Spinal Disorders: Fundamentals of Diagnosis and Treatment Part 106 pptx

Recapitulation Epidemiology. Approximately 40% of patients with rheumatoid arthritis show pathology in the cervical spine, mainly the atlantoaxial segment. Pathogenesis. The translational instability between axis and atlas might be painful and leads in the long term to myelopathic changes duetochronictrau- matization of the myelon. Ongoing osseous resorp- tion of the lateral masses of the atlas causes upward migration of the dens into the foramen magnum. In the subaxial cervical spine, the inflammatory process causes instability and deformity. Clinical presentation. The instability and deformity are mostly associated with the corresponding clini- cal symptoms: pain and neurological signs in dif- ferent stages. However, it has to be kept in mind that these patients are used to tolerating pain and that often other problems of the joints are more prominent. The pathology of the cervical spine may progress unnoticed in these cases. Diagnostic work-up. Every patient with RA should have a lateral flexion radiography of the cervical spine performed as a screening investigation at least every 3–5 years (according to the aggressivity of the disease). In cases of manifest instability or de- formity, a neurophysiological work-up and MRI should be performed. Non-operative treatment. If surgery is not indicat- ed, the patient should be given regular observation with neurophysiological examinations, radiographs and MRI. Operative treatment. Neck pain is the most com- mon indication for surgery, but neurological symp- toms with myelopathy or radicular deficits might be the primary cause for surgery. It should be kept in mind that clinical assessment in rheumatoid patients might be extremely difficult since previous surgery on various articulations of the extremities makes in- terpretation of clinical findings difficult. Neurophysi- ological investigation is a suitable means for obtain- ing objective results. Stabilization of the atlantoaxial segment is the most common procedure for treat- ment of atlantoaxial instability. It is performed by screw fixation technique from a posterior approach. In the case of severe occipitocervical dislocation, the fixation should be extended to the occiput. Persis- tent dislocation or compression by the dislocated dens should be treated by transoral decompression. In the subaxial spine, instabilities may be treated by posterior plate fixation with lateral mass screws or pedicle screws. Concomitant narrowing of the spinal canal should be approached by anterior decompres- sion with corpectomy and/or posterior laminecto- my. The timing of surgery in rheumatoid patients is crucial to obtaining satisfactory clinical results. Key Articles Boden SC, Dodge LD, Bohlmann HH, Recht ine GL (1993) Rheumatoid arthritis of the cervical spine. Long term analysis with predictors of paralysis and recovery. J Bone Joint Surg 75-A(9):1282 –1297 The authors report their experience in treating 73 patients with rheumatoid arthritis with an average follow-up of 7 years. The authors highlight that the most important predictor of the potential for neurological recovery after the operation was the preoperative poste- rior atlanto-odontoid interval. In patients who had paralysis due to atlantoaxial subluxa- tion, no recovery occurred if the posterior atlanto-odontoid interval was less than 10 mm, whereas recovery of at least one neurological class always occurred when the posterior atlanto-odontoid interval was at least 10 mm. If basilar invagination was superimposed, clinically important neurological recovery occurred only when the posterior atlanto- odontoid interval was at least 13 mm. All patients who had paralysis and a posterior atlanto-odontoid interval or diameter of the subaxial canal of 14 mm had complete motor recovery after the operation. Crockard HA, Pozo JL, Ransford AO, Stevens JM, Kendall BE, Essigman WK (1986) Transoral decompression and posterior fusion for rheumatoid atlanto-axial subluxa- tion. J Bone Joint Surg 68B(3):350 – 356 In this landmark paper, Crockard et al. describe a surgical technique for transoral ante- rior decompression and posterior occipitocervical fusion, which removes both bony and soft-tissue causes of compression and allows early mobilization without major external fixation. 