Artificial Disk Replacement for Radiculopathy and Myelopathy

Leonard K. Kibuule

Jeffrey S. Fischgrund

Jean-Jacques Abitbol

Patients with cervical spine-related problems may often present to the physician with notable complaints of neck pain. Axial neck pain may be the initial presenting symptom of a disease process, with other, sometimes more subtle, clinical manifestations. Neuromuscular pain is a symptom that can occur at any point in life and is a common occurrence among individuals, especially those who are relatively well educated (1). In some adult populations, the lifetime prevalence of neck pain has been shown to be as high as 54% (1). In North America, the lifetime prevalence is 66%, and 5% of the population has disabling pain at any given time (2). The exact etiology of neck pain remains controversial. Contributors to pain include pathology to the cervical disks, facet joints, and nerve fiber endings (3,4).

On the other hand, radiculopathy, or pain radiating into the upper extremity, has been shown to occur with less frequency. Radhakrishnan et al. (5) evaluated a 14-year population-based data set from Rochester, Minnesota, and revealed the annual incidence of cervical radiculopathy to be 83/100,000. This study also showed that a common cause of radiculopathy was degenerative cervical spondylosis. Other contributing factors to radiculopathy include additional patient comorbid conditions. People stricken with endocrinopathies, such as diabetes, are also more susceptible to a compressive neuropathy. Patients may also present with shoulder pain from adhesive capsulitis in the region, sensory and motor deficits, and diminished reflexes. When radiculopathy does occur, it is usually the result of a compressive lesion to the nerve root at the affected disk level. This is the case in about 80% of individuals (6).

Like radiculopathy, cervical spondylosis can also cause myelopathy. Myelopathy is usually the result of spinal cord compression. Some causes of myelopathy include a decrease in the space available for the spinal cord, changes in the morphology of the cord itself in response to surrounding biomechanical alterations, or alterations in local vascular supply to the cord. These alterations are not always static in nature but can be precipitated by dynamic shifts in the cervical spine as well. Loss of space available for the spinal canal can occur during maneuvers involving flexion or lateral bending, a change that may not be evident with standard imaging techniques. Many clinicians and scientists have attempted to determine the exact relationship between the space available for the spinal cord and its link to myelopathy. Scientists have found that most normal adults will have an anteroposterior diameter that measures around 17 to 18 mm (7). Those who have a diameter of 13 mm or less are said to have a congenitally narrowed spinal column. As the diameter decreases, the area available for the neural tissues at a given level may become compromised. This compression can cause the neural tissues in the area to be irritated, inflamed, or, even worse, permanently damaged. In addition to risks of neurologic compression, vascular channels that supply blood locally may also be at risk. As blood vessels experience pressure from surrounding structures, vessel walls become more permeable and surrounding edema can occur (8). Distal neural tissue may see a decline in nutrient flow from vessels compressed more proximally. This disruption may lead local tissue to rely more heavily on less efficient collateral blood flow.

Animal studies have shown that changes in vascular flow around the spinal cord can lead to similar neurologic changes (9). Other experiments have revealed that vascular ischemia, coupled with mechanical compression, can produce effects of symptoms similar to cervical myelopathy in human beings (8). Penning et al. (10) in 1986 demonstrated that concentric compression of the spinal cord in a narrow, stenotic canal proved to produce long tract signs only after the cross-sectional area of the cord had been reduced by about 30% to a value of about 60 mm² or less. Morishita studied the risks factors associated with a congenitally narrowed spinal canal and how it may contribute to future development of cervical spondylotic myelopathy. He reviewed the cervical MRI of 295 symptomatic patients and evaluated their spondylotic grades, cervical kinematics, and segmental mobility. His results suggest that cervical spinal canal diameter of less than 13 mm may be associated with an increased risk for development of pathologic changes in cervical intervertebral disks and further cervical spinal stenosis (7).

TABLE 134.1 Nurick Classification of Disability from Cervical Myelopathy

Grade I	No difficulty in walking
Grade II	Mild gait involvement not interfering with employment
Grade III	Gait abnormality preventing employment
Grade IV	Able to walk only with assistance
Grade V	Chairbound or bedridden

Patients afflicted with cervical spondylosis who present with axial neck pain and/or radiculopathy will often initially treat themselves symptomatically before seeking medical attention. Insidious neck pain may be the initial presenting symptom depending on the duration of the disease process. Traumatic injuries of the cervical spine can cause cervical disk herniation, root impingement, or direct compression of the cord. Radicular pain or associated myelopathy may result.

