Ian A. F. Stokes

ISB recommendation on definitions of joint coordinate system of various joints for the reporting of human joint motion-part I: ankle, hip, and spine

The Standardization and Terminology Committee (STC) of the International Society of Biomechanics (ISB) proposes a general reporting standard for joint kinematics based on the Joint Coordinate System (JCS), first proposed by Grood and Suntay for the knee joint in 1983 (J. Biomech. Eng. 105 (1983) 136). There is currently a lack of standard for reporting joint motion in the field of biomechanics for human movement, and the JCS as proposed by Grood and Suntay has the advantage of reporting joint motions in clinically relevant terms. In this communication, the STC proposes definitions of JCS for the ankle, hip, and spine. Definitions for other joints (such as shoulder, elbow, hand and wrist, temporomandibular joint (TMJ), and whole body) will be reported in later parts of the series. The STC is publishing these recommendations so as to encourage their use, to stimulate feedback and discussion, and to facilitate further revisions. For each joint, a standard for the local axis system in each articulating bone is generated. These axes then standardize the JCS. Adopting these standards will lead to better communication among researchers and clinicians.

Are animal models useful for studying human disc disorders / degeneration?

Intervertebral disc (IVD) degeneration is an often investigated pathophysiological condition because of its implication in causing low back pain. As human material for such studies is difficult to obtain because of ethical and government regulatory restriction, animal tissue, organs and in vivo models have often been used for this purpose. However, there are many differences in cell population, tissue composition, disc and spine anatomy, development, physiology and mechanical properties, between animal species and human. Both naturally occurring and induced degenerative changes may differ significantly from those seen in humans. This paper reviews the many animal models developed for the study of IVD degeneration aetiopathogenesis and treatments thereof. In particular, the limitations and relevance of these models to the human condition are examined, and some general consensus guidelines are presented. Although animal models are invaluable to increase our understanding of disc biology, because of the differences between species, care must be taken when used to study human disc degeneration and much more effort is needed to facilitate research on human disc material.

The effects of abdominal muscle coactivation on lumbar spine stability.

Study Design. A biomechanical model of the lumbar spine was used to calculate the effects of abdominal muscle coactivation on spinal stability. Objectives. To estimate the effects of abdominal muscle coactivation on lumbar spine stability, muscle fatigue rate, and lumbar spine compression forces. Summary of Background Data. The activation of human trunk muscles has been found to involve coactivation of antagonistic muscles, which has not been adequately predicted by biomechanical models. Antagonistic activation of abdominal muscles might produce flexion moments resulting from abdominal pressurization. Qualitatively, antagonistic activity also has been attributed to the need to stabilize the spine. Methods. Spinal loads and spinal stability were calculated for maximum and submaximum (40%, 60% and 80%) efforts in extension and lateral bending using a previously published, anatomically realistic biomechanical model of the lumbar spine and its musculature. Three different antagonistic abdominal muscle coactivation patterns were imposed, and results were compared with those found in a model with no imposed coactivation. Results. Results were quantified in terms of the sum of cubed muscle stresses (∑σm3, which is related to the muscle fatigue rate), the maximum compressive loading on the lumbar spine, and the critical value of the muscle stiffness parameter (q) required for the spine to be stable. Forcing antagonistic coactivation increased stability, but at the cost of an increase in ∑σm3 and a small increase in maximum spinal compression. Conclusions. These analyses provide estimates of the effects of antagonistic abdominal muscle coactivation, indicating that its probable role is to stabilize the spine.

Compression-induced changes in intervertebral disc properties in a rat tail model.

STUDY DESIGN An Ilizarov-type apparatus was applied to the tails of rats to assess the influence of immobilization, chronically applied compression, and sham intervention on intervertebral discs of mature rats. OBJECTIVES To test the hypothesis that chronically applied compressive forces and immobilization cause changes in the biomechanical behavior and biochemical composition of rat tail intervertebral discs. SUMMARY OF BACKGROUND DATA Mechanical factors are associated with degenerative disc disease and low back pain, yet there have been few controlled studies in which the effects of compressive forces on the structure and function of the disc have been isolated. METHODS The tails of 16 Sprague-Dawley rats were instrumented with an Ilizarov-type apparatus. Animals were separated into sham, immobilization, and compression groups based on the mechanical conditions imposed. In vivo biomechanical measurements of disc thickness, angular laxity, and axial and angular compliance were made at 14-day intervals during the course of the 56-day experiment, after which discs were harvested for measurement of water, proteoglycan, and collagen contents. RESULTS Application of pins and rings alone (sham group) resulted in relatively small changes of in vivo biomechanical behavior. Immobilization resulted in decreased disc thickness, axial compliance, and angular laxity. Chronically applied compression had effects similar to those of immobilization alone but induced those changes earlier and in larger magnitudes. Application of external compressive forces also caused an increase in proteoglycan content of the intervertebral discs. CONCLUSIONS The well-controlled loading environment applied to the discs in this model provides a means of isolating the influence of joint-loading conditions on the response of the intervertebral disc. Results indicate that chronically applied compressive forces, in the absence of any disease process, caused changes in mechanical properties and composition of tail discs. These changes have similarities and differences in comparison with human spinal disc degeneration.

