Aims. A variety of surgical methods and strategies have been demonstrated for
A number of causes have been advanced to explain the destructive discovertebral (Andersson) lesions that occur in ankylosing spondylitis, and various treatments have been proposed, depending on the presumed cause. The purpose of this study was to identify the causes of these lesions by defining their clinical and radiological characteristics. We retrospectively reviewed 622 patients with ankylosing spondylitis. In all, 33 patients (5.3%) had these lesions, affecting 100 spinal segments. Inflammatory lesions were found in 91 segments of 24 patients (3.9%) and traumatic lesions in nine segments of nine patients (1.4%). The inflammatory lesions were associated with recent-onset disease; a low modified Stoke ankylosing spondylitis spine score (mSASSS) due to incomplete bony ankylosis between vertebral bodies; multiple lesions; inflammatory changes on MRI; reversal of the inflammatory changes and central bony ankylosis at follow-up; and a good response to anti-inflammatory drugs. Traumatic lesions were associated with prolonged disease duration; a high mSASSS due to complete bony ankylosis between vertebral bodies; a previous history of trauma; single lesions; nonunion of fractures of the posterior column; acute kyphoscoliotic deformity with the lesion at the apex; instability, and the need for operative treatment due to that instability. It is essential to distinguish between inflammatory and traumatic
Introduction: Pseudoarthrosis in Ankylosing spondylitis is often misdiagnosed as infection. It is a slow progressing lesion resulting in a kyphosis and slow onset weakness of the lower limbs. We are presenting our strategy and experience in treating 9 patients with such a lesion. Method: 9 patients age range from 40–55 years who presented with pseudoarthrosis of the ankylosed spine underwent back-front surgery during 2001–204. 6 patients had dorsal spine lesion, 2 had dorso-lumbar junctional lesion and 1 had cervico-dorsal junctional lesion. 8/9 patients had insidious onset with progressive weakness of both lower limb. 1 patient had an acute onset with deformity. 7/9 patients had neurodeficit (Frankel C) 1/9 had complete paraplegia. All patients underwent posterior kyphosis correction and decompression of the spinal cord. During posterior decompression 8/9 patients had an incidental dural tear due to adherence fractured lamina. The dura was repaired primarily or patch graft. 5/9 patients had single stage back and front surgery. The rest of the patients had staged surgery. The front surgery was excision of the tough fibrotic psuedoarthosis and reconstruction using strut graft/cage. Results: Average duration of surgery was 4 ½ hours (3 ½ to 6 hours). Blood loss was 800 ml (600–1300 ml). All patients required blood transfusion. Primary dural repair was done in 7/8 cases, patch graft in 3/8 cases, ceiling with fusion glue and fat graft in 1 patient. 5 patients who had less that 1000 ml blood loss during posterior surgery had same stage anterior reconstruction. Rest of the patient had 2 staged surgery. 4/9 patients had previous THR B/L. All patients showed rapid improvement in the neurological status and at 3 months follow up all were Frankel E. Conclusion: The surgical outcome of the ankylosing spondylitis patients with