MMT book chapter

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MMT book chapter

ARTICLE IN PRESS
Manual Therapy 10 (2005) 242–255
www.elsevier.com/locate/math
Masterclass
Diagnosis and classification of chronic low back pain disorders:
Maladaptive movement and motor control impairments as
underlying mechanism
Peter O’Sullivana,b,
a
Body-logic Physiotherapy, 146 Salvado Rd, Wembley, WA 6014, Australia
School of Physiotherapy, Curtin University of Technology, Perth, Western Australia
b
Received 3 April 2005; accepted 9 July 2005
Abstract
Low back pain (LBP) is a very common but largely self-limiting condition. The problem arises however, when LBP disorders do
not resolve beyond normal expected tissue healing time and become chronic. Eighty five percent of chronic low back pain (CLBP)
disorders have no known diagnosis leading to a classification of ‘non-specific CLBP’ that leaves a diagnostic and management
vacuum. Even when a specific radiological diagnosis is reached the underlying pain mechanism cannot always be assumed. It is now
widely accepted that CLBP disorders are multi-factorial in nature. However the presence and dominance of the patho-anatomical,
physical, neuro-physiological, psychological and social factors that can influence the disorder is different for each individual.
Classification of CLBP pain disorders into sub-groups, based on the mechanism underlying the disorder, is considered critical to
ensure appropriate management. It is proposed that three broad sub-groups of CLBP disorders exist. The first group of disorders
present where underlying pathological processes drive the pain, and the patients’ motor responses in the disorder are adaptive.
A second group of disorders present where psychological and/or social factors represent the primary mechanism underlying the
disorder that centrally drives pain, and where the patient’s coping and motor control strategies are mal-adaptive in nature. Finally it
is proposed that there is a large group of CLBP disorders where patients present with either movement impairments (characterized
by pain avoidance behaviour) or control impairments (characterized by pain provocation behaviour). These pain disorders are
predominantly mechanically induced and patients typically present with mal-adaptive primary physical and secondary cognitive
compensations for their disorders that become a mechanism for ongoing pain. These subjects present either with an excess or deficit
in spinal stability, which underlies their pain disorder. For this group, physiotherapy interventions that are specifically directed and
classification based, have the potential to impact on both the physical and cognitive drivers of pain leading to resolution of the
disorder. Two case studies highlight the different mechanisms involved in patients with movement and control impairment disorder
outlining distinct treatment approaches involved for management. Although growing evidence exists to support this approach,
further research is required to fully validate it.
r 2005 Elsevier Ltd. All rights reserved.
1. The need to classify CLBP disorders
Low back pain (LBP) is common with up to 80% of
people reporting LBP over their life time (Dillingham,
1995). The majority of acute LBP disorders resolve
Corresponding author at: Body-logic Physiotherapy, 146 Salvado
Rd, Wembley, WA 6014, Australia.
E-mail address: [email protected].
1356-689X/$ - see front matter r 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.math.2005.07.001
within a 4 week period although recurrence is common
(Croft et al., 1998). A small number of disorders
(10–40%) become chronic and represent a major cost
burden for society (Dillingham, 1995; Croft et al., 1998).
In spite of the small number of pathological conditions
that can give rise to back pain, most cases (85%) are
classified as ‘‘non-specific’’ because a definitive diagnosis
cannot be achieved by current radiological methods
(Dillingham, 1995). Even when a specific diagnosis is
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P. O’Sullivan / Manual Therapy 10 (2005) 242–255
made, the validity of the diagnosis can often be
questioned. This leaves a diagnostic and management
vacuum (Leboeuf-Yde et al., 1997). This situation
commonly results in the ‘‘signs and symptoms’’ of
the disorder being treated without consideration for
the underlying basis or mechanism for the pain
disorder.
It is well recognized that the classification of chronic
low back pain (CLBP) disorders into homogenous
groups, and the application of specific interventions
tailored for these groups is likely to enhance treatment
efficacy (Leboeuf-Yde et al., 1997). It is also well
established that LBP is a multi-dimensional problem
(Borkan et al., 2002; McCarthy et al., 2004). These
dimensions consist of pathoanatomical, neurophysiological, physical and psychosocial factors (Waddell, 2004).
To date, the majority of studies that relate to the
classification of back pain have focused only on a single
dimension of the problem, rather than consideration
being given to all dimensions of LBP (Ford et al., 2003).
