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Manual Therapy 10 (2005) 1420 www.elsevier.com/locate/math

Review article

Can acute low back pain result from segmental spinal buckling during sub-maximal activities? A review of the current literature
Richard Preussa,b, Joyce Funga,b,
a

McGill University School of Physical and Occupational Therapy, 3630 Prom. Sir William Osler, Montreal, Canada H3G 1Y5 b Jewish Rehabilitation Hospital Research Centre (site of CRIR), 3205 Place Alton Goldbloom, Laval, Canada H7V 1R2 Received 18 December 2003; received in revised form 16 July 2004; accepted 18 August 2004

Abstract This paper provides a review of the current literature supporting the hypothesis that segmental spine buckling resulting in tissue damage may be a primary cause of sudden onset low back pain, even during activities that are sub-maximal with respect to loading and muscle activation. While a temporal link exists, it is supported primarily by anecdotal and clinical reports. More pertinent to this review is the biological plausibility of segmental spine buckling as a mechanism of acute injury, supported by modelling studies as well as current knowledge of tissue mechanics and neurophysiology. One antithesis, however, is the low incidence of low back injuries reported during sub-maximal tasks. In order to account for this discrepancy, several predisposing factors are addressed, both constant and situation-dependent, which may contribute to the occurrence of segmental spinal buckling during sub-maximal activities. r 2004 Elsevier Ltd. All rights reserved.
Keywords: Low back pain; Soft tissue injuries; Joint instability

Contents 1. 2. 3. 4. 5. 6. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Spine stability and buckling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Buckling and tissue injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Tissue injury and sudden onset LBP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Predisposing factors to spinal buckling and tissue injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
Corresponding author. Jewish Rehabilitation Hospital Research Centre, 3205 Place Alton Goldbloom, Laval, Quebec, Canada H7V 1R2. Tel.: +1 450 688 9550; fax: +1 450 688 3673. E-mail address: joyce.fung@mcgill.ca (J. Fung).

1356-689X/$ - see front matter r 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2004.08.006

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1. Introduction While low back injuries often occur during heavy lifting, or in extreme postures, many patients with low back pain (LBP) will describe an initial onset of symptoms during seemingly benign activities, requiring minimal or sub-maximal efforts. This apparent paradox is further perplexed by the fact that these individuals may regularly participate in activities requiring much greater efforts than those encountered at the time of the injury. Physicians, physiotherapists, and other health care professionals involved in the treatment of LBP are then faced with the task of explaining how an injury could occur under these sub-maximal conditions. This review is intended to address the question of whether there exists a credible basis for the hypothesis that episodes of sudden onset LBP can result from tissue damage caused by spinal buckling during activities that are sub-maximal with respect to loading and muscle activation. In short, we will attempt to establish a plausible causative link between segmental spine buckling, tissue damage, and sudden onset LBP under submaximal conditions. It is obviously not feasible to reproduce this type of injury sequence experimentally, due to ethical concerns, as well as a general lack of consistency and doseresponse relationship (i.e. the incidence of sudden onset LBP during sub-maximal activity is presumably quite low, since nearly all daily activities take place at sub-maximal levels). There are, however, some potential causative links that can be drawn from temporality and biological plausibility, combined with a general coherence of ndings from numerous experimental and modelling studies. Addressing the temporal relationship between submaximal activities and sudden onset LBP is particularly difcult, as there may not be a simple causeeffect relationship between these two events, but more likely a chain of events for which each link must be in place before the end effect can occur. As such, we must rely on clinical and anecdotal evidence to establish temporality. McGill (2002), and Cholewicki and McGill (1996), discuss clinical reports of low back injuries related to simple tasks such as picking up a pencil from the oor. Further, these authors hypothesize that injuries occurring during sub-maximal tasks are due to a transient segmental buckling (i.e. the segment will briey exceed its maximum safe range of motion), similar to a mechanism that has been observed using video uoroscopy under more strenuous conditions (Cholewicki and McGill, 1996). They suggest that this segmental buckling behaviour may occur as the result of a temporary loss of stability at the segment, possibly resulting from a transient loss of coordination or control of one or more intersegmental muscles. It is important to note, however, that this behaviour was observed under very high loading conditions, and as such remains a hypothetical