Mechanical conditions that accelerate intervertebral disc degeneration: overload versus immobilization.

Study Design. A review of the literature on macromechanical factors that accelerate disc degeneration with particular focus on distinguishing the roles of immobilization and overloading. Objective. This review examines evidence from the literature in the areas of biomechanics, epidemiology, animal models, and intervertebral disc physiology. The purpose is to examine: 1) what are the degeneration-related alterations in structural, material, and failure properties in the disc; and 2) evidence in the literature for causal relationships between mechanical loading and alterations in those structural and material properties that constitute disc degeneration. Summary of Background Data. It is widely assumed that the mechanical environment of the intervertebral disc at least in part determines its rate of degeneration. However, there are two plausible and contrasting theories as to the mechanical conditions that promote degeneration: 1) mechanical overload; and 2) reduced motion and loading. Results. There are a greater number of studies addressing the “wear and tear” theory than the immobilization theory. Evidence is accumulating to support the notion that there is a “safe window” of tissue mechanical conditions in which the discs remain healthy. Conclusions. It is concluded that probably any abnormal loading conditions (including overload and immobilization) can produce tissue trauma and/or adaptive changes that may result in disc degeneration. Adverse mechanical conditions can be due to external forces, or may result from impaired neuromuscular control of the paraspinal and abdominal muscles. Future studies will need to evaluate additional unquantified interactions between biomechanics and factors such as genetics and behavioral responses to pain and disability.

Mechanical modulation of vertebral body growth. Implications for scoliosis progression.

Study Design. The authors developed a rat‐tail model to investigate the hypothesis that vertebral wedging during growth in progressive spinal deformities results from asymmetric loading in a “vicious cycle.” Objectives. To document growth curves with axial compression or distraction applied to tail vertebrae to determine whether compression load slows growth and distraction accelerates it. Summary of Background Data. Progression of skeletal deformity during growth is believed to be governed by the Hueter‐Volkmann law, but there is conflicting evidence to support this idea. Methods. Twenty‐eight 6‐week‐old Sprague‐Dawley rats were assigned to one of three groups: compression loading, distraction loading, or sham (apparatus applied without loading). Under general anesthesia, two 0.7‐mm diameter stainless steel percutaneous pins were used to transfix each of two vertebrae. The pins were glued to 25‐mm diameter external ring fixators. Springs (load rate, 35 g/mm) were installed on three stainless steel threaded rods that were passed through holes in each ring and compressed with nuts to apply compression or distraction forces between 25‐75% of bodyweight. Vertebral growth rates in μm/day were measured by digitizing the length of the vertebrae images in radiographs taken 0, 1, 3, 5, 7, and 9 weeks later. Results. The loaded vertebrae grew at 68% of control rate for compressed vertebrae and at 114% for distracted vertebrae. (Differences statistically significant, P < 0.01 by analysis of variance.) For the compressed vertebrae, the pinned vertebrae, which were loaded at one of their two growth cartilages, grew at a reduced rate (85%), although this effect was not apparent for the distraction animals. Conclusions. The findings confirm that vertebral growth is modulated by loading, according to the Hueter‐Volkmann principle. The quantification of this relationship will permit more rational design of conservative treatment of spinal deformity during the adolescent growth spurt.

