of experts composed of medical and surgical specialists treating patients with SCI formulated the following questions: 1) What is the epidemiology of pediatric spinal cord injury and fractures?; 2) Are there unique features of pediatric SCI which distinguish the pediatric SCI population from adult SCI?; 3) Is there evidence to support the use of neuroprotective approaches, including hypothermia and steroids, in the treatment of pediatric SCI? A systematic review of the literature using multiple databases was undertaken to evaluate these three specific questions. A search strategy composed of specific search terms (Spinal Cord Injury, Paraplegia, Quadriplegia, tetraplegia, lapbelt injuries, seatbelt injuries, cervical spine injuries and Pediatrics) returned over 220 abstracts that were evaluated and by two observers. Relevant abstracts were then evaluated and papers were graded using the Downs and Black method. A table of evidence was then presented to a panel of experts using a modified Delphi approach and the following recommendation was then formulated using a consensus approach: Pediatric patients with traumatic SCI have different mechanisms of injury and have a better neurological recovery potential when compared to adults. Patients with SCI before their adolescent growth spurt have a high likelihood of developing scoliosis. Because of these differences, traumatic SCI should be highly suspected in the presence of abnormal neck or neurological exam, a high-risk mechanism of injury or a distracting injury even in the absence of radiological anomaly.     

Chronic activity-based therapy does not improve body composition,insulin-like growth factor-I,adiponectin, or myostatin in persons with spinal cord injury

Spinal cord injury (SCI) induces dramatic changes in body composition including reductions in fat-free mass (FFM) and increases in fat mass (FM).

Objective

To examine changes in body composition in response to chronic activity-based therapy (ABT) in persons with SCI.

Design

Longitudinal exercise intervention.

Methods

Seventeen men and women with SCI (mean age = 36.1 ± 11.5 years) completed 6 months of supervised ABT consisting of load bearing, resistance training, locomotor training, and functional electrical stimulation. At baseline and after 3 and 6 months of ABT, body weight, body fat, and FFM were assessed using dual-energy X-ray absorptiometry, and fasting blood samples were obtained to assess changes in insulin-like growth factor-I (IGF-I), adiponectin, and myostatin.

Results

Across all subjects, there was no change (P > 0.05) in body weight, percent body fat, or FFM of the leg, arm, or trunk, whereas whole-body FFM declined (P = 0.02, 50.4 ± 8.4 to 49.2 ± 7.4 kg). No changes (P = 0.21–0.41) were demonstrated in IGF-I, adiponectin, or myostatin during the study.

Conclusions

Chronic ABT focusing on the lower extremity does not slow muscle atrophy or alter body fat, body mass, or regional depots of FFM in persons with SCI. Further, it does not induce beneficial changes in adiponectin, myostatin, or IGF-I. Alternative exercise-based therapies are needed in SCI to reverse muscle atrophy and minimize the onset of related health risks.     

Chronic spinal compression model in minipigs: a systematic behavioral, qualitative, and quantitative neuropathological study

The goal of the present study was to develop a porcine spinal cord injury (SCI) model, and to describe the neurological outcome and characterize the corresponding quantitative and qualitative histological changes at 4-9 months after injury. Adult Gottingen-Minnesota minipigs were anesthetized and placed in a spine immobilization frame. The exposed T12 spinal segment was compressed in a dorso-ventral direction using a 5-mm-diameter circular bar with a progressively increasing peak force (1.5, 2.0, or 2.5?kg) at a velocity of 3?cm/sec. During recovery, motor and sensory function were periodically monitored. After survival, the animals were perfusion fixed and the extent of local SCI was analyzed by (1) post-mortem MRI analysis of dissected spinal cords, (2) qualitative and quantitative analysis of axonal survival at the epicenter of injury, and (3) defining the presence of local inflammatory changes, astrocytosis, and schwannosis. Following 2.5-kg spinal cord compression the animals demonstrated a near complete loss of motor and sensory function with no recovery over the next 4-9 months. Those that underwent spinal cord compression with 2 kg force developed an incomplete injury with progressive partial neurological recovery characterized by a restricted ability to stand and walk. Animals injured with a spinal compression force of 1.5?kg showed near normal ambulation 10 days after injury. In fully paralyzed animals (2.5?kg), MRI analysis demonstrated a loss of spinal white matter integrity and extensive septal cavitations. A significant correlation between the magnitude of loss of small and medium-sized myelinated axons in the ventral funiculus and neurological deficits was identified. These data, demonstrating stable neurological deficits in severely injured animals, similarities of spinal pathology to humans, and relatively good post-injury tolerance of this strain of minipigs to spinal trauma, suggest that this model can successfully be used to study therapeutic interventions targeting both acute and chronic stages of SCI.     

