Chapter 14 Definition and Assessment of Dysfunctional Segmental Motion
The spine is responsible for providing a smooth motion of the trunk in all planes of motion, while protecting the neural structures. The smallest unit of the spine that exhibits the biomechanical characteristics of the spinal column is termed a motion segment or functional spinal unit (FSU), and is composed of two vertebral bodies and a disc.
Normal motion of vertebral bodies relative to each other is provided by the soft connective tissue, such as the intervertebral discs and ligaments. Ligaments can only resist tensile loading owing to their fibrous hierarchical structures. Normal motion of the healthy spine is realized through the harmonic interaction of the ligaments with the unique design of gross spinal anatomy. During sagittal motion, for instance, dorsal ligaments (posterior longitudinal, capsule, interspinous, and supraspinous ligaments) are activated in flexion while the others are at rest. In extension, the anterior longitudinal ligament and, to varying degrees, the capsular ligaments, are stretched while the others are at rest.
This functional order of the ligaments is orchestrated by the center of rotation of the FSU, which is located toward the dorsal one third of the disc space in the healthy spine. The line connecting the centers of rotation for all vertebral levels is termed the neutral axis of the spine. A load passing through this line would theoretically cause pure compression of the spine, with no rotation and bending moment. Moreover, in flexion, ligaments dorsal to this axis would be stretched and those ventral would be lax. Similarly, in extension, ligaments ventral to this axis would be stretched and those dorsal would be lax. Any change in the location of the neutral axis would influence the function of the ligaments, and vice versa.
The contribution of the disc to spinal motion is more complex than that of the ligaments. In a healthy disc, the gel-like nucleus is filled with water, thanks to the water-trapping proteoglycans. It is nearly incompressible and is pressurized in the unloaded state. When loaded, the nucleus resists compression by pushing against the end plates and the surrounding anulus fibrosus. The anular lamellae, which are compacted and pressurized by the transverse loads exerted by the nucleus, become stiffer and capable of resisting compressive loading exerted by the vertebral bodies. With the aforementioned in mind, it is noted that the water content of the disc plays a key role in maintenance of disc height and FSU biomechanics.
Dysfunction of a motion segment refers to the functional state of the disc associated with pathologic or abnormal motion segment biomechanics. The most common cause of such dysfunction is disc interspace degenerative changes. With dysfunctional segmental motion, “mechanical pain” may arise. Mechanical back pain is characterized as a deep and agonizing pain that is worsened with loading and relieved with unloading. This triad (deep and agonizing, worsened by loading the spine, and improved by unloading the spine) clinically characterizes mechanical pain and represents the clinical correlate of dysfunctional segmental motion.
Degenerative changes initially influence the structural elements of the spine, particularly the disc. These changes, in turn, result in pathologic motion of the FSU. The most striking biomechanical reflection of degenerative changes is observed in the stiffness characteristics of FSU motion. The loss of water content in the nucleus pulposus results in a decreased central disc interspace pressure. This results in a less taut anulus fibrosus and a decrease in the ability of anular layers to withstand applied compressive and tensile forces. In advanced stages of the degenerative cascade, the anulus fibrosus loses its mechanical strength because of fissures and clefts in the lamellae. The overall effect of these changes is a diminution of stiffness and a resultant laxity of the FSU.
Biomechanical evaluation of the FSU is achieved mainly through cadaveric specimen studies. Much of the body of knowledge regarding spinal biomechanics is based on in vitro assessment of specimens obtained from fresh-frozen cadavers. Specimens, stripped of musculature, are loaded to predetermined bending load levels to quantify the biomechanical response of the FSU. Although limited, the in vitro analysis of FSU motion can be highly controlled and detailed. Numerous researchers studying in vitro FSU biomechanics have shown that the response of the FSU to external loading is associated with two characteristic flexibility zones: the neutral zone (NZ) and the elastic zone (EZ). The NZ is a segment of the flexibility curve within which small loads can generate large displacements. The EZ is a segment within which lesser displacements result from greater load application—without causing mechanical injury to the spine. The sum of the two zones (neutral plus elastic zones) comprises the total range of motion (ROM) of the spine under physiologic loading conditions.
It has been suggested that the width of the NZ is the best indicator of spinal instability (due either to injury or degeneration).1–5 Panjabi et al. studied the influence of traumatic ligamentous injury on the stability of the thoracolumbar spine.6 They demonstrated that both ROM and the NZ increased after destabilizing trauma. However, the NZ was observed to be a more sensitive indicator of instability.
