Although the frequency of lumbar lesions in RA is not considered to be as low as previously described, their natural course has not been elucidated because there have been only a few systemic reports (1–3
). This is likely due to the occasional difficulty in differentiation of RA-specific lesions from osteoporotic fractures of the vertebral body and degenerative spondylolisthesis. Moreover, complications such as cervical myelopathy and articular lesions of the lower extremities make neurological diagnosis more difficult (2
RA-associated lumbar lesions are roughly divided into vertebral lesions, facet joint lesions, and intervertebral disc lesions. These lesions must be differentiated from spondylosis deformans and osteoporosis lesions. Vertebral lesions (defined as rheumatoid nodules of the vertebral bodies) were reported in 1952 by Baggenstoss et al. who observed them in autopsy patients (4
). Facet joint lesions were described by Lawrence et al. (6
). In the present study, we defined RA lumbar lesions as rheumatoid nodules of the vertebral bodies (4
), vertebral collapse without previous trauma (5
), disc space narrowing without osteophyte formation, end-plate erosion (2
), and segmental instability associated with facet joint destruction (6
). End-plate erosion was obvious in all of the six patients. The occurrence of RA lesions in the vertebral bodies and intervertebral disc (which has no synovial tissue) was attributed to enthesopathy by Shichikawa et al. (12
). In most of the reported cases of RA lumbar lesions, neurological symptoms are caused by spinal canal stenosis, stemming from vertebral lesions leading to vertebral collapse (4
) or from facet joint lesions leading to segmental instability (6
). There are very few cases of foraminal stenosis. Heywood reported a case of L4 radiculopathy attributable to a L4/5 facet joint lesion (8
), yet he did not describe the pathogenesis clearly.
Myelography and postmyelographic CT scans cannot be used to establish a diagnosis of foraminal stenosis, which can be detected in MRI and SRG. In four of the six cases of our series, however, MRI failed to detect foraminal stenosis. One possible reason is that the nerve root compression is not detected by recumbent MRI because the pain was relieved in the recumbent but not the sitting or standing position. In contrast, an invasive examination, SRG, detected the nerve root compression attributable to the superior articular process of the lower vertebra in all patients. Furthermore, SRG was very useful in the functional diagnosis based on pain reproduction at the time of nerve root puncture and blocking effect in RA cases where the neurological diagnosis cannot be easily established. This seemed to be a characteristic feature of RA in terms of arthritis. We assumed that the pathogenesis of foraminal stenosis in the lumbar spine of RA patients is the compression of the nerve root by the superior articular process of the lower vertebra; this is caused by vertical instability of the facet joint when facet joint lesions are associated with disorders in the vertebral body and the intervertebral disc. Impaired nerve roots due to foraminal stenosis are most frequently reported to be present at L5 in spondylosis (13
), whereas L4 was the most common site for nerve root impairment in RA.
With regard to surgical treatment, Crawford et al. stated that RA patients who undergo an instrumented lumbar fusion can expect a slightly higher complication rate than patients without RA, which may be related to osteopenia and immunosuppression (3
). Inaoka et al. performed posterior lumbar interbody fusion on seven RA patients and reported that collapse of graft occurred in one patient, migration of pedicle screw in two, instability of adjacent level in three, and collapse of adjacent vertebra in four (14
). Fusion surgery might be performed in view of the pathogenesis of lumbar radiculopathy caused by foraminal stenosis in RA, but it was often difficult to employ fusion surgery with instrumentation because most of the patients in our series were in poor general condition or had severe osteoporosis. We performed posterior decompression without fusion in three cases; short-term outcomes were favourable though one patient was re-operated for secondary radiculopathy. Symptoms of radiculopathy were reduced by posterior decompression of the affected nerve root with partial resection of superior articular process which served as a compression factor.