mechanism to explain onset of LBP under sub-maximal conditions. This hypothesis, and the question of how this buckling behaviour might occur during sub-maximal tasks, brings us to the main focus of this review: the issue of biological plausibility. To explore the biological plausibility of this injury sequence, it is important to rst address the concept of buckling as it relates to spine stability, and how the segmental buckling phenomenon discussed above might occur, particularly at the relatively low loads that are associated with sub-maximal activities. Secondly, it must be demonstrated that spine buckling under these conditions can be associated with tissue injury. Finally, a link must be drawn between tissue injury and sudden onset LBP. Further, to fully address the question above, we must also address the issue of the general lack of consistency and low doseresponse relationship for this hypothetical injury sequence. To do this, factors that might predispose an individual to spinal buckling, tissue injury and LBP will be briey addressed.

2. Spine stability and buckling The concepts of equilibrium and stability are related to the energy of a system (for a review, the reader is referred to McGill and Cholewicki, 2001). Much of the stability of the spine comes from the potential of the periarticular structures to store elastic energy, based on the stiffness of those structures. Each joint possesses some inherent stability due to the stiffness of the ligaments and joint capsule. More importantly, however, the periarticular musculature can impart a large degree of stability on the joint. Muscles can provide stability to a joint through their stiffness, which is related not only to the biomechanical properties of the muscle, but also to the level of muscle activation or force (Bergmark, 1989; Cholewicki and McGill, 1995). As such, co-activation of the periarticular muscles can provide a large increase in stability to the joint, and with the full complement of the stabilizing musculature working coherently, stability can be achieved even under very high loading conditions (Gardner-Morse et al., 1995; Cholewicki and McGill, 1996). In the frontal plane, the spine has been compared to an Euler column with a uniform modulus of elasticity (Crisco and Panjabi, 1992). This system is similar to the mast of a sailboat, whose stays exhibit high stiffness under tension. The stays of the mast are analogous to the global muscle system of the spine: muscles with no direct vertebral attachments, such as Rectus Abdominis. Like the stays of the mast, it is these global muscles that provide the bulk of the stiffness to the spinal column as a whole (Cholewicki and McGill, 1996). Unlike a ships mast, however, the spine is made up of several individual

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segments. To maintain a uniform modulus of elasticity for the spine, therefore, muscles with direct attachments to individual vertebrae, such as Multidus, must provide stiffness to the intervertebral joints. This is referred to as the local muscle system. In order to meet both the equilibrium and stability requirements of the lumbar spine, a balance must be met between the activity of the large, global muscles, and that of the smaller, local muscles (Bergmark, 1989; Cholewicki and McGill, 1996). With regards to transient segmental buckling, however, it is the activity of the local muscles that is of primary interest. Modelling studies have found that inactivity of the local, intersegmental musculature will lead to instability and buckling at the affected segment at loads similar to the critical load of the ligamentous lumbar spine (88 N), regardless of the muscle activity at the other segments, or at the global level (Crisco and Panjabi, 1991; Cholewicki and McGill, 1996). By this reasoning, faulty motor control at the level of the local muscle system may lead to inappropriate levels of muscle force and stiffness at a given spine segment, and may compromise segmental stability at that level (McGill and Cholewicki, 2001). This compromised stability may, in turn, allow for transient intersegmental buckling, as described by McGill (2002). This is characterized by the segment briey exceeding its safe physiological range of motion, leading to loading of the surrounding soft tissues (ligaments, intervertebral disc, etc.). This phenomenon contrasts with the global buckling behaviour that would occur for an Euler column of uniform stiffness. In the sagittal plane, the normal spinal curvature alters the global buckling behaviour of the spine. Under conditions of uniform stiffness, an excessive vertical load will simply increase the spines normal curvature in the sagittal plane, rather than causing a uniform buckling behaviour, as in the frontal plane. Patwardhan et al. (1999) have suggested that the local, intersegmental musculature may act to change the direction of the force vector applied to the spine in the sagittal plane, to produce an internal compressive force tangential to the curve of the spine in this plane. This follower load not only prevents excessive change in the spine curvature, but has been shown to enhance the load carrying capacity of the spine, in both the frontal (Patwardhan et al., 2001) and sagittal (Patwardhan et al., 1999) planes, well into the physiological range. If the force vector created by the follower load were to deviate from its ideal path in the sagittal plane, however, a bending moment would result, causing excessive exion or extension at the affected segment. As such, faulty segmental motor control, at the level of the local muscle system, can once again be seen as a potential cause of excessive intersegmental motion under load: in other words, segmental spine buckling.