Intracanal pressure in compressive spinal cord injury: reduction with hypothermia

Most cases of human spinal cord injury (SCI) are accompanied by continuing cord compression. Experimentally, compression results in rapid neurological decline over hours, suggesting a rise in intracanal pressure local to the site of injury. The aim of this study was to measure the rise in local intracanal pressure accompanying progressive canal occlusion and to determine the relationship between raised intracanal pressure and neurological outcome. We also aimed to establish whether hypothermia was able to reduce raised intracanal pressure. We demonstrate that, following SCI in F344 rats, local intracanal pressure remains near normal until canal occlusion exceeds 30% of diameter, whereupon a rapid increase in pressure occurs. Intracanal pressure appears to be an important determinant of neurological recovery, with poor long-term behavioural and histological outcomes in animals subject to 8?h of 45% canal occlusion, in which intracanal pressure is significantly elevated. In contrast, good neurological recovery occurs in animals with near normal intracanal pressure (animals undergoing 8?h of 30% canal occlusion or those undergoing immediate decompression). We further demonstrate that hypothermia is an effective therapy to control raised intracanal pressure, rapidly reducing elevated intracanal pressure accompanying critical (45%) canal occlusion to near normal. Overall these data indicate that following SCI only limited canal narrowing is tolerated before local intracanal pressure rapidly rises, inducing a sharp decline in neurological outcome. Raised intracanal pressure can be controlled with hypothermia, which may be a useful therapy to emergently decompress the spinal cord prior to surgical decompression.     

A phase I/IIa clinical trial of a recombinant Rho protein antagonist in acute spinal cord injury

Multiple lines of evidence have validated the Rho pathway as important in controlling the neuronal response to growth inhibitory proteins after central nervous system (CNS) injury. A drug called BA-210 (trademarked as Cethrin(?)) blocks activation of Rho and has shown promise in pre-clinical animal studies in being used to treat spinal cord injury (SCI). This is a report of a Phase I/IIa clinical study designed to test the safety and tolerability of the drug, and the neurological status of patients following the administration of a single dose of BA-210 applied during surgery following acute SCI. Patients with thoracic (T2-T12) or cervical (C4-T1) SCI were sequentially recruited for this dose-ranging (0.3?mg to 9?mg Cethrin), multi-center study of 48 patients with complete American Spinal Injury Association assessment (ASIA) A. Vital signs; clinical laboratory tests; computed tomography (CT) scans of the spine, head, and abdomen; magnetic resonance imaging (MRI) of the spine, and ASIA assessment were performed in the pre-study period and in follow-up periods out to 1 year after treatment. The treatment-emergent adverse events that were reported were typical for a population of acute SCI patients, and no serious adverse events were attributed to the drug. The pharmacokinetic analysis showed low levels of systemic exposure to the drug, and there was high inter-patient variability. Changes in ASIA motor scores from baseline were low across all dose groups in thoracic patients (1.8±5.1) and larger in cervical patients (18.6±19.3). The largest change in motor score was observed in the cervical patients treated with 3?mg of Cethrin in whom a 27.3±13.3 point improvement in ASIA motor score at 12 months was observed. Approximately 6% of thoracic patients converted from ASIA A to ASIA C or D compared to 31% of cervical patients and 66% for the 3-mg cervical cohort. Although the patient numbers are small, the observed motor recovery in this open-label trial suggests that BA-210 may increase neurological recovery after complete SCI. Further clinical trials with Cethrin in SCI patients are planned, to establish evidence of efficacy.     

