Management of complex pediatric and adolescent spinal deformity.

OBJECT: The authors sought to analyze prospectively the outcome of surgery for complex spinal deformity in the pediatric and young adult populations. METHODS: The authors evaluate all pediatric and adolescent patients undergoing operative correction of complex spinal deformity from December 1997 through July 1999. No patient was lost to follow-up review (average 21.1 months). There were 27 consecutive pediatric and adolescent patients (3-20 years of age) who underwent 32 operations. Diagnoses included scoliosis (18 idiopathic, five nonidiopathic) and four severe kyphoscoliosis. Operative correction and arthrodesis were achieved via 21 posterior approaches (Cotrel-Dubousset-Horizon), seven anterior approaches (Isola or Kaneda Scoliosis System), and two combined approaches. Operative time averaged 358 minutes (range 115-620 minutes). Blood loss averaged 807 ml (range 100-2,000 ml). Levels treated averaged 9.1 (range three-16 levels). There was a 54% average Cobb angle correction (range 6-82%). No case was complicated by the patient's neurological deterioration, loss of somatosensory evoked potential monitoring, cardiopulmonary disease, donor-site complication, or wound breakdown. There was one case of hook failure and one progression of deformity beyond the site of surgical instrumentation that required reoperation. There were 10 minor complications that did not significantly affect patient outcome. No patient received undirected banked blood products. There was a significant improvement in cosmesis, and no patient experienced continued pain postoperatively. All patients have been able to return to their preoperative activities. CONCLUSIONS: Compared with other major neurosurgical operations, segmental instrumentation for pediatric and adolescent spinal deformity is a safe procedure with minimal morbidity and there is a low risk of needing to use allogeneic blood products.

Nonoperative management of acute spinal cord injury.

Advances in transport, imaging, and stabilization of the injured patient have made the topic of acute management more important than ever in patients with spinal cord injury. Optimal treatment requires prompt delivery of care for life-threatening respiratory and hemodynamic events in a manner that will not further damage the unstable spinal elements. The application of these treatment principles broadly to injured patients is necessitated by our inability to determine, on an acute basis, those patients who might eventually recover meaningful neurologic function from those who will not. Therefore, nonoperative management of acute spinal cord injury requires consideration of two goals: 1) the preservation of the patient's life and 2) optimizing the potential for recovery of neurologic function. The first consideration requires not only an understanding of the novel systemic consequences of spinal cord injury but also of treatments directed at combating them. The second includes the application of resuscitative measures without further damaging the spinal cord and, in some cases, the use of traction and immobilization. In the past these efforts were aimed primarily at increasing the survival rate of patients with spinal cord injury, whereas current care may also play an important role in the eventual recovery of neurologic function. Despite many advances in our understanding of the basic mechanisms of paralysis, clinical management of spinal cord injury remains a significant challenge and one that requires continuing efforts at improving acute and postacute therapies.

Clinical measurement, statistical analysis, and risk-benefit: controversies from trials of spinal injury.

BACKGROUND: The National Acute Spinal Cord Injury Studies have been a series of trials assessing the role of pharmacologic agents in the prevention of secondary neuronal damage after acute spinal cord injury. METHODS: The trials were multicenter randomized, controlled studies. RESULTS: Two trials have demonstrated the efficacy of high-dose methylprednisolone in improving neurologic and functional recovery and have shown a reassuring safety profile. CONCLUSION: This study responds to a recent commentary on these trials and examines in particular the roles of clinical measurement, statistical analysis, and risk benefit in assembling evidence for or against innovative therapies.

Progesterone is neuroprotective after acute experimental spinal cord trauma in rats.