While it is clear that the local musculature must play a role in maintaining the stability of the spine, the question remains: how can a loss of stability occur during activities that are sub-maximal with respect to loading and muscle activation, even in individuals capable of performing tasks requiring much higher levels of exertion? The answer to this appears to be related to the observation that the neuromuscular system of the spine does not maintain a constant safety margin for stability during different tasks (Cholewicki and McGill, 1996). Perturbations to the spine may, in fact, be met in two ways (Bergmark, 1989; Stokes et al., 2000; Cholewicki et al., 2000): either through preset levels of stiffness and stability, such as those achieved through preparatory, feedforward muscle contraction (Hodges and Richardson, 1997a,b), or through an active modulation of muscle force and stiffness in response to perturbation, via afferent feedback (Cresswell et al., 1994; Thomas et al., 1998; Brown et al., 2003). By pre-activating the trunk musculature, the stiffness and stability of the spine are increased, decreasing the need for an active response to a transient perturbation (Stokes et al., 2000). Using a detailed model of the spine, and incorporating actual electromyographic (EMG) data, Cholewicki and McGill (1996) found that the stiffness and stability of the spine was increased during more demanding tasks (as dened by joint compression force), but diminished during periods of low muscular activity. In fact, the lowest levels of stability occurred when there was no demand for high muscle forces, such as in upright standing, or prior to a lifting task. Under these conditions, only low levels of trunk muscle co-activation are present (Cholewicki et al., 1997), with preset levels of stability depending predominantly on the passive structures of spine. It has been suggested that this reects a strategy used by the neuromuscular system to conserve energy, and to maintain muscle contraction below levels likely to cause muscle fatigue or pain (Cholewicki and McGill, 1996; Cholewicki et al., 1997). As a result, the margin of safety for stability in these sub-maximal situations will be narrow, and even small perturbations may require increased and well-coordinated muscle activity to maintain spine stability. Further, the neuromuscular coordination that is required to maintain joint stability appears to be quite complex. Using the elbow to represent an inverted penduluma simple model for joint stabilityStokes and Gardner-Morse (2000) noted that different strategies could be used, under vertical loading conditions, to maintain stable equilibrium. These strategies were based on variations in posture and muscle activation, each with trade-offs between stability and physiological costs. Similarly, different patterns of muscle activation have been noted during slow exionextension of the trunk, illustrating not only the potential for more than one

