ARTICLE IN PRESS

Manual Therapy 10 (2005) 14–20

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. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

2. Spine stability and buckling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

3. Buckling and tissue injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

4. Tissue injury and sudden onset LBP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

5. Predisposing factors to spinal buckling and tissue injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

6. 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
 ARTICLE IN PRESS
R. Preuss, J. Fung / Manual Therapy 10 (2005) 14–20
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 buck-
ling, tissue damage, and sudden onset LBP under sub-
maximal 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 ‘‘dose–response’’ 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 findings from
numerous experimental and modelling studies.
Addressing the temporal relationship between sub-
maximal activities and sudden onset LBP is particularly
difficult, as there may not be a simple cause–effect
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 floor.
Further, these authors hypothesize that injuries occur-
ring during sub-maximal tasks are due to a transient
segmental buckling (i.e. the segment will briefly exceed
its maximum safe range of motion), similar to a
mechanism that has been observed using video fluoro-
scopy under more strenuous conditions (Cholewicki and
McGill, 1996). They suggest that this segmental buck-
ling 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, how-
ever, that this behaviour was observed under very high
loading conditions, and as such remains a hypothetical
15
mechanism to explain onset of LBP under sub-maximal
conditions. This hypothesis, and the question of how
this buckling behaviour might occur during sub-max-
imal 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 first 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 ‘‘dose–response’’ relationship for
this hypothetical injury sequence. To do this, factors
that might predispose an individual to spinal buckling,
tissue injury and LBP will be briefly 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, how-
ever, 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 periarti-
cular 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 ship’s
mast, however, the spine is made up of several individual
 ARTICLE IN PRESS
16 R. Preuss, J. Fung / Manual Therapy 10 (2005) 14–20
segments. To maintain a uniform modulus of elasticity
for the spine, therefore, muscles with direct attachments
to individual vertebrae, such as Multifidus, 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 briefly 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 spine’s 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, interseg-
mental 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 physio-
logical 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 flexion 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 Richard-
son, 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 defined
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 (Cho-
lewicki et al., 1997), with preset levels of stability
depending predominantly on the passive structures of
spine. It has been suggested that this reflects 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—
pendulum—a simple model for joint stability—Stokes
and Gardner-Morse (2000) noted that different strate-
gies 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 flexion–extension of the trunk,
illustrating not only the potential for more than one
 ARTICLE IN PRESS
R. Preuss, J. Fung / Manual Therapy 10 (2005) 14–20
motor strategy to satisfy equilibrium and stability
requirements, but also the potential for error as a result
of the system’s 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 insufficient
force generation in even one muscle might lead to a
transient, segmental insufficiency, potentially resulting
in segmental buckling, even under sub-maximal condi-
tions.
The potential for neuromuscular error with regards to
spine stability may be further increased when prepara-
tory, 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 Multifidus, 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 finding, 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 in-
creased 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 parti-
cularly 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
17
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 non-
reversible deformation first 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 activ-
ities 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 first sign of
ligament damage in the spine can occur at bending
moments of only 60 Nm, with complete failure occurring
at 140–185 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 result-
ing 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 reflexive 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 reflexive
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 fit 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, there-
fore, to link tissue injury to segmental buckling in the
spine. The first 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
 ARTICLE IN PRESS
18 R. Preuss, J. Fung / Manual Therapy 10 (2005) 14–20
second is a result of the neuromuscular system’s attempt
to stabilize a segment by activating the small, interseg-
mental 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 confirmed 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 final 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
briefly 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
fibrosis. 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
inflammatory 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 sub-
maximal 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-max-
imal 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 ade-
quate pre-stability to the segment, or to respond
appropriately with muscle activation to a perturbation.
The first 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 feed-
back. Cognitive factors, uniformly described by Horak
(1996) as ‘‘central set’’, are likely to affect both of these
mechanisms for neuromuscular control of spine stabi-
lity. These may involve issues such as intent, concentra-
tion and fatigue, prior experience with a task, or
environmental conditions and distractions, each of
which has been shown to influence 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 identified
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 ligamento-
muscular stabilizing system of the spine (Solomonow et
al., 1998, 1999) describes a means by which somatosen-
sory feedback from the spinal ligaments helps to
monitor segmental movement and activate the para-
spinal 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 influence 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 Multifidus, and possibly other
muscles (Solomonow et al., 1998, 1999). Solomonow et
al. (1999) have demonstrated that laxity in the suprasp-
inal 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
 ARTICLE IN PRESS
R. Preuss, J. Fung / Manual Therapy 10 (2005) 14–20
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 floor). 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 flexed 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 flexed, 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 flexed postures.
Finally, it is possible that an individual may possess
certain traits that might predispose them to neuromus-
cular insufficiencies with respect to spine stability. The
interdependence of activity between individual trunk
muscles (Cholewicki and VanVliet, 2002) leaves open
the potential for inefficient 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, how-
ever, it is unclear whether this compromised control is a
cause or a consequence of the LBP.
19
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 sup-
ports the existence of a temporal relationship, physiol-
ogy 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 ‘‘dose–response’’ 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 financial support from the Fonds
de la recherché en santé du Québec (FRSQ), the
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.
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