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PubMed1983

Radiological assessment of thoracolumbar spinal injuries.

The vertebrae of the thoracolumbar junction are extremely vulnerable to serious injury. Spontaneous reduction of these unstable fractures or dislocations often occurs, making radiological diagnosis of the full extent of these injuries difficult. The technique of radiological examination applicable is described, and important radiological signs are emphasized. The anatomical factors predisposing the thoracolumbar junction to trauma and the mechanism of injury are briefly described.

Fractures, Bone↗
PubMed1980

The diagnostic value of the anteroposterior radiograph for thoracolumbar spinal injuries.

Identification of fractures of the posterior elements of thoracolumbar vertebrae is important because these fractures render the spine unstable. Technically it is difficult to demonstrate the posterior elements on a supine lateral radiograph in patients with multiple injuries. Careful inspection of the posterior vertebral structures on the anteroposterior view will reveal valuable information. Three radiological signs--interpediculate widening, increased interspinal distance and the appearance of 'Chance' fractures--are discussed.

Fractures, Bone↗
PubMedDate not supplied

Thoracolumbar spinal injuries. A comparative study of recumbent and operative treatment in 100 patients.

Internal fixation of fractures of the thoracolumbar spine with early ambulation is evaluated in this study of 100 patients with 106 fractures, 34 of which were treated by recumbency, 13 with Meurig-Williams plates, and 59 with Harrington rods. Fracture reduction in the recumbent group was 14% unsatisfactory and 82% satisfactory; only one fracture was anatomically reduced. After plating, 38% of fracture reductions were unsatisfactory and 61% satisfactory. Harrington rod reduction and internal fixation resulted in 67% anatomic, 31% satisfactory, and 2% unsatisfactory reductions. Neurologic improvement in partial lesions was 53% with Harrington rods and 44% with recumbent treatment. For paraplegic patients the time between treatment and wheelchair mobilization was reduced from 10.5 weeks with recumbent treatment to 5.3 weeks with Harrington instrumentation. Rehabilitation time for ambulatory candidates was decreased from 7.1 weeks to 2.5 weeks. Complications were reduced from 18% in the recumbent group to 7% in the Harrington rod groups. By using the three above-three below, rod long/fuse short approach rather than the two above-two below with fusion over the length of the rods technique, the number of anatomic reductions was increased from 70% to 82% and the length of the fusion decreased from 4.8 levels to 1.4 levels.

Adolescent↗
PubMedDate not supplied

[Respiratory obstruction caused by retropharyngeal hematoma secondary to cervical spinal injury. Report of a case].

A case of severe airway obstruction secondary to retropharyngeal hematoma in a young multiple trauma patient with a stable occipitoatloid capsular-ligamentous injury is reported. The onset of mechanical obstruction occurred eight hours after the trauma requiring emergent oral intubation, and lasted seventeen days. The initial lateral cervical spine radiograph was negative, whereas the second one performed 7 hours after and initially underestimated, showed a large prevertebral soft tissue swelling. The initial difficult radiological diagnosis of trauma is described, and the therapeutic implications are discussed.

Adult↗
PubMed2000

Pharmacological interventions for acute spinal cord injury.