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motor strategy to satisfy equilibrium and stability requirements, but also the potential for error as a result of the systems complexity (Cholewicki et al., 1997). The relative contribution to spine stability provided by each trunk muscle, in fact, appears to depend not only on the direction and magnitude of trunk loading, but also on the activity of the other trunk muscles (Cholewicki and VanVliet, 2002). One possible exception to this rule is the Transversus Abdominis (TrA), which appears to be controlled independently of the other trunk muscles during the preparatory activation that precedes limb movement, and whose activation does not appear to depend on the direction of that movement (Hodges and Richardson, 1999b). Despite this apparent independent, feedforward control of the TrA, the mechanical effect that this muscle has on the stability of the spine cannot be independent from that provided by the other muscles of the trunk. As a result, faulty activation or insufcient force generation in even one muscle might lead to a transient, segmental insufciency, potentially resulting in segmental buckling, even under sub-maximal conditions. The potential for neuromuscular error with regards to spine stability may be further increased when preparatory, feedforward muscle activation cannot be used. Following a perturbation, an active response based on afferent feedback may be required from both the global and local musculature in order to maintain upright posture and spine stability. Moseley et al. (2003) have recently demonstrated that the Lumbar Multidus, an important muscle in the local muscle system of the spine, may respond differently to a perturbation when its timing cannot be anticipated. While this does not necessarily represent an abnormal nding, it may represent a potential disadvantage of the stabilizing system of the spine when feedback control must be relied upon primarily to maintain spine stability. This increased reliance on feedback control may also exist, to a certain degree, even when a perturbation is expected, but when its metrics cannot be predicted, or when its metrics are incorrectly predicted (van Dieen and de Looze, 1999). This situation of external spine loading, with unpredictable timing, magnitude, or direction, is particularly important in light of the potentially high compressive forces that may accompany the global muscle response to external perturbation (Mannion et al., 2000).

3. Buckling and tissue injury From the discussion in the previous section, it seems plausible that segmental instability and buckling of the spine can occur under sub-maximal conditions, likely as a result of faulty motor control. The next issue of

relevance to this discussion, therefore, is whether this segmental buckling can result in tissue injury. The threshold of clinically relevant mechanical tissue damage is likely to be the elastic limit at which nonreversible deformation rst occurs (Adams and Dolan, 1995). This limit can be easily reached when a tissue is loaded rapidly, such as during transient loss of segmental stability resulting in buckling. During activities that are sub-maximal with respect to muscle activation, however, one would also expect the loads on the spine to be fairly small in magnitude, possibly precluding certain forms of injury, and/or allowing some degree of buckling without a resulting injury. This may not, however, be the case. For example, McGill (2002) reports that a man lifting a 27 kg weight held in the hands, using a squat style lift, can experience extensor reaction moments in the low back of 450 Nm, and a compressive load on the lumbar spine of 7000 N. This is particularly important given that the rst sign of ligament damage in the spine can occur at bending moments of only 60 Nm, with complete failure occurring at 140185 Nm (Adams and Dolan, 1995). Based on these values, injury could result if only a fraction of the load experienced during this relatively light lift was transferred to the periarticular ligaments of the spine. Another proposed mechanism of tissue injury resulting from intersegmental buckling is that, in an effort to regain spine stability as segmental buckling is occurring, the neuromuscular system might seek to activate preferentially the small intrinsic muscles spanning the unstable joint, as recruitment of larger global muscles would increase the load on the spine, potentially magnifying the effects of the buckling (Cholewicki and McGill, 1996). Conversely, the recruitment of intrinsic muscles may be required as a result of, or in concert with, a reexive overreaction of the global trunk muscles to unexpected loading (Mannion et al., 2000). There is a limit, however, to the stability that can be achieved by activating the small, intrinsic muscles of the spine, as the load that these muscles are capable of withstanding is low compared to their global counterparts (related to the cross-sectional area of the muscles) (Bergmark, 1989). Consequently, a compensatory or reexive strategy used by the neuromuscular system to prevent buckling might itself result in muscle injury if the stresses placed on the muscles exceed the limits that these tissues are able to withstand. This type of response would t into the category of bodily response, described as one of the top 10 mechanisms of injury in workplace accidents (Liberty Mutual, 2003). Two biologically plausible mechanisms exist, therefore, to link tissue injury to segmental buckling in the spine. The rst is injury occurring as a direct result of stresses placed on the periarticular tissues during segmental buckling, which may exceed the elastic limits of these tissues even under relatively low loads. The

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second is a result of the neuromuscular systems attempt to stabilize a segment by activating the small, intersegmental muscles of the spine, potentially leading to excessive stresses in these muscles. While direct evidence of these injuries may not exist in the literature, possibly due to the fact that a diagnosis of soft tissue injury in the back is rarely conrmed with diagnostic imaging, a clinical diagnosis of muscle strain, or joint sprain, is common in patients presenting with LBP (Micheli and Wood, 1995).