The radicular pain is usually distributed in a dermatomal pattern associated with the afflicted cervical nerve root. Pain, burning, tingling, and numbness in the region are common symptoms. Ongoing pain or increasing difficulty with manifestations of myelopathy may lead patients to seek the evaluation more expediently.

Patients who have true myelopathy may have a constellation of presenting symptoms. Some may have clumsiness to their hands or lower extremities. Others may have difficulty with balance or an awkward gait (6). The Nurick system (Table 134.1) (11) for grading spondylotic myelopathy was developed as an objective way to assess patients based on their gait abnormality. Shortfalls of this grading system have lead to other classification schemes in the hopes of providing a comprehensive and accurate descriptor of a complex process occurring within the cervical spine (7,12). As the pathology progresses, the clinical symptoms may continue to worsen as well. Reflexes may be impacted. The inverted radial reflex, the Hoffmann reflex, and the extensor plantar reflex may appear as signs of an underlying process of cervical myelopathy. These signs should encourage the clinician to obtain further diagnostic testing if not already anticipated in the workup of the patient. Prolonged delays in diagnosis and treatment may ultimately lead to further weakness, atrophy, and possible loss of function.

CLASSICAL TREATMENT OF CERVICAL SPINE PATHOLOGY

Like some conditions of the lumbar spine, cervical radiculopathy without evidence of neurologic decline should initially be treated conservatively (13). Nonoperative care can be attempted if patients present with pain and no objective evidence of weakness or neurologic deficit. If presenting within 3 to 4 weeks of symptoms, a trial of nonsteroidal anti-inflammatory medication, corticosteroids, muscle relaxants, antidepressants, and/or physical therapy may be initiated if clinically tolerable. This treatment may be coupled with a brief period of rest or alteration in activities that exacerbate the condition. Even with a clearly defined cervical disk herniation, patients will often improve with simple conservative care. For those whose symptoms persist for several weeks and with objective evidence of the etiology of the pain, for some, steroid injections in and around the area of compression may be beneficial. When nonoperative management has been exhausted and symptoms persist or neurologic deficits exist, then operative management with decompression may be indicated. Currently, indications for surgery for cervical radiculopathy include (a) persistent or recurrent arm pain, nonresponsive to a trial of conservative treatment (3 months); (b) progressive neurologic deficit; (c) static neurologic deficit associated with significant radicular pain; and (d) confirmatory imaging studies consistent with the patient’s clinical findings (13).

For patients who have been managed with conservative care and are not experiencing relief, more invasive procedures may be explored. Symptoms of axial neck pain or radiculopathy from discogenic pathology may be treated with operative management. Objective findings on MRI or other diagnostic study (i.e., CT myelogram, provocative diskography) should be established before pursuit of operative treatment. The clinician should look to correlate the results of all diagnostic studies with clinical presentations. Any ambiguous results should be reassessed or additional testing undertaken to diminish any doubt of the operative level. Patients with findings of myelopathy or progressive motor deficit should be evaluated relatively aggressively. Studies have shown risk of permanent neurologic damage in patients with prolonged deficits. Myelopathy can progress in a stepwise fashion over time (13). Patients with severe, progressive symptoms are potential candidates for operative management. In determining intervention, the surgeon should consider duration of symptoms, likelihood of neurologic recovery, operative risks versus benefit, and any associated comorbidities. In a prospective study by Kadanka et al. (14), patients with mild-to-moderate nonprogressive or slowly progressive myelopathy were found to have similar outcomes after either nonoperative or operative treatment.

