Why a mechanical disc?

Abstract

Low back pain secondary to degenerative disc disease is an overwhelming and growing problem in the United States and Western countries. Most degenerative disc disease can be treated nonoperatively. There are, however, substantial numbers of patients who have not benefited from exhaustive nonoperative treatments and subsequently seek surgical solutions to their incapacitating back pain. Lumbar fusion for back pain and/or leg pain associated with degenerative disc disease is considered the gold standard by which other treatments are judged.

A challenge to spinal fusion for degenerative disc disease is now being offered in the form of the artificial disc. The implantation of an artificial lumbar disc allows for maintenance or restoration of physiologic movement at affected segments. A major long-term complication of spinal fusion is degeneration of a disc adjacent to the fused segments. Theoretically, the maintenance of motion could minimize development of adjacent disc degeneration as seen with spinal fusion. It is interesting to note that fusion of the hip or knee is not considered a primary procedure, but fusion is a primary procedure for the lumbar spine.

Four artificial lumbar discs are discussed in this article. Early results are promising in terms of clinical results and movement, but long-term follow-up clinical trials must be done in order to gain an accurate comparison with spinal fusion. Trials are currently ongoing.

The clinical results up to now and the potential for maintaining lumbar mobility throughout life warrant continuation of this surgical procedure.

Introduction

Symptomatic lumbar disc degeneration is an overwhelming problem in the United States as well as in the remaining world population. It is well documented that approximately 70% of US citizens experience a minimum of one important episode of low back pain during their lifetime [1], [2]. Significantly, degenerative disc disease (DDD) is now the leading cause of pain and disability in adults in the United States. Health care for this patient population represents a large socioeconomic impact, with estimates of over $34 billion in annual health costs in the United States. This cost does not include indirect economic losses from lost wages and diminished productivity, estimated to be $16 billion [3].

Most degenerative disc disease can be treated nonoperatively. There are, however, substantial numbers of patients who have not benefited from exhaustive nonoperative treatments and subsequently seek surgical solutions to their incapacitating back pain. Therefore, it is not uncommon for operative treatment to be offered to patients. The spinal fusion rate in the U.S. has been rising steadily between 1979 and 1990 [4]. The rate of lumbar fusion operations in men rose from 17/100,000 in the period from 1979–1981 to 28/100,000 in the period between 1988–1990. In women, the figures rose from 12/100,000 in the period from 1979–1981 to 21/100,000 in the period from 1988–1990. In 1990 alone, there were approximately 46,500 lumbar spinal fusion surgeries performed in the United States. That figure rose to 72,000 in 1993 [5].

Fusion of the lumbar spine is indicated for a wide range of problems, often performed in conjunction with decompressive procedures or for spinal deformity or instability of the spine. Fusions without decompression have also been offered to patients for the treatment of axial back pain secondary only to degenerative disc disease. Spine surgeons have recognized over the years that fusion for this diagnosis (DDD) is not as successful as decompressive procedures for radicular complaints, with or without the addition of fusion [6], [7].

Although fusion has been performed in the lumbar spine for approximately 100 years, its persistent application in degenerative disc disease represents somewhat of an anachronism. For end stage degeneration of other joints, such as the hip or knee, one would perform joint replacement arthroplasty; fusion would never be considered as the primary procedure. It is only in the spine that fusion still represents the primary procedure for treatment of an end stage symptomatic degeneration, in this setting, of the lumbar joint complex. Even when a fusion is offered to patients with hip or knee arthritis as a type of “salvage” procedure, the surgeon recognizes there are potential long-term complications to the adjacent mobile segments. For example, hip arthrodesis has well documented complications of ipsilateral knee pain and increases in lower back pain [8], [9], [10]. Therefore, inherent to all musculoskeletal fusions is a steady unavoidable negative consequence to motion segments adjacent to fused joints.

The rationale for fusion is the relief of axial back pain through acceleration of the lumbar degenerative cascade to its end stage. In the earliest phase of physiologic lumbar disc degeneration, the disc loses height secondary to biomechanical changes in the nucleus. The normal ratio of disc glycoproteins, chondroitin sulfate and keratin sulfate, begins to invert. Because the chondroitin sulfate molecules are much more hydrophilic than the keratin sulfate molecules, the nuclear material macroscopically loses water content and consequently fails to maintain proper disc height [11], [12], [13]. This is clearly visible on magnetic resonance imaging T2-weighted images as a change from bright white images to the darkened images characteristic of “black disc disease.” With even modest decreases in disc height, proper tension significantly lessens in the surrounding annular structures, resulting in what Kirkaldy-Willis [14] characterized as a transient period of “hypermobility” of the motion segment. It is during this hypermobility period that the disc is especially susceptible to injuries, such as annular tears and frank herniations. Clinical manifestations during the hypermobility period include episodes of back pain, leg pain or both.