STUDY DESIGN: A standardized rat contusion model was used to test the hypothesis that progesterone significantly improves neurologic recovery after a spinal cord injury that results in incomplete paraplegia. OBJECTIVES: To compare the effect of progesterone versus a variety of control agents to determine its effectiveness in promoting neurologic recovery after an incomplete rat spinal cord injury. SUMMARY OF BACKGROUND DATA: Progesterone is a neurosteroid, possessing a variety of functions in the central nervous system. Exogenous progesterone has been shown to improve neurologic function after focal cerebral ischemia and facilitates cognitive recovery after cortical contusion in rats. METHODS: A standardized rat contusion model of spinal cord injury using the New York University impactor that resulted in rats with incomplete paraplegia was used. Forty mature male Sprague-Dawley rats were randomly assigned to four groups: laminectomy with sham contusion, laminectomy with contusion without pharmacologic treatment, laminectomy with contusion treated with dimethylsulfoxide and dissolved progesterone, and laminectomy with contusion treated with dimethylsulfoxide. Functional status was assessed weekly using the Basso-Beattie-Bresnehan (BBB) locomotor rating scale for 6 weeks, after which the animals were killed for histologic studies. RESULTS: Rats treated with progesterone had better outcomes (P = 0.0017; P = 0.0172) with a BBB score of 15.5, compared with 10.0 in the dimethylsulfoxide control group and 12.0 in the spinal cord contusion without pharmacologic intervention group. This was corroborated in histologic analysis by relative sparing of white matter tissue at the epicenter of the injury in the progesterone-treated group (P < 0.05). CONCLUSIONS: Rats treated with progesterone had a better clinical and histologic outcome compared with the various control groups. These results indicate potential therapeutic properties of progesterone in the management of acute spinal cord injury.

Anterior lumbar fusion with titanium threaded and mesh interbody cages.

The authors report their experience with 42 patients in whom anterior lumbar fusion was performed using titanium cages as a versatile adjunct to treat a wide variety of spinal deformity and pathological conditions. These conditions included congenital, degenerative, iatrogenic, infectious, traumatic, and malignant disorders of the thoracolumbar spine. Fusion rates and complications are compared with data previously reported in the literature. Between July 1996 and July 1999 the senior authors (C.I.S., R.P.N., and M.J.R.) treated 42 patients by means of a transabdominal extraperitoneal (13 cases) or an anterolateral extraperitoneal approach (29 cases), 51 vertebral levels were fused using titanium cages packed with autologous bone. All vertebrectomies (27 cases) were reconstructed using a Miami Moss titanium mesh cage and Kaneda instrumentation. Interbody fusion (15 cases) was performed with either the BAK titanium threaded interbody cage (in 13 patients) or a Miami Moss titanium mesh cage (in two patients). The average follow-up period was 14.3 months. Seventeen patients had sustained a thoracolumbar burst fracture, 12 patients presented with degenerative spinal disorders, six with metastatic tumor, four with spinal deformity (one congenital and three iatrogenic), and three patients presented with spinal infections. In five patients anterior lumbar interbody fusion (ALIF) was supplemented with posterior segmental fixation at the time of the initial procedure. Of the 51 vertebral levels treated, solid arthrodesis was achieved in 49, a 96% fusion rate. One case of pseudarthrosis occurred in the group treated with BAK cages; the diagnosis was made based on the patient's continued mechanical back pain after undergoing L4-5 ALIF. The patient was treated with supplemental posterior fixation, and successful fusion occurred uneventfully with resolution of her back pain. In the group in which vertebrectomy was performed there was one case of fusion failure in a patient with metastatic breast cancer who had undergone an L-3 corpectomy with placement of a mesh cage. Although her back pain was immediately resolved, she died of systemic disease 3 months after surgery and before fusion could occur. Complications related to the anterior approach included two vascular injuries (two left common iliac vein lacerations); one injury to the sympathetic plexus; one case of superficial phlebitis; two cases of prolonged ileus (greater than 48 hours postoperatively); one anterior femoral cutaneous nerve palsy; and one superficial wound infection. No deaths were directly related to the surgical procedure. There were no cases of dural laceration and no nerve root injury. There were no cases of deep venous thrombosis, pulmonary embolus, retrograde ejaculation, abdominal hernia, bowel or ureteral injury, or deep wound infection. Fusion-related complications included an iliac crest hematoma and prolonged donor-site pain in one patient. There were no complications related to placement or migration of the cages, but there was one case of screw fracture of the Kaneda device that did not require revision. The authors conclude that anterior lumbar fusion performed using titanium interbody or mesh cages, packed with autologous bone, is an effective, safe method to achieve fusion in a wide variety of pathological conditions of the thoracolumbar spine. The fusion rate of 96% compares favorably with results reported in the literature. The complication rate mirrors the low morbidity rate associated with the anterior approach. A detailed study of clinical outcomes is in progress. Patient selection and strategies for avoiding complication are discussed.