BACKGROUND: Acute spinal cord injury is a devastating condition typically affecting young people with a preponderance of males. Pharmacological treatment in the early hours of the injury is aimed at reducing the extent of permanent paralysis during the rest of the patient's life. OBJECTIVES: To review randomized trials of pharmacological therapies for acute spinal cord injury. SEARCH STRATEGY: The review draws on the search strategy developed by the Cochrane Injuries Group. In addition, files of the National Acute Spinal Cord Injury Study have been reviewed. SELECTION CRITERIA: All published or unpublished randomized controlled trials of pharmacological treatment for acute spinal cord injury in any language. DATA COLLECTION AND ANALYSIS: Data have been abstracted from original trial reports. For the NASCIS, Japanese and French trials, additional data (e.g. SDs) have been obtained from the original authors. MAIN RESULTS: There are few trials in this area of medical care. Only one therapy has been extensively studied, methylprednisolone sodium succinate, which has been shown to improve neurologic outcome up to one year post injury if administered within 8 hours of injury and in a dose regimen of: bolus 30mg/kg administered over 15 minutes with a maintenance infusion of 5.4 mg/kg per hour infused for 23 hours. The initial North American trial was replicated in a Japanese trial but not in the one from France. Data has been obtained from the latter study to permit appropriate meta-analysis of all three trials. This analysis indicates significant recovery in motor function after methylprednisolone therapy. A more recent trial indicates that if methylprednisolone therapy is given for an additional 24 hours (for a total of 48 hours), additional improvement in motor neurologic function and functional status is observed. This is particularly observed if treatment cannot be started until between 3 to 8 hours after injury. The same methylprednisolone therapy has been found effective in whiplash injuries and a modified regimen found to improve recovery after surgery for lumbar disc disease. REVIEWER'S CONCLUSIONS: High dose methylprednisolone steroid therapy is the only pharmacological therapy shown to have efficacy in a Phase Three randomized trial when it can be administered within 8 hours of injury. High dose methylprednisolone has been accepted as standard therapy in many countries. A recent trial indicates additional benefit by extending the maintenance dose from 24 to 48 hours if start of treatment must be delayed to between 3 and 8 hours after injury. There is an urgent need for more randomized trials of pharmacological therapy for acute spinal cord injury.

Anti-Inflammatory Agents↗
PubMed2003

Vascular endothelial growth factor improves functional outcome and decreases secondary degeneration in experimental spinal cord contusion injury.

Spinal cord injury leads to acute local ischemia, which may contribute to secondary degeneration. Hypoxia stimulates angiogenesis through a cascade of events, involving angiogenesis stimulatory substances, such as vascular endothelial growth factor (VEGF). To test the importance of angiogenesis for functional outcome and wound healing in spinal cord injury VEGF165 (proangiogenic), Ringer's (control) or angiostatin (antiangiogenic) were delivered locally immediately after a contusion injury produced using the NYU impactor and a 25 mm weight-drop. Rats treated with VEGF showed significantly improved behavior up to 6 weeks after injury compared with control animals, while angiostatin treatment lead to no statistically significant changes in behavior outcome. Furthermore, VEGF-treated animals had an increased amount of spared tissue in the lesion center and a higher blood vessel density in parts of the wound area compared with controls. These effects were unlikely to be due to increased cell proliferation as determined by bromo-deoxy-uridine-labeling. Moreover, VEGF treatment led to decreased levels of apoptosis, as revealed by TUNEL assays. In situ hybridization demonstrated presence of mRNA for VEGF receptors Flt-1, fetal liver kinase-1, neuropilin-1 and -2 in several important cellular compartments of the spinal cord. The different experiments indicate that beneficial effects seen by acute VEGF delivery was attributable to protection/repair of blood vessels, decreased apoptosis and possibly also by other additional effects on glial cells or certain neuron populations.

Analysis of Variance↗
PubMed2002

Strategies for regeneration and repair in spinal cord traumatic injury.

Spinal cord injury is frequently followed by the loss of supraspinal control of sensory, autonomic and motor functions at the sublesional level. In order to enhance recovery in spinal cord-injured patients, we have developed three fundamental strategies in experimental models. These strategies define in turn three chronological levels of postlesional intervention in the spinal cord. Neuroprotection soon after injury using pharmacological tools to reduce the progressive secondary injury processes that follow during the first week after the initial lesion. This strategy was conducted up to clinical trials, showing that a pharmacological therapy can reduce the permanent neurological deficit that usually follows an acute injury of the central nervous system (CNS). A second strategy, which is initiated not long after the lesion, aims at promoting axonal regeneration by acting on the main barrier to regeneration of lesioned axons: the glial scar. Finally a mid-term substitutive strategy is the management of the sublesional spinal cord by sensorimotor stimulation and/or supply of missing key afferents, such as monoaminergic systems. These three strategies are reviewed. Only a combination of these different approaches will be able to provide an optimal basis for potential therapeutic interventions directed to functional recovery after spinal cord injury.