For a classification system to be clinically useful it
should be based on identifying the underlying mechanism(s) driving the disorder, in order to guide targeted
interventions, which in turn should predict the outcome
of the disorder.
2. Models for the diagnosis and classification of CLBP
Current approaches or models used for the diagnosis
and classification of CLBP have tended to only focus on
a single dimension of the disorder, limiting their validity
(Ford et al., 2003). The following overview is not
designed to be exhaustive, but highlights to the clinician
the strengths and weaknesses of these different
approaches.
2.1. Patho-anatomical model
The traditional medical approach to diagnosis of
CLBP has been from a pathoanatomical perspective
(Nachemson, 1999). The findings of intervertebral disc
(IVD) and facet joint degeneration, annular tears, IVD
prolapse, spondylolisthesis, foraminal and spinal stenosis with associated nerve pain are commonly assumed to
be related to back pain (and in some cases associated
neurogenic pain), with interventions provided on the
basis of this assumption (Nachemson, 1999).
However, the problem with pathoanatomical diagnoses for CLBP is that many ‘abnormal’ findings are
also commonly observed in the pain free population and
pathoanatomical findings correlate poorly with levels of
pain and disability (Nachemson, 1999). Frequently, little
consideration is given to the confounding impact of
psycho-social, neuro-physiological and physical factors
that may co-exist and contribute to the underlying basis
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of these disorders (Nachemson, 1999). Because of this,
even when a specific pathoanatomical diagnosis can
been made, there is still a need to classify the disorder
based on the mechanism(s) that drive the pain disorder
to ensure appropriate management.
2.2. Peripheral pain generator model
More recently there has been a focus on the
identification of the painful structure (peripheral pain
generator) based on the patient’s history, area of pain,
clinical examination findings and diagnostic blocks
(Donatelli and Wooden, 1989; Laslett and Williams,
1994; Schwarzer et al., 1994; Bogduk, 1995; Bogduk,
2004). This has led to studies that have reported that the
majority of chronic back pain originates in the IVD
(45%), with a smaller number of subjects with facet
joint (20%) and sacro-iliac joint (15%) pain (Bogduk,
1995). These studies have led to diagnostic and
therapeutic procedures to identify, block or denervate
the nociceptive source (Bogduk, 2004). The major
limitation of this treatment model is that it treats the
symptom of pain without consideration for the underlying mechanism or cause of the pain generation,
and these approaches frequently only result in short
term pain relief and lack broad therapeutic utility
(Nachemson, 1999).
2.3. Neuro-physiological model
An increased focus on the study of the nervous system
and its involvement in pain disorders has documented
complex biochemical and neuro-modulation changes at
a peripheral, as well as at spinal cord and cortical levels
(Flor and Turk, 1984; Flor et al., 1997; Moseley, 2003;
Wright and Zusman, 2004). This has highlighted that
pain can be generated and maintained at a peripheral
level, as well as centrally at both spinal cord and cortical
levels. Central sensitisation of pain which is manifest in
most CLBP disorders (to varying degrees) can occur
secondary to sustained peripheral noniceptive input
resulting in changes at spinal cord and cortical levels
(Zusman, 2002). This can be both amplified and
inhibited by fore-brain descending input (see psychosocial section) (Zusman, 2002). As well as this there is
growing evidence that the nervous system undergoes
changes to its cortical mapping and possesses a
pain ‘memory’ which may leave it pre-sensitized to
the exacerbation and recurrence of pain (Zusman,
2002). This new knowledge has lead to an increased
focus on medical interventions to inhibit both
peripheral and central processing of pain (Bogduk,
2004), as well as psychological and cognitive interventions to reduce the forebrain facilitation of pain
(Woby et al., 2004).
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2.4. Psychosocial model
The focus on the nervous systems’ role in pain
modulation has coincided with increasing research
investigating the impact of psychological and social
factors on the modulation of pain and in particular, their
capacity to increase the central nervous system mediated
drive of pain via the forebrain (Linton, 2000; Zusman,
2002; Waddell, 2004). Mal-adaptive coping strategies
such as negative thinking, pathological fear and abnormal anxiety regarding pain, avoidant behaviour, catastrophizing and hyper-vigilance have been shown to be
associated with high levels of pain, disability and muscle
guarding (Frymoyer et al., 1985; Main and Watson,
1996; Nachemson, 1999; Linton, 2000). Social factors
such as the compensation system, work place disputes,
work and family tensions and cultural issues affecting
beliefs reinforce the psychological factors that can
increase the central drive of pain (Nachemson, 1999).
