Thoracic cord compression caused by disk herniation in Scheuermann’s disease: A case report and review of the literature

We present the case of a 14-year-old male with Scheuermann’s disease and significant neurological deficit due to thoracic disk herniation at the apex of kyphosis. He was treated with an anterior decompression, anterior and posterior fusion in the same setting using plate, cage and a segmental instrumentation system. The patient had an excellent outcome with complete neurological recovery

Staged surgical treatment for severe and rigid scoliosis

<p>Abstract</p> <p>Background</p> <p>A retrospective study of staged surgery for severe rigid scoliosis. The purpose of this study was to evaluate the result of staged surgery in treatment of severe rigid scoliosis and to discuss the indications.</p> <p>Methods</p> <p>From 1998 to 2006, 21 cases of severe rigid scoliosis with coronal Cobb angle more than 80° were treated by staged surgeries including anterior release and halo-pelvic traction as first stage surgery and posterior instrumentation and spinal fusion as second stage. Pedicle subtraction osteotomy(PSO) was added in second stage according to spine rigidity. Among the 21 patients, 8 were male and 13 female with an average age of 15.3 years (rang from 4 to 23 years). The mean pre-operative Cobb angle was 110.5° (80°-145°) with a mean spine flexibility of 13%. Radiological parameters at different operative time points were analyzed (mean time of follow-up: 51 months).</p> <p>Results</p> <p>External appearance of all patients improved significantly. The average correction rate was 65.2% (ranging from 39.8% to 79.5%) with mean correction loss of 2.23° at the end of follow-up. No decompensation of trunk has been found. Mean distance between the midline of C7 and midsacral line was 1.19 cm ± 0.51. Two patients had neurological complications: one patient had motor deficit and recovered incompletely.</p> <p>Conclusion</p> <p>Staged operation and halo-pelvic traction offer a safe and effective way in treatment of severe rigid scoliosis. Patients whose Cobb angle was more than 80° and the flexibility of the spine was less than 20% should be treated in this way, and those whose flexibility of the spine was less than 10% and the Cobb angle remained more than 70° after 1st stage anterior release and halo-pelvic traction should undergo pedicle subtraction osteotomy (PSO) in the second surgery.</p

Sacral dome resection and single-stage posterior reduction in the treatment of high-grade high dysplastic spondylolisthesis in adolescents and young adults

OBJECTIVE: The description of the operation technique and retrospective review of 15 consecutive patients who were treated by posterior sacral dome resection and single-stage reduction with pedicle screw fixation for high-grade, high-dysplastic spondylolisthesis. MATERIALS AND METHODS: All the patients had high-grade, high-dysplastic spondylolisthesis L5 and were treated by posterior sacral dome resection and posterior single-stage reduction from L4-S1. The average age at the time of surgery was 17.3 (11-28) years. The average follow-up time is 5.5 (2-11.6) years. Clinical and radiological data were retrospectively reviewed. RESULTS: Spondylolisthesis was reduced from average 99% preoperative to 29% at the last follow-up. L5 incidence improved from 74° to 56°, the lumbosacral angle improved from 15° kyphosis to 6° lordosis, lumbar lordosis decreased from 69° to 53° from preoperative to the last follow-up. While pelvic incidence of 77° remained unchanged, sacral slope decreased from 51° to 46° and pelvic tilt increased from 25° to 30°. Clinical outcome was subjectively rated to be much better than before surgery by 14 out of 15 patients. Four out of 15 patients had temporary sensory impairment of the L5 nerve root which resolved completely within 12 weeks. There were no permanent neurological complications or no pseudarthrosis. CONCLUSION: The sacral dome resection is a shortening osteotomy of the lumbosacral spine which allows a single-stage reduction of L5 without lengthening of lumbosacral region in high-grade spondylolisthesis, which helps to avoid neurological complications. This is a safe surgical technique resulting in a good multidimensional deformity correction and restoration of spino-pelvic alignment towards normal values with a satisfactory clinical outcome

Spinal stenosis subsequent to juvenile lumbar osteochondrosis

This paper describes eight patients with spinal stenosis associated with marked osteochondrous changes in the vertebral bodies due to juvenile lumbar osteochondrosis (Scheuermann's disease). In no case was the midsagittal or interpedicular diameter of the spinal canal indicative of bony stenosis. On the other hand, in the myelograms the sagittal diameter of the dural sac was in all cases significantly narrowed, a diagnostic sign of central spinal stenosis. Therefore, myelography should always be contemplated when osteochondrous changes are present and spinal stenosis is suspected clinically regardless of whether the spinal canal diameters are normal in plain films.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46799/1/256_2004_Article_BF00204096.pd

Contribution of Cystine-Glutamate Antiporters to the Psychotomimetic Effects of Phencyclidine

Altered glutamate signaling contributes to a myriad of neural disorders, including schizophrenia. While synaptic levels are intensely studied, nonvesicular release mechanisms, including cystine–glutamate exchange, maintain high steady-state glutamate levels in the extrasynaptic space. The existence of extrasynaptic receptors, including metabotropic group II glutamate receptors (mGluR), pose nonvesicular release mechanisms as unrecognized targets capable of contributing to pathological glutamate signaling. We tested the hypothesis that activation of cystine–glutamate antiporters using the cysteine prodrug N-acetylcysteine would blunt psychotomimetic effects in the rodent phencyclidine (PCP) model of schizophrenia. First, we demonstrate that PCP elevates extracellular glutamate in the prefrontal cortex, an effect that is blocked by N-acetylcysteine pretreatment. To determine the relevance of the above finding, we assessed social interaction and found that N-acetylcysteine reverses social withdrawal produced by repeated PCP. In a separate paradigm, acute PCP resulted in working memory deficits assessed using a discrete trial t-maze task, and this effect was also reversed by N-acetylcysteine pretreatment. The capacity of N-acetylcysteine to restore working memory was blocked by infusion of the cystine–glutamate antiporter inhibitor (S)-4-carboxyphenylglycine into the prefrontal cortex or systemic administration of the group II mGluR antagonist LY341495 indicating that the effects of N-acetylcysteine requires cystine–glutamate exchange and group II mGluR activation. Finally, protein levels from postmortem tissue obtained from schizophrenic patients revealed significant changes in the level of xCT, the active subunit for cystine–glutamate exchange, in the dorsolateral prefrontal cortex. These data advance cystine–glutamate antiporters as novel targets capable of reversing the psychotomimetic effects of PCP