Animals↗
PubMed1983

Modulation of urinary bladder function with thyrotropin-releasing hormone in patients with spinal cord injuries during the spinal shock phase.

Injury to the spinal cord is associated with large increases in plasma beta-endorphin immunoreactivity. To investigate the effect on vesical function of thyrotropin-releasing hormone (TRH), 13 patients with spinal injury were studied during the spinal shock phase. In seven of them (Group A), after basal cystometry together with anal sphincter electromyography (EMG), 1 mg of TRH was administered intravenously as a bolus dose, followed by 1 mg infused over 5 minutes. After the administration of the bolus dose of TRH, cystometry + EMG was repeated (Study I). These seven cases received TRH 1 mg intravenously 12 hourly for the next three days. On day 4, after basal cystometry + EMG, TRH was administered as above and the urodynamic study was repeated (Study II). Detrusor pressure (Pdct) with bladder filled to 800 ml (or upto tolerance) and bladder compliance were noted. Six cases underwent study I alone and received normal saline instead of TRH (Group B). After TRH in group A, the mean (+/- SE) Pdct increased by 10 +/- 3 cm H2O (p less than 0.05) in study I and by 10 +/- 3 cm H2O (p less than 0.05) in study II whereas the mean compliance decreased by 37 +/- 20 ml/cm H2O (NS) in study I and by 44 +/- 18 ml/cm H2O (p less than 0.05) in study II. In group B, the mean Pdct decreased by 1 +/- 2 cm H2O (NS) and the mean compliance increased by 1 +/- 2 ml/cm H2O (NS) in the post-normal saline study. These results show that TRH may improve bladder function in patients with injury-induced spinal shock by increasing detrusor pressure and by decreasing bladder compliance.

Adult↗
PubMed2006

Amikacin dosing and monitoring in spinal cord injury patients: variation in clinical practice between spinal injury units and differences in experts' recommendations.

The objective of this article was to determine the current practice on amikacin dosing and monitoring in spinal cord injury patients from spinal cord physicians and experts. Physicians from spinal units and clinical pharmacologists were asked to provide protocol for dosing and monitoring of amikacin therapy in spinal cord injury patients. In a spinal unit in Poland, amikacin is administered usually 0.5 g twice daily. A once-daily regimen of amikacin is never used and amikacin concentrations are not determined. In Belgium, Southport (U.K.), Spain, and the VA McGuire Medical Center (Richmond, Virginia), amikacin is given once daily. Whereas peak and trough concentrations are determined in Belgium, only trough concentration is measured in Southport. In both these spinal units, modification of the dose is not routinely done with a nomogram. In Spain and the VA McGuire Medical Center, monitoring of serum amikacin concentration is not done unless a patient has renal impairment. In contrast, the dose/interval of amikacin is adjusted according to pharmacokinetic parameters at the Edward Hines VA Hospital (Hines, Illinois), where amikacin is administered q24h or q48h, depending on creatinine clearance. Spinal cord physicians from Denmark, Germany, and the Kessler Institute for Rehabilitation (West Orange, New Jersey) state that they do not use amikacin in spinal injury patients. An expert from Canada does not recommend determining serum concentrations of amikacin, but emphasizes the value of monitoring ototoxicity and nephrotoxicity. Experts from New Zealand recommend amikacin in conventional twice- or thrice-daily dosing because of the theoretical increased risk of neuromuscular blockade and apnea with larger daily doses in spinal cord injury patients. On the contrary, experts from Greece, Israel, and the U.S. recommend once-daily dosing and determining amikacin pharmacokinetic parameters for each patient. As there is considerable variation in clinical practice across spinal units and experts differ on ideal dosing and monitoring of amikacin therapy in spinal cord injury patients, there is an urgent need to develop best-practice guidelines.

Amikacin↗
PubMed2000

Chronic pain after spinal cord injury: a survey of practice in spinal injury units in the USA.

