Intermittent neurogenic claudication as a result of lumbar spinal stenosis accounts for between 3% and 14% of patients complaining of low back pain who attend a specialist (1,2,3). Therefore, this is not an inconsiderable health care problem, causing significant disability to the patient and cost to society. The clinical symptoms, cause, and treatment of the problem are well documented and are generally attributed to lumbar spinal stenosis resulting in nerve root compression at one or more levels (4,5,6,7). Facet joint specific pain is exacerbated by extension and relived by flexion or lying in the recumbent position (8,9). During extension the load on the facet joints is increased, resulting in narrowing of the spinal canal and nerve root canals, and deformity of the joint capsule with or without resultant pressure on the adjacent nerve root (9,10).

The stability of the spinal column is dependent on the individual motion segments acting together. The load-bearing structures of each segment are the vertebral body and the two facet joints. Loading between adjacent vertebral bodies is transmitted both by the intervertebral disc between the vertebrae and the facet joints between each pedicle. If any part of a motion segment is damaged, abnormal, altered loading will result on the other structures. Degenerative disease of the intervertebral disc resulting in reduction in disc height is recognized as a cause of altered stress on the facet joints, which in turn may result in narrowing of the spinal canal at that level (11,12,13). Facet joint degeneration has been shown to accelerate disc degeneration, as a result of destabilization of the motion segment (14). Long-term intervertebral disc and facet joint degeneration is recognized as a precursor of spondylolisthesis (9,10,11).

The treatment of patients with intermittent neurogenic claudication varies depending on the severity of the symptoms and will usually begin conservatively and include analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), physiotherapy, spinal manipulative treatment, and epidural steroid injection. Those who fail to respond to conservative treatment may be offered decompressive surgery by way of laminectomy with or without a spinal fusion technique. The success of decompressive surgery is very variable, with risks of surgical complication and may be associated with the need for reoperation (15,16,17). Analysis of 74 published studies of surgery for spinal stenosis found the success rate for a good outcome varied from 26% to 100% (18).

With the knowledge that extension exacerbates spinal stenosis and exit foraminal narrowing, a simple minimally invasive implant for preventing this has been developed (X STOP Interspinous Process Decompression System, St. Francis Medical Technologies Inc., Almeda, CA). The implant prevents narrowing of the spinal canal and neural foramina in extension. It is placed between the spinous processes from a lateral approach through the interspinous ligament. It is held in place by the interspinous ligament posteriorly, the lamina anteriorly, and by two wings on the implant laterally (Fig. 24.1).

Cadaveric studies have shown that the implant does increase the cross-sectional area of the spinal canal as well as widen the exit foramina (19) (Fig. 24.2). In another study, the implant significantly reduced the mean peak pressure, contact area, and force pressures at the implanted level (20). The 1- and 2-year follow-up studies of a prospective, randomized multicenter study conclude that the X STOP provides an effective treatment for patients suffering from lumbar spinal stenosis, offering a minimally invasive alternative to both conservative treatment and decompressive surgery (21,22).