Despite this advanced knowledge there is debate regarding the relative contribution of these factors to pain
disorders and whether these factors predispose, or are as
a result of a pain disorder. In contrast positive factors
such as adaptive coping strategies, appropriate pacing
and distraction (reduced hypervigilance) can have a
descending inhibitory effect on pain via the forebrain
(Zusman, 2002). Certainly there is evidence that cognitive behavioural interventions are effective in reducing
disability in specific groups with non-specific CLBP
(Woby et al., 2004), however there appears to be a
growing trend within physiotherapy to classify most
patients with non-specific CLBP as primarily psychosocial driven due to a lack of an alternative diagnosis.
Although all CLBP disorders have psychological and
social impact with associated cognitive issues related to
the disorder, it appears that only a small sub-group exist
where these factors become the dominant or primary
pathological basis for the disorder.
2.5. Mechanical loading model
Both high and low levels of physical activity are
reported to be risk factors for LBP while moderate levels
of activity appear protective (Newcomer and Sinaki,
1996; Balague et al., 1999). Mechanical factors are
usually reported to be associated with the initial
development of LBP and are frequently reported to
contribute to the recurrence of LBP and the exacerbation of CLBP. These factors include; sustained low load
postures and movements (such as sitting, standing,
bending and twisting), exposure to whole body vibration, high loading tasks (such as repeated lifting and
bending), as well as sudden and repeated spinal loading
in sports specific and manual work situations (Pope and
Hansen, 1992; Adams et al., 1999; Nachemson, 1999;
Abenhaim et al., 2000; McGill, 2004). These different
mechanical exposures are also influenced by ergonomic
and environmental factors (McGill, 2004), such as
seating design, lifting technique, work place design and
sporting equipment. Individual physical factors such as
where in its range a spinal articulation is loaded (neutral
zone vs. elastic zone), reduced trunk muscle strength and
endurance, impaired flexibility, ligamentous laxity and
motor control dysfunction as well as anthropometric
considerations have also been reported to be associated
with LBP (Adams et al., 1999; Abenhaim et al., 2000;
McGill, 2004; Dankaerts et al., 2005b; O’Sullivan et al.,
2005). Although little direct evidence supports the
efficacy of ergonomic interventions for the management
of LBP, there is little doubt that physical factors such as
sustained end range spinal loading, lifting with flexion
and rotation, exposure to vibration and specific sporting
activities involving cyclical end range loading of the
spine (especially combined with rotation) do negatively
impact on the musculo-skeletal system and have the
potential to cause ongoing peripheral nociceptor sensitization (Adams et al. 1999; Nachemson, 1999; Abenhaim et al., 2000; Burnett et al., 2004; McGill, 2004).
2.6. Signs and symptoms model
The area and nature of pain, impairments in spinal
movement and function, changes in segmental spinal
mobility (hyper and hypo), as well as pain responses to
mechanical stress (provocation tests) and movement
(peripheralisation and centralisation of pain with
repeated movement) have formed the basis for classifying LBP disorders (McKenzie, 1981; Maitland, 1986;
McKenzie, 2000). These approaches are based on
biomechanical and pathoanatomical models and have
lead to the assessment and treatment of signs and
symptoms associated with CLBP (McKenzie, 1981;
Maitland, 1986; McKenzie, 2000). Evidence for the
efficacy of these approaches for the management of
CLBP disorders remains limited (Maher et al., 1999;
Abenhaim et al., 2000; Bogduk, 2004). This may in part
be due to the limitations of the research design for some
of these studies, as well as a neglect to account for the
complex biopsychosocial nature of chronic pain disorders (Elvey and O’Sullivan, 2004).
2.7. Motor control model
There has been an increased focus on the management
of CLBP from a motor control perspective (Richardson
and Jull, 1995; O’Sullivan, 1997, 2000; Sahrmann, 2001).
While it is well recognized that movement and motor
control impairments exist with CLBP disorders, they are
highly variable and their presence does not establish
cause and effect. Movement and motor control impairments are known to occur secondary to the presence of
pain (Hodges and Moseley, 2003; Van-Dieen et al.,
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2003). Pathological processes such as neurogenic and
radicular pain, neuropathic and centrally mediated
pain and inflammatory disorders result in adaptive or
protective altered motor behaviour in response to pain
(Hall and Elvey, 1999; Elvey and O’Sullivan, 2004).
