Ankylosing Spondylitis and Spinal Cord Injury: Origin, Incidence, Management, and Avoidance

W. Bradley Jacobs, M.D.; Michael G. Fehlings, M.D., Ph.D., F.R.C.S.C.


Neurosurg Focus. 2008;24(1):E12 

In This Article

Abstract and Introduction


Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease that primarily affects the vertebral column and sacroiliac joints. Over time, the disease process promotes extensive remodeling of the spinal axis via ligamentous ossification, vertebral joint fusion, osteoporosis, and kyphosis. These pathological changes result in a weakened vertebral column with increased susceptibility to fractures and spinal cord injury (SCI). Spinal cord injury is often exacerbated by the highly unstable nature of vertebral column fractures in AS. A high incidence of missed fractures in the ankylosed spine as well as an increased incidence of spinal epidural hematoma also worsens the severity of SCI. Spinal cord injury in AS is a complex problem associated with high morbidity and mortality rates, which can be attributed to the severity of the injury, associated medical comorbidities, and the advanced age of most patients with AS who suffer an SCI. In this paper the authors outline the factors that increase the incidence of vertebral column fractures and SCI in AS and discuss the management of SCI in patients with AS. Primary prevention strategies for SCI in patients with AS are outlined as well.


Ankylosing spondylitis is the major subtype of an interrelated group of seronegative rheumatic spondyloarthritides that also includes psoriatic spondyloarthritis, reactive spondyloarthritis, spondyloarthritis associated with inflammatory bowel disease, and undifferentiated spondyloarthritis.[10] Ankylosing spondylitis primarily affects the axial skeleton (sacroiliac joints and spinal column) and is a chronic lifelong disease that often starts in young adults, with the age at onset being < 30 years in 80% of patients.[18] The usual disease pattern is one of slow and steady progression, and as such, complications of AS, such as spinal fractures, are not frequently manifested until much later in life. The incidence of AS is between 0.5 and 14 per 100,000 people per year, whereas the prevalence is between 0.1 and 1.4%.[9] Men are affected approximately twice as often as women.[18]

The seronegative spondyloarthropathies have a genetic predisposition related to the major histocompatibility complex Class I molecule HLA-B27. Ninety to 95% of patients with AS are positive for HLA-B27, but AS develops in only 5% of HLA-B27-positive individuals.[11,41] This finding suggests that other, as yet unidentified, genetic and environmental factors also play a significant role in the pathogenesis of AS.

The diagnosis of AS is made on the basis of both radiographic and clinical factors known as the modified New York criteria ( Table 1 ).[40] Central to the diagnosis is the presence of sacroiliitis, as defined on radiography or MR imaging. The degree of sacroiliitis is graded from 0 to 4, with the grade corresponding to radiographically demonstrated normal joints, suspicious changes, minor changes, moderate changes, and ankylosis, respectively. Inflammatory back pain is the central clinical feature of AS. In a controlled study Rudwaleit and colleagues[35] developed diagnostic criteria to help delineate inflammatory back pain as occurs in AS and other spondyloarthritides from other types of back pain. The fulfillment of any 2 of their 4 criteria suggests a diagnosis of inflammatory back pain: 1) morning stiffness lasting more than 30 minutes; 2) improvement of back pain with activity and not rest; 3) awakening due to back pain during the second half of the night; and 4) alternating buttock pain.

In addition to inflammation in the axial skeleton, peripheral arthritis, enthesitis, and anterior uveitis can occur in AS. Manifestations in other organ systems, such as the pulmonary, cardiovascular, or renal systems, are rare but do occur; when present, they can have significant repercussions on the health status of the patient with AS.


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