OBJECTIVE: To determine the current practice regarding assessment and management of patients with chronic pain after spinal cord injury (SCI) in the United States of America (USA). METHODS: A postal questionnaire sent to the medical directors of 12 spinal injury units in the USA. RESULTS: A response was received from eight of the 12 units. Chronic pain was considered a significant problem amongst patients with SCI. There was inconsistency of opinion regarding prevalence estimates, investigation and management of chronic pain after SCI; but classification systems for pain were remarkably similar amongst units. Most felt that there was a need for further information, although only one unit said it was presently conducting research into the subject. CONCLUSION: Our survey has demonstrated the uncertainty that exists amongst USA specialists dealing with pain after SCI, and strengthens the case for more research into the subject with a view to developing guidelines for care.

Chronic Disease↗
PubMed2006

The cellular inflammatory response in human spinal cords after injury.

Spinal cord injury (SCI) provokes an inflammatory response that generates substantial secondary damage within the cord but also may contribute to its repair. Anti-inflammatory treatment of human SCI and its timing must be based on knowledge of the types of cells participating in the inflammatory response, the time after injury when they appear and then decrease in number, and the nature of their actions. Using post-mortem spinal cords, we evaluated the time course and distribution of pathological change, infiltrating neutrophils, monocytes/macrophages and lymphocytes, and microglial activation in injured spinal cords from patients who were 'dead at the scene' or who survived for intervals up to 1 year after SCI. SCI caused zones of pathological change, including areas of inflammation and necrosis in the acute cases, and cystic cavities with longer survival (Zone 1), mantles of less severe change, including axonal swellings, inflammation and Wallerian degeneration (Zone 2) and histologically intact areas (Zone 3). Zone 1 areas increased in size with time after injury whereas the overall injury (size of the Zones 1 and 2 combined) remained relatively constant from the time (1-3 days) when damage was first visible. The distribution of inflammatory cells correlated well with the location of Zone 1, and sometimes of Zone 2. Neutrophils, visualized by their expression of human neutrophil alpha-defensins (defensin), entered the spinal cord by haemorrhage or extravasation, were most numerous 1-3 days after SCI, and were detectable for up to 10 days after SCI. Significant numbers of activated CD68-immunoreactive ramified microglia and a few monocytes/macrophages were in injured tissue within 1-3 days of SCI. Activated microglia, a few monocytes/macrophages and numerous phagocytic macrophages were present for weeks to months after SCI. A few CD8(+) lymphocytes were in the injured cords throughout the sampling intervals. Expression by the inflammatory cells of the oxidative enzymes myeloperoxidase (MPO) and nicotinamide adenine dinucleotide phosphate oxidase (gp91(phox)), and of the pro-inflammatory matrix metalloproteinase (MMP)-9, was analysed to determine their potential to cause oxidative and proteolytic damage. Oxidative activity, inferred from MPO and gp91(phox) immunoreactivity, was primarily associated with neutrophils and activated microglia. Phagocytic macrophages had weak or no expression of MPO or gp91(phox). Only neutrophils expressed MMP-9. These data indicate that potentially destructive neutrophils and activated microglia, replete with oxidative and proteolytic enzymes, appear within the first few days of SCI, suggesting that anti-inflammatory 'neuroprotective' strategies should be directed at preventing early neutrophil influx and modifying microglial activation.

Adolescent↗
PubMed2005

Tissue displacement and impact force are important contributors to outcome after spinal cord contusion injury.

Spinal cord contusion injury in rodents is widely used as a model for spinal cord trauma in humans. Several biomechanical variables can influence injury outcome. In this work, we have assessed the influence of impact force and displacement of the spinal cord at the time of contusion injury on the severity of locomotor deficits and histopathological changes. Our work indicates that there is a linear relationship between force and tissue displacement, and that both these factors contribute to injury outcome. Furthermore, our work also suggests that setting narrow limits for the actual force applied (+/-5 kdyn) and tissue displacement (within a 200 microm range) will yield more consistent outcomes and provide greater sensitivity in detecting changes, regardless of the type of impactor device used.

Animals↗