低剂量他克莫司治疗大鼠急性脊髓损伤的实验研究

目的：探讨低剂量他克莫司（tacrolimus，又名FK506）对大鼠急性脊髓损伤是否具有神经保护作用。方法：雄性Wistar大鼠72只，随机分为假手术组（12只）、损伤组（30只）和FK506治疗组（30只）。采用Allen’s打击法致伤大鼠T10脊髓，假手术组仅做椎板切除术。FK506治疗组在脊髓损伤后5min一次性经尾静脉注射FK5060．3mg／kg，其余两组以相同方法给予等量生理盐水。致伤后30min、6h、24h、48h、72h取伤段脊髓组织行病理观察及原位末端标记法（TUNEL）检测神经细胞凋亡，伤后1、3、7、14、21d行脊髓功能BBB评分和斜板实验。结果：伤后3、7、14、21d，FK506治疗组斜板实验和BBB评分明显优于损伤组，两组间比较差异有显著性（P〈0．05）；伤后各时间点FK506治疗组脊髓损伤区出血坏死较损伤组轻；伤后6、24、48、72h神经细胞凋亡FK506治疗组较损伤组明显减少，两组间比较差异有显著性（P〈0．05）。结论：在大鼠急性脊髓损伤后早期应用低剂量他克莫司（0．3mg/kg）治疗对神经具有保护作用，可减少神经细胞凋亡，减轻脊髓继发性损伤，促进脊髓功能恢复。     

早期脊髓复苏在急性颈脊髓损伤治疗中的临床意义

目的：评价早期脊髓复苏在急性颈脊髓损伤治疗中的意义。方法：106例急性颈脊髓损伤患者，其中脊髓完全性损伤21例，脊髓不完全性损伤85例。早期脊髓复苏方案包括：（1）维持呼吸道通畅和足够有效的血容量，维持平均动脉血压100mmHg以上，血氧饱和度在95％以上；（2）应用大剂量甲基强的松龙或地塞米松等药物治疗；（3）行颅骨牵引制动或复位颈椎；（4）早期进行颈椎减压植骨融合内固定术；（5）术后早期应用高压氧治疗。结果：死亡7例，失访5例，94例获得12～52个月的随访。随访病例中69例患者神经功能获得改善。其中完全性损伤组有效率为23.3％，不完全性损伤组有效率为74．1％，总有效率为65．1％。结论：颈脊髓损伤后早期复苏治疗是保留和恢复残留脊髓神经功能较为有效的措施。     

Recovery from a spinal cord injury: significance of compensation, neural plasticity, and repair

Clinical recovery after a lesion of the central nervous system (CNS) can be attributed to mechanisms of functional compensation, neural plasticity, and/or repair. The relative impact of each of these mechanisms after a human spinal cord injury (SCI) has been explored in a prospective European multi-center study in 460 acute traumatic SCI subjects. Functional (activities of daily living and ambulatory capacity), neurological (sensory-motor deficits), and spinal conductivity (motor- and somato-sensory evoked potentials) measures were repeatedly followed over 12 months. In accordance with previous studies, complete SCI subjects (cSCI; n = 217) improved in activities of daily living unrelated to changes of the neurological condition, while incomplete SCI subjects (iSCI; n = 243) showed a greater functional and neurological recovery. The functional recovery in iSCI subjects was not related to an improvement of spinal conductivity, as reflected in unchanged latencies of the evoked potentials. This is in line with animal studies, where spinal conductivity of damaged spinal tracts has been reported to remain unchanged. These findings support the assumption that functional recovery occurs by compensation, especially in cSCI and by neural plasticity leading to a greater improvement in iSCI. Relevant repair of damaged spinal pathways does not take place.     

Change in Neuroplasticity-Related Proteins in Response to Acute Activity-Based Therapy in Persons With Spinal Cord Injury

Background:

Activity-based therapy (ABT) focuses on regaining motor and sensory function below the level of the lesion in persons with a spinal cord injury (SCI). This is accomplished through repetitive training of specific motor tasks. Research has shown that ABT may increase neuroplasticity in the rat and human spinal cord.

Objective:

The primary aim of this study was to examine acute alterations in neuroplasticity-related proteins during ABT in persons with SCI.

