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Mark W. Fox, Burton M. Onofrio, and John E. Kilgore

fracture. 18 This study reviews patients with ankylosing spondylitis who were surgically treated for complications of their disease in order to identify the different spinal disorders observed and to better define their management. Criteria for selecting external immobilization versus surgical stabilization with or without decompression are discussed. In addition, the surgical techniques, intraoperative difficulties, and complications observed in these complex cases are reviewed. Clinical Material and Methods Patient Population During the period between 1984

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Alexander A. Khalessi, Bryan C. Oh, and Michael Y. Wang

discussion of relevant studies. Discussion will proceed from general considerations in AS, namely diagnosis and disease monitoring, to nonpharmacological management tools and available medications. Surgical management of AS will be discussed elsewhere. Medical Management of Ankylosing Spondylitis Outcomes Assessment: Patient Diagnosis and Disease Monitoring Assessment of patients with AS represents a multifactorial challenge in terms of systemic manifestations (axial, peripheral, etheseal, and extraarticular symptoms and signs) and longitudinal variation (active

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Mohammed F. Shamji, Mohammed Bafaquh, and Eve Tsai

( Table 1 ) provides insight into the underlying disease pathogenesis and may permit the development of novel avenues of treatment. TABLE 1 Genetic associations with ankylosing spondylitis Gene Group Products HLA-B27 HLA-B27 non–HLA-B27 MHC genes HLA-B60 HLA-B61 HLA-DRB1*01, B1*04 HLA-DR8 LMP-2, LMP-7 HSP-70 non-MHC genes IL-1 gene cluster CYP2D6 TGFβ Human Leukocyte Antigen–B27 Human leukocyte antigen–B27 is an MHC Class I molecule that is encoded on chromosome 6; although it is

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Jaypal Reddy Sangala, Elias Dakwar, Juan Uribe, and Fernando Vale

nonsurgical management of this entity. In this article we give an overview of the current evidence-based nonsurgical management of AS. Relevant pathophysiology of the disease is reviewed to underscore the targets of the various pharmacological agents. Pathology and Site of Action of Pharmacological Agents Ankylosing spondylitis is a chronic, immune-mediated inflammatory disease that is associated with inflammation in the sacroiliac joints, the axial skeleton, entheses, peripheral joints, uvea, and other structures. The initial pathological changes are initiated by

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Wolf Rosenkranz

I n 1961, Bowie and Glasgow 1 described three patients with long-standing ankylosing spondylitis who gradually developed disturbances of the anal and vesicular sphincters associated with loss of sensation in the sacral dermatomes. In one case the lumbar myelogram reportedly showed prominent diverticuli along the lumbar nerve sheaths; in another a myelogram done in the supine position revealed pooling of the contrast medium at indentations at each vertebral level. Since 1961, eight additional cases of ankylosing spondylitis complicated by the cauda equina

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Carroll Osgood, Louis G. Martin, and Elliott Ackerman

T he high incidence of neurological deficits in patients with ankylosing spondylitis or “bamboo spine” who suffer cervical fracture dislocation is not generally appreciated. Two cases are presented. Case Reports Case 1 A 47-year-old man whose spine had been fused in marked flexion from ankylosing spondylitis since 1944 was injured in an automobile accident on December 22, 1969. When seen at a local hospital he had pain and numbness in the left arm and a fracture of C6–7, but was otherwise neurologically intact. He was placed in a Thomas collar and

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Daniel J. Hoh, Paul Khoueir, and Michael Y. Wang

. References 1 Belanger TA , Milam RA IV , Roh JS , Bohlman HH : Cervico-thoracic extension osteotomy for chin-on-chest deformity in ankylosing spondylitis . J Bone Joint Surg Am 87 : 1732 – 1738 , 2005 2 Ben-David B , Haller G , Taylor P : Anterior spinal fusion complicated by paraplegia. A case report of a false-negative somatosensory-evoked potential . Spine 12 : 536 – 539 , 1987 3 Bhojraj SY , Dasgupta D , Dewoolkar LV : One-stage “front” and “back” correction for rigid cervical kyphosis. A safer technique of correction for a

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Patrick W. Hitchon, Aaron M. From, Matthew D. Brenton, John A. Glaser, and James C. Torner

A nkylosing spondylitis, associated with the presence of the serum HLA-B27 antigen and sacroiliitis, is prevalent in 0.1% of the general population, reaching a reported maximum prevalence of 1.5% in caucasians in the United States. Ankylosing spondylitis is characterized by ossification of the spinal discs, joints, and ligaments. Syndesmophytes form across the disc spaces culminating with osseous fusion of the entire spine and the formation of the ankylosed or bamboo spine. Affecting all levels of the spine, ankylosing spondylitis manifests with symptoms of

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Gregory W. Albert and Arnold H. Menezes

A nkylosing spondylitis is one of the spondyloarthropathies, a group of chronic inflammatory diseases that primarily affect the axial skeleton. 2 Importantly for neurosurgeons, one of the hallmarks of ankylosing spondylitis is spine disease. New bone forms syndesmophytes bridging the vertebral bodies and facet joints, leading to ankylosis of the spine. Patients with ankylosing spondylitis are at high risk for developing osteoporosis, microfractures of the spine, and traumatic fractures. When fractures do occur, there is a much higher incidence of

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Cauda equina syndrome of long-standing ankylosing spondylitis

Case report and review of the literature

Micam W. Tullous, Holger E. I. Skerhut, Jim L. Story, Willis E. Brown Jr., Eduardo Eidelberg, Mohammad R. Dadsetan, and John R. Jinkins

antigen. The primary pathological site of ankylosing spondylitis is at the insertion of ligaments and capsules on bone, whereas in rheumatoid disease the essential pathology resides within the synovium. 7 In addition to spinal symptomatology, some patients may exhibit a peripheral arthropathy and regions of insertional tendonitis. Other nonmusculoskeletal manifestations of the disease include uveitis, chronic prostatitis, pulmonary fibrosis, cardiac valvular disease, and amyloidosis. 7 Neurological complications include solitary nerve root lesions, 9, 14, 24