OPERATIVE MANAGEMENT

Traditionally, treatment of cervical discogenic pathology has involved anterior cervical discectomy and fusion (ACDF) with plate instrumentation. The treatment of cervical disk herniations by ACDF was first popularized by Smith and Robinson in 1958 (Smith G, The treatment of certain cervical spine disorders by ventral removal of the intervertebral disc and interbody fusion. J Bone Joint Surg Am 1958;40:607-624.). Fusion procedures are performed through a ventral approach with a goal to decompress the neuroforamen and provide structural stability to the adjacent vertebral bodies. Their initial indications for surgical treatment were failure of conservative treatment with persistent upper extremity radicular symptoms. This procedure involves the introduction of a structural bone graft (although recently use of polyetheretherketone and other bone graft substitutes has been popularized) with or without rigid fixation accomplished with a ventral plate.
Fusion of the segment is intended to eliminate motion at the index level and encourage healing of the vertebral bodies in a position where the neuroforamen is open and remains patent.

Anterior cervical decompression and fusion, however, is a procedure that carries its own inherent risks as well. The fusion of two or more adjacent vertebral bodies creates stresses and changes the mechanics within the cervical spine. For instance, ACDF has been shown to alter the normal biomechanics of adjacent levels and may contribute to the development of adjacent segment disease (ASD), although this is a highly controversial area and there is no definitive evidence that fusion increases the development of ASD (15). In a study by Hilibrand et al. (16), he found that 26.9% of patients had symptomatic ASD at 10 years. Goffin et al. (17) followed patients postoperatively who had had an ACDF and found nearly 92% of individuals had ASD at 5 years. Gore and Sepic (18) followed patients for a mean of 21 years after their initial ACDF and reported 16% required additional surgery for symptomatic adjacent segment degeneration. While many studies showing increased degeneration at other segments following surgical fusion, other studies showed the development of similar amounts of ASD after nonfusion foraminotomy surgery. What is not known is the incidence of adjacent segment breakdown even without fusion, otherwise known as the natural history of progressive degeneration. Several studies have also shown increased intradiskal pressures above and below a cervical fusion (15). Other research has revealed increased abnormal kinematic motion at adjacent levels as well (15). It is likely that these degenerative changes are not solely caused by a change in mechanics resulting from fusion, but the literature implies that both the natural history of cervical degeneration, in combination with increases in biomechanical stress, may all play a role in this phenomenon. All of these investigations have lead to increasing concerns for further degenerative changes not only for adjacent levels but for the index level being treated as well.

Other issues with cervical fusion include challenges with obtaining a solid fusion itself. The hope is a solid fusion will be achievable in 100% of individual. Unfortunately, this desire is not the reality. The risk of pseudarthrosis is a real complication and has been shown to increase with multiple attempted fusion levels (7). Bohlman showed a 13% pseudarthrosis rate at an average 6-year follow-up of patients, and this rate increased to 27% for multilevel fusions (2). Attempts have been made to increase the fusion rates in the cervical spine by altering various variables involved in the process. Surgeons have tried various interbody devices (allograft vs. autograft vs. PEEK), use of different load cervical plates (load sharing vs. static vs. no plate at all), postoperative cervical collar use, and recently the use of different biologic agents (bone morphogenic protein [bmp-2] vs. demineralized bone matrix vs. autograft). Although the use of iliac crest bone graft shows the most favorable rates of fusion, it is also not without its own risks (19). Issues such as donor-site complications have caused many surgeons to seek alternative surgical techniques. The risk of neurovascular injury, fracture, chronic pain, infection, and abdominal herniation (2) have convinced many surgeons to consider PEEK or other bone substitutes in combination with biologics instead of traditional autograft bone (20). A review of 1,191 iliac crest harvest cases showed postoperative complications in 20% of patients and 55% with subsequent chronic donor-site pain at 1-year follow-up (21). While some surgeons have moved to using allograft bone or synthetic substitutes, the cost of these alternatives will continue to still pose a challenge. Others believe that one answer to that challenge is cervical disk arthroplasty.

CERVICAL ARTHROPLASTY

HISTORICAL PERSPECTIVE

Recently, scientists have focused their efforts on total disk replacement (TDR) and how this can successfully be applied to the cervical spine. Cervical TDR, if performed successfully, would in theory avert many of the risks and complications associated with anterior cervical decompression and fusion. Traditional autograft harvest for fusion and their associated complications, although not widely performed today, would not need to be entertained. Adequate decompression would still be the primary surgical goal, but an attempt to maintain more physiologic kinematics of the cervical spine and hopefully prevent/delay ASD would be an added bonus of such a device. Currently, there are three cervical disk arthroplasty devices that have been approved by the US Food and Drug Administration (FDA) for clinical use, while several others are still under Investigational Device Exemption (IDE) and in clinical trial studies. There is hope that this new technology will provide a good alternative to traditional fusion methodology and provide a positive long-term impact in the treatment of cervical radiculopathy and myelopathy. However, until these devices are perfected, their development will be met with challenges both clinically and from a design standpoint.