Methods:

Volunteers were current participants in an ABT program and consisted of 12 men and 3 women (age, 31.8 ± 10.9 years) with chronic SCI (injury duration, 63.9 ± 54.4 months). A single 2-hour bout of ABT consisted of standing load bearing, body weight-supported treadmill training, whole body vibration, and functional electrical stimulation. Blood samples were obtained at baseline and immediately after completion of each modality to determine serum levels of brain-derived neurotrophic factor (BDNF), prolactin, and cortisol.

Results:

One-way analysis of variance (ANOVA) with repeated measures was used to examine differences in proteins over time. Results revealed baseline levels of BDNF (2.37 ± 1.41 ng/mL) that were lower than previous research has demonstrated in persons with SCI. No change in BDNF or cortisol was found, although prolactin was significantly reduced in response to ABT.

Conclusion:

Despite the length of the bout, acute changes in BDNF were not observed. Whether different intensities or modalities of ABT may promote acute increases in serum BDNF in individuals with SCI remains to be determined and further study is merited.Key words: BDNF, cortisol, exercise, prolactin, rehabilitation, spinal cord injuryRecent research demonstrates that exercise after spinal cord injury (SCI) may increase neuroplasticity in the rat and cycling. Exercise-mediated alterations in BDNF seem to be intensity-dependent, as no change in BDNF was shown during mild exercise versus human spinal cord.^1,2 However, the mechanisms more intense workloads. In addition, prolactin explaining this neuroplasticity are still relatively unexplored. Data from animal studies suggest that neurotrophic factors released during exercise may be a contributing factor. One such protein is brain-derived neurotrophic factor (BDNF), which is found in the brain and periphery. It promotes synaptic plasticity and neuronal growth in noninjured animals and alters motoneuron survival in animals with SCI. Increased levels of BDNF were demonstrated in healthy adults exercising at 55% and 75% maximal workload (Wmax),⁹ as well as in individuals with multiple sclerosis performing 30 minutes of moderate has been identified as a possible mediator of neuroplasticity in the spinal cord as it serves as a marker of serotonergic activation during exercise.¹² In a previous study, prolactin was increased (P < .05) in response to time trial arm ergometry in SCI athletes, yet mild exercise did not induce changes in prolactin. Whether this discrepant response of prolactin to exercise occurs in other individuals with SCI remains to be determined.Exercise also tends to increase cortisol release that may impact neurogenesis via an inhibition of growth in the hippocampus and/or through regulation of BDNF. Nevertheless, it has been suggested that this enhanced stressor response may have little effect upon neuroplasticity; as no correlation has been revealed between BDNF and cortisol, further study is warranted.It is not known whether acute exercise induces significant changes in neurotrophins in men and women with SCI, as only one study has examined this issue. Rojas-Vega et al required previously trained elite male athletes (VO₂max = 34.5 mL/kg/ min) with SCI from T4-T12 to complete a 42-km hand-biking time trial during which blood samples were obtained to measure concentrations of BDNF, cortisol, and prolactin.¹³ Results demonstrated increased (P < .05) BDNF with initiation of exercise, although postexercise values were similar to baseline. Postexercise measures of cortisol and prolactin were also higher (P < .05) than baseline levels. The population that was studied is relatively unique and exercise performed is atypical of common practice in the rehabilitation of persons with SCI, so it remains to be determined whether similar acute increases in neurotrophins would be revealed in less active individuals completing different exercise modalities.Activity-based therapy (ABT) consisting of high-volume training focusing on the core and lower extremities has recently been identified as an effective technique to promote functional recovery in this population.^17–19 The primary aim of this study was to examine acute changes in BDNF, cortisol, and prolactin during a prolonged bout of ABT in men and women with SCI. Individual changes in these proteins were also examined to better understand how different rehabilitation modalities may affect neuroplasticity. These data have the potential to impact the neurorehabilitation of persons with SCI. It was hypothesized that exercise would elicit significant acute changes in BDNF and cortisol as previously demonstrated in this population.¹³     

