Biomechanics of back pain
TL;DR: A mechanistic account of back pain is offered which attempts to incorporate all of the most important recent advances in spinal research, and the concept of ‘functional pathology’ is introduced, according to which, back pain can arise because postural habits generate painful stress concentrations within innervated tissues, even though the stresses are not high enough to cause physical disruption.
Abstract: This paper offers a mechanistic account of back pain which attempts to incorporate all of the most important recent advances in spinal research. Anatomical and pain-provocation studies show that severe and chronic back pain most often originates in the lumbar intervertebral discs, the apophyseal joints, and the sacroiliac joints. Psychosocial factors influence many aspects of back pain behaviour but they are not important determinants of who will experience back pain in the first place. Back pain is closely (but not invariably) associated with structural pathology such as intervertebral disc prolapse and endplate fractures, although age-related biochemical changes such as those revealed by a 'dark disc' on MRI have little clinical relevance. All features of structural pathology (including disc prolapse) can be re-created in cadaveric specimens by severe or repetitive mechanical loading, with a combination of bending and compression being particularly harmful to the spine. Structural disruption alters the mechanical environment of disc cells in a manner that leads to cell-mediated degenerative changes, and animal experiments confirm that surgical disruption of a disc is followed by widespread disc degeneration. Some people are more vulnerable to spinal degeneration than others, largely because of their genetic inheritance. Age-related biochemical changes and loading history can also affect tissue vulnerability. Finally the concept of 'functional pathology' is introduced, according to which, back pain can arise because postural habits generate painful stress concentrations within innervated tissues, even though the stresses are not high enough to cause physical disruption.
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TL;DR: To suggest how intervertebral disc degeneration might be distinguished from the physiologic processes of growth, aging, healing, and adaptive remodeling, and to simplify the issue of causality.
Abstract: and Introduction Abstract Study Design: Review and reinterpretation of existing literature. Objective: To suggest how intervertebral disc degeneration might be distinguished from the physiologic processes of growth, aging, healing, and adaptive remodeling. Summary of Background Data: The research literature concerning disc degeneration is particularly diverse, and there are no accepted definitions to guide biomedical research, or medicolegal practice. Definitions: The process of disc degeneration is an aberrant, cell-mediated response to progressive structural failure. A degenerate disc is one with structural failure combined with accelerated or advanced signs of aging. Early degenerative changes should refer to accelerated age-related changes in a structurally intact disc. Degenerative disc disease should be applied to a degenerate disc that is also painful. Justification: Structural defects such as endplate fracture, radial fissures, and herniation are easily detected, unambiguous markers of impaired disc function. They are not inevitable with age and are more closely related to pain than any other feature of aging discs. Structural failure is irreversible because adult discs have limited healing potential. It also progresses by physical and biologic mechanisms, and, therefore, is a suitable marker for a degenerative process. Biologic progression occurs because structural failure uncouples the local mechanical environment of disc cells from the overall loading of the disc, so that disc cell responses can be inappropriate or aberrant. Animal models confirm that cell-mediated changes always follow structural failure caused by trauma. This definition of disc degeneration simplifies the issue of causality: excessive mechanical loading disrupts a disc's structure and precipitates a cascade of cell-mediated responses, leading to further disruption. Underlying causes of disc degeneration include genetic inheritance, age, inadequate metabolite transport, and loading history, all of which can weaken discs to such an extent that structural failure occurs during the activities of daily living. The other closely related definitions help to distinguish between degenerate and injured discs, and between discs that are and are not painful.
1,463 citations
Cites background or methods from "Biomechanics of back pain"
...Reprinted with permission from Churchill Livingstone; 2002.(4) 2155 What is Disc Degeneration? • Adams and Roughley...
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...Reprinted with permission from Churchill Livingstone; 2002.(4) Figure 7....
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...Reprinted with permission from Churchill Livingstone; 2002.(4) 2154 Spine • Volume 31 • Number 18 • 2006...
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...Radial fissures progress outward from the nucleus, usually posteriorly or posterolaterally,(47) and this process can be simulated in cadaveric discs by cyclic loading in bending and compression.(4) Radial fissures are associated with nucleus “degeneration,”(47,49) but it is not clear which comes first....
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...Reprinted with permission from Churchill Livingstone; 2002.(4) Figure 4....
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TL;DR: 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.