Surface EMG electrodes do not accurately record from lumbar multifidus muscles

OBJECTIVE This study investigated whether electromyographic signals recorded from the skin surface overlying the multifidus muscles could be used to quantify their activity. DESIGN Comparison of electromyography signals recorded from electrodes on the back surface and from wire electrodes within four different slips of multifidus muscles of three human subjects performing isometric tasks that loaded the trunk from three different directions. BACKGROUND It has been suggested that suitably placed surface electrodes can be used to record activity in the deep multifidus muscles. METHODS We tested whether there was a stronger correlation and more consistent regression relationship between signals from electrodes overlying multifidus and longissimus muscles respectively than between signals from within multifidus and from the skin surface electrodes over multifidus. RESULTS The findings provided consistent evidence that the surface electrodes placed over multifidus muscles were more sensitive to the adjacent longissimus muscles than to the underlying multifidus muscles. The R(2) for surface versus intra-muscular comparisons was 0.64, while the average R(2) for surface-multifidus versus surface-longissimus comparisons was 0.80. Also, the magnitude of the regression coefficients was less variable between different tasks for the longissimus versus surface multifidus comparisons. CONCLUSIONS Accurate measurement of multifidus muscle activity requires intra-muscular electrodes. RELEVANCE Electromyography is the accepted technique to document the level of muscular activation, but its specificity to particular muscles depends on correct electrode placement. For multifidus, intra-muscular electrodes are required.

1980 Volvo award in clinical sciences. Assessment of patients with low-back pain by biplanar radiographic measurement of intervertebral motion.

Abnormalities of intervertebral joint motion including hypermobility, reduced mobility, torsional abnormality, and displacement of the center of rotation have been associated with degenerative change. However, measurement of these signs in plane X-ray films is handicapped by the three-dimensional motion and geometry of the spine. This study aimed to relate three-dimensional motion of the joints to their pathological state. We have used biplanar radiography to measure intervertebral motion during voluntary movements by patients with low back pain. Primary (or intentional) and coupled motions were measured by a refined technique, along with disc shear and facet joint motion. Abnormalities were found, especially in the “coupled” motions which were related to narrowed disc space, and to proximity to previous fusions. There was asymmetry of motion specific to joints with herniated nucleus pulposus.

Quantitative anatomy of the lumbar musculature.

This paper describes the anatomy of the musculature crossing the lumbar spine in a standardized form to provide data generally suitable for static biomechanical analyses of muscle and spinal forces. The muscular anatomy from several sources was quantified and transformed to the mean bony anatomy of four young healthy adults measured from standing stereo-radiographs. The origins, insertions and physiological cross-sectional area (PCSA) of 180 muscle slips which act on the lumbar spine are given relative to the bony anatomy defined by the locations of 12 thoracic and five lumbar vertebrae, and the sacrum, and the shape and positions of the 24 ribs. The broad oblique abdominal muscles are each represented by six vectors and an appropriate proportion of the total PCSA was assigned to each to represent the muscle biomechanics.

Growth Plate Mechanics and Mechanobiology. A Survey of Present Understanding

The longitudinal growth of long bones occurs in growth plates where chondrocytes synthesize cartilage that is subsequently ossified. Altered growth and subsequent deformity resulting from abnormal mechanical loading is often referred to as mechanical modulation of bone growth. This phenomenon has key implications in the progression of infant and juvenile musculoskeletal deformities, such as adolescent idiopathic scoliosis, hyperkyphosis, genu varus/valgus and tibia vara/valga, as well as neuromuscular diseases. Clinical management of these deformities is often directed at modifying the mechanical environment of affected bones. However, there is limited quantitative and physiological understanding of how bone growth is regulated in response to mechanical loading. This review of published work addresses the state of knowledge concerning key questions about mechanisms underlying biomechanical modulation of bone growth. The longitudinal growth of bones is apparently controlled by modifying the numbers of growth plate chondrocytes in the proliferative zone, their rate of proliferation, the amount of chondrocytic hypertrophy and the controlled synthesis and degradation of matrix throughout the growth plate. These variables may be modulated to produce a change in growth rate in the presence of sustained or cyclic mechanical load. Tissue and cellular deformations involved in the transduction of mechanical stimuli depend on the growth plate tissue material properties that are highly anisotropic, time-dependent, and that differ in different zones of the growth plate and with developmental stages. There is little information about the effects of time-varying changes in volume, water content, osmolarity of matrix, etc. on differentiation, maturation and metabolic activity of chondrocytes. Also, the effects of shear forces and torsion on the growth plate are incompletely characterized. Future work on growth plate mechanobiology should distinguish between changes in the regulation of bone growth resulting from different processes, such as direct stimulation of the cell nuclei, physico-chemical stimuli, mechanical degradation of matrix or cellular components and possible alterations of local blood supply.