Mimura et al. studied multidirectional flexibility of FSUs with a variety of degeneration grades.7 They observed that the ROM decreased in the sagittal and lateral planes and increased in axial rotation. In addition, they noted an increase in the laxity at the joint, which was associated with the instability index (the ratio of the NZ to the ROM; i.e., the NZ ratio).
Tanaka et al. investigated the effect of degeneration on the flexibility of 114 FSUs obtained from 47 cadaveric lumbar spines.8 They categorized specimens in five degeneration grades based on radiographic (MRI) and cryomicrotome section analyses. All specimens were tested biomechanically for flexion, extension, lateral bending, and axial rotation. Rotations and translations were recorded. Both techniques seemed to be in an agreement regarding the advanced stages of degeneration, more so than for early stages. The investigators did not report any data regarding the NZ, but did demonstrate that the upper lumbar FSUs were associated with a significantly increased ROM (in rotations and translations) during sagittal bending and axial rotation as the degeneration progressed toward grade IV. ROM decreased at the grade V level. For the lower lumbar FSUs, ROM increased up to the grade III level of degeneration, followed by a decrease at grades IV and V. This observation was statistically significant only during axial rotation and lateral bending.
Schmidt et al. investigated the stiffness of cadaveric lumbar motion segments with radial tears in discs detected by MRI and cryomicrotome sections under sagittal, lateral, and axial rotations.9 They used normal control specimens (n = 4) and degenerated specimens (n = 16) with radial tears in the anulus. Specimens with radial tears exhibited loss of stiffness at varying degrees in all planes of motion.
Zhao et al. studied the effect of the depressurized nucleus fibrosus with end plate disruption on FSU motion characteristics.10 Twenty-one thoracolumbar motion segments, of which four were normal, were studied. Sixteen specimens had pre-existing moderate degeneration, and one had pre-existing severe degeneration. All specimens were tested for bending motion using an eccentric (i.e., off-axis) axial loading mechanism. The investigators loaded the specimen in creep (i.e., prolonged exposure to a constant load) to remove the water content from the nucleus and then loaded the specimen in compression-to-failure to generate end plate disruption, which simulated advanced degeneration. They monitored their procedures by pressure measurements within the disc. The comparison of the flexibility tests before and after the degeneration-inducing maneuvers demonstrated that there were substantial increases in NZ and ROM as well as the instability index (NZ/ROM) in flexion and lateral bending.
Fujiwara et al. studied the effects of disc degeneration and facet joint osteoarthritis on the segmental flexibility of the lumbar spine.11 They graded the degeneration (grades I to V) of 110 lumbar motion segments obtained from 19 female and 25 male cadavers using MRI films and biomechanical tests. They observed an increase in ROM in axial rotation, flexion, and extension as the degeneration advanced (grades II to IV), followed by a decrease at degeneration grade V. In lateral bending, ROM increased at grade III and decreased in more advanced levels. This observation was true for both sexes.
Gay et al. studied the effect of degeneration on spinal flexibility during stepwise loading and continuous loading conditions in an in vitro evaluation.12 The NZ and ROM have been observed to be larger with stepwise loading compared with continuous loading.13 The effect of degeneration on spinal flexibility had not previously been studied for both assessment techniques in the same experimental model. Gay et al. demonstrated that the NZ and ROM, assessed using both stepwise and continuous loading techniques, showed a trend similar to that observed with macroscopic evaluation of disc degeneration. In other words, spinal flexibility increased with degeneration up to grade III and decreased at grade IV.
Oxland et al. investigated the relationship between bone density, disc degeneration, and flexibility in cadaveric spinal specimens.14 They demonstrated a significant increase in ROM in axial rotation, as well as a significant decrease in the NZ in lateral bending, as the degeneration grade increased. There were no significant changes observed in ROM and NZ associated with degeneration level during sagittal motion. In this study, the investigators used axial loading during bending testing to simulate muscle forces, which may have influenced the alterations of the NZ.
There are ample data supporting the destructive effect of degeneration on spinal stability (at least at the early stages of the degeneration cascade). Evidence, however, is lacking regarding characterization of NZ and ROM behavior changes that occur with degeneration, despite strong theoretical foundations. The causes of this deficiency may lie in the variation in biomechanical testing protocols from laboratory to laboratory, the subjectivity associated with grading degeneration, and the adaptive changes in the FSU in response to disc degeneration.