Abstract: 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.
297 citations
Cites background from "Biomechanics of back pain"
...In this way, mechanical injuries weaken the disc, increasing the risk of further injury, and a vicious cycle of accumulating injury that outstrips the disc’s capability for biologic repair develops.(2,3) In a contrasting hypothesis for the mechanical pathogenesis of disc degeneration, it is suggested that hypomobility of the disc produces adaptive changes that may cause tissue weakness and degeneration, subsequent pain, and further reduced motion, again in a vicious cycle as was proposed for the case of articular cartilage....
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TL;DR: The diagnostic accuracy of the clinical examination and clinical reasoning process was superior to the sacroiliac joint pain provocation tests alone, and a specific clinicalexamination and reasoning process can differentiate between symptomatic and asymptomatic sac roiliac joints.
Abstract: Research suggests that clinical examination of the lumbar spine and pelvis is unable to predict the results of diagnostic injections used as reference standards. The purpose of this study was to assess the diagnostic accuracy of a clinical examination in identifying symptomatic and asymptomatic sacroiliac joints using double diagnostic injections as the reference standard. In a blinded concurrent criterion-related validity design study, 48 patients with chronic lumbopelvic pain referred for diagnostic spinal injection procedures were examined using a specific clinical examination and received diagnostic intraarticular sacroiliac joint injections. The centralisation and peripheralisation phenomena were used to identify possible discogenic pain and the results from provocation sacroiliac joint tests were used as part of the clinical reasoning process. Eleven patients had sacroiliac joint pain confirmed by double diagnostic injection. Ten of the 11 sacroiliac joint patients met clinical examination criteria for having sacroiliac joint pain. In the primary subset analysis of 34 patients, sensitivity, specificity and positive likelihood ratio (95% confidence intervals) of the clinical evaluation were 91% (62 to 98), 83% (68 to 96) and 6.97 (2.70 to 20.27) respectively. The diagnostic accuracy of the clinical examination and clinical reasoning process was superior to the sacroiliac joint pain provocation tests alone. A specific clinical examination and reasoning process can differentiate between symptomatic and asymptomatic sacroiliac joints. [Laslett M, Young SB, Aprill CN and McDonald B (2003): Diagnosing painful sacroiliac joints: A validity study of a McKenzie evaluation and sacroiliac provocation tests. Australian Journal of Physiotherapy 49: 89-97]
264 citations
Cites background from "Biomechanics of back pain"
...…SIJ (Dreyfuss et al 1996, Maigne et al 1996, Schwarzer et al 1995a, Slipman et al 1998), and that only fluoroscopically-guided contrastenhanced anaesthetic injection is of diagnostic value (Adams et al 2002, Dreyfuss et al 1996, Maigne et al 1996, Merskey and Bogduk 1994, Schwarzer et al 1995a)....
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TL;DR: A new musculoskeletal model for the lumbar spine that includes the abilities to predict joint reactions, muscle forces, and muscle activation patterns is described in this paper and can be integrated with existing OpenSim models to build more comprehensive models of the human body.
Abstract: A new musculoskeletal model for the lumbar spine is described in this paper. This model features a rigid pelvis and sacrum, the five lumbar vertebrae, and a rigid torso consisting of a lumped thoracic spine and ribcage. The motion of the individual lumbar vertebrae was defined as a fraction of the net lumbar movement about the three rotational degrees of freedom: flexion–extension lateral bending, and axial rotation. Additionally, the eight main muscle groups of the lumbar spine were incorporated using 238 muscle fascicles with prescriptions for the parameters in the Hill-type muscle models obtained with the help of an extensive literature survey. The features of the model include the abilities to predict joint reactions, muscle forces, and muscle activation patterns. To illustrate the capabilities of the model and validate its physiological similarity, the model’s predictions for the moment arms of the muscles are shown for a range of flexion–extension motions of the lower back. The model uses the OpenSim platform and is freely available on https://www.simtk.org/home/lumbarspine to other spinal researchers interested in analyzing the kinematics of the spine. The model can also be integrated with existing OpenSim models to build more comprehensive models of the human body.