4. Tissue injury and sudden onset LBP The nal link in the chain of events described in the hypothesis above is the relationship between tissue injury and the sudden onset of LBP. As this topic has been explored extensively in the literature, it will only be briey addressed here. For example, Bogduk (1983) provides a brief review of the nerve supply to the lumbar spine, establishing a list of possible sources of primary LBP. Free nerve endings, which act as nociceptors, are found in essentially all of the spine structures that are innervated, including the muscles, the ligaments, the facet joint capsules, and the outer layers of the annulus brosis. As such, damage to any of these structures can result in an almost instantaneous onset of pain due to mechanical irritation of these free nerve endings. Further, a more gradual onset of pain, over the course of several hours, can occur as a result of the inammatory process that accompanies tissue injury (Evans, 1980).

5. Predisposing factors to spinal buckling and tissue injury While anecdotal evidence supports the temporal relationship between sudden onset LBP and submaximal activities, and coherent evidence appears to support the biological plausibility of sudden onset LBP resulting from segmental buckling and tissue injury, the lack of consistency in this injury mechanism can affect the establishment of a causal relationship. Evidently, intersegmental spine buckling does not occur every time an individual engages in activities involving sub-maximal loading and trunk muscle activation. As such, the causal relationship between this type of activity and spine buckling must involve other predisposing factors. As discussed above, intersegmental buckling during sub-maximal activity is likely the result of some error in neuromuscular control, failing either to provide adequate pre-stability to the segment, or to respond appropriately with muscle activation to a perturbation. The rst possibility, inadequate pre-stability, would point to an error in the feedforward control of the spine

musculature, while the second would indicate some error in muscle activation modulated by afferent feedback. Cognitive factors, uniformly described by Horak (1996) as central set, are likely to affect both of these mechanisms for neuromuscular control of spine stability. These may involve issues such as intent, concentration and fatigue, prior experience with a task, or environmental conditions and distractions, each of which has been shown to inuence the neuromuscular response to a given task. Errors in feedforward control may also occur at a subconscious level. Abnormalities in the feedforward activation of the TrA, apparently independent of the cognitive factors described above, have been identied in subjects with LBP (Hodges and Richardson, 1996, 1999a). It is unclear, however, if these abnormalities are a cause or consequence of the LBP. What is clear, is that a change in the feedforward activation of the trunk musculature can change the pre-stability of the spine, potentially leading to increased reliance on afferent feedback to maintain spine stability. Given the response time of the trunk muscles to perturbation (Moseley et al., 2003) and the necessary electromechanical delay prior to force generation, it would appear that a certain degree of feedforward control must be necessary to avoid injury above a certain threshold of loading and perturbation velocity. Errors in feedback modulation of spine stability can also occur for a variety of reasons. The ligamentomuscular stabilizing system of the spine (Solomonow et al., 1998, 1999) describes a means by which somatosensory feedback from the spinal ligaments helps to monitor segmental movement and activate the paraspinal musculature to maintain and/or restore stability. It has, in fact, been suggested that this modulation of muscle activity may be the key role of the ligamentous complex of the spine (Solomonow et al., 1998, 1999), which provides little stability in the absence of the musculature (Panjabi et al., 1989; Cholewicki and McGill, 1996). Low threshold mechanoreceptors in the ligaments likely inuence muscle activity via the fusimotor system, while high threshold receptors may exert effects directly onto the alpha motorneurons (Dyhre-Poulson and Krogsgaard, 2000). In the spine, such connections exist from mechanoreceptors in the various spinal ligaments, and likely from the discs and facet joint capsules, to the Multidus, and possibly other muscles (Solomonow et al., 1998, 1999). Solomonow et al. (1999) have demonstrated that laxity in the supraspinal ligament of cats, secondary to cyclic loading, leads to a decrease in the periarticular muscle activation normally associated with the loading of this structure. As such, activities leading to viscoelastic creep in the spinal ligaments, such as prolonged or cyclic loading, may decrease the effectiveness of this neuromuscular stabilizing mechanism, predisposing an individual to