CD11d Antibody Treatment Improves Recovery in Spinal Cord-Injured Mice

Acute administration of a monoclonal antibody (mAb) raised against the CD11d subunit of the leukocyte CD11d/CD18 integrin after spinal cord injury (SCI) in the rat greatly improves neurological outcomes. This has been chiefly attributed to the reduced infiltration of neutrophils into the injured spinal cord in treated rats. More recently, treating spinal cord-injured mice with a Ly-6G neutrophil-depleting antibody was demonstrated to impair neurological recovery. These disparate results could be due to different mechanisms of action utilized by the two antibodies, or due to differences in the inflammatory responses between mouse and rat that are triggered by SCI. To address whether the anti-CD11d treatment would be effective in mice, a CD11d mAb (205C) or a control mAb (1B7) was administered intravenously at 2, 24, and 48?h after an 8-g clip compression injury at the fourth thoracic spinal segment. The anti-CD11d treatment reduced neutrophil infiltration into the injured mouse spinal cord and was associated with increased white matter sparing and reductions in myeloperoxidase (MPO) activity, reactive oxygen species, lipid peroxidation, and scar formation. These improvements in the injured spinal cord microenvironment were accompanied by increased serotonin (5-HT) immunoreactivity below the level of the lesion and improved locomotor recovery. Our results with the 205C CD11d mAb treatment complement previous work using this anti-integrin treatment in a rat model of SCI.     

Lower extremity functional electrical stimulation cycling promotes physical and functional recovery in chronic spinal cord injury

Abstract

Objective

To examine the effect of long-term lower extremity functional electrical stimulation (FES) cycling on the physical integrity and functional recovery in people with chronic spinal cord injury (SCI).

Design

Retrospective cohort, mean follow-up 29.1 months, and cross-sectional evaluation.

Setting

Washington University Spinal Cord Injury Neurorehabilitation Center, referral center.

Participants

Twenty-five people with chronic SCI who received FES during cycling were matched by age, gender, injury level, and severity, and duration of injury to 20 people with SCI who received range of motion and stretching.

Intervention

Lower extremity FES during cycling as part of an activity-based restorative treatment regimen.

Main outcome measure

Change in neurological function: motor, sensory, and combined motor–sensory scores (CMSS) assessed by the American Spinal Injury Association Impairment scale. Response was defined as ≥1 point improvement.

Results

FES was associated with an 80% CMSS responder rate compared to 40% in controls. An average 9.6 CMSS point loss among controls was offset by an average 20-point gain among FES subjects. Quadriceps muscle mass was on average 36% higher and intra/inter-muscular fat 44% lower, in the FES group. Hamstring and quadriceps muscle strength was 30 and 35% greater, respectively, in the FES group. Quality of life and daily function measures were significantly higher in FES group.

Conclusion

FES during cycling in chronic SCI may provide substantial physical integrity benefits, including enhanced neurological and functional performance, increased muscle size and force-generation potential, reduced spasticity, and improved quality of life.     

The impact of specialized centers of care for spinal cord injury on length of stay, complications, and mortality: a systematic review of the literature

Specialized centers of care for spinal cord injury (SCI) were first established in 1944 in England. The objective of these centers is to improve care and neurological recovery of patients suffering from a spinal cord injury. An interdisciplinary group of experts composed of medical and surgical specialists treating patients with SCI formulated the following questions: (1) Is there any evidence to suggest that specialized centers of care in SCI decrease the length of patient stay? and (2) Is there evidence that specialized centers of care for SCI reduce mortality and secondary complications? A systematic review of the current evidence was performed using multiple databases to answer these two specific questions. Two independent reviewers graded each paper using the Black and Downs method. Recommendations were then formulated based on the evidence available and were reviewed by a panel of experts using a modified Delphi approach. Two recommendations were formulated and both received complete agreement from a panel of experts. The first recommendation is "Early transfer of a patient with traumatic SCI to a specialized center of care should be done promptly to decrease overall length of stay." The second recommendation is "Early transfer of patients with traumatic SCI to an integrated multidisciplinary specialized center of care decreases overall mortality, and the number and severity of complications."     

