European Spine Journal 2018 (Jan); 27 (1): 145153 ~ FULL TEXT
Alan Breen, Alexander Breen
Faculty of Science and Technology,
Poole, BH12 5BB, UK.
PURPOSE: Evidence of intervertebral mechanical markers in chronic, non-specific low back pain (CNSLBP) is lacking. This research used dynamic fluoroscopic studies to compare intervertebral angular motion sharing inequality and variability (MSI and MSV) during continuous lumbar motion in CNSLBP patients and controls. Passive recumbent and active standing protocols were used and the relationships of these variables to age and disc degeneration were assessed.
METHODS: Twenty patients with CNSLBP and 20 matched controls received quantitative fluoroscopic lumbar spine examinations using a standardised protocol for data collection and image analysis. Composite disc degeneration (CDD) scores comprising the sum of Kellgren and Lawrence grades from L2S1 were obtained. Indices of intervertebral motion sharing inequality (MSI) and variability (MSV) were derived and expressed in units of proportion of lumbar range of motion from outward and return motion sequences during lying (passive) and standing (active) lumbar bending and compared between patients and controls. Relationships between MSI, MSV, age and CDD were assessed by linear correlation.
RESULTS: MSI was significantly greater in the patients throughout the intervertebral motion sequences of recumbent flexion (0.29 vs. 0.22, p = 0.02) and when flexion, extension, left and right motion were combined to give a composite measure (1.40 vs. 0.92, p = 0.04). MSI correlated substantially with age (R = 0.85, p = 0.004) and CDD (R = 0.70, p = 0.03) in lying passive investigations in patients and not in controls. There were also substantial correlations between MSV and age (R = 0.77, p = 0.01) and CDD (R = 0.85, p = 0.004) in standing flexion in patients and not in controls.
CONCLUSION: Greater inequality and variability of motion sharing was found in patients with non-specific low back pain (CNSLBP) than in controls, confirming previous studies and suggesting a biomechanical marker for the disorder at intervertebral level. The relationship between disc degeneration and MSI was augmented in patients, but not in controls during passive motion and similarly for MSV during active motion, suggesting links between in vivo disc mechanics and pain generation.
KEYWORDS: Back pain; Diagnosis; Fluoroscopy; Kinematics; Spinal injuries
From the FULL TEXT Article:
Concepts of lumbar spine stability cover a range of complexity.
Intervertebral angle change (IV-RoM) is not now
thought to be very useful, due to wide population variations,
although range of translation is generally preferred
by spinal surgeons who assess for instability.  These
measures, although of questionable validity, are nevertheless
accessible from plain radiographs. To probe more
deeply and investigate more subtle forms of instability,
continuous intervertebral motion measures are needed. 
For the assessment of mechanical destabilisation of the
spine caused by injury, the intervertebral neutral zone is
thought to be the most sensitive measure.  Although its
measurement has been generally confined to cadaveric
studies, the advancing sophistication of quantitative fluoroscopic
systems (QF) is beginning to provide a surrogate
in vivo measure in the form of slope of the intervertebral
rotation-time curve (also known as the attainment rate). 
Chronic, non-specific low back pain (CNSLBP) is
widely considered to be at least partially of mechanical
origin, due to its susceptibility to movement and position. It
is also considered to be related to intervertebral disc
degeneration.  However, no reliable diagnostic tool
that could help a clinician to determine if a disc is the
source of the pain in patients with chronic LBP is currently
available.  Instead, relationships between trunk myoelectric
activity, co-ordination and directional preference
are more prevalent in the clinical biomechanics literature.  However, without an assessment of the relationship
between segmental mechanics and pain, identification
of biomechanical markers in CNSLBP will remain elusive.
While the in vivo investigation of intervertebral loading
is still problematical, kinematic studies are becoming more
common.  The lumbar spine is a kinetic chain that
requires the sharing of motion between levels during
bending. Various aspects of intervertebral motion sharing
have been investigated in cadaveric studies  in
plain radiographic studies in vivo  and in continuous
radiographic studies. [3, 5, 8, 20, 2530] Most of these
have studied motion onset and displacement; however, two
that studied displacement [4, 24] and one that studied
pattern variations , found differences between patients
with CNSLBP and controls.
Intervertebral motion pattern variation studies are of
interest because they provide more information than end of
range studies and can be more readily applied to contemporary
concepts of spine stability. Reeves and Cholewicki  identified impaired restraint and performance in the
passive and active intervertebral subsystems as subset
measures of subtle instability, where restraint is the ability
of a system to resist an imposed perturbation and performance
is the ability to return to the original position once
the perturbation has been removed. In the lumbar spine, the
average range of differences in the sharing of motion by
each intervertebral level over the sequence reflects the
inequality of restraint across levels (MSI) (Fig. 1). Its
variability throughout the motion (MSV), may be considered
as an expression of intervertebral motion control.
In assessing the possible role of intervertebral motion
sharing in CNSLBP, Mellor et al.  investigated the
variability of recumbent intervertebral passive motion
sharing and found it to be greater in patients with CNSLBP
than in controls. Therefore, it was thought as a possible
biomechanical marker for CNSLBP. These studies only
addressed motion sharing variability (control) and not
equality of restraintand their replication has not been
attempted until now. They also did not account for the
effects of disc degeneration. We, therefore, attempted to
replicate these studies, adding a measure of motion sharing
inequality, investigating motion under load and incorporating
disc degeneration as a possible source of interaction
with these measures.