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segmental instability, particularly during activities in which the pre-stability provided by the periarticular musculature is low (i.e. sub-maximal activities such as picking up a pencil from the oor). This becomes all the more important, given that prolonged loading of spinal ligaments decreases their resistance to loading by 42% in just 5 min, and 67% in 1 h (Adams and Dolan, 1995). As a result, intersegmental buckling preceded by a prolonged exed posture (for example, in subjects who sit all day at work), not only decreases the likelihood of an appropriate, feedback modulated muscle response, but also substantially increases the likelihood of ligament injury. Several other factors can also affect the spine muscles directly. Muscle fatigue, in addition to affecting muscle force and various aspects of the myoelectric signal (e.g. Roy et al., 1989), has also been shown to have a deleterious effect on proprioception (Taimela et al., 1999), likely due to the same factors that affect the ability of the muscle to generate mechanical force and stiffness when fatigued. Vibration (as experienced when operating heavy machinery, driving, etc.), in addition to its mechanical effects on tissue (i.e. cyclic loading), will also affect the function of dynamic muscle spindle la afferents (Cordo et al., 1998), with this effect persisting for some time following prolonged vibration (Rogers et al., 1985; Thompson and Belanger, 2002). A exed, or horizontal orientation of the trunk, in addition to altering the normal mechanical alignment of the spine, may also decrease spine proprioceptive acuity to some degree (Jakobs et al., 1985; Preuss et al., 2003), possibly as a result of altered feedback from mechanoreceptors in the load-bearing structures of the spine. This is all the more relevant, given that injuries during sub-maximal activities often occur in exed postures. Finally, it is possible that an individual may possess certain traits that might predispose them to neuromuscular insufciencies with respect to spine stability. The interdependence of activity between individual trunk muscles (Cholewicki and VanVliet, 2002) leaves open the potential for inefcient coordination patterns of activation due to inappropriate central commands, structural or muscular asymmetries, articular tropisms, etc. These same traits, or sequelae from previous injuries, such as untreated local muscle atrophy (Hides et al., 1994, 1996), may also predispose certain individuals to developing chronic pain following an initial incident of LBP. Such subjects have been observed to have poorer postural control in the lumbar spine (Radebold et al., 2001), and longer trunk muscle reaction times in response to perturbation (Radebold et al., 2000, 2001), both of which are indicative of compromised neuromuscular control. Once again, however, it is unclear whether this compromised control is a cause or a consequence of the LBP.

6. Conclusion Based on the factors discussed above, it is reasonable to conclude that there exists a strong basis for the hypothesis that episodes of sudden onset LBP can result from tissue damage caused by spinal buckling during sub-maximal activities. While anecdotal evidence supports the existence of a temporal relationship, physiology and modelling studies support its biological plausibility, based on both the mechanics of the system and its neuromuscular behaviour. In order to explain the low consistency and doseresponse relationship, however, it is necessary to consider several predisposing factors, both constant and situation-dependent, which might contribute to the occurrence of segmental spinal buckling during sub-maximal activities. When designing treatment or preventative programs for LBP, therefore, it is essential to address not only the issue of spine stability and neuromuscular control, but also the possible factors that might predispose the individual to episodes of transient segmental instability.

Acknowledgements R. Preuss receives nancial support from the Fonds en sante du Que bec (FRSQ), the de la recherche Canadian Institutes of Health Research and from the Richard H. Tomlinson Fellowship Endowment of McGill University. J. Fung is a chercheur-boursier of the FRSQ and a William Dawson Scholar of McGill University. We thank Dr. Ian Stokes for his guidance and valuable feedback.