1054 Section Tumors and Inflammation Key Articles Dvorak J, Grob D, Baumgartner H, Gschwend N, Grauer W, Larsson S (1989)Functional evaluation of the spinal cord by magnetic resonance imaging in p atients with rheuma- toid arthritis and instability of upper cervical spine. Spine 14(10):1057 – 1064 This study describes the imaging findings in patients with atlanto-axial instability due to rheumatoid arthritis and provides recommendations for surgical treatment. Matsunaga S, Sakou T, Onishi T, Hayashi K, Taketomi E, Sunahara N, Komiya S (2003) Prognosis of patients with up per cervical lesions ca used by rheumatoid arthritis: com- parisonofoccipitocervicalfusionbetweenC1 laminectomy and nonsurgical manage- ment. Spine 15(28):1581 – 1587 In a matched controlled comparative study, non-surgical treatment and occipitocervical fusion associated with C1 laminectomy were evaluated in patients with upper cervical lesions caused by rheumatoid arthritis. The authors concluded that occipitocervical fusion associated with C1 laminectomy for patients with rheumatoid arthritis is useful for decreasing nuchal pain, reducing myelopathy, and improving prognosis. CombeB,LandeweR,LukasC,BolosiuHD,BreedveldF,DougadosM,EmeryP,Ferrac- cioli G, Hazes JM, Klareskog L, Machold K, Martin-Mola E, Nielsen H, Silman A, Smolen J, Yazici H (2007) EULAR recommendations for the management of early arthritis: report of a task force of the European Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis 66:34 – 45 Excellent review on the conservative treatment of rheumatoid arthritis with recommen- dations on the management of early rheumatoid arthritis References 1. Almeida Mdo S, et al. (2005) Epidemiological study of patients with connective tissue dis- eases in Brazil. Trop Doct 35(4)206–9 2. Boden SC, et al. (1993) Rheumatoid arthritis of the cervical spine. Long term analysis with predictors of paralysis and recovery. J Bone Joint Surg 75A(9):1282–1297 3. Brooks AL, Jenkins EG (1978) Atlanto-axial arthrodesis by the wedge compression method. J Bone Joint Surg 60A:279–284 4. Crockard HA, et al. (1986) Transoral decompression and posterior fusion for rheumatoid atlanto-axial subluxation. J Bone Joint Surg 68B(3):350–356 5. Dvorak J, et al. (1989) Functional evaluation of the spinal cord by magnetic resonance imag- ing in patients with rheumatoid arthritis and instability of upper cervical spine. Spine 14(10):1057–1064 6. Dvorak J, et al. (1993) Clinical validation of functional flexion/extension radiographs of the cervical spine. Spine 18(1):120–127 7. Edwards CJ, et al. (2005) The changing use of disease-modifying anti-rheumatic drugs in individuals with rheumatoid arthritis from the United Kingdom General Practice Research Database. Rheumatology (Oxford) 44(11)1394–1398 8. Gallie WE (1939) Fractures and dislocations of the cervical spine. Am J Surg 46A:495–499 9. Goel A, Laheri V (1994) Plate and screw fixation for atlanto-axial subluxation. Technical report. Acta Neurochir 129:47–53 10. Grob D (2000) Atlantoaxial immobilization in rheumatoid arthritis: a prophylactic proce- dure? Eur Spine J 9:404–409 11. Grob D, et al. (1992) Biomechanical evaluation of four different posterior atlantoaxial fixa- tion techniques. Spine 17(5):480–490 12. Grob D, et al. (1994) The role of plate and screw fixation in occipitocervical fusion in rheu- matoid arthritis. Spine 19:2545–2551 13. Grob D, Schütz U, Plötz G (1999) Occipitocervical fusion in patients with rheumatoid arthritis. Clin Orthop 366:46–53 14. Harms J, Melcher RP (2001) Posterior C1–C2 fusion with polyaxial screw and rod fixation. Spine 26(22):2467–71 15. Kraus DR, et al. (1991) Incidence of subaxial subluxation in patients with generalized rheu- matoid arthritis who have had previous occipital cervical fusions. Spine 16(10S):486–489 16. Magerl F, Seemann P (1986) Stable posterior fusion of the atlas and axis by transarticular screw fixation. Cervical Spine 1:322–327 17. Mannion AF, Elfering A (2006) Predictors of surgical outcome and their assessment. Eur Spine J 15(Suppl 1)93–108 Rheumatoid Arthritis Chapter 37 1055 18. Matsunaga S, et al. (2003) Prognosis of patients with upper cervical lesions caused by rheu- matoid arthritis: comparison of occipitocervical fusion between C1 laminectomy and non- surgical management. Spine 15(28):1581–1587 19. Ono K, Ebara S, Fuji T (1987) Myelopathy hand. J Bone Joint Surg 69B:215–219 20. Ranawat CS, et al. (1979) Cervical spine fusion in rheumatoid arthritis. J Bone Joint Surg 61A:1003–1010 21. Shimizu T, Shimada H, Shirakura K (1993) Scapulohumeral reflex (Shimizu). Its clinical sig- nificance and testing maneuver. Spine 18(15):2182–2190 1056 Section Tumors and Inflammation 38 Ankylosing Spondylitis Thomas Liebscher, Kan Min, Norbert Boos Core Messages ✔ Ankylosing spondylitis (AS) is a systemic, inflammatory, seronegative rheumatoid disease ✔ Ankylosing spondylitis in 90 % of cases is asso- ciated with HLA-B27 ✔ The male/female ratio is 2– 7:1 ✔ The onset of the disease is usually between 15 and 35 years of age, and it can take up to 10 years before