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Clinical Review: Focused
The Role of the Lumbar Multifidus in Chronic Low
Back Pain: A Review
Michael D. Freeman, PhD, MPH, DC, Mark A. Woodham, DC,
Andrew W. Woodham, BA
Low back pain (LBP), a highly prevalent problem in society, is often a recurrent condition.
Recent advances in the understanding of the biomechanics of LBP have highlighted the
importance of muscular stabilization of the “neutral zone” range of motion in the low back.
The lumbar multifidus muscles (LMM) are important stabilizers of this neutral zone, and
dysfunction in these muscles is strongly associated with LBP. The dysfunction is a result of
pain inhibition from the spine, and it tends to continue even after the pain has resolved,
likely contributing to the high recurrence rate of LBP. Persisting LMM dysfunction is
identified by atrophic replacement of multifidus muscle with fat, a condition that is best
seen on magnetic resonance imaging. Muscle training directed at teaching patients to
activate their LMM is an important feature of any clinical approach to the LBP patient with
demonstrated LMM dysfunction or atrophy.
PM R 2010;2:142-146
INTRODUCTION
Low back pain (LBP) is a highly prevalent problem in society; approximately 60% to 80% of
the population will experience an episode of LBP during their lifetime, and 60% to 86% of
these people will have more than one episode of LBP [1,2]. A relatively recent shift in the
view of LBP has gone from classifying it as a self-limited acute condition to a recurrent
syndrome [3]. The purpose of this review is to discuss the role of the lumbar multifidus
muscles (LMM) in recurrent LBP, as well as to discuss literature-based clinical approaches to
assessment and treatment of multifidus dysfunction.
Spinal stabilization therapy has been observed to be more effective over time in treating
LBP than minimal intervention and exercise therapy alone, and has also been observed to
reduce pain, disability, and medication intake, as well as recurrence rates [4,5].Asa
consequence, treatment focus has shifted to reactivation and strengthening of the smaller
muscles of the spine to improve long-term stabilization of the vertebral column.
Biomechanical research has increased the understanding of mechanisms of low back
injury and pain, specifically regarding the ability to stabilize the “neutral zone” of the lumbar
spine with tonic muscle control. Panjabi [6] has described the neutral zone as the part of the
range of intervertebral motion, measured from the neutral position, in which spinal motion
can occur with minimal nonmuscular passive resistance from the spine. Suni and colleagues
[2] described a randomized controlled trial of a neuromuscular training program directed at
neutral zone stabilization on a population of patients with recent back injury. These authors
demonstrated a significant decrease in the intensity of LBP in the treatment group that was
not seen in the control group, and concluded that control of the lumbar neutral zone was an
important component of LBP and disability prevention.
MULTIFIDUS FUNCTION
It is well established that the LMM are important stabilizers of the lumbar neutral zone; Wilke et
al [7] found that the actions of the multifidi account for more than two thirds of the stiffness of
the spine when in the neutral zone. In comparison with all lumbar muscles, the LMM are short
and stout, with a high cross-sectional area (CSA) and short muscle fibers. Furthermore, these
M.D.F. Department of Public Health and Pre-
ventive Medicine, Oregon Health and Science
University School of Medicine 1234 SW 18
th
Ave, Portland, OR 97205. Address correspon-
dence to: M.F.; e-mail: forensictrauma@
gmail.com
Disclosure: nothing to disclose
M.A.W. Private practice, Tacoma, WA
Disclosure: nothing to disclose
A.W.W. Department of Genetic, Molecular,
and Cellular Biology, University of Southern
California, Los Angeles, CA
Disclosure: nothing to disclose
Disclosure Key can be found on the Table of
Contents and at www.pmrjournal.org
Submitted for publication May 15, 2009;
accepted November 19.
PM&R © 2010 by the American Academy of Physical Medicine and Rehabilitation
1934-1482/10/$36.00 Vol. 2, 142-146, February 2010
Printed in U.S.A. DOI: 10.1016/j.pmrj.2009.11.006
142
authors found that at the foundation of this high CSA was a high
mass, which allows for packing of a large number of muscle
fibers into relatively small space. This morphology allows the
LMM to produce very large forces over a small operating range,
and makes the LMM ideally suited for stability as opposed to
motion [8,9]. Functionally, the LMM are divided into deep and
superficial fibers, with deep fibers spanning 2 vertebral seg-
ments and functioning tonically, and the superficial fibers span-
ning 3 to 5 levels and functioning phasically [10,11]. This
arrangement makes the deep fibers of the LMM anatomically
and biomechanically well suited for stabilization.