References
Adams M, Dolan P. Recent advances in lumbar spinal mechanics and their clinical signicance. Clinical Biomechanics 1995;10:319. Bergmark A. Stability of the lumbar spine: a study in mechanical engineering. Acta Orthopaedica Scandinavica Supplemental 1989;230:154. Bogduk N. The innervation of the lumbar spine. Spine 1983;8:28693. Brown S, Haumann M, Potvin J. The responses of leg and trunk muscles to sudden unloading of the hands: implications for balance and spine stability. Clinical Biomechanics 2003;18:81220. Cholewicki J, McGill S. Relationship between muscle force and stiffness in the whole mammalian muscle: a simulation study. Journal of Biomechanical Engineering 1995;117:33942. Cholewicki J, McGill S. Mechanical stability of the in vivo lumbar spine: implications for injury and chronic low back pain. Clinical Biomechanics 1996;11:115. Cholewicki J, VanVliet J. Relative contribution of trunk muscles to the stability of the lumbar spine during isometric exertions. Clinical Biomechanics 2002;17:99105. Cholewicki J, Panjabi M, Khachatryan A. Stabilizing function of trunk exor-extensor muscles around a neutral spine posture. Spine 1997;22:220712.

ARTICLE IN PRESS
20 R. Preuss, J. Fung / Manual Therapy 10 (2005) 1420 McGill S, Cholewicki J. Biomechanical basis for stability: an explanation to enhance clinical utility. Journal of Orthopaedic and Sports Physical Therapy 2001;31:96100. Micheli L, Wood R. Back pain in young athletes: signicant differences from adults in causes and patterns. Archives of Pediatrics and Adolescent Medicine 1995;149:158. Moseley G, Hodges P, Gandevia S. External perturbation of the trunk in standing humans differentially activates components of the medial back muscles. Journal of Physiology 2003;547.2:5817. Panjabi M, Abumi K, Duranceau J, Oxland T. Spinal stability and intersegmental muscle forces: a biomechanical model. Spine 1989;14:1949. Patwardhan A, Havey R, Meade K, Lee B, Dunlap B. A follower load increases the load-carrying capacity of the lumbar spine in compression. Spine 1999;24:10039. Patwardhan A, Meade K, Lee B. A frontal plane model of the lumbar spine subjected to a follower load: implications for the role of muscles. Journal of Biomechanical Engineering 2001;123:2127. Preuss R, Grenier S, McGill S. The effect of test position on lumbar spine position sense. Journal of Orthopaedic and Sports Physical Therapy 2003;33:738. Radebold A, Cholewicki J, Panjabi M, Patel T. Muscle response pattern to sudden trunk loading in healthy individuals and in patients with chronic low back pain. Spine 2000;25:94754. Radebold A, Cholewicki J, Polzhofer G, Greene H. Impaired postural control in the lumbar spine is associated with delayed muscle response times in patients with chronic idiopathic low back pain. Spine 2001;26:72430. Rogers D, Bendrups A, Lewis M. Disturbed proprioception following a period of muscle vibration in humans. Neuroscience Letters 1985;57:14752. Roy S, De Luca C, Casavant D. Lumbar muscle fatigue and chronic lower back pain. Spine 1989;14:9921001. Solomonow M, Zhou B, Baratta R, Lu Y, Harris M. Biomechanics of increased exposure to lumbar injury caused by cyclic loading: part 1. Loss of reexive muscular stabilization. Spine 1999;24: 242634. Solomonow M, Zhou B, Harris M, Lu Y, Baratta R. The ligamentomuscular stabilizing system of the spine. Spine 1998;23:255262. Stokes I, Gardner-Morse M. Strategies used to stabilize the elbow joint challenged by inverted pendulum loading. Journal of Biomechanics 2000;33:73743. Stokes I, Gardner-Morse M, Henry S, Badger G. Decrease in trunk muscular response to perturbation with preactivation of lumbar spinal musculature. Spine 2000;25:195764. Taimela S, Kankaanpaa