the diagnosis is made ✔ The imaging modalities of choice are standard radiographs and MRI. Computed tomography is useful for diagnosing occult fractures and for preoperative planning ✔ Ankylosing spondylitis is treated non-opera- tively by analgesics, anti-inflammatory drugs and physiotherapy ✔ Spinal surgery is only indicated if conservative treatment has failed to prevent spinal deformi- ties and instabilities or in the case of disc space infections ✔ The surgical techniques for treating spinal deformity, instabilities and infections depend on the localization and etiology of the pathol- ogy ✔ Surgical techniques include lumbar closing wedge (pedicle subtraction) osteotomies, mul- tisegmental posterior wedge osteotomy, cervi- cal opening or closing wedge osteotomies ✔ Meticulous preoperative planning of the osteo- tomy is mandatory ✔ Unstable fractures with neurological dysfunc- tions at the cervical spine are stabilized from a combined anterior and posterior approach. In the lumbar spine, the surgery is most fre- quently done from posterior ✔ Surgical interventions for ankylosing spondyli- tis are prone to complications Epidemiology Spondyloarthropathies are chronic systemic inflammatory rheumatic disorders Spondyloarthropathies (SPAs) are systemic and chronic inflammatory rheu- matic disorders with involvement of the axial skeleton or asymmetrical arthritis of large joints of the lower extremities. SPAs are divided into five subcategories: ankylosing spondylitis psoriatic arthritis reactive arthritis inflammatory bowel disease related arthritis undifferentiated spondyloarthropathy Ankylosing spondylitis is the most common form of SPA Ankylosing spondylitis (AS) is the most common form of SPAaffecting the whole spine [7, 17, 20, 105]. The final result is a kyphosis of the whole column with sag- ittal imbalance ( Case Introduction). Besides spinal ankylosis, inflammatory lesions, bony erosions, discitis and loss of bone mineral density (BMD) can occur during the process of this disease. AS was described for the first time by Vladimir von Bechterew in 1893 [9]. The description was initially based on clinical symp- Tumors and Inflammation Section 1057 a b Case Introduction A 42-year-old male had suffered from ankylosing spondylitis for over 10 years and developed a progressive ankylosis of the entire spine. Despite intensive physiotherapy, the patient developed an increasing sagittal deformity and loss of his verticalgaze( a). When shaking hands, he was unable to look at his counterpart, which was quite disturbing in his job. The standing lateral radiograph demonstrates a significant loss of lumbar lordosis ( b). Since the pathology was predomi- nantly located in the lumbar spine, a lumbar closing wedge osteotomy at L3 was suggested and carried out. toms and the spinal deformity. With the advance of radiography, it was possible to document the articular changes. AS is associated with chronic inflammation of the: sacroiliac joints vertebral column osteoarthritis of the large joint (hip, knee and shoulder joints) extra-articular disorders including enthesitis and uveitis AS more frequently occurs in males Ankylosing spondylitis occurs more frequently in the male population with a ratio of between 2 and 7 to 1 [28, 31, 43, 49, 53, 79, 105]. The prevalence rate in Europe and North America ranges between 0.1 and 1.4/100000 and regionally 1058 Section Tumors and Inflammation c d e Case Introduction (Cont.) Postoperative radiographs (c, d) demonstrate an excellent correction and alignment of the spine with recreation of lum- bar lordosis. At a 2-year follow-up, the patient was very satisfied with the result, able to look straight ahead and fully func- tional in his job ( e). The onset of disease is usually between 15 and 35 years of age can rise up to 8.2/100000 [87]. The onset of disease is usually between 15 and 35 years. Up to 10 years can pass before the diagnosis is made [40, 43, 49, 79]. This delay in diagnosis is due to the initially non-specific clinical symptoms (e.g., low back pain) and lack of early pathognomonic imaging findings. During the later disease stage, inflammatory spinal lesions can be found which most commonly occur in the thoracic and lumbar spine [8, 105]. Aseptic spondylodis- AS is characterized by progressive kyphosis with segmental instability, asep- tic discitis and osteoporosis citis is an erosive lesion of the disc and vertebral body without infection or trauma, first described by Andersson in 1937 [2]. Clinical and radiographic find- ings demonstrate a progressive vertebral and discovertebral kyphosis with seg- mental instability [99, 103]. The prevalence of aseptic discitis is about 18% of patients with AS [61]. Almost