Effect of VEGF and CX43 on the promotion of neurological recovery by hyperbaric oxygen treatment in spinal cord–injured rats

Background contextSpinal cord injury (SCI) is a serious health issue that may result in high health care costs, with additional social and psychological burdens. Hyperbaric oxygen (HBO) treatment has been found to be beneficial for neurological recovery; however, the underlying mechanisms are yet to be characterized.PurposeThe aim of this study was to investigate the mechanisms of HBO treatment in SCI by measuring the expression levels of vascular endothelial growth factor (VEGF) and Connexin43 (CX43) in the injured spinal cord tissue.Study design/settingAn experiment animal study of rats undergoing SCI and HBO treatment.MethodsThe spinal cord injury model was established in rats, which were randomly divided into the following four groups: (1) the sham-operated group (SH), (2) the sham-operated and hyperbaric oxygen treatment group (SH+HBO), (3) the spinal cord injury group (SCI), and (4) the spinal cord injury and hyperbaric oxygen treatment group (SCI+HBO). For groups of SH+HBO and SCI+HBO, the animals received 1 hour of HBO at 2.0 ATA in 100% O2 twice per day for 3 days and then daily for the following days consecutively after surgery. After operation, neurological assessments were performed, the spinal cord tissue samples were harvested for histopathological evaluation, Western blot and real-time polymerase chain reaction analysis.ResultsThe Basso-Bettie-Bresnahan scores were significantly improved in the SCI+HBO group compared with the SCI group on the postoperative 7th and 14th days. The histology scores were significantly decreased by HBO treatment compared with that in the SCI group on the postoperative 3rd, 7th, and 14th days. Western blot analysis and real-time polymerase chain reaction revealed that the expression level of vascular endothelial growth factor (VEGF) in the SCI+HBO group was significantly increased compared with the SCI group. The protein expression level of CX43 and its mRNA level in the SCI+HBO group were significantly decreased on the postoperative 3rd and 7th days, whereas its expression was significantly increased by HBO treatment on the postoperative 14th day compared with the SCI group.ConclusionsHBO treatment improved neurological recovery when applied after SCI. The expression level changes of VEGF and CX43 may contribute to the further understanding on the molecular mechanisms of HBO treatment on SCI.     

芬苯达唑对大鼠脊髓损伤后免疫反应和运动功能恢复的影响

目的：观察芬苯达唑对脊髓损伤大鼠的CD45R阳性B细胞、IgG免疫反应以及运动功能恢复的影响。方法将75只成年雌性SD大鼠随机分为假手术组、模型对照组和芬苯达唑组,每组25例。假手术组、模型对照组术前4周给予常规啮齿动物饲料喂食（含18%蛋白质的饲料）,芬苯达唑组术前4周给予加入芬苯达唑的常规啮齿动物饲料喂食。用Allen法构建脊髓损伤模型,分别于术后第1、7、14、21、28天行Basso?Beatti?Bresnahan（BBB）运动功能评估,利用免疫组化检测损伤部位脊髓组织中IgG的表达水平,利用免疫荧光检测脊髓损伤部位CD45R阳性B细胞的信号水平。结果脊髓损伤后,模型对照组和芬苯达唑组的BBB评分均显著低于假手术组（均P＜0.05）,随着时间的延长,两组的BBB运动评分均逐渐有所恢复,但仍低于假手术组;脊髓损伤后第1天,模型对照组与芬苯达唑组的BBB运动评分分别为（3.10±0.29）分、（3.23±0.48）分,差异尚无统计学意义;而在脊髓损伤后的第7、14、21、28天,芬苯达唑组的BBB评分均高于模型对照组,差异均有统计学意义（均P＜0.05）。免疫组化检查证实损伤部位脊髓标本的IgG水平显著升高,第7天开始,芬苯达唑组各个时间点的IgG免疫反应水平均低于模型对照组,差异均有统计学意义（均P＜0.05）。免疫荧光检查证实脊髓损伤后损伤部位脊髓节段CD45R阳性B细胞信号水平显著升高,第7天开始,芬苯达唑组各个时间点脊髓损伤部位的CD45R阳性B细胞的信号水平均低于模型对照组,差异均有统计学意义（均P＜0.05）。结论芬苯达唑预处理可降低脊髓组织中IgG的表达水平及脊髓损伤部位的CD45R阳性B细胞的信号水平,促进脊髓损伤后的神经功能恢复。     