As decreases in disc height progress, the hypermobility phase gradually evolves into one of two distinct patterns. The first is frank subluxation of the disc space, as demonstrated either by spondylolisthesis or retrolisthesis. Instability in either a forward or backward direction is mostly determined by the specific orientation of the lumbar facets at each level, inherent mobility of the specific disc space and, finally, by the location of the disc along the normal lordotic arch of the entire lumbar spine [15], [16]. The lower lumbar discs have a predisposition to spondylolisthesis, whereas the upper lumbar discs have a predisposition to retrolisthesis. Deviations from these patterns are probably secondary to facet orientation. The second pattern of evolution from the hypermobility phase results in axial settling of the disc space without subluxation. In this pattern, the disc space collapse is unavoidably accompanied by loss of the normal lordosis that is normally provided by the well-hydrated nucleus and taut annular structures [14], [17].

Whether subluxation occurs or not, as the disc space collapses further, the motion segment stiffens from increased osteophyte formation and facet arthrosis. As the motion segment progressively stiffens, the patient's segmental backache may start to disappear. Unfortunately, as one motion segment stiffens, it results in adjacent segment hypermobility, thereby accelerating the degeneration of that segment [18], [19], [20], [21]. Biomechanical studies have also demonstrated that rigid immobilization of one segment of the spine will lead to hypermobility of segments above and below the fused segment [20]. This phenomenon is more problematic if the newly affected level is already in a “hypermobility phase” secondary to early stage DDD. Hence, the degenerative cascade in lumbar disc disease is not confined to individual motion segment but proceeds with consequences up and down the entire lumbar spine.

Although significant end stage loss of motion may seem beneficial for longstanding back pain, the concomitant encroachment on the spinal canal by disc bulge, redundant ligamentum flavum and osteophyte formation may result in spinal stenosis symptoms of radicular pain, neurogenic claudication, neurologic deficit and possibly recurrence or persistence of back pain. In the normal course of human pathophysiology, the end stage of disc degeneration occurs very late in life when the consequences to the remaining functional motion segments are minimized because of limited anticipated life expectancy.

The goal and direct effect of spinal fusion is to provide axial back pain relief by accelerating the lumbar segments chosen for fusion to the end stage of the degenerative cascade. Fusion, ideally performed, should also allow adequate room for the neural elements and preservation of the normal sagittal alignment.

Fusion once achieved, however, may result in symptomatic accelerated degeneration of the adjacent segments above or below the fused levels for the young patient and even elderly patients [18], [19], [20], [21] (Fig. 1). Finnegan et al. [22] showed that as many as 29% of patients who have had fusions in the past will have a return of pain. This pain is usually caused by adjacent segment disease that additionally burdens the spine. The “increased workload” performed by the adjacent segments is the causative factor in accelerated degeneration and further subsequent pain.

Despite the aforementioned problems, lumbar fusion remains the gold standard for the surgical treatment of axial back pain secondary to symptomatic degenerative disc disease that is unrelieved by exhaustive conservative measures. Although controversy has surrounded fusion for this diagnosis, Fritzell et al. [23] won the 2001 Volvo Award by proving that patients with discogenic pain have better outcomes after successful spinal fusions over a similar group who continued conservative treatments. There are many varied methods of obtaining a fusion in the lumbar spine in degenerative disc disease. Historically, the first fusions were posterior fusions, which progressed over time to posterolateral fusions. Anterior lumbar fusions were popularized during the 1960s. Methods of obtaining an anterior interbody fusion from a posterior approach, such as with a posterolateral interbody fusion or transforaminal lumbar interbody fusion, are also well known and frequently performed. Anterior interbody fusions in association with posterior instrumentation with or without fusion have been widely used in an attempt to obtain a higher fusion rate, restore disc height, indirectly decompress neural structures and maintain proper sagittal alignment [24], [25], [26]. Fusion across a disc space after restoring normal lordosis has been thought to possibly aid in reducing the incidence of adjacent segment degeneration.

The most critical problem regarding fusion surgery for axial back pain is the persistent disassociation between the radiographic appearance of a successful fusion and clinical demonstration of relief of the patient's pain with a return to normal function. Whereas modern surgical techniques can easily achieve a 95% radiographic fusion, clinical success lags behind with occurrence in the 60% to 80% range [27]. This disassociation between radiographic evaluation and clinical success has been a prime motivator for surgeons to look for alternative means to fusion. Even if fusion provides effective pain relief postoperatively, the surgeon knows the patient still has the risk of a return of pain resulting from subsequent adjacent segment problems!