257 citations
Cites background from "Biomechanics of back pain"
...Lower back pain has been posited to originate from biomechanical-based deficits (Adams 2004; McGill et al. 2000; White and Panjabi 1978b). For this reason, musculoskeletal models are of great interest to back pain researchers as they provide an inexpensive and efficient method to determine features such as muscle activation patterns, joint torques and forces, contributions of passive and active stiffness elements, and optimal posture, among others, which can be used to differentiate the motion of subjects with and without lower back pain. The complexities of the muscle architecture for the spine and interpatient variability in the spine and vertebral joint geometries, among others, naturally cause the development of these models to be both time-consuming and difficult. Despite these challenges, several models of the human lumbar spine have been presented in the literature (Bogduk et al. 1992a; Cholewicki et al. 1995; de Zee et al. 2007; El-Rich et al. 2004; Huynh et al. 2010; Lambrecht et al. 2009; McGill and Norman 1987; Shirazi-Adl 1991; Stokes and GardnerMorse 1995). Chronologically, these models typically show increased complexity and realism. The model presented in the present paper extends this body of work in two manners. First, the detailed lumbar muscle anatomy is combined with the musculotendon force-generating parameters elaborated on extensively in Zajac (1989). Second, the model is based on the open-source platform OpenSim (Delp et al....
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...Lower back pain has been posited to originate from biomechanical-based deficits (Adams 2004; McGill et al. 2000; White and Panjabi 1978b)....
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TL;DR: Evidence suggests that there may be interdependence between force and repetition with respect to MSD risk, and fatigue failure studies of musculoskeletal tissues show a pattern of failure that mirrors theMSD risk observed in epidemiological studies.
Abstract: Objective: Our aims were (a) to perform a system atic literature review of epidemiological studies that examined the interaction of force and repetition with respect to musculoskeletal disorder (MSD) risk, (b) to assess the relationship of force and repetition in fatigue failure studies of musculoskeletal tissues, and (c) to synthesize these findings. Background: Many epidemiological studies have examined the effects of force and repetition on MSD risk; however, relatively few have examined the interaction between these risk factors. Method: In a literature search, we identified 12 studies that allowed evaluation of a forcerepetition interaction with respect to MSD risk. Identified studies were subjected to a methodological quality assessment and critical review. We evaluated laboratory studies of fatigue failure to examine tissue failure responses to force and repetition. Results: Of the 12 epidemiological studies that tested a Force × Repetition interaction, 10 reported evidence of interaction. Based on these results, the suggestion is made that force and repetition may be interdependent in terms of their influence on MSD risk. Fatigue failure studies of musculoskeletal tissues show a pattern of failure that mirrors the MSD risk observed in epidemiological studies. Conclusions: Evidence suggests that there may be interdependence between force and repetition with respect to MSD risk. Repetition seems to result in modest increases in risk for lowforce tasks but rapid increases in risk for highforce tasks. This interaction may be representative of a fatigue failure process in affected tissues.
219 citations
References
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19 Mar 2004
TL;DR: The problem diagnostic triage pain and disability back pain through history the epidemiology of back pain risk factors the clinical course of low back pain the physical basis of simple backache.
Abstract: 1. The Problem 2. Diagnostic Triage 3. Pain and Disability 4. The History of Back Pain 5. The Size of the Problem 6. Risk Factors 7. The Clinical Course of Simple Backache 8. The Physical Basis of Simple Backache 9. Physical Impairment 10. Illness Behavior 11. Psychological Distress
1,653 citations
TL;DR: Three matrix turnover phases are identified and evidence is illustrated for a lack of increased synthesis of aggrecan and type II procollagen, but also by an increase in collagen type II denaturation and type I Procollagen synthesis, both dependent on age and grade of tissue degeneration.
Abstract: Very little is known about the turnover of extracellular matrix in the human intervertebral disc. We measured concentrations of specific molecules reflecting matrix synthesis and degradation in predetermined regions of 121 human lumbar intervertebral discs and correlated them with ageing and Thompson grade of degeneration. Synthesis in intervertebral discs, measured by immunoassay of the content of a putative aggrecan biosynthesis marker (846) and the content of types I and II procollagen markers, is highest in the neonatal and 2-5-yr age groups. The contents of these epitopes/molecules progressively diminished with increasing age. However, in the oldest age group (60-80 yr) and in highly degenerated discs, the type I procollagen epitope level increased significantly. The percentage of denatured type II collagen, assessed by the presence of an epitope that is exposed with cleavage of type II collagen, increased twofold from the neonatal discs to the young 2-5-yr age group. Thereafter, the percentage progressively decreased with increasing age; however, it increased significantly in the oldest group and in highly degenerate discs. We identified three matrix turnover phases. Phase I (growth) is characterized by active synthesis of matrix molecules and active denaturation of type II collagen. Phase II (maturation and ageing) is distinguished by a progressive drop in synthetic activity and a progressive reduction in denaturation of type 11 collagen. Phase III (degeneration and fibrotic) is illustrated by evidence for a lack of increased synthesis of aggrecan and type II procollagen, but also by an increase in collagen type II denaturation and type I procollagen synthesis, both dependent on age and grade of tissue degeneration.