half (40–50%) of the patients with mild AS exhibit osteopenic or osteoporotic lumbar vertebrae [6, 94, 107]. Severe complications of osteoporosis and loss of trabecular bone are spinal fractures subsequent to The prevalence of spinal fractures is about 5 % and increases with age minor trauma. The prevalence of spinal fracture is about 5% and increases with age [40]. It reaches about 15% at the age of 42 years and older [40]. Unilateral Ankylosing Spondylitis Chapter 38 1059 AS also frequently affects hips, knee and shoulder joints inflammationoflargediarthrodialjointssuchaships,kneesandshouldersisa common symptom of SPA. Hip joints are affected in 57% of patients [37]. The prevalence of unilateral shoulder arthritis in patients with AS is estimated to be between 30% and 58%. Approximately 25% of AS patients even suffer from bilat- eral shoulder arthritis [37, 38, 43]. Besides changes in physical function, other areas also affect the quality of life such as [12]: psychological domain [67] social domain economic aspects A disease duration of 15 years is associated with a 50% inability to work Afteradiseasedurationof15years,about50%ofpatientsareusuallynolonger able to work full time [43]. Up to 80% of patients suffer from daily pain and more than 60% need to take painkillers daily [43]. In addition, anxiety and depression are correlated with the degree of disorder [45, 67]. Pathogenesis Genetic factors play a key role Despite intensive research, the pathogenesis of AS is not yet clear [19]. There is increasing evidence that AS is genetically linked. The association of AS and the The pathogenesis of AS is not clear HLA -B27 gene is well known. HLA-B27 can be found in up to 90% of patients with AS [49, 79, 105]. The HLA-B27 gene is mapped to the major histocompatibil- ity complex (MHC) class I region on the short arm of chromosome 6 [55]. There are24subtypesofHLA-B27 [54, 55]. The subtype HLA-B27 05 is most common worldwide. Twin studies have shown that AS is passed on to the next generation with a higher incidence for monozygotic than for dizygotic or even heterozygotic parent-child pairs [24, 49]. Since 80–90% of all HLA-B27 carriers do not develop AS, it is widely assumed that more genetic factors are involved [87]. HLA subtype carriers B27 06 (found in the Southeast Asian population) and B27 09 (Sardinian population) do not develop AS [54, 55], which also strongly indicates the exis- tence of other genetic factors. Whole genome mapping and within-family studies have demonstrated a link between AS and other non-HLA -B27 genes mainly on the short arm of chromosome 6 [23, 62, 89, 93]. Bacterial infections may trigger autoimmune responses An infection-based pathogenesis of AS has been the subject of critical debate [19, 41, 66, 96]. Antigenic peptides are thought to derive from bacterial proteins (P.aeruginosa,E.coliand Bacillus megaterium) which have a similar alignment of amino acids like peptides inside articular joints [41, 66]. HLA-B27 restricted CD8-T lymphozytes are suspected of identifying the bacterial protein as a target and thereafter could also aim at peptide structures inside the sacroiliac joint or vertebral column resulting in an autoimmune reaction with inflammatory signs. The finding that reactive arthritis is triggered by genitourinary infections with Chlamydia trachomatis or by enteritis caused by gram-negative enterobacteria (e.g., Shigella, Salmonella, Yersinia andCampylobacter) supports this hypothesis, but the evidence for triggering infections in other spondylarthopathies is limited [19]. Inflammatory reactions play a key role in the pathogenesis The detailed pathogenetic mechanisms have yet to be elucidated for associ- ated bone mineral density loss, bony lesions as well as the formation of new bone material ending up in ankylosis. It is assumed that new bone formations are independent of local inflammatory processes [66]. On the other hand, there is some evidence that persistent inflammation might be an etiologic factor of bone lossinAS[65].Consequencesofbonelossare(occult)fracturesandpseudar- throsis, in which microscopically necrotic bone material and cartilage can be observed besides vascular fibrous tissue [39]. The existence of an aseptic discitis supports an inflammatory origin for bony changes. CD3+ lymphocytes and IgA 1060 Section Tumors and Inflammation positive plasma cells have been identified in vertebral bones and the surrounding soft tissue affected by aseptic discitis [76]. Bloodmarkers for inflammation(CRP, ESR) are found elevated in aseptic discitis as well [61, 76]. After local inflamma- tory processes, disc replacing fibrous tissue and cartilaginous nodules have been identified in later stages of aseptic