In recent years, the usefulness of dynamic analysis of
spinal disorders has become more apparent. For example,
Shiba et al.  found that by examining dynamic, as
opposed to static global sagittal alignment at the beginning
and end of a gait sequence in patients with degenerative
lumbar kyphoscoliosis, loss of global sagittal alignment at
the end of the gait sequence was more readily detected.
The present studies bring to three the number of cohorts
in which uneven continuous motion sharing has been found
to be greater in CNSLBP patients than in controls. In the
present study, uneven passive restraint across the lumbar
spine (MSI) was greater in patients with CNSLBP than in
pain free controls. There would seem to be at least two
possible explanations for this. The first is that unequal
restraint (MSI) could add to increased muscle metabolic
demands during activities of daily living causing recurrent
muscle pain.  The second may relate to the rapid
accelerations associated with inadequate restraint at an
injured level, which has been suggested to be a nociceptive
pain generator producing a single point of pain. This could
also cause motion sharing inequality. [36, 37]
It is notable that age and disc degeneration were substantially
correlated with uneven passive motion sharing
(MSI) in the back pain patients and hardly at all in the
controls in Cohort 1. This suggests that CNSLBP is linked
to disc degeneration when there is uneven restraint in the
passive subsystem. Barz et al. put forward a new conceptual
model of CNSLBP that links such structural degeneration
with mechanical compensation and stability. 
Thus, more evenly shared restraint (MSI), despite the
presence of degenerative change, may be seen as the result
of structural compensation that allows the individual relative
freedom from symptoms.
In contrast, in weight bearing active flexion in patients, the
correlations found between age, disc degeneration and
increased variability of motion sharing (MSV) suggests relationships with control in the active subsystem. However, the
finding that motion sharing variability (MSV) was not greater
in patients during active weight bearing motion may have
been due to the stabilising influence of the trunk muscles
during active bending. Thus, control of MSV may be an
important factor in the avoidance ofCNSLBP.This possibility
could be explored by future research using the above techniques
in combinationwith electromyography.  However,
Von Forell et al. found, using finite element modelling,
stresses on the spinal holding elements would generally be
lower when not all lumbar discs are degenerated. 
It is uncertain whether these relationships are causative
or consequent to back pain, or both. The above suggested
relationships to rapid accelerations and/or increased muscle
metabolic demands are possible explanations for a causative
effect. For example, in the recumbent studies, it is
difficult to conceive how pain alone could have selectively
affected passive segmental restraint when muscle electrical
activity was minimal. 
Recent research by Lao et al.  supported the
hypothesis of Kirkaldy-Willis  that disc degeneration
has different effects on intervertebral motion at different
stages. Contemporaneous discographic and profilometry
studies have supported the hypothesis that painful discs are
also usually disrupted.  The strong associations found
here between disc degeneration and uneven intervertebral
motion in patients, but not in controls, seem consistent with
this. It is also consistent with other recent research, which
found that disc degeneration was associated with low back
pain, especially when associated with end-plate signal
change. [11, 44, 45] However, unlike the present work,
these studies used MRI disc degeneration grading, while
radiographic grading based on structural aspects rather than
biochemical changes may be better correlated with pain
when considered alongside intervertebral motion patterns.
The other two main biological generators of CNSLBP
are chemical and neuroplastic. Circulating inflammatory
markers have been found in such patients  and it may
be hypothesised that the greater the unevenness of motion
sharing, the greater the likely prevalence of rapid displacements during physical tasks causing the release of
cytokines from failing holding elements.
Central sensitisation seems to be a consequence of many
factors that are linked to the experience of having chronic
pain; however, the role of nociception, once it has become
embedded, is less clear.  Exercise in the treatment of
chronic pain has neurological as well as mechanical
effects, making its monitoring by brain mapping a variable
of interest for comparison with changes in the above
mechanical factors with treatment.  Future work could,
therefore, usefully compare MSI and MSV in passive
recumbent and active weight bearing motion in patients
and controls to monitor their responses to physical
The main limitation of these studies is their small numbers.
However, the strength and significance of the correlations
and replication of previous work suggests that the relationships
found should be robust. Many clinicians would
prefer weight bearing motion studies to be conducted using
free bending rather than with the pelvis constrained to
capture natural motion patterns. However, this makes
comparison between participant groups difficult, as it
introduces sources of extraneous uncontrolled variation,
including that from large hip joint motions.  It would
also have been useful to have obtained both recumbent and
weight bearing sequences for both patients and controls in
Cohort 2, but this was not possible owing to missing data
and will need to wait for the future studies.
Lastly, imaging studies that use image intensifiers are
associated with a radiation dose; however, image acquisition
times for such studies are considerably less protracted
than in clinical procedures, resulting in smaller doses.
Mellor, reported a mean effective radiation dose of
0.561 mSv for the four sequences which were used with
Cohort 1 in the present studies. This is approximately half
the dose of a conventional plain radiographic examination
of the lumbar spine. 
This research confirms and extends the results of previous
studies [8, 24, 29] that found abnormalities of shared
intervertebral motion to be consistent with having
CNSLBP and suggests possible mechanisms for this. It also
suggests routes for improved understanding of the role of
disc degeneration in common back pain in which degeneration
may be considered a pain source when it is associated
with uneven motion sharing and end-plate signal
change. The results open a route to the study of motion
sharing as a moderator of outcomes and of prognosis in
clinical studies and its role among other known biological
factors, such as muscle metabolic demands and chemical
markers. However, further confirmatory work is still
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