Psychological processes such as stress, fear, anxiety,
depression, hysteria, and somatisation are also known to
disrupt motor behaviour (Frymoyer et al., 1985; Hodges
and Moseley, 2003). Attempts to ‘‘normalize’’ movement or motor control impairments or treat dysfunction
in the spinal muscles in many of these disorders would
be inappropriate and ineffective due to the nonmechanical basis of these disorders.
There is however growing evidence that CLBP
disorders do exist where mal-adaptive movement and
motor control impairments appear to result in ongoing
abnormal tissue loading and mechanically provoked
pain (Burnett et al., 2004; Dankaerts et al., 2005b;
O’Sullivan et al., 2005). Following an acute episode of
low back pain (when tissue healing would have normally
occurred), ongoing mal-adaptive motor control behaviour provides a basis for ongoing peripherally driven
nociceptor sensitisation leading to a chronic pain state.
These disorders are amenable to tailored physiotherapy
interventions directed at their specific physical and
cognitive impairments (O’Sullivan et al., 1997a–c; Stuge
et al., 2004).
2.8. Biopsychosocial model
What is clear from the scientific literature and clinical
practice, is that a multi-dimensional approach to dealing
with CLBP based on a biopsychosocial model is
required (Elvey and O’Sullivan, 2004; McCarthy et al.,
2004; Waddell, 2004). The relative contribution of the
different dimensions and their dominance associated
with a CLBP disorder will differ for each patient. The
role of the treating clinician is to consider all dimensions
of the disorder based on an interview, thorough physical
examination (assessing all aspects of the neuromusculosketetal system) combined with review of radiological
imaging, medical tests and screening questionnaires
(Elvey and O’Sullivan, 2004; O’Sullivan, 2004; Waddell,
2004) (Fig. 1). A clinical reasoning process allows
determination of which factors are dominant in the
disorder and whether the patient has adapted to the
disorder in a positive or negative manner. Consideration
of all the factors outlined allows for a diagnosis and
mechanism based classification guiding management of
the disorder (Elvey and O’Sullivan, 2004) (Fig. 1).
3. Diagnosis and classification of back pain
The Quebec task force classification system provides a
logical approach for the diagnosis and classification of
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LBP disorders within a biopsychosocial framework
(Spitzer, 1987; Abenhaim et al., 2000; Waddell, 2004).
Under this framework red flags are considered in a
diagnostic triage. The patient is screened for yellow flags
or non-organic features suggestive of psychological and/
or social factors dominating in the disorder. Under this
classification system, disorders can be diagnosed as
specific (especially nerve root pain) or non-specific, and
staged (acute, sub-acute and chronic).
3.1. Diagnosis: specific and non-specific CLBP disorders
Specific pathoanatomical diagnoses, although critical
for the understanding of many disorders, require further
classification. For example, a diagnosis of lumbar spine
stenosis (central or foraminal/lateral—chronic stage)
may be associated with an adaptive (protective) motor
response associated with a functional reduction of the
lumbar lordosis with associated lumbar multifidus
inhibition, to unload sensitized neural tissue. In this
case attempts to normalize the motor control impairments would result in exacerbation and deterioration of
the disorder. On the other hand the same diagnosis may
be associated with a mal-adaptive motor response,
represented by a functional increase in lumbar lordosis
with associated back muscle guarding, resulting in
further neural compromise and direct aggravation of
the disorder. In this case normalising the motor control
impairments (to functionally reduce the lumbar lordosis) would be indicated and effective. This proposed
classification (into adaptive/mal-adaptive motor control
responses) directly influences whether the patients’
specific disorder is amenable for physiotherapy management that is aimed at normalising the motor control
impairments or not. Alternatively, this diagnosis may be
associated with a dominance of psychosocial factors and
associated dominant central nervous system sensitisation, compromising the potential success of both
conservative physiotherapy and surgical interventions.
In this case the same specific diagnosis may present with
a different classification, reflecting a different underlying
pain mechanism and therefore indicating a different
intervention (Elvey and O’Sullivan, 2004).
Eighty-five percent of CLBP disorders do not have a
specific diagnosis (Dillingham, 1995). These disorders
are labelled ‘non-specific CLBP’ disorders and represent
a large group of ‘tissue strains’ and ‘sprains’ that have
not resolved beyond normal tissue healing time (Abenhaim et al., 2000). This group has been broadly classified
based on the area of pain and defined as somatic
referred or radicular in nature (Abenhaim et al., 2000).