M, Luoto S. The effect of lumbar fatigue on the ability to sense a change in lumbar position: a controlled study. Spine 1999;24:13227. Thomas J, Lavender S, Corcos D, Andersson G. Trunk kinematics and trunk muscle activity during rapidly applied load. Journal of Electromyography and Kinesiology 1998;8:21525. Thompson C, Belanger M. Effects of vibration in inline skating on the Hoffman reex, force and proprioception. Medicine & Science in Sports & Exercise 2002;34:203744. van Dieen J, de Looze M. Directionality of anticipatory activation of trunk muscles in a lifting task depends on load knowledge. Experimental Brain Research 1999;128:397404. Cholewicki J, Simons A, Radebold A. Effects of external trunk loads on lumbar spine stability. Journal of Biomechanics 2000;33:137785. Cordo P, Burke D, Gandevia S, Hales J. Mechanical neural and perceptual effects of tendon vibration. In: Latash M, editor. Progress in Motor Control: Vol. 1. Human Kinetics, New York, 1998. p. 15171. Cresswell A, Oddsson L, Thorstensson A. The inuence of sudden perturbations on trunk muscle activity and intra-abdominal pressure while standing. Experimental Brain Research 1994;98:33641. Crisco J, Panjabi M. The intersegmental and multisegmental muscles of the lumbar spine: a biomechanical model comparing lateral stabilizing potential. Spine 1991;16:7939. Crisco J, Panjabi M. Euler stability of the human ligamentous lumbar spine. Part 2: Experiment. Clinical Biomechanics 1992;7:2732. Dyhre-Poulson P, Krogsgaard R. Muscular reexes elicited by electrical stimulation of the anterior cruciate ligament in humans. Journal of Applied Physiology 2000;89:21915. Evans P. The healing process at the cellular level: a review. Physiotherapy 1980;66:2569. Gardner-Morse M, Stokes I, Laible J. Role of muscles in lumbar spine stability in maximum extension efforts. Journal of Orthopaedic Research 1995;13:8028. Hides J, Richardson C, Jull G. Multidus muscle recovery is not automatic after resolution of acute, rst-episode low back pain. Spine 1996;21:27639. Hides J, Stokes M, Saide M, Jull G, Cooper D. Evidence of lumbar multidus muscle wasting ipsilateral to symptoms in patients with acute/subacute low back pain. Spine 1994;19:16572. Hodges P, Richardson C. Inefcient muscular stabilization of the lumbar spine associated with low back pain: a motor control evaluation of transversus abdominis. Spine 1996;21:264050. Hodges P, Richardson C. Contraction of the abdominal muscles associated with movement of the lower limb. Physical Therapy 1997a;77:13244. Hodges P, Richardson C. Feedforward contraction of transversus abdominis in not inuenced by the direction of arm movement. Experimental Brain Research 1997b;114:36270. Hodges P, Richardson C. Altered trunk muscle recruitment in people with low back pain with upper limb movement at different speeds. Archives of Physical Medicine and Rehabilitation 1999a;80: 100512. Hodges P, Richardson C. Transversus abdominis and the supercial abdominal muscles are controlled independently in a postural task. Neuroscience Letters 1999b;265:914. Horak F. Adaptation of automatic postural responses. In: Bloedel J, Ebner T, Wise S, editors. The acquisition of motor behavior in vertebrates. Cambridge: The MIT Press; 1996. p. 5785. Jakobs T, Miller J, Schultz A. Trunk position sense in the frontal plane. Experimental Neurology 1985;90:12938. Liberty Mutual: Workplace Safety Index. Online reference, 2003 http://www.eorm.com/ezine/pp5/WorkPlaceSafetyIndex2003.pdf Mannion A, Adams M, Dolan P. Sudden and unexpected loading generates high forces on the lumbar spine. Spine 2000;25:84252. McGill S. Low back disorders: evidence-based practice and rehabilitation. Windsor: Human Kinetics; 2002.