跳水致颈髓损伤早期综合治疗的疗效评价

[目的]探讨跳水致颈髓损伤早期综合治疗的临床效果。[方法]2001～2005年27例跳水致颈脊髓损伤患者，其中脊髓完全性损伤15例，脊髓不完全性损伤12例。早期综合治疗方案包括：（1）全身治疗：维持呼吸道通畅和有效循环血容量，保证收缩压在90mmHg以上；血氧饱和度在90％以上；（2）早期应用大剂量甲基强的松龙或地塞米松等药物治疗；（3）颅骨牵引制动或颈椎复位；（4）早期进行手术减压植骨融合内固定术；（5）术后早期行高压氧治疗。术后定期复查x线片观察损伤节段的稳定性和植骨融合率以及有无内固定并发症。以ASIA分级标准和感觉、运动评分判定脊髓神经功能恢复情况。[结果]27例患者随访6～36个月，平均28个月；本组病例无术中、术后并发症，切口愈合良好；术后3个月复查x线片，损伤节段稳定，植骨融合良好，无钢板断裂、螺钉松动脱落等现象。13例患者神经功能获得改善，总有效率为48．1％，其中完全性损伤组有效率为20％，不完全性损伤组有效率为83．3％。完全性损伤患者ASIA分级变化不明显，但其评分较入院时可有相应的增加，不完全性损伤患者ASIA分级和感觉运动评分均有明显的提高。[结论]颈髓损伤后早期综合治疗可以促进脊髓神经功能恢复。     

Effect of Acrylamide on Neurological Recovery Following Spinal Cord Injury in Rats

Summary  Acrylamide (ACR) is a cumulative neurotoxin which causes axonal degeneration in animals and man. Industrial workers exposed to ACR have been reported to suffer from a variety of central and peripheral neuropathological symptoms including numbness of hands and feet, skin peeling and muscular weakness of legs. These reports suggest that the body burden of ACR may be a risk factor in recovery patterns following neurotrauma. The present study was designed to assess the effect of ACR on neurological recovery following spinal cord injury (SCI) in rats.  Male Sprague-Dawley rats weighing 200–230 g were anaesthetised with chloral hydrate and laminectomy was performed at T 7–8 level leaving the dura intact. A compression plate (2.2×5.0 mm) loaded with a weight of 35 g was placed on the exposed cord for 5 minutes. Animals were divided into seven groups of eight rats each. The animals in Group 1 served as control whereas rats in Group 2 underwent laminectomy alone (sham). The rats in Group 3 to 6 were subjected to SCI as mentioned above. Animals in Groups 4, 5 and 6 also received ACR in the doses of 10 mg/kg, 20 mg/kg and 40 mg/kg, i.p., respectively in addition to SCI, whereas the rats in Group 7 received ACR alone at a dose of 40 mg/kg body weight. The first dose of ACR was given 30 minutes before SCI, followed by daily administration of drug for 7 days. Post traumatic neurological recovery was recorded daily for 10 days using a modified Tarlov score, inclined plane test and sensory and vocal score. Electrophysiological changes were assessed using somatosensory and corticomotor evoked potentials. The animals were sacrificed at different time intervals and the injured site of the spinal cord was analysed for lipid hydroperoxides (LPH), conjugated dienes (CD) and glutathione (GSH). Neuropathological changes in the spinal cord were assessed using light microscopy. The rats exposed to compression injury alone showed a maximum neurological deficit at 24 hr and then a gradual recovery was observed over a period of 10 days. The rats treated with ACR along with SCI showed poor or no recovery over a period of 10 days. Our electrophysiological and histopathological studies also confirmed that concomitant exposure to ACR produces a significant deleterious effect on the recovery from SCI. SCI induced increase in oxidative stress (increase in LPH and CD and decrease in GSH) is also exacerbated by ACR suggesting a role of free radicals.  The results of this study suggest that increased body burden of ACR may retard the recovery from neurotrauma or even lead to permanent disability.     

骨髓间充质干细胞治疗脊髓损伤的研究进展

骨髓间充质干细胞以其良好的增殖和多向分化能力,取材方便,易于分离培养和自体移植无免疫源性等特征而成为细胞移植治疗脊髓损伤研究的重点之一。目前已证实蛛网膜下腔注射是最理想的骨髓间充质干细胞治疗途径。早期临床应用骨髓间充质干细胞移植是安全的,对脊髓损伤的修复作用是肯定的,其作用机制可能与骨髓间充质干细胞的替代作用、神经营养作用、抑制免疫反应及促进轴突再生等有关。