946 citations
"Biomechanics of back pain" refers background in this paper
...The large proteoglycan molecules that bind water into the tissue become increasingly fragmented, and some fragments are lost, so that the tissue becomes increasingly dehydrated.(45) This process is particularly marked in the nucleus, which becomes steadily more fibrous as proteoglycans are replaced by fibrous proteins including collagen....
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TL;DR: The authors' finding of isolated nerve fibres that express substance P deep within diseased intervertebral discs and their association with pain suggests an important role for nerve growth into the interverTEbral disc in the pathogenesis of chronic low back pain.
917 citations
TL;DR: The sacroiliac joint is a significant source of pain in patients with chronic low back pain and warrants further study, and its prevalence, validity, and the validity of pain provocation are established.
Abstract: Study Design.This was a cross-sectional analytic study.Objectives.In relation to pain from the sacroiliac joint, this study sought to establish 1) its prevalence, 2) the validity of pain provocation, 3) whether any arthrographic abnormalities predict a response to joint block, and 4) whether certain
876 citations
Additional excerpts
...Similar techniques have shown that the sacro-iliac joints are a major source of symptoms in approximately 30% of patients with chronic back pain below the level of L5-S1....
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...Similar techniques have shown that the sacro-iliac joints are a major source of symptoms in approximately 30% of patients with chronic back pain below the level of L5-S1.(12)...
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TL;DR: A multiple logistic regression model was developed, based on biomechanical plausibility, and indicated that a combination of five trunk motion and workplace factors distinguished between high and low risk of occupationally-related low back disorder risk well (odds ratio: 10.7).
Abstract: Current ergonomic techniques for controlling the risk of occupationally-related low back disorder consist of static assessments of spinal loading during lifting activities. This may be problematic because several biomechanical models and epidemiologic studies suggest that the dynamic characteristics of a lift increase spine loading and the risk of occupational low back disorder. It has been difficult to include this motion information in workplace assessments because the speed at which trunk motion becomes dangerous has not been determined. An in vivo study was performed to assess the contribution of three-dimensional dynamic trunk motions to the risk of low back disorder during occupational lifting in industry. More than 400 repetitive industrial lifting jobs were studied in 48 varied industries. Existing medical and injury records in these industries were examined so that specific jobs historically categorized as either high-risk or low-risk for reported occupationally-related low back disorder could be identified. A triaxial electrogoniometer was worn by workers and documented the three-dimensional angular position, velocity, and acceleration characteristics of the lumbar spine while workers lifted in these high-risk or low-risk jobs. Workplace and individual characteristics were also documented for each of the repetitive lifting tasks. A multiple logistic regression model was developed, based on biomechanical plausibility, and indicated that a combination of five trunk motion and workplace factors distinguished between high and low risk of occupationally-related low back disorder risk well (odds ratio: 10.7). These factors included 1) lifting frequency, 2) load moment, 3) trunk lateral velocity, 4) trunk twisting velocity, and 5) the trunk sagittal angle. This analysis implies that by suitably varying these five factors observed during the lift collectively, the odds of high-risk group membership may decrease by almost 11 times. The predictive power of this model was found to be more than three times greater than that of current lifting guidelines. This study, though not proving causality, indicates an association between the biomechanical factors and low back disorder risk. This model could be used as a quantitative, objective measure to design the workplace so that the risk of occupationally-related low back disorder is minimized.
839 citations
"Biomechanics of back pain" refers background in this paper
...Mechanical influences must be important because specific types of mechanical loading constitute the greatest known risk factors for acute disc prolapse,(1) and for low back pain in general.(2) However, there is growing evidence that back pain is a phenomenon which affects both mind and body....
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