MULTIFIDUS ATROPHY AND LOW BACK
PAIN
A number of prior investigations have described the LMM
atrophy and replacement by fat after low back injury, a patho-
logic process that is closely correlated with LBP. Kjaer and
colleagues [12] evaluated the lumbar magnetic resonance imag-
ing (MRI) results for 412 adult and 442 adolescent subjects in a
cross-sectional study of LMM atrophy. These authors catego-
rized the degree of observed atrophy in the LMM as none, slight,
and severe, and correlated the findings with complaints of LBP.
They found that fat infiltrations of the LMM were strongly
associated with LBP in adults, and that the association was
independent of body mass index (BMI).
Kader et al [13] performed a retrospective study of 78
patients with LBP and either with or without leg pain. The
authors assessed the correlation between MRI changes in the
LMM and leg pain. It was reported that LMM atrophy was
present in 80% of the patients with LBP and that there was a
significant correlation between LMM atrophy and referred
leg pain. The authors theorized that LMM atrophy may be
caused by dorsal ramus syndrome, which has been described
as LBP with referred leg pain, produced by irritation of
anatomic structures supplied by the dorsal ramus nerve, ie,
the facet joints and LMM. The authors further concluded that
abnormalities of the LMM may explain referred leg pain in
the absence of other MRI abnormalities.
Hides et al [14] described a study of 26 subjects with unilat-
eral LBP, some with referred lower extremity pain. The authors
assessed LMM atrophy among the subjects using ultrasound
imaging, noting marked asymmetry of the LMM that was local-
ized to a single vertebral level in most cases. The authors noted
that the level of LMM asymmetry correlated with the neurologic
level of the symptoms in 24 of the 26 subjects in the study.
IMAGING OF MULTIFIDUS ATROPHY
There are numerous publications describing the morpho-
logic assessment of the LMM using MRI, computed tomog-
raphy (CT), and ultrasound (US).
Kader et al [13] used MRI in evaluating LMM atrophy,
which they defined as muscular replacement with fat and
fibrous tissues. The authors established a ranked grading
scale for LMM atrophy consisting of mild, moderate, and
severe, corresponding to atrophy in less than 10% of CSA of
the LMM, more than 10% and less than 50%, and more than
50%, respectively (Figures 1-3). Two readers assessed the
degree of LMM atrophy among the subjects, with good inter-
observer agreement noted.
Kjaer et al [12] described the blinded assessment of LMM
atrophy in 854 MRI scans of adults and adolescents using a
grading scale similar to that used by Kader et al [13]. The
authors found good intraobserver and interobserver agree-
ment among the readers for the adult group. The authors
noted that fatty infiltration after LMM atrophy could be
measured in a noninvasive manner using MRI.
Barker et al [15] performed MRI on 50 patients presenting
to a back pain clinic with unilateral persisting LBP. The
authors measured the CSAs of the left and right psoas and
LMM and correlated their findings with the distribution and
duration of symptoms among the subjects. A significant
positive correlation between the side of LMM atrophy and the
distribution of the LBP was found, as well as between the
degree of atrophy and the duration of the symptoms.
CT has been evaluated as a relatively lower-cost and more
accessible alternative to MRI for assessment of LMM atrophy.
Danneels et al [16] described a study of CT assessment of 32 LBP
patients and 23 active volunteers. The study design included CT
of the CSA of the LMM at 3 levels. The authors found macro-
scopic atrophic changes in the LMM in 80% of the patients with
LBP, and that the atrophy in the LMM at the lowest levels of the
lumbar spine correlated significantly with LBP status. The au-
thors concluded that the most important finding from their
study was the finding of a significant correlation between LMM
atrophy and radicular and nonradicular leg pain.
The utility and reliability of US relative to MRI scanning,
have also been evaluated as a means of assessing LMM CSA.
Hides et al [17] compared the CSA assessment of the LMM
among healthy young adults using MRI and US, following a
strict protocol The authors determined that LMM CSA could
be measured as accurately with US as with MRI, although
they did not assess the ability of US to discriminate the degree
of atrophy in the LMM.