A new technique for the surgical management of unstable thoracolumbar burst fractures: a modification of the anterior approach and an outcome comparison to traditional methods.

This study was conducted to determine the safety, efficacy, and complication rate associated with the anterior approach in the use of a new titanium mesh interbody fusion cage for the treatment of unstable thoracolumbar burst fractures. The experience with this technique is compared with the senior authors' (C.S., R.W., and M.S.) previously published results in the management of patients with unstable thoracolumbar burst fractures. Between 1996 and 1999, 21 patients with unstable thoracolumbar (T12-L3) burst fractures underwent an anterolateral decompressive procedure in which a titanium cage and Kaneda device were used. Eleven of the 21 patients had sustained a neurological deficit, and all patients improved at least one Frankel grade (average 1.2 grades). There was improvement in outcome in terms of blood loss, correction of kyphosis, and pain, as measured on the Denis Pain and Work Scale, in our current group of patients treated via an anterior approach when compared with the results in those who underwent a posterior approach. In our current study the anterior approach was demonstrated to be a safe and effective technique for the management of unstable thoracolumbar burst fractures. It offers superior results compared with the posterior approach. The addition of the new titanium mesh interbody cage to our previous anterior technique allows the patient's own bone to be harvested from the corpectomy site and used as a substrate for fusion, thereby obviating the need for iliac crest harvest. The use of the cage in association with the Kaneda device allows for improved correction of kyphosis and restoration of normal sagittal alignment in addition to improved functional outcomes.

Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up. Results of the third National Acute Spinal Cord Injury randomized controlled trial.

OBJECT: A randomized double-blind clinical trial was conducted to compare neurological and functional recovery and morbidity and mortality rates 1 year after acute spinal cord injury in patients who had received a standard 24-hour methylprednisolone regimen (24MP) with those in whom an identical MP regimen had been delivered for 48 hours (48MP) or those who had received a 48-hour tirilazad mesylate (48TM) regimen. METHODS: Patients for whom treatment was initiated within 3 hours of injury showed equal neurological and functional recovery in all three treatment groups. Patients for whom treatment was delayed more than 3 hours experienced diminished motor function recovery in the 24MP group, but those in the 48MP group showed greater 1-year motor recovery (recovery scores of 13.7 and 19, respectively, p=0.053). A greater percentage of patients improving three or more neurological grades was also observed in the 48MP group (p=0.073). In general, patients treated with 48TM recovered equally when compared with those who received 24MP treatments. A corresponding recovery in self care and sphincter control was seen but was not statistically significant. Mortality and morbidity rates at 1 year were similar in all groups. CONCLUSIONS: For patients in whom MP therapy is initiated within 3 hours of injury, 24-hour maintenance is appropriate. Patients starting therapy 3 to 8 hours after injury should be maintained on the regimen for 48 hours unless there are complicating medical factors.

Surgical treatment of thoracolumbar fractures.

