Clinical spinal instability and low back pain

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Abstract

Clinical instability is an important cause of low back pain. Although there is some controversy concerning its definition, it is most widely believed that the loss of normal pattern of spinal motion causes pain and/or neurologic dysfunction. The stabilizing system of the spine may be divided into three subsystems: (1) the spinal column; (2) the spinal muscles; and (3) the neural control unit. A large number of biomechanical studies of the spinal column have provided insight into the role of the various components of the spinal column in providing spinal stability. The neutral zone was found to be a more sensitive parameter than the range of motion in documenting the effects of mechanical destabilization of the spine caused by injury and restabilization of the spine by osteophyle formation, fusion or muscle stabilization. Clinical studies indicate that the application of an external fixator to the painful segment of the spine can significantly reduce the pain. Results of an in vitro simulation of the study found that it was most probably the decrease in the neutral zone, which was responsible for pain reduction. A hypothesis relating the neutral zone to pain has been presented. The spinal muscles provide significant stability to the spine as shown by both in vitro experiments and mathematical models. Concerning the role of neuromuscular control system, increased body sway has been found in patients with low back pain, indicating a less efficient muscle control system with decreased ability to provide the needed spinal stability.

Introduction

Low back pain (LBP) is a common medical problem. There is a 50–70% chance of a person having LBP pain during his or her lifetime, [3] with a prevalence of about 18%. [28] In the industrialized societies, LBP is expensive costing an estimated $15 to $50 billion per year in the USA [2], [12], [25], [44]. Specific causes for most LBP are not known. Although negative social interaction (for example, dissatisfaction at work) has been found to relate to chronic LBP, a significant portion of the problem is of mechanical origin. It is often referred to as clinical spinal instability [26].

Clinical spinal instability is controversial and not well understood. White and Panjabi defined clinical instability of the spine as the loss of the spine’s ability to maintain its patterns of displacement under physiologic loads so there is no initial or additional neurologic deficit, no major deformity, and no incapacitating pain [46]. Appropriately performed clinical studies of patients with spine pain and documented clinical instability would be ideal for testing this hypothesis. However, carrying out such studies is difficult. Biomechanical studies have provided some important and useful understanding. Before we go further, it is helpful to differentiate between mechanical instability and clinical instability. The former defines inability of the spine to carry spinal loads, while the latter includes the clinical consequences of neurological deficit and/or pain.

Clinical instability of the spine has been studied in vivo since 1944 when Knutsson, using functional radiographs, attempted to relate LBP to retro-displacement of a vertebra during flexion [20]. There have been several similar studies over the past 50 years, but the results have been unclear. In association with back or neck pain, some investigators found increased motion [7], [8], [11], [21], whereas others found decreased motion [9], [19], [39], [40]. Some reasons for the uncertainties have been the variability in the voluntary efforts of the subjects to produce spinal motion, the presence of muscle spasm and pain during the radiographic examination, lack of appropriate control subjects matched in age and gender, and the limited accuracy of in vivo methods for measuring motion. These problems, although not insurmountable, are difficult to resolve in a clinical setting.

The first systematic approach to the analysis of mechanical stability of the spine was undertaken by us using an in vitro biomechanical model of the cervical spine [31], [47]. Fresh cadaveric functional spinal units (two adjacent vertebrae with interconnecting disk, ligaments, and facet joints, but devoid of musculature) were loaded either in flexion or extension, and the anatomic elements (disk, ligaments, and facet joints) were transected either from anterior to posterior or from posterior to anterior. This study resulted in the development of a checklist for the diagnosis of lumbar spine instability [46].

The lumbar spine checklist uses several elements, such as biomechanical parameters, neurologic damage and anticipated loading on the spine (Table 1). A point value system is used to determine clinical stability or instability. The anterior elements include the posterior longitudinal ligament and all anatomic structures anterior to it (two points). The posterior elements are all anatomic structures posterior to the posterior longitudinal ligament (two points). Intervertebral translation (two points) is measured either on flexion-extension or resting radiographs. Rotation (two points) is measured either on flexion–extension radiographs or on resting radiographs. Damage to the cauda equina is given three points, and anticipated high loading on the spine is given one point. If the sum of the points is five or more, then the spine is considered clinically unstable. This systematic approach to the assessment of clinical instability is an important tool for the clinician, and a prospective controlled study to validate the predictions of the checklist would be beneficial.

Section snippets

The spinal stabilizing system

It has been conceptualized that the overall mechanical stability of the spinal column, especially in dynamic conditions and under heavy loads, is provided by the spinal column and the precisely coordinated surrounding muscles. As a result, the spinal stabilizing system of the spine was conceptualized by Panjabi to consist of three subsystems: spinal column providing intrinsic stability, spinal muscles, surrounding the spinal column, providing dynamic stability, and neural control unit

The spinal column

Biomechanical studies under controlled laboratory conditions have provided some insight into the role of spinal column components (disk, ligaments and facets) in providing spinal stability. The load–displacement curve is often used as a measure of physical properties of the spinal column or any other structure. The curve may be linear or nonlinear. In manmade structures, such as a steel spring, the load displacement curve is often linear, i.e. the ratio of the load applied and the displacement

The spinal muscles

The importance of muscles in stabilizing the spinal column is quite obvious when a cross-section of the human body is viewed at the lumbar level (Fig. 5). Not only is the total area of the cross-sections of the numerous muscles surrounding the spinal column much bigger than the area of the spinal column, but the muscles have significantly larger lever arms than those of the intervertebral disc and ligaments. The muscles provide mechanical stability to the spinal column. Euler, a Swiss

The control unit

The etiology of LBP in most patients is not known, as mentioned earlier. It may be hypothesized that a certain percentage of these patients may have suboptimal neuromuscular control, especially under dynamic conditions. A few studies have specifically looked at this aspect of LBP. In one of the first studies of this kind, the sway of the center of gravity of the body in patients with spinal canal stenosis was determined [16]. The patients were challenged to exercise until claudication occurred,

A hypothesis of pain, motion and stabilization

Based on the definition of clinical spinal instability presented earlier, the instability hypothesis assumes a relationship between abnormal intervertebral motion and LBP. The corollary to this hypothesis is that a decrease in the intervertebral motion in a patient with LBP may result in reduced pain. In fact, this is the basis for low back treatments involving surgical fusion, muscle strengthening and muscle control training. We conducted a biomechanical experiment to test this hypothesis [38].

Manohar M. Panjabi obtained his undergraduate degree in mechanical engineering from Birla College of Engineering, Pilani, India, and his PhD degree in machine design from Chalmers University of Technology, Gothenburg, Sweden. He has held various faculty positions at Yale University. He is currently a professor in the Departments of Orthopaedics and Rehabilitation, and Mechanical Engineering, director of Biomechanics Research Laboratory. His research interest focuses on human spine, especially

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    Manohar M. Panjabi obtained his undergraduate degree in mechanical engineering from Birla College of Engineering, Pilani, India, and his PhD degree in machine design from Chalmers University of Technology, Gothenburg, Sweden. He has held various faculty positions at Yale University. He is currently a professor in the Departments of Orthopaedics and Rehabilitation, and Mechanical Engineering, director of Biomechanics Research Laboratory. His research interest focuses on human spine, especially the basic understanding of its function, injuries and clinical problems, which may be addressed advantageously with the biomechanical tools.

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