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HomeHealth articlesrheumatoid arthritis of the cervical spineWhat Is Cervical Spine Rheumatoid Arthritis?

Rheumatoid Arthritis of the Cervical Spine - Symptoms, Diagnosis, and Treatment

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Rheumatoid arthritis affects the cervical spine and results in instability, erosion, and thickening of the spine. Read the article to know more.

Medically reviewed by

Dr. Anuj Gupta

Published At January 24, 2023
Reviewed AtApril 18, 2023

Introduction

Rheumatoid arthritis (RA) is a long-standing inflammatory disease that chiefly affects the bones, ligaments, and synovial joints. It profoundly affects the spine, causing musculoskeletal and neurovascular deficits. Cervical involvement is a progression of intense chronic synovitis that leads to bone erosions, ligament laxity, and finally clinical and radiological instability.

Who Is Susceptible to Cervical Spine RA?

About 0.8% of the white population in the United States and Europe are affected by rheumatoid arthritis, 40 to 88% of which report neck pain. The prevalence of cervical involvement in RA cases is between 43 to 86%, with around 7 to 34% of the patients presenting with neurological deficits. It is estimated that about 36% of patients with preexisting spinal instability end up with neurological deficits.

What Are the Types of Cervical Spine RA?

Rheumatoid abnormalities in the cervical spine can be categorized into three types:

  • Atlantoaxial Instability (AAI) or Atlantoaxial Subluxation (AAS) - AAI or AAS is the most common variant, which can be a fixed deformity and can be partially or completely reducible.

  • Superior Migration of the Odontoid (SMO) - Superior migration of the odontoid, also known as cranial settling, is the second most common deformity presenting with pseudo-basilar invagination, or vertical or upward translocation of the odontoid.

  • Subaxial Subluxation - Subaxial subluxation, the least common deformity, is seen on multiple levels producing a step-ladder deformity.

What Is the Pathophysiology of Cervical Spine RA?

The progressive synovial inflammation leads to the involvement of the cervical spine. A complex interaction between genetic, environmental, and immunological factors contributes to the pathophysiology of cervical involvement of the spine. Patients with predisposing conditions like HLA-DR4 and DR-1 activating antigen-presenting cells, along with various environmental factors, stimulate the CD4+ T-cells. These CD4+ cells activate B-lymphocytes to produce plasma cells, which then secrete autoantibodies- Rh-factor and anti-CCP, further accelerating inflammation.

Furthermore, activated T-cells stimulate the macrophages, which release cytokines like TNF-α, IL-1, and IL6. TNF-α promotes leukocyte influx and activates fibroblasts which then secrete matrix metalloproteinases (MMPs) that break down the articular cartilage. TNF-α also activates osteoclast differentiation and bone resorption. The combined process of cartilage and bone degradation is an immune-modulated mechanism. An uncontrolled progression of the mechanism can cause instability of the spinal column due to ligament damage causing laxity, compression, or improper blood supply of the spinal cord.

What Are the Signs and Symptoms of Cervical Spine RA?

The clinical manifestations are: joint arthropathy (joint pains), atrophy or wasting of the muscles, declined range of motion, compression-associated neural deficit, and poor functional status. Neck pain at the craniocervical junction is the most common presentation.

Compression of the greater occipital nerves as they pass between C1 and C2 is attributed to occipital headaches. Greater auricular nerve compression can result in the ear or mastoid pain. The patient may present with crepitation (creaking joints) or a sensation of their head “falling forward” with flexion.

Due to neurological deficit, the patient may present with muscle atrophy (wasting), weakness, limb paresthesias, bowel and bladder problems, over-reactive body reflexes, spasticity (increased muscle tone and stiffness), increased Hoffman's reflex, abnormal plantar reflex signs, abnormal abdominal reflexes, and unable to perceive self-movements. Patients with a compression in the upper spinal cord and cervicomedullary junction present with an electric shooting sensation that runs down the back, on neck flexion, often accompanied by a palpable 'clunk' (Lhermitte's sign).

Severe cervicomedullary junction compressions may develop abnormalities in the lower cranial nerves causing dysphagia (inability to swallow) from the vagus and glossopharyngeal nerve compression, dysarthria (speaking difficulties) from hypoglossal nerve compression, loss of facial sensation, or facial pain from the nucleus of the spinal trigeminal tract compression, syringomyelia, and even locked-in syndrome or sudden death. Other symptoms observed from various regions and degrees of compression are signs of vertebrobasilar insufficiencies, such as tinnitus, vertigo, visual disturbance, and dysphagia.