Many studies indicate that spinal canal decompression and stabilization lead to improved neurologic recovery in patients with incomplete neurologic deficits. It is recognized that surgical stabilization of unstable thoracolumbar injuries with complete neurologic deficit or without deficit reduces hospital stay, improves spinal alignment, shortens rehabilitation, and results in fewer medical complications. Unfortunately, many aspects of management remain controversial. For many injuries, more than one treatment method has been shown to be efficacious, although certain injuries have improved outcome with specific treatment modalities. This article is an overview of indications for surgery, operative approaches, types of instrumentation, and treatment options for specific thoracolumbar injuries.

Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study.

OBJECTIVE: To compare the efficacy of methylprednisolone administered for 24 hours with methyprednisolone administered for 48 hours or tirilazad mesylate administered for 48 hours in patients with acute spinal cord injury. DESIGN: Double-blind, randomized clinical trial. SETTING: Sixteen acute spinal cord injury centers in North America. PATIENTS: A total of 499 patients with acute spinal cord injury diagnosed in National Acute Spinal Cord Injury Study (NASCIS) centers within 8 hours of injury. INTERVENTION: All patients received an intravenous bolus of methylprednisolone (30 mg/kg) before randomization. Patients in the 24-hour regimen group (n=166) received a methylprednisolone infusion of 5.4 mg/kg per hour for 24 hours, those in the 48-hour regimen group (n=167) received a methylprednisolone infusion of 5.4 mg/kg per hour for 48 hours, and those in the tirilazad group (n=166) received a 2.5 mg/kg bolus infusion of tirilazad mesylate every 6 hours for 48 hours. MAIN OUTCOME MEASURES: Motor function change between initial presentation and at 6 weeks and 6 months after injury, and change in Functional Independence Measure (FIM) assessed at 6 weeks and 6 months. RESULTS: Compared with patients treated with methylprednisolone for 24 hours, those treated with methylprednisolone for 48 hours showed improved motor recovery at 6 weeks (P=.09) and 6 months (P=.07) after injury. The effect of the 48-hour methylprednisolone regimen was significant at 6 weeks (P=.04) and 6 months (P=.01) among patients whose therapy was initiated 3 to 8 hours after injury. Patients who received the 48-hour regimen and who started treatment at 3 to 8 hours were more likely to improve 1 full neurologic grade (P=.03) at 6 months, to show more improvement in 6-month FIM (P=.08), and to have more severe sepsis and severe pneumonia than patients in the 24-hour methylprednisolone group and the tirilazad group, but other complications and mortality (P=.97) were similar. Patients treated with tirilazad for 48 hours showed motor recovery rates equivalent to patients who received methylprednisolone for 24 hours. CONCLUSIONS: Patients with acute spinal cord injury who receive methylprednisolone within 3 hours of injury should be maintained on the treatment regimen for 24 hours. When methylprednisolone is initiated 3 to 8 hours after injury, patients should be maintained on steroid therapy for 48 hours.

Treatment with genetically engineered fibroblasts producing NGF or BDNF can accelerate recovery from traumatic spinal cord injury in the adult rat.

We tested the hypothesis that NGF or BDNF can protect damaged neural structures following spinal cord injury. Spinal contusions were produced in adult rats by a weight drop method. Thereafter, unmodified Rat 1 fibroblasts or fibroblasts engineered to secrete NGF or BDNF were injected into the injury site. Weekly assessments of recovery were made for 6 weeks using a locomotor rating scale. All rats were immediately paraplegic, then began to recover. At 1 week after injury, the ratings of locomotor performance in rats implanted with NGF- or BDNF-secreting fibroblasts were significantly increased over those of rats implanted with unmodified fibroblasts. This trend toward enhanced recovery persisted during the duration of the experiment, although the difference became smaller. Histological examination after 6 weeks showed a larger cross-sectional area of spinal cord at the maximal injury site in the animals treated with NGF or BDNF. These results demonstrate a significant biological effect of treatment with neurotrophins in traumatic spinal cord injury.

Transoral-transpharyngeal approach to the craniocervical junction.