Since the 1950s, clinicians have pondered with the concept of artificial disk replacement in the spine. In 1950, Nachemson performed biomechanical studies after injecting cadaveric disks with self-hardening liquid silicone rubber (22). Later in 1973, Stubstad et al. (23) developed several designs in the shape of a disk made from elastic polymer. Stubstad took his concept one step further and even undertook a primate study. Many of the early designs somewhat mimicked the fluid-like mechanics of the human cervical spine, and they experimented with various compressible types of plastics and polymers. Since Nachemson’s experiment in 1950, not a decade has gone by without a new concept for a disk replacement device and with each a new set of challenges. Fernstrom (24) was the first to implant an artificial device into the cervical spine in 1966. He utilized spherical metallic balls in an attempt to reproduce the “ball joint” mechanism of the disk. These balls were implanted in over 250 patients, but the technology was later abandoned because the devices caused hypermobility and tended to erode into the vertebral end plate and vertebral body (23). Even Fernstrom (24) himself admitted poor results. Today, the FDA scrutinizes new medical devices prior to any approved release for use by the medical community (25). Newer devices
have been developed, have been approved, and have seen moderate success since the inception of this technology years ago. Routinely at the annual meeting of the Cervical Spine Research Society, clinicians present their experience with the use of various arthroplasty devices. At the 29th annual meeting, Robertson et al. (26) presented a series of 15 patients with radiculopathy and/or myelopathy who had received the Bristol prosthesis. He reported satisfactory motion of the prosthesis at 2 years follow-up and an improvement in neurologic symptoms.

FIXATION, BIOMECHANICS, AND OTHER CHALLENGES

As artificial cervical disk technology continues to mature, new challenges related to these devices will emerge. Designers today are faced with the laborious task of developing devices that are more reliable than their predecessors, are safe for clinical use, and still accomplish the intended surgical goals related to the patient’s cervical pathology. In an effort to minimize some of these complications, it is important for surgeons who use these devices to recognize their various limitations and understand the various options currently available.

Cervical disk arthroplasty is intended to recreate the native intervertebral disk height and preserve cervical range of motion. A healthy native cervical disk provides support for physiologic loads, allows for fluid mechanical range of motion, and provides adequate space for exiting nerve roots. These characteristics are often compromised with cervical disease. Clinical radiculopathy and myelopathy can result from compression of neural tissue from osteophytes, ligament hypertrophy, or other soft tissue structures. For a successful surgical procedure, adequate decompression must not be compromised despite the decision to perform a cervical arthroplasty. Traynelis and Haid (27) commented that ideally, an artificial disk should recreate the properties of the native cervical disk and last the lifetime of the patient. This device should maintain the proper intervertebral spacing, recreate the appropriate lordotic contour of the cervical spine, and maintain the stability for the adjacent structures even after insertion. An additional desirable characteristic of native disks is their inherent shock absorption properties. A replacement device should have material characteristics, which limit any physiologic mismatch with the surrounding tissue (28). If a significant mismatch exists at the bone-implant interface, bone resorption and stress shielding may occur or, even worse, implant failure. Alteration of loads may also adversely affect adjacent structures and compromise the longevity of the device. For instance, abnormal loading of facets may theoretically lead to facet arthrosis and alter the biomechanical characteristics of the device. Pimenta (29) recently presented a study, which revealed that 8% of facets showed signs of arthrosis by CT scan in patients implanted with a porous coated motion (PCM) disk arthroplasty at 5-year follow-up. Facets not only contribute strength and stability to the spine but they can also be a pain generator if damaged. These struc tures and other surrounding soft tissues should be manipulated carefully to minimize trauma and prevent the possibility of future derangement.

Only gold members can continue reading. Log In or Register to continue