discitis [27, 61]. Bone marrow from zygapo- physeal joints demonstrates persistent inflammation even in those patients with long-standing disease. The findings of increased numbers of T cells and B cells and neoangiogenesis suggest that these features play a role in the pathogenesis of AS [3]. Stages of pathological changes include inflamma- tory responses, proliferative bone sclerosis and ankylosis with increasing deformity Pathological changes ofthevertebralcolumnduetoASoccurinthreeconsecu- tive or side by side stages: First, there is an inflammatory process with bony ero- sions and destruction of vertebrae and discs. The development of square vertebral bodies is shown to be based on a combination of a destructive osteitis and repair [5]. These changes initially are noted in the whole spine yet more frequently are seen in the lower thoracic spine [8, 105]. Second, a proliferatory bone sclerosis develops followed by a reactive bone formation with syndesmophytes. These changes are slow in growth throughout the whole spine followed by kyphotic defor- mation and progressive sagittal imbalance of the spine. Third, the spine deformity will increase to an ankylosing process and end in a so-called bamboo spine. The rationale of conservative therapy is to protract the consequences of inflammation and osteoporosis and defer structural damage to the affected bones. The finding of abundant tumor necrosis factor (TNF)- message in affected joints provides the rationale for the therapeutic use of TNF- inhibitors [18, 19]. A strategy of continuous use of non-steroidal anti-inflammatory drugs (NSAIDs) has been shown to reduce radiographic progression in symptomatic patients with AS, without increasing toxicity substantially [102]. Early treatment therefore appears essential for a good clinical outcome [15, 71]. Clinical Presentation History The diagnosis is often delayed Ankylosing spondylitis predominantly affects the mobility of the vertebral col- umn, joint function and pain. This entity is sometimes difficult to diagnose par- ticularly during the onset of the disease. Quite often the diagnosis is therefore delayed. It is important to consider the diagnosis of AS in patients who present with early symptoms such as: morning stiffness pain in the pelvic region (sacroiliac joints) pain at night decreasing pain during movement musculoskeletal pain at varying locations fatigue loss of body weight subfebrile temperature When AS has become manifest, the disease affects the function and mobility of the spine and diarthrodial joints and results in pain. The cardinal sy mptoms are: Inflammatory back pain is a hallmark “inflammatory” back pain typical arthritis pain (pain at night and stiffness in the morning) progressive spinal stiffness progessive hyperkyphosis (inability to look straight ahead) Ankylosing Spondylitis Chapter 38 1061 Table 1. Criteria for inflammatory back pain morning stiffness > 30 min improvement in back pain with exercise but not with rest awakening because of back pain during thesecondhalfofthenight alternating buttock pain The criteria are fulfilled if at least two of four of the parameters are present [80] Inflammatory pain is among the first symptoms and the key clinical sign of AS. The criteria [80] for inflammatory back pain in younger patients (<50 years) are shown in Table 1. Rudwaleit reported that none of the single parameters sufficiently differenti- ated AS from mechanical low back pain. Several sets of combined parameters proved to be well balanced between sensitivity and specificity. If at least two of the aforementioned four parameters were fulfilled (positive likelihood ratio 3.7), a sensitivity of 70.3% and a specificity of 81.2% was found. If at least three of the four parameters were fulfilled, the positive likelihood ratio increased to 12.4 [80]. Additional symptoms are: enthesitis (e.g., Achilles tendon, plantar fascia) anterior uveitis pulmonary, cardial and bowel inflammation Typical concomitant disorders or extra-articular manifestations have been observed to be part of AS: painful tendinopathy, acute anterior uveitis (AAU), pulmonary and cardial inflammation, e.g., aortitis, and bowel disease. The fre- quency, duration and intensity of these concomitant disorders varies individu- AS is a systemic disease ally. The prevalence of AAU is between 33% and 49% [21, 25, 43]. AS is perceived as a systemic disease. Physical Findings Ankylosing spondylitis is a potentially progressive disease. The first symptoms of AS are mild and non-specific. The physical findings are often non-specific Frequent physical findings are: pain provocation of sacroiliac joints (positive Mennell test) decreased spinal mobility (Schober and Ott