The Stabilizing System of the Spine. Part I. Function, Dysfunction, Adaptation, and Enhancement (Fragment)

Manohar M. Panjabi. Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, New Haven, Connecticw U.S.A.


Presented here is the conceptual basis for the assertion that the spinal stabilizing system consists ofthree subsystems. The vertebrae, discs, and ligaments constitute the passive subsystem. All muscles and tendons surrounding the spinal column that can apply forces to the spinal column constitute the active subsystem. The nerves and central nervous system comprise the neural subsystem, which determines the requirements for spinal stability by monitoring the various transducer signals, and directs the active subsystem to provide the needed stability. A dysfunction of a component of any one of the subsystems may lead to one or more of the following three possibilities: (a) an immediate response from other subsystems to successfully compensate, (b) a long-term adaptation response of one or more subsystems, and (c) an injury to one or more components of any subsystem. It is conceptualized that the first response results in normal function, the second results in normal function but with an altered spinal stabilizing system, and the third leads to overall system dysfunction, producing, for example, low back pain. In situations where additional loads or complex postures are anticipated, the neural control unit may alter the muscle recruitment strategy, with the temporary goal of enhancing the spine stability beyond the normal requirements. Low back pain is a well-recognized problem of the lation and resulting in substantial social loss (2,I I,23, 37). Because the etiology is unknown for most types of low back pain (38), it is not surprising that many of the present treatments are relatively ineffective. Spinal instability is considered to be one of the important causes of low back pain but is poorly defined and not well understood (24). The basic concept of spinal instability is that abnormally large intervertebral motions cause either compression and/or stretching of the inflamed neural elements or abnormal deformations of ligaments, joint capsules, annular fibers, and end-plates, which are known to have significant density of nocioceptors (41). In both situations, the abnormally large intervertebral motions may produce pain sensation. Knutsson (19) was probably the first to propose a mechanical parameter as an indicator of spinal instability: the retrodisplacement (anterior to posterior translation) of a vertebra observed on lateral radiographs while flexing the spine from the extended position. There is some recent evidence to support these observations of increased motion being related to low back problems (12,20,40). Other studies have found a mixed set of results. Decreased motion was found by Pearcy et al. (34) and Dvorak et al. (8) in low back pain patients with degenerative changes in the spine. ln the same study, Dvorak et al. (8) reported increased motion in younger athletic patients with back pain. Both hypo- and hypermobility of the spine’ as measured by the range of motion without regard to the direction of vertebral fiiovements, have been proposed by another hypothesis of spinal instability (18). In addition to the abnormal magnitudes (larger or smaller than normal), the motion quality is another parameter. Abnormally large dispersion of the centers of rotation during flexion, extension, and lateral bending have been suggested as signs of spinal instability, both in an in vitro model (35) and in low back pain patients (7). Seligman et al. (36), also using the concept of the center of rotation and experimental results of an in vitro study, suggested that the increased length of the path of the centers of rotation during flexion/extension may be a predictor of spinal instability. There may also be motion quality abnormalities. Pearcy et al. (33) found coupled axial rotations and lateral bending motions during flexion/extension in low back pain patients as compared with the control group. Similar observations concerning the coupled torques also have been made (32). Thus, there have been several attempts made in the past to relate the clinical problem of low back pain to an abnormality in intervertebral motion. Although some useful information has been gathered, there are contradictory observations and hypotheses. To make progress on this clinically important problem of spinal instability, new hypotheses must be developed, and, driven from the hypotheses, new types of motion information must be obtained. A better understanding of the workings of the spinal stabilizing system may also be useful in this respect.