All the radiographic and clinical evaluations were completed both before THR surgery and 3 months following the surgery during routine follow up.
During the last 2 decades it has been recognized that scoliosis may start de novo during adult life as a result of advanced degenerative disc disease, osteoporosis or both. In some the degenerative process is superimposed on a previous adolescent curve. Aside from the disfigurement caused by the spinal deformity, pain and disability are usually the major clinical problem. The prevalence of adult scoliosis rises with age: from 4% before age 45, 6% at age 59 to 15% in-patients older than 60 years. More than two thirds of the patients are females and the prevalence of right lumber curves is higher than in comparable series of patients with adolescent scoliosis. Adult scoliosis is characterized by vertebral structural changes with translatory shifts i.e. lateral olisthesis accompanied by degenerative disc and facet joint arthrosis. Although the magnitude of these curves is usually mild (20–30 degrees) lateral spondylolisthesis is observed frequently. It is also common to observe degenerative spondylolisthesis in patients with degenerative lumbar scoliosis. The annual rate of curve progression ranges from 0.3 to 3%. Patients present with a history of a spinal deformity accompanied by loss of lumbar lordosis, trunk imbalance and significant mechanical back pain. Pain may arise not only from degenerative disc disease and facet arthritis leading to symptoms of spinal stenosis, but also from muscle fatigue due to the altered biomechanics secondary to a deformity in the coronal and sagittal planes. Root entrapment is common and occurs more often on the concavity of the curve. Symptoms of neurogenic claudication are also common in adults with lumbar scoliosis. Non-operative care includes exercises, swimming, NSAIDs, and occasional epidural injections. Brace treatment can be tried as well. Curve progression as well as axial or radicular pain not responding to non-operative care are indications for surgical intervention. Surgery may include decompression alone or in conjunction with curve correction and stabilization. Posterior instrumentation may be supplemented with interbody cages. Fusion is usually carried down to L5 but occasional instrumentation to the sacropelvis is mandatory. Problems with a high pseudoarthrosis rate are common with sacral fixation. Even in the best of hands a long recovery period (6–12 month) and moderate pain relief should be expected. As summarized by Dr. Bradford “despite recent advancements evaluation and successful management of patients with adult spinal deformity remains a significant challenge”
We report four patients with unilateral postpartum sacroiliitis presenting with agonising unilateral pain, an elevated ESR, elevated alkaline phosphatase levels, leucocytosis and positive bone scans. The diagnosis of a non-infectious inflammatory cause was supported by the postpartum onset, the response to non-steroidal anti-inflammatory drugs, negative aspiration cultures in two cases and the lack of changes in the sacroiliac joints on long-term follow-up radiographs.
We report four children aged two to nine years with traumatic tears of the transverse ligament of the atlas and atlanto-axial subluxation. This is extremely rare in this age group since trauma usually causes a skeletal rather than a ligamentous injury. The injuries resulted from falls or motor vehicle accidents, with considerable delay in diagnosis. Flexion radiographs showed atlas-dens intervals (ADI) of 6, 7, 8 and 13 mm; all four patients were treated by posterior fusion at C1-C2 after the failure of conservative treatment. In one child with quadriparesis and a fixed ADI of 13 mm, transoral anterior resection of the odontoid was performed before the fusion. Diagnosis of this traumatic lesion requires a high level of suspicion. Conservative treatment is likely to fail; surgical stabilisation is indicated.
We report two cases of Serratia marcescens infection at the sites of spinal fractures and emphasise the fact that neurological deterioration soon after spinal fracture may be due to acute vertebral osteomyelitis.
Reports of spondylolysis in vertebrae other than those of the lower lumbar spine are rare. We report 32 patients with upper lumbar spondylolysis who have been studied clinically, radiologically and scintigraphically. Twenty patients had bilateral lesions, and seven of those with unilateral lesions had structural changes or anomalies in the opposite posterior arch. Positive scans were found to be associated with a short clinical history, and indicated stress-related lesions. Our findings suggest that mechanical factors may play a role in the aetiology of spondylolysis in the upper lumbar spine similar to that which they play in the lower lumbar spine, and that local structural anomalies may contribute to abnormal loading of these vertebrae.