Rheumatoid Arthritis-Induced Lateral Atlantoaxial Subluxation With Multiple Vertebrobasilar Infarctions

Study Design. Case report. Objective. To highlight the probability that lateral atlantoaxial subluxation (AAS) exists in patients with rheumatoid arthritis (RA) and induces vertebrobasilar infarctions that are more foregrounded than compressive myelopathy. Summary of Background Data. Although lateral subluxation is a well-known subtype of AAS, a case of cerebral ischemia associated with lateral AAS has not been reported before. Methods. A 52-year-old male with a 6-year history of RA had a sudden onset of visual field defect and mild right cerebellar ataxia. Head magnetic resonance imaging revealed acute multiple infarctions in the vertebrobasilar area, and magnetic resonance angiography revealed stenosis of the left vertebral artery (VA). Lateral radiograph of the cervical spine in the neutral position revealed atlanto-occipital assimilation and anterior AAS. T2-weighted sagittal images on cervical magnetic resonance imaging revealed high signal intensity in the spinal cord at C1-C2. Cerebral angiography revealed right VA occlusion and severe stenosis of the left V3 segment of VA. Three-dimensional computed tomography angiography of the craniovertebral junction revealed lateral AAS, which was due to severe erosive changes of the facet joints, and the left V3 portion was stenosed by a bony component. During conservative therapy, the patient experienced left occulomotor nerve palsy due to a second stroke. Results. Two months later, the patient underwent occipitocervical posterior fusion with an iliac bone graft. His postoperative course was uneventful, and the left VA stenosis disappeared. At the 45-month follow-up, he had no further infarctions. Bony fusion was radiologically confirmed, and 3-dimensional computed tomography angiography revealed good patency of the affected left VA. Conclusion. In patients with RA, the potential risk of AAS should be recognized. Lateral AAS in particular may induce cerebral ischemia by positional VA occlusion in advanced stages of the disease.