REFLEX INHIBITION MODEL OF LOCALIZED
MULTIFIDUS ATROPHY
Macintosh et al [11] described the morphology of the LMM
by means of the dissection of 12 adult cadaver spines. In
contrast to previous determinations that each LMM is inner-
vated by a number of spinal nerves, these authors found that
the LMM is divided into 5 distinct myotomes that are each
innervated by a single spinal segment. They found that all
muscle fibers attaching to the spinous process or lamina of a
particular vertebra are segmentally innervated by the same
nerve; the medial branch of the dorsal ramus that originates
143PM&R Vol. 2, Iss. 2, 2010
inferior to the respective vertebra (Figure 4). Thus, the mus-
cle that moves a given spinal segment is supplied by the nerve
for that segment. The authors postulated that from an ana-
tomic perspective, the shared innervation of the zygapophy-
seal joints means that pain emanating from these joints could
result in a reflex inhibition of the LMM at the same level.
Indahl et al [18] noted that the injection of saline into the
zygapophyseal joint in a porcine model resulted in decreased
activity of the multifidus muscle. They concluded that the
effect of the injection was to activate a stretch reflex in the
joint capsule, which in turn excited inhibitory interneurons
in the spinal cord, which in turn inhibited the motor neurons
and decreased the muscle response. The authors inferred that
LMM atrophy seen in the human spine is a result of reflex
inhibition caused by afferent feedback from the zygapophy-
seal joint, which in turn impedes the voluntary activation of
the LMM. The authors pointed to their results as evidence
that multifidus atrophy seen in back pain patients is more
likely a result of dysfunction rather than disuse. The authors
postulated that inhibitory discharges from the zygapophyseal
joints may explain the efficacy of manual medical approaches
to back pain such as manipulation and mobilization directed
at the zygapophyseal joints.
Hodges et al [19] demonstrated, also in a porcine model,
the rapid onset of LMM atrophy within 3 days after an
experimentally induced nerve root injury. After transection
of the medial branch of the L3 nerve root, the ipsilateral LMM
CSA adjacent to the L4, L5, and L6 spinous processes was
reduced by 13%, 20%, and 12%, respectively, by 72 hours
after injury. The changes were isolated to the side of injury;
there were no differences in the CSA or muscular activity
levels of the contralateral LMM, as determined by US assess-
ment. The authors also investigated the changes in the LMM
after experimentally induced disk injury in the porcine
model. A stab wound was introduced to the left anterolateral
aspect of the L3-4 intervertebral disk, and this was followed
by focal atrophy and a reduction of the CSA of the left LMM
by 17%. The authors opined that it was unlikely that the
injury resulted from LMM denervation (owing to nerve root
injury) as the atrophy was only at the level of the disk,
whereas single nerve roots innervate three levels of LMM. The
authors noted that the posttraumatic changes in the LMM
noted in their study were undoubtedly attributable to a
reduction in neural drive to the muscle, but that the mecha-
nism that accounted for the reduction was unclear.
Hides et al [20] provided further evidence that the pattern
of LMM atrophy is local rather than general in a study that
compared multifidus size and bilateral symmetry between
chronic LBP patients and healthy asymptomatic subjects. The
authors reported that at the L4 and L5 levels, asymptomatic
subjects were found to have significantly larger multifidus
muscles in comparison with chronic LBP patients. They also
found that the greatest asymmetry was seen at the L5 verte-
bral level in patients with unilateral pain presentations. The
authors concluded that their findings support a clinical ap-
proach to LBP that uses exercise therapy that focuses on
localized muscle impairments.
Wallwork et al [21] demonstrated that LMM atrophy was
associated with a reduction in the ability to voluntarily con-
tract the muscle. The authors used diagnostic US to measure
contractions of the LMM by comparing the thickness of the
muscle at rest to when it was contracted. Study subjects with
chronic LBP and LMM atrophy demonstrated significantly
decreased ability to perform isometric contractions of their
LMM. These study results reinforced the findings of prior
authors and emphasized the clinical perspective that rehabil-
itation in LBP patients may need to target localized impair-
ments in motor control.
MULTIFIDUS ATROPHY TREATMENT
Danneels et al [4] assessed the efficacy of 3 different treat-
ment modalities on multifidus CSA in chronic LBP patients.
A group of 59 patients were randomly allocated to one of 3
programs: stabilization training, stabilization training com-
bined with dynamic resistance, and stabilization training
combined with dynamic-static resistance. Using CT scan-
ning, LMM CSAs were measured before and after 10 weeks of
training. The CSA of the LMM muscle was significantly
increased at all vertebral levels only in the dynamic-static
resistance training group. The authors concluded that the
static holding component between concentric and eccentric
contraction phases was critical to induction of muscle re-
growth.