The transoral-transpharyngeal approach is a reliable and technically sound method for gaining anterior extradural exposure to the craniocervical junction. We report 23 patients undergoing this approach for pathology lying between the inferior clivus and third cervical vertebra. Pathology included 6 patients with congenital malformations of the odontoid process, 4 patients with basilar invagination caused by rheumatoid arthritis, 2 patients with atlantoaxial subluxation caused by Down's syndrome, and 1 each with Chiari I malformation, pseudogout of C1/C2, ossification of the posterior longitudinal ligament, and chronic dens dislocation caused by trauma. Malignant tumors included 4 chordomas, 2 giant cell tumors of C1-C3, and 1 chondrosarcoma. Orotracheal intubation without tracheotomy was used in 22 patients. Sixteen of these 22 patients were extubated either immediately or within 24 hours. Six complications occurred in 5 patients and included a palatal dehiscence in 2, delayed oropharyngeal hemorrhage, prolonged endotracheal intubation because of severe tongue edema, and 1 case each of meningitis and aspiration pneumonia responsive to intravenous antibiotics. No deaths, local infections, or postoperative cerebrospinal fluid leaks occurred. Neurologic symptoms of cord compression improved or stabilized in all patients. The transoral-transpharyngeal approach is an effective means for extradural decompression of the anterior craniocervical junction and for exposure of selected tumors at this site.

Immunolocalization of heat shock protein after fluid percussive brain injury and relationship to breakdown of the blood-brain barrier.

We have previously developed a model of mild, lateral fluid percussive head injury in the rat and demonstrated that although this injury produced minimal hemorrhage, breakdown of the blood-brain barrier was a prominent feature. The relationship between posttraumatic blood-brain barrier disruption and cellular injury is unclear. In the present study we examined the distribution and time course of expression of the stress protein HSP72 after brain injury and compared these findings with the known pattern of breakdown of the blood-brain barrier after a similar injury. Rats were subjected to a lateral fluid percussive brain injury (4.8-5.2 atm, 20 ms) and killed at 1, 3, and 6 h and 1, 3, and 7 days after injury. HSP72-like immunoreactivity was evaluated in sections of brain at the light-microscopic level. The earliest expression of HSP72 occurred at 3 h postinjury and was restricted to neurons and glia in the cortex surrounding a necrotic area at the impact site. By 6 h, light immunostaining was also noted in the pia-arachnoid adjacent to the impact site and in certain blood vessels that coursed through the area of necrosis. Maximal immunostaining was observed by 24 h postinjury, and was primarily associated with the cortex immediately adjacent to the region of necrosis at the impact site. This region consisted of darkly immunostained neurons, glia, and blood vessels. Immunostaining within the region of necrosis was restricted to blood vessels. HSP72-like immunoreactivity was also noted in a limited number of neurons and glia in other brain regions, including the parasagittal cortex, deep cortical layer VI, and CA3 in the posterior hippocampus.(ABSTRACT TRUNCATED AT 250 WORDS)

Instrumentation of the occipital-atlantal-axial (c0-c1-c2) complex.

Few areas of spinal surgery present a greater challenge than management of occipitocervical abnormalities. This is due to the simultaneous presence of two commanding, yet conflicting treatment principles. First, decompression and protection of the spinal cord at this level is synonymous with the presevation of life itself. Second, however, the degree of cervical movements at this junction is unprecedented in the spine, requiring the preservation movement yet stabilization of discrete motion segemnts. The interrelation of these two critical functions is realized in the complex arrangement of the C0- C1-C2 anatomic configuration. The occipitocervical junction is responsible for 50% of the 90 degrees of head rotation. In addition, 10-15 degrees of flexion and extension are added to the subaxial cervical spine by C0-C1-C2.This duality of function is the primary reasin for the complexity of the facet joints in this location. No lateral bending occurs at this level.

Breakdown of the blood-brain barrier after fluid percussion brain injury in the rat: Part 2: Effect of hypoxia on permeability to plasma proteins.