However this diagnostic/classification system is of
limited clinical value as it does not identify the underlying mechanism driving the pain disorder, and consequently there is no clear direction for specific
management (Padfield and Butler, 2002).
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246
Social factors
- relationships – family, friends, work
- work structure
- medical advice
- support structures
- compensation – emotional, financial
- cultural factors
- socio-economic factors
Genetic factors
Patho-anatomical factors
- potentially influencing all
other domains
- structural pathology
- identify peripheral pain generator
(IVD / Zt joint / SI Jt / neural tissue / myo-fascial /
connective tissue)
Physical factors
Psychological factors
- personality type
- beliefs & attitudes
- hypervigilance
- coping strategies – confronter vs
avoider
- pacing
- emotions - fear / anxiety / depression
/ anger
- iIlness behaviour
Pain
Neuro-physiological factors
- peripheral sensitisation
- central sensitisation
- sympathetic nervous system activity
- somatic complaints
- ‘passive’ structure competence (hypermobility)
- developmental factors
- mechanism of injury
- disorder history and stage
- area of pain – local / generalised / referred
- pain behaviour – directional / centralisation
- mechanical vs non-mechanical provocation
- articular mobility
- neural tissue provocation testing
- neurological examination
- motor control / myo-fascial considerations
- adaptive vs mal-adaptive motor response
- movement impairments (directional)
- motor control impairments (directional)
- activity levels / conditioning / strength /
muscle endurance
- work / home environment / lifestyle
- ergonomic factors
Fig. 1. Factors that need consideration within a biopsychosocial framework, for the diagnosis and classification of CLBP disorders.
3.2. Classification of CLBP
Due to the shortcomings of the current models, it is
clear that both specific and non-specific CLBP disorders
require further classification based on a biopsychosocial
construct. There are a number of key clinical indicators
regarding pain area and behaviour, which provide an
important insight into the different mechanisms underlying and driving a pain disorder, allowing classification
to be made. Considered simplistically, the presence of
localized and anatomically defined pain associated with
specific and consistent mechanical aggravating and
easing factors, suggest that physical/mechanical factors
are likely to dominate the disorder resulting in a primary
peripheral nociceptive drive. Correlation between clinical examination and pathoanatomical findings is critical
to determine their significance and relationship to the
disorder. If pain is constant, non-remitting, widespread
and is not greatly influenced by mechanical factors (or
minor mechanical factors result in an exaggerated and
disproportionate pain response), then inflammatory or
centrally driven neurophysiological factors (such as
altered central pain processing) are likely to dominate
the disorder. High levels of anxiety, hypervigilance, fear
and emotional stress presenting as primary aggravating
or precipitating factors in the disorder, highlight the
influence of psychological and in some cases social
factors indicating the dominant forebrain drive of pain
in a disorder (Linton, 2000). Understanding a patient’s
social circumstances, work environment, lifestyle factors
and beliefs regarding their disorder is also critical
(Waddell, 2004). Whether the patient has active or
passive coping strategies in managing their disorder, and
whether they pace themselves is important in understanding their capacity to actively manage their pain
(Bergstrom et al., 2001). In reality most disorders will be
associated with a combination of these factors, and the
role of the clinician is to consider the balance and
dominance of them in the disorder (Fig. 1).
It is proposed that there are three broad sub-groups of
patients that present with disabling CLBP associated
with movement and control impairments (Fig. 4).
(1) The first sub-group is represented by disorders
where high levels of pain and disability, as well as
movement and/or control impairments are secondary
and adaptive to an underlying pathological process.
These include red flag disorders, specific pathoanatomical disorders in some circumstances (such as IVD
prolapse, spinal and foraminal stenosis with associated
radicular pain 7 neurological deficits, internal disc
disruption with associated inflammatory pain, ‘unstable’
grade 2–4 spondylolisthesis), inflammatory pain disorders, neuropathic and centrally or sympathetically
mediated pain disorders. These patients present with
antalgic movement patterns and altered motor control
that is driven directly by the pain disorder. The therapist
will quickly determine this as attempts to ‘normalize’
these motor control and movement impairments results
in exacerbation or non-resolution of the disorder, as
these impairments are adaptive and driven by pathological processes. If the pathological process resolves with
time or secondary to specifically targeted interventions
(i.e. appropriate medical and/or surgical management
when indicated), the signs and symptoms (e.g. motor
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control and movement impairments) related to the
disorder resolve.
