Three Pathways between the Sacroiliac Joint and Neural Structures Exist

At the beginning of this century, pain from the sacroiliac joints had been considered the main source of low back pain and radiculopathy. Since the discovery and acceptance of the lumbar-disk-complex model of radicular back pain, the theory that the sacroiliac joint contributes to a low back pain syndrome remains controversial and poorly understood as part of a broad category of nondiscogenic low back pain.

Fortin et al present in this issue of the AJNR (page 1429) an intriquing hypothesis asserting that pathways of communication exist between the sacroiliac joints and several neural structures. Tracing extravasation patterns on sacroiliac arthrograms and postarthrogram CT, the authors have delineated pathways in which contrast material from the sacroiliac joint communicates posteriorly with the first dorsal foramima, ventrally with the lumbosacral plexus, and dorsally along the sacral ala to the fifth lumbar epiradicular sheath. Drawing from the discogenic model of low back pain, the authors suggest that sacroiliac capsular irritation and cytokine release may cause adjacent neural insult by these communications. Furthermore, the variety of structures these pathways lead to may in turn explain the variety of symptoms and signs possible from sacroiliac disease.

Sacroiliac arthrography is an uncommon procedure in most radiology departments that often falls between specialty lines of neuroradiology, musculoskeletal radiology, and body imaging, because patients with sacroiliac pain come from a variety of orthopedic, neursurgical, neurologic, and rehabilitation specialty referrals. Most of these procedures include injection of anesthetic or corticosteroids, with any reduction of a patient's symptoms indicating the sacroiliac joint as the source of pain. Extravasation is very common in these procedures, and the patterns of extravasation described by the authors frequently are observed in clinical practice. Furthermore, although the validity of pain reproduction and reduction with anesthetic in the setting of extravasation may be challenged, it nonetheless occurs. The notion that these communications by arthrography provide the mechanism for pain arising from sacroiliac disease is unproved but still attractive.

Among the most frustrating conditions in medicine is atypical or nonradicular low back pain. Unlike the patient with persistent low back pain and a radiculopathy matching a structural lesion seen at imaging, in which one may be relatively confident of a relationship between that finding and symptoms, patients with atypical lumbosacral junction pain frustrate clinicians and radiologists. Without radicular symptoms, or with a radiculopathy that does not match a structural lesion, a scenario occurs in which management often is directed by the results of provocative injections of disks, facets, and sacroiliac joints. To make matters worse, asymptomatic imaging abnormalities are common at the lumbosacral junction, including disk herniations causing nerve compression that may misdirect treatment. Sifting through the significant and insignificant imaging findings of the spine and sacroiliac joints in light of a complicated or inconsistent clinical history of low back pain is a very difficult challenge. In this setting, Fortin's observations may provide a starting point to reexamine the nature of atypical radicular pain, particularly with close correlation of injection data and specific pain patterns. Previous work by the author correlating pain maps from sacroiliac injection in volunteers and patient-drawn pain maps in individuals with atypical lumbosacral pain warrant a close read by anyone imaging or treating patients in whom lumbosacral and sacroiliac pain must be differentiated.

Despite this, caution must be used before one should accept the authors' hypothesis. The precise mechanism of pain from any joint may involve not only capsular irritation, but also direct subchondral bone irritation through cartilage loss and marrow edema. In patients with seronegative spondyloarthropathies involving the sacroiliac joints, as well as in individuals with post-traumatic and degenerative sacroiliac pain, the subchondral plate frequently is compromised, and this mechanism cannot be disregarded. Indeed, one could argue that stimulation of subchondral, pressure-sensitive pain receptors in bone could account for much of the local pain observed in sacroiliac disease, with communication to adjacent neural structures accounting only for the radicular component in those individuals with mixed local and radicular pain. This would not account, however, for the authors' prior observation of pain in an identical distribution in asymptomatic volunteers undergoing sacroiliac arthrography, assuming the volunteers had intact sacroiliac joint surfaces.

Even with the exact mechanism of pain remaining unproved, the article reinforces the role of provocative tests in the diagnosis of atypical low back pain, and provides an avenue for further investigation toward rational diagnosis and treatment of this vexing clinical problem.