test) anterior sagittal imbalance (plumbline falling in front of the hip joint) coronal spinal imbalance (less frequently) reduced chest expansion during inspiration and expiration after a chronic progression loss of body height A neurological examination of the upper and lower extremities is mandatory to diagnose neural compression. In the presence of severe back pain, it is manda- Rule out spinal instability or an occult fracture in cases of severe back pain tory to rule out a spinal instability or an occult fracture [34, 42] in order to pre- vent neurological deterioration due to epidural bleeding or secondary fracture displacement [77, 78]. Compensatory balance adjustment occurs in the cranial segments of the cervical spine as a direct consequence of the AS associated col- umn stiffening. Furthermore, an increased force effect for the small vertebral joints can be observed with the risk of atlanto-occipital subluxation or even a ver- tebral dislocation. Pain, stiffness and reduced range of motion in peripheral joints can occur at any stage of the disease. A thorough examination of the large diarthrodial joints and the search for enthesopathies is compulsory in addition to the mandatory clinical examination of the spine [37, 38]. 1062 Section Tumors and Inflammation Diagnostic Work-up Early diagnosis can improve treatment outcome The ultimate goal is to diagnose AS as early as possible so as to start an appropri- ate therapy. When AS is suspected, a thorough diagnostic assessment must be enforced because early diagnosis can improve treatment outcome. A positive familyhistoryandreportsoftypicalarthritissymptomssuchaspainatnightand stiffness in the morning can be helpful. In addition to the physical examination, the diagnostic work-up comprises laboratory investigations, including HLA-B27 determination and imaging studies. Laboratory Investigations The most important laboratory investigations are: C-reactive protein (CRP) elevated erythrocyte sedimentation rate (ESR) white blood cell count (WBC) determination of HLA-B27 only in symptomatic patients Inflammatory markers are sensitive but non-specific These inflammation markers are sensitive but non-specific [35, 36, 68, 69]. Occa- sionally, a light anemia can be observed. The sensitivity of HLA-B27 determina- tion is about 90% but the specificity is low since up to 80% of HLA-B27 carriers do not suffer from AS [43, 49, 54]. The laboratory examination could evolve to a better diagnostic tool through the identification of non-major histocompatibility complex (n-MHC) “genetic susceptibility factors” in AS using gene mapping techniques [23, 55, 62]. Imaging Studies Besides the typical clinical signs and laboratory investigations, the imaging stud- ies are essential for the early diagnosis of AS. However, imaging findings of acute inflammation, or bony alterations of sacroiliac joints (SI joints) or vertebral col- umn, can be absent in the early stages of AS ( Fig. 1). Imaging studies of the spine are essential to: make the diagnosis of AS exclude fractures, spondylolisthesis or Andersson lesions assess sagittal imbalance monitor progress of the disease assess the treatment effect Signs of acute inflammation and bony alterations can be absent in early stages Clinical examinations are complemented by various imaging studies (X-ray, CT, MRI and bone scan). However, whole-body MR imaging will more and more be used to monitor inflammatory spinal lesions at an early or an active stage of dis- ease. The possibility of evaluating shoulder and hip joints together with the axial skeleton is the major advantage of whole-body MRI [105]. Standard Radiographs Standard radiography remains the mainstay of diagnostic imaging Standard radiographs of the spine and sacroiliac joints (SIJs) remain the main- stay of diagnostic imaging for AS ( Fig. 1a). The hallmark of AS is a sacroiliitis and at a later stage ankylosis of the SIJs ( Fig. 1a–c). Radiologic alterations of the SIJs are differentiated by the modified New York classification [97] into four grades ( Table 2). Ankylosing Spondylitis Chapter 38 1063 . complications of osteoporosis and loss of trabecular bone are spinal fractures subsequent to The prevalence of spinal fractures is about 5 % and increases with age minor trauma. The prevalence of spinal. with long-standing disease. The findings of increased numbers of T cells and B cells and neoangiogenesis suggest that these features play a role in the pathogenesis of AS [3]. Stages of pathological changes. chronic progression loss of body height A neurological examination of the upper and lower extremities is mandatory to diagnose neural compression. In the presence of severe back pain, it is manda- Rule out spinal