Clinical studies have demonstrated that hypoxia after severe brain injury is common and significantly worsens neurologic outcome. We have, therefore, developed a rat model of posttraumatic hypoxic injury in order to identify the pathophysiologic responses after head injury that are worsened by this secondary insult. We examined the effect of hypoxia after brain injury on permeability of the blood-brain barrier to plasma proteins. Animals were divided into two experimental groups: group I (impact alone) and group IH (impact plus hypoxia). Rats were subjected to a lateral fluid percussive brain injury (4.8-5.2 atm). Animals in group IH were exposed to hypoxic conditions (10% O2) for 45 min immediately after injury. In each group, vascular permeability to endogenous immunoglobulins (IgG) and to horseradish peroxidase (HRP) was examined at the light microscopic level. IgG was immunolocalized in brain sections at 1-24 h after injury. In other studies, HRP was given i.v. either before impact or 10 min before killing. Permeability to this protein was assessed at 1-72 h after injury. The distribution of extravasated proteins was similar between the experimental groups at 1 h postinjury. Pronounced abnormal permeability to IgG and HRP (given before impact) occurred in discrete regions throughout both the ipsilateral and contralateral hemispheres. By 6 h after injury, a differential response of the blood-brain barrier was noted between groups I and IH. Widespread leakage of proteins was observed in the injured hemisphere in group IH. This finding was in sharp contrast to group I, in which extravasated proteins remained more localized in the injured hemisphere. The time course for reestablishment of the blood-brain barrier to HRP (given before killing) was determined. The impact site remained permeable to HRP up to at least 72 h postinjury within groups I and IH. In group I, the blood-brain barrier was reestablished in the parasagittal cortex and deep cortical layer by 6 h postinjury. In contrast, the blood-brain barrier in group IH was not restored in similar brain regions until 24 h postinjury. These studies demonstrate that (1) hypoxia after brain injury exacerbates the regional breakdown of the blood-brain barrier to circulating proteins, (2) this influence of hypoxia on permeability is not apparent immediately after injury but rather is expressed at 6 h after injury, and (3) hypoxia after traumatic brain injury delays recovery of the blood-brain barrier. These findings suggest that secondary posttraumatic hypoxia contributes to the vascular pathogenesis of brain injury.

Breakdown of the blood-brain barrier after fluid percussive brain injury in the rat. Part 1: Distribution and time course of protein extravasation.

Experimental brain injury is associated with marked vasogenic edema, as evidenced by an increase in brain water content. This prominent and widespread response raises questions about the vulnerability of microvasculature in the brain to injury. In the present report we further characterize the vascular response by evaluating the integrity of the blood-brain barrier to circulating proteins. Vascular permeability to endogenous immunoglobulins (IgG) and to the protein horseradish peroxidase (HRP) was examined after a lateral, fluid percussive brain injury in the rat. In study 1 IgG was immunolocalized in brain sections 1-24 hr after injury. In studies 2 and 3 HRP was given intravenously either before impact (study 2) or 10 min before sacrifice (study 3). Permeability to this protein was assessed at 1-6 hr (study 2) or at 1-72 hr (study 3) after injury. In studies 1 and 2 the extravascular accumulation of proteins was evaluated. Pronounced abnormal permeability to IgG and HRP occurred within the first hour after injury and was widespread throughout both hemispheres. The intensity of immunostaining for IgG increased with time up to 24 hr after injury. In contrast, maximal extravascular accumulation of HRP occurred within the first hour after injury. In study 3 the time course for re-establishment of the blood-brain barrier to HRP was determined. Maximal permeability occurred at 1 hr after injury. At 24 hr abnormal permeability was restricted to the impact site and this area remained permeable up to 72 hr after injury. In summary this study demonstrates that breakdown of the blood-brain barrier to plasma proteins is a prominent feature of experimental brain injury. This abnormal permeability is characterized by its transient expression and widespread distribution. The time course for re-establishment of the blood-brain barrier to circulating proteins is most delayed at the impact site.