A randomized controlled trial performed by Van et al [22]
used real-time visual feedback by means of US to improve the
isometric contraction capability of the LMM in healthy sub-
Figure 1. Mild multifidus muscle atrophy, per Kader et al [13]
grading criteria (less than 10% of CSA of muscle replaced with
fat).
144 Freeman et al ROLE OF THE LUMBAR MULTIFIDUS IN CHRONIC LOW BACK PAIN
jects. The authors applied motor learning principles to train
the subjects in voluntary contraction of the multifidus and
gave verbal feedback to one group, and verbal and visual
feedback to the other. They found that providing the subjects
with visual feedback of their performance resulted in better
quality muscle contraction of the LMM as well as better
memory of how to contract the multifidi after reassessment a
week later.
Sung [23] evaluated the question of whether an exercise
program designed to increase the ability to contract the LMM
improves functional status or reduces LBP. This author de-
scribed a short-term cohort study that assessed the effect of a
4-week spinal stabilization exercise program in a group of
LBP patients, reporting a significant improvement in LMM
function, as well as a reduction in LBP disability.
Hides et al [5] described the effects of stabilization training
on LMM CSA among elite athletes (cricketers) with LBP,
concluding that LMM atrophy can exist in highly active, elite
athletes. The authors demonstrated that the stabilization
training increased the CSA of the LMM, and that the training
was associated with a decrease in symptoms of LBP. Their
results showed that specific training that aims at activation of
the LMM is associated with both an increase in functional
status and a reduction in LBP.
In an earlier study by Hides et al [24], the authors dem-
onstrated that LMM function recovery is not necessarily
associated with the resolution of painful symptoms in LBP
patients. The authors studied a group of 39 patients with a
first episode of acute unilateral LBP and corresponding uni-
lateral segmental inhibition of the LMM. The patients were
randomly allocated to 2 groups, only one of which performed
specific exercises designed to reactivate the LMM through
facilitating an isometric contraction of these muscles. The
group that did not perform the exercises had decreased LMM
size at a 10-week follow-up examination even though they
had resumed normal levels of activity and had a remission of
painful symptoms, whereas the group that performed the
isometric contractions showed more rapid and complete
LMM recovery. The authors suggested that the continued
dysfunction of the LMM in such patients may be one reason
for the high recurrence rates of LBP after an initial episode.
MacDonald et al [25] assessed muscular control of long
and short LMM fibers in 15 recurrent LBP patients and 19
control subjects. The authors used EMG to determine
whether LMM control at the L5 level differed between the
groups. They found that there were changes in motor control
of the LMM among the patients that primarily affected the
shorter fibers, and that these changes were greater on the
previously painful side of the low back. These findings sup-
port the use of a specifically designed stabilization exercise
program directed toward the LMM and specifically the
deeper shorter fibers that serve to stabilize the spine. The
authors concluded that the abnormal pattern of muscle con-
trol they observed may leave the spine vulnerable to reinjury,
thus predisposing the spine to recurrent episodes of LBP. The
authors postulated that the observed motor control problem
among the recurrent LBP patients implied that pain and
functional performance should not be the only outcome
measures after an acute episode of LBP.
CONCLUSIONS
The LMM are important stabilizers of the lumbar spine neu-
tral zone, and atrophy of the muscle decreases the ability to
Figure 2. Moderate multifidus muscle atrophy, per Kader et al
[13] grading criteria (more than 10% but less than 50% of CSA
of muscle replaced with fat).
Figure 3. Severe multifidus atrophy, per Kader et al [13] grad-
ing criteria (more than 50% of CSA of muscle replaced with
fat).
145PM&R Vol. 2, Iss. 2, 2010
control the neutral zone and is strongly associated with LBP.
This atrophy appears to help perpetuate an inhibitory feed-
back loop that begins with pain in the spine, possibly stem-
ming from the intervertebral disks or zygapophyseal joints,
followed by reflex inhibition of the multifidus, and then
atrophy and fatty replacement of the muscle. Amelioration of
the LBP does not necessarily result in resumption of normal
LMM function, and decreased LMM function is likely impli-
cated in recurrent LBP. Muscle training directed at teaching
patients to activate their LMM is an important feature of any
clinical approach to the patient with LBP who demonstrates
LMM dysfunction or atrophy.
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Transverse Process
Spinous Process
Intervertebral Disc
Facet Joint
Medial Branch of
The Dorsal Ramus
Multifidus Muscle
Figure 4. Schematic representation of orientation and inner-
vation of a lumbar multifidus muscle.
146 Freeman et al ROLE OF THE LUMBAR MULTIFIDUS IN CHRONIC LOW BACK PAIN