Multiple occurrences of clots in the vertebrobasilar artery have also been reported in patients with severe cervical instability causing pinching of the vertebral arteries. Other characteristic findings include vertical nystagmus and Cheyne-Stokes respirations, especially in patients with advanced brainstem compression.

What are the Diagnostic Criteria for Rheumatoid Arthritis of the Cervical Spine?

Diagnostic Criteria to Determine the Level of Neurological Deficit:

  • Class I: No insufficiency.

  • Class II: A subjective weakness with hyperreflexia and dysesthesia.

  • Class IIIa: An objective weakness with long tract signs, but the patient can walk.

  • Class IIIb: An objective weakness with long tract signs with a disability to walk or feed oneself, quadriparesis.

Diagnostic Criteria to Determine the Level of Functional Deficit:

  • Class I: No disability.

  • Class II: Adequate for normal activities, despite the handicap of discomfort or limited motion.

  • Class III: Limited to only a few or none of the duties.

  • Class IV: Incapacitated or confined to a wheelchair.

How to Diagnose Cervical Spine RA?

  • Lateral flexion and extension radiographs should be ordered. AAI deformity is determined using the measurements of the anterior atlantodental interval (AADI) and the posterior atlantodental interval (PADI).

  • AADI is greater than 3 mm and increases and decreases on flexion and extension, respectively. AADI of more than 8 mm requires surgery.

  • PADI less than 13 or 14 mm is indicative of surgery, as values below 14 mm indicate compression of the spinal cord.

  • The open-mouth view is used to assess lateral AAS. A lateral asymmetry displacement of the atlas along the axis beyond 2 mm indicates AAS due to the collapse of the lateral atlas mass or fractures of the dens.

  • Subaxial subluxation (SAS) is diagnosed by measuring the amount of listhesis (slippage) between adjacent vertebrae. A Listhesis of 3.5 to 4 mm is diagnostic of SAS.

  • MRI shows evidence of spinal compression in all patients with cervical spine RA with the space for the cord below 13 mm.

  • The cervicomedullary angle, as measured by MRI, is more than 135° which is an indicator of cord distortion.

  • CT scans are used for quantitative studies of AADI and PADI.

  • A contrast CT scan shows excellent details of the bones and detects spinal cord compression from the synovial pannus.

How to Treat or Manage Cervical Spine RA?

Non-surgical management: use of collars may prevent deformity.

Surgical Management:

  • Atlantoaxial Subluxation: If the deformity is reducible, then fusion of the posterior atlantoaxial can be done by modified Gallie fusion, Brooks fusion, and C1-C2 trans-articular screw fixation (gives immediate multidirectional stability).Irreducible deformity and posterior neural compression in patients can be treated by C1 laminectomy and trans-articular stabilization. Patients with irreducible bony anterior compression may undergo decompression by an anterior transoral approach. Patients with irreducible ventral craniovertebral junction (CVJ) lesions can be treated with endoscopic endonasal odontoidectomy (EEO) with anterior C1 arch sparing. Healthier patients (Class I and II of neurological deficit) can be treated with just atlantoaxial stabilization and fusion, even with irreducible deformity.

  • Superior Migration of the Odontoid: Preoperatively, gradual cervical traction can be used for reduction. Occipitocervical fusion is the surgical choice of treatment. This requires securing a tricortical bone graft with wire loops, cement or metal mesh, contoured rods, plates, and screws. Occipitocervical fusion with plating involves screw placement into the pedicles of C2 under fluoroscopic guidance with a pre-contoured plate. Irrespective of the technique used, autologous bone grafting should always be performed. A ventral route provides reliable decompression in patients with anterior compression.

  • Subaxial Subluxation: Most patients with this kind of deformity can be treated by posterior cervical fusion with bone autograft. Internal fixation with wires, plate-screw, or rod-screw allows for mobilization at early stages and improves rates of fusion. Irreducible subluxations, with or without neurologic deficits, may best be treated with just anterior decompression and fusion or in conjunction with posterior fusion.

  • Combined Subluxations: Some patients present with upper cervical involvement combined with early sub-axial subluxation. Surgical management in such patients involving the fusion should be extended to include the involved sub-axial segments to prevent early degeneration of borderline subluxations below a rigid cervical fusion.

Conclusion

The goal of preventive treatment is limited to preventing the progression of RA into the cervical spine. The spinal involvement detection may be incidental in RA patients. Early detection is the key to avoiding surgical interventions. So, an interdepartmental approach to diagnosis, early intervention, management, and surgical intervention is a must to create a streamlined treatment regime.

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Dr. Anuj Gupta
Dr. Anuj Gupta

Spine Surgery

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