Instability

The rationale for fusing the painful motion segment has been the concept of instability.⁶ Understanding and diagnosis of clinical instability remains controversial. When abnormal motion is present on flexion-extension radiographs, especially in the setting of spondylolisthesis, fusion is accepted as a reasonable option.⁷ By this standard, relatively few patients with low back pain have overt subjective or objective evidence of instability, however. Pope and Panjabi⁸ suggested that instability is a mechanical entity and is defined as a loss of stiffness to a given load. Biomechanical and radiologic studies using open magnetic resonance imaging (MRI) in flexion and extension have shown, however, that segmental motion either does not change significantly with disc degeneration⁹^–¹¹ or may decrease except during early stages of disc degeneration.¹²

Mulholland and Sengupta ¹³ suggested that spinal instability does not mean “increased motion” as commonly misunderstood,^8,¹⁴ but rather it indicates abnormal load distribution across the vertebral endplate. The pathologic changes within the disc space may result in abnormal transmission of load across the endplates. It has been well established in other weight-bearing joints that abnormal load transmissions result in degenerative changes, and the resultant pain may be diminished by a properly placed osteotomy to realign the joint forces and redistribute the loads.¹⁵ The normal disc consists of a homogeneous gel of collagen and proteoglycan. The normal disc is isotropic, similar to a fluid-filled bag, a property that allows it to transmit load uniformly across the vertebral endplates.¹³

Disc degeneration alters the isotropic properties of the disc. The disc becomes nonhomogeneous, with areas of fragmented and condensed collagen, cartilage fragments, fluid, and gas.¹⁶ Load transmission over the endplates becomes uneven. The nucleus becomes depressurized, and an increasingly larger load is transmitted through the anulus, which leads to splitting and inward folding of the anulus.¹⁷ The central area of the endplate overlying the depressurized nucleus now transmits lesser load, and corresponding endplate changes, such as destruction, thinning of the trabeculae, and thinning of the cartilaginous endplate,^18,¹⁹ may be noted. Focal loading of the endplate cartilage and subchondral bony trabeculae can occur with certain positions, leading to a sharp increase in back pain. This situation is analogous to a “stone in the shoe” causing high spot loading and pain, a concept proposed by Mulholland and Sengupta.¹³

This concept explains the clinical sign of instability catch as experienced by patients with mechanical back pain secondary to disc degeneration during flexion-extension movement. This hypothesis also explains why manipulation of the lumbar spine by a chiropractor may occasionally dislodge the fragment from its weight-bearing position, bringing an immediate relief of acute low back pain.¹³ Mulholland and Sengupta’s hypothesis of abnormal loading as the primary cause of mechanical back pain was supported by a close association of abnormal disc pressure profiles with positive discography with pain provocation.²⁰ A pressure profilometry study by McNally and Adams²¹ revealed the anisotropic properties of the degenerated disc. This study showed that the pattern of loading, rather than the absolute levels of loading, was related to pain generation in the degenerated spine. The concept may also help explain the lack of correlation between degrees of disc degeneration and back pain because individual anatomic and consequential load transmission changes vary from one person to another. With advancing age, the continued progression of these changes results in the disc becoming more collagenized and homogeneous. The very aged disc may distribute loads more evenly again, resulting in a degree of spontaneous relief of pain with time.²²

Panjabi ²³ described spinal stability in vivo as a function of three subsystems: (1) the spinal column, (2) the spinal muscles, and (3) the neural control unit. In vivo, spinal muscle action and neural control may be equal or more important spinal stabilizers, but the focus of surgical treatment of back pain has been the passive stability provided by the spinal column itself. Instability in the spinal column may result from damage or degeneration of bone, joints, or ligaments, which may be characterized by an increased motion in its early stages. By the time the pain becomes severe enough to consider surgical intervention, the total range of motion is often diminished or abnormal in quality.²⁴ Panjabi²³ redefined spinal instability as an abnormal motion often accompanied by an increased neutral zone motion caused by ligament laxity, even when the range of motion is diminished. Panjabi used the analogy of a marble rolling on a soup bowl (Fig. 53–1).

FIGURE 53–1 Panjabi’s ²³ analogy of a “marble on a soup bowl,” explaining relationship between spinal instability and change in range of motion. A, Intact spine. The marble can move with little resistance across neutral zone (NZ) but faces increasing resistance toward elastic zone (EZ). B, Unstable motion segment. The bowl is flat allowing the marble to move to and fro with little resistance—that is, increased NZ with no increase in EZ. C, Stabilized segment. A smaller cup reduces primarily NZ, with minimal reduction of EZ movement. D, Stabilized segment—but too much loss of motion, which is undesirable. E, Uneven stabilization—with different stiffness in two directions, which is again undesirable.

There is no real conflict between the abnormal motion (Panjabi) versus abnormal load distribution (Mulholland) theories of spinal instability. These two factors may be interrelated. An abnormal motion may cause abnormal load distribution, which may cause pain. It may be anticipated that if an abnormal motion does not cause abnormal load distribution, it may not be associated with pain production, and this explains why many back discs do not hurt.

Definitions

In recent years, many devices have been introduced for spine instrumentation without fusion, which are collectively known as motion preservation devices. There are subtle differences among these stabilization devices.

Prosthetic devices are designed to replace anatomic structures in the motion segment, retaining or restoring their function. Total disc replacement devices and nucleus replacement devices (PDN; Raymedica, Inc., Minneapolis, MN) are examples in this group. Facet replacement devices such as TFAS (Archus Orthopedics, Inc., Redmond, WA) and TOPS (Impliant, Inc., Princeton, NJ) are often presented as posterior dynamic stabilization (PDS) devices. They are truly prosthetic devices, however, which require excision of the facet joints. These devices replace the function of the facet joints in terms of providing stability and motion.

Stabilization devices are instrumentation for control of motion or load bearing or both; in contrast to prosthetic devices, they do not require excision of any anatomic part of the motion segment. Dynamic stabilization or soft stabilization devices are inserted between pedicle screws and are often described as pedicle screw–based PDS devices. Interspinous process distraction (IPD) devices are floating devices, which do not require bony anchorage.

Semirigid fixation is the term used to describe devices intended for achieving solid fusion without the stress-shielding effect of conventional rigid fixation. These are often flexible metallic devices of various designs, as opposed to conventional fusion rods, which offer no mobility at the instrumented segment. Typical devices in this category include Isobar TTL (Scient’x, Inc., West Chester, PA) and Accuflex (Globus Medical, Inc., Audubon, PA).

Soft fusion is a newer term that refers to posterior spinal fusion with minimal stiffness. Some biomechanical and clinical studies indicate the rigidity of lumbar fusion may vary depending on fusion techniques.^25,²⁶ The theory behind the concept of soft fusion is that intertransverse process fusions using PDS devices may achieve a less rigid fusion compared with conventional rigid fusion with fusion rods or interbody devices and may be less detrimental to the adjacent segment. At this time, there is no clinical evidence supporting the concept of soft fusion. This concept has evolved from the fact that many PDS devices obtain U.S. Food and Drug Administration (FDA) approval under 510K for spinal fusion only and not for nonfusion stabilization. Use of these devices as dynamic stabilization devices without fusion represents off-label use.

Design Rationale for Dynamic Stabilization Devices

During the last decade, almost every possible flexible system has been introduced as a potential dynamic stabilization system. Most devices were introduced with no biomechanical data or any clinical evidence of efficacy for even their primary goal. Clinical applications of these devices often extend beyond their primary indication. As expected, questions have been raised about their clinical efficacy, biomechanical basis of design rationale, and mechanism of action.

Biomechanical Goals for Posterior Dynamic Stabilization

Motion Preservation

The primary goal of dynamic stabilization is to preserve motion. It is intended to preserve as much normal motion as possible, while limiting abnormal motion. Some degree of loss of motion is inevitable with application of any PDS device. Because clinical instability occurs mostly during the neutral zone motion, the key to stabilization should be restriction of the neutral zone while preserving the elastic zone motion as much as possible. Because neutral zone motion represents ligament laxity, all PDS systems, by virtue of motion restriction, automatically reduce the neutral zone regardless of their mechanism of action. This automatic reduction of the neutral zone explains why most of the devices claim clinical success in relieving back pain at least in the short-term.

When the range of motion is abnormally increased, usually in translation, after laminectomy, the goal of a PDS device should be to restore a normal range and quality of motion. Normally, it is unlikely that a dynamic stabilization device would increase the range of motion of a degenerated segment, unless it induces a favorable biologic reaction to the disc and facet joint by offloading these structures. Rarely, it may be expected that the device may restore the collapsed disc space height by distraction, however, and eventually may increase the range of motion toward normal. Without anterior support of the disc, the systems could be expected to fail, and the disc space could collapse again.

Load Transmission

The mechanism of pain relief with dynamic stabilization may be unloading the disc and the facet joints by load sharing, preventing abnormal load distribution and high spot loading.¹³ How much load should be shared by the device is unclear. It may be assumed, however, that the device would reduce the intradiscal pressure by the magnitude of load sharing.

Resistance to Fatigue Failure

The most important challenge for dynamic stabilization devices is to survive against fatigue failure, despite allowing continued motion. Fatigue failure is common, even with the much stronger implants such as fusion rods, in case of fusion failure. The key to survival against fatigue for a much weaker PDS device is appropriate quality and quantity of motion restriction and load sharing so that the device is never exposed to an abnormal large load.

The motion restriction should be uniform throughout the range of motion. If the device may cause too much restriction of motion in any direction, most commonly acting like an extension stop, the device may be exposed to repeatedly unusually high stress in extension and may eventually fail (Fig. 53–2). Similarly, the load sharing should be uniform throughout the range of motion. If the device may unload the disc too much in one direction, often in extension, the device has to bear unusually high load during that motion and is likely to fail (Fig. 53–3).

FIGURE 53–2 Dynesys (Zimmer Spine, Inc., Warsaw, IN) restricts flexion too much, equivalent to rigid fixation, but permits near-normal extension in cadaveric spine.

(Adapted from Schmoelz W, Huber JF, Nydegger T, et al: Dynamic stabilization of the lumbar spine and its effects on adjacent segments: An in vitro experiment. J Spinal Disord Tech 16:418-423, 2003.)

FIGURE 53–3 Intradiscal pressure changes with flexion-extension motion. Normally, pressure at center of disc increases in flexion and extension. Stabilization with Dynesys (Zimmer Spine, Inc., Warsaw, IN) restores disc pressure in flexion to normal, but unloads disc completely and behaves similar to total load-bearing structure, without sharing any load with disc.

(From Schmoelz W, Huber JF, Nydegger T, et al: Influence of a dynamic stabilisation system on load bearing of a bridged disc: An in vitro study of intradiscal pressure. Eur Spine J 15:1276-1285, 2006.)

The fatigue property of a fusion device is normally tested in an American Society for Testing and Materials (ASTM) standard spine model consisting of two plastic cubes as vertebral bodies but nothing to represent anatomic structures such as the disc or the facet joints. The fatigue property of a dynamic stabilization device may be inadequately tested in this model because the devices are meant for sharing the load with the existing anatomic structures. An indirect assessment of fatigue property may be performed by study of the instant axis of rotation and intradiscal pressure changes.

Normally, the disc pressure increases in flexion and extension and is lowest in neutral position. A PDS device ideally should permit an increase in the disc pressure in flexion and extension but to a smaller magnitude owing to load sharing (see Fig. 53–3). If the disc pressure does not increase at all, particularly in extension, it may indicate that the device is acting like a total load-bearing structure during extension rather than as a load-sharing structure. Similarly, a mismatch in the location of the instant axis of rotation of the device and the motion segment is another predictor of fatigue failure of the device.

Nonmetallic devices may deform, soften, and creep to adapt to the kinematics of the motion segment and survive fatigue better, at the cost of reduced efficacy over time. Is creep and softening of a nonmetallic device a disadvantage? One may argue that dynamic stabilization may stimulate a favorable biologic response to repair the motion segment, and its subsequent creep or softening is truly an advantage, when its function is over. Conversely, metallic spring devices may retain their mechanical property over a long time but are more subject to fatigue failure should there be any mismatch in the kinematics. Fatigue failure of a nonmetallic device may not be recognized radiologically unless there is screw loosening or breakage, but failure of a metallic device cannot hide.

Pedicle-to-Pedicle Distance Excursion

A normal pedicle-to-pedicle excursion during flexion-extension may be 6 to 9 mm, less in lateral bending, and minimal in rotation (Fig. 53–4). The device should permit a normal pedicle-to-pedicle distance excursion to permit normal range of motion and ensure that the device should not act as a “motion stopper” in any direction. Only a few dynamic stabilization devices can accommodate such a large degree of flexibility.

FIGURE 53–4 A, Pedicle-to-pedicle distance from flexion to extension may be 8 to 9 mm to preserve normal motion. B, Dynamic stabilization (Transition; Globus Medical Inc., Audubon, PA) may need to permit excursion of pedicle screw heads by same magnitude.

(From Sengupta DK: Use of posterior motion-sparing instrumentation and interspinous devices for the treatment of degenerative disorders of the lumbar spine. In Shen F, Shaffrey C [eds]: Arthritis and Arthroplasty: The Spine. Elsevier, in press.)