eMedicine Specialties > Orthopedic Surgery > Spine

Rheumatoid Spondylitis

Author: Michael J Vives, MD, Associate Professor, Department of Orthopedics, Division of Spine Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey
Coauthor(s): Steven R Garfin, MD, Professor, Chair, Department of Orthopedics, University of California at San Diego Medical Center
Contributor Information and Disclosures

Updated: Aug 26, 2008

Introduction

History of the Procedure

The most common sites of rheumatoid arthritis (RA) are the metatarsophalangeal joints, followed by the metacarpophalangeal joints and the cervical spine (ankylosing spondylitis, rheumatoid spondylitis). Much of the understanding of spinal afflictions in RA was advanced by studies published in the 1950s and 1960s.1 In 1951, Davis and Markley detailed medullary compression as a cause of death in patients with RA.2 In 1969, Mathews reported that 25-30% of patients with RA who were admitted to the hospital had radiographic evidence of cervical spine involvement.3

Problem

Rheumatoid spondylitis (ankylosing spondylitis) primarily affects the cervical spine. Affliction of the thoracic or lumbar spine is rare. The anatomic abnormalities occur as a consequence of the destruction of synovial joints, ligaments, and bone. Abnormalities of the rheumatoid cervical spine generally can be grouped into 3 categories. Atlantoaxial instability (AAI) or atlantoaxial subluxation (AAS) is the most common. AAS can be a fixed deformity or can be partially or fully reducible. Superior migration of the odontoid (SMO) is the next most common abnormality and has alternately been referred to as cranial settling, pseudobasilar invagination, or vertical/upward translocation of the odontoid.4 The third and least commonly seen deformity is subaxial subluxation. This may be seen at multiple levels, producing a stepladder deformity. The 3 deformities may be seen in isolation, or combined involvement may occur.

Frequency

Rheumatoid arthritis (RA) affects 0.8% of the white population in the United States and Europe. Neck pain is reported in 40-88% of patients with RA. The prevalence of cervical spine involvement (rheumatoid spondylitis, ankylosing spondylitis) in RA ranges from 25-80%, depending on the diagnostic criteria applied.5 However, only 7-34% of patients with RA have a neurologic deficit. A substantial number of patients with radiographic instability or neck pain do not develop neurologic deficits.6,7,8

Involvement of the cervical spine typically begins early in the disease process and often parallels the extent of peripheral disease. Of the 3 types of involvement, AAI is the most common, occurring in up to 49% of patients.9 While most of these subluxations are anterior, approximately 20% are lateral and approximately 7% are posterior. SMO is seen in up to 38% of patients with RA. Subaxial subluxation is seen as a discrete pathologic entity in 10-20% of patients.

Subaxial subluxation also develops after previous upper cervical fusions.10,11 In one series of 79 patients, 36% developed subaxial subluxation an average of 2.6 years following occipitocervical fusion, and 5.5% experienced subaxial subluxation an average of 9 years following atlantoaxial fusion.10

Pathophysiology

Recent theories on the pathogenesis of rheumatoid arthritis (RA) suggest that the synovial cells of these patients chronically express an antigen that triggers the production of rheumatoid factor, an immunoglobulin molecule directed against other autologous immunoglobulins. An inflammatory response is initiated, involving immune complex formation, activation of the complement cascade, and infiltration of polymorphonuclear leukocytes. The proliferating fibroblasts and inflammatory cells produce granulation tissue, known as rheumatoid pannus, within the synovium. The pannus produces proteolytic enzymes capable of destroying adjacent cartilage, ligaments, tendons, and bone. The destructive synovitis results in ligamentous laxity and bony erosion with resultant cervical instability and subluxation.

Atlantoaxial subluxation results from erosive synovitis in the atlantoaxial, atlanto-odontoid, and atlanto-occipital joints and the bursa between the odontoid and the transverse ligament (see Image 1). The superior migration of the odontoid is attributed to erosion and bone loss in the occipitoatlantal and atlantoaxial joints (see Image 2). Subaxial subluxation results from destruction of the facets, intervertebral discs, and interspinous ligaments. Unlike degenerative disease, involvement of C2-C3 and C3-C4 is common, and osteophytes seldom are seen.

Presentation

Rheumatoid involvement of the cervical spine (rheumatoid spondylitis, ankylosing spondylitis) is just one element in a systemic disease process. Cervical involvement often correlates with the degree of hand and wrist erosion. Cervical involvement also has been associated with the presence of rheumatoid nodules and the use of corticosteroids. Classically, craniocervical neck pain often is associated with occipital headaches.

Compression of the C2 sensory fibers supplying the nucleus of the spinal trigeminal tract can cause facial pain. Compression of the C2 sensory fibers supplying the greater auricular nerve may result in ear pain. Occipital neuralgia results from compression of the C2 sensory fibers supplying the greater occipital nerve. A history of myelopathic symptoms should be sought carefully. Patients may experience weakness, decreased endurance, gait difficulty, paresthesias of the hands, and loss of fine dexterity. Patients with involvement may experience urinary retention and, eventually, incontinence.

Vertebrobasilar insufficiency may be found, particularly in patients with atlantoaxial instability (AAI). Complaints may include vertigo, loss of equilibrium, visual disturbances, tinnitus, and dysphagia. Similar symptomatology can also be caused by mechanical compression of the brainstem. In some patients, neck motion can elicit shocklike sensations through the torso or into the extremities (ie, Lhermitte sign).

The physical inventory of these patients frequently is confounded by the severity of their peripheral rheumatoid involvement. Weakness in these patients can also be due to tenosynovitis, tendon rupture, muscular atrophy, peripheral nerve entrapment, or articular involvement, making neurologic impairment less obvious. Signs of myelopathy should raise suspicion of cervical involvement. Rarely, cranial nerve dysfunction can occur secondary to compression of the medullary nuclei by the odontoid. Other rare findings in patients with advanced brainstem compression include vertical nystagmus and Cheyne-Stokes respirations.

The Ranawat classification can be used to categorize patients with rheumatoid myelopathy based on their clinical history and physical findings (see below).12 This classification has some utility in determining potential for neurologic recovery following surgery.

The Ranawat classification of neurologic deficit is as follows:

  • Class I - No neural deficit
  • Class II - Subjective weakness, dysesthesias, and hyperreflexia
  • Class IIIA - Objective weakness and long-tract signs; patient remains ambulatory
  • Class IIIB - Objective weakness and long-tract signs; patient no longer ambulatory

Indications

Numerous investigators have attempted to elucidate the natural history of rheumatoid arthritis (RA) as it affects the cervical spine (rheumatoid spondylitis, ankylosing spondylitis), with wide variation in their findings.13,14,15,16,17 Depending on the diagnostic criteria applied, the prevalence of cervical involvement in RA ranges from 25-80%. The likelihood of cervical involvement appears to increase with the duration of rheumatic disease. Because neurologic deficit is seen only in 7-34% of cases, many patients with pain and radiographic criteria for instability do not develop neurologic sequelae. However, 10% of patients with RA may die from brainstem compression that is unrecognized before their sudden death.18

The identification of a subset of patients with impending neurologic deficit has been elusive due to the poor correlation of neurologic symptoms with radiographic indicators of instability. Therefore, universally accepted surgical indications have been slow to develop.

Contraindications

Contraindications to surgery for rheumatoid spondylitis (ankylosing spondylitis) include medical conditions that suggest the patient would not tolerate the stress of surgery, such as unstable angina or a recent myocardial infarction or stroke. Active infection with likely bacteremia would also be a relative contraindication to surgery, especially in the setting of planned instrumentation. The patient's medical condition should be optimized prior to proceeding with any planned surgical intervention.

More on Rheumatoid Spondylitis

Overview: Rheumatoid Spondylitis
Workup: Rheumatoid Spondylitis
Treatment: Rheumatoid Spondylitis
Follow-up: Rheumatoid Spondylitis
Multimedia: Rheumatoid Spondylitis
References
Further Reading
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Further Reading

Rituximab for the treatment of rheumatoid arthritis.
National Institute for Health and Clinical Excellence (NICE) - National Government Agency [Non-U.S.].  2007 Aug.  26 pages.  NGC:005902

Abatacept for the treatment of rheumatoid arthritis.
National Institute for Health and Clinical Excellence (NICE) - National Government Agency [Non-U.S.].  2008 Apr.  29 pages.  NGC:006483
 

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Keywords

rheumatoid spondylitis, ankylosing spondylitis, Bekhterev arthritis, Marie-Strumpell spondylitis, rhizomelic spondylitis, rheumatoid arthritis, RA, atlantoaxial subluxation, AAS, subaxial subluxation, atlantoaxial instability, AAI, superior migration of the odontoid, SMO

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Contributor Information and Disclosures

Author

Michael J Vives, MD, Associate Professor, Department of Orthopedics, Division of Spine Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey
Michael J Vives, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons and North American Spine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Steven R Garfin, MD, Professor, Chair, Department of Orthopedics, University of California at San Diego Medical Center
Steven R Garfin, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, North American Spine Society, Orthopaedic Research Society, and Western Orthopaedic Association
Disclosure: Nothing to disclose.

Medical Editor

Lee H Riley III, MD, Chief, Division of Orthopedic Spine Surgery, Assistant Professor, Departments of Orthopedic Surgery and Neurosurgery, Johns Hopkins University
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

William O Shaffer, MD, Professor, Vice-Chairman and Residency Program Director, Department of Orthopedic Surgery, University of Kentucky at Lexington
William O Shaffer, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, International Society for the Study of the Lumbar Spine, Kentucky Medical Association, Kentucky Orthopaedic Society, North American Spine Society, Southern Medical Association, and Southern Orthopaedic Association
Disclosure: DePuySpine 1997-2007 (not presently) Royalty Consulting; DePuySpine 2002-2007 (closed) Grant/research funds SacroPelvic Instrumentation Biomechanical Study; DePuyBiologics 2005-2008 (closed) Grant/research funds Healos study just closed; No present Industry grants or funds. None None

CME Editor

Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital
Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of Physicians of Indian Origin, American College of International Physicians, and American College of Surgeons
Disclosure: Nothing to disclose.

Chief Editor

Mary Ann E Keenan, MD, Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of Orthopedic Surgery, Hospital of the University of Pennsylvania
Mary Ann E Keenan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, American Society for Surgery of the Hand, and Orthopaedic Rehabilitation Association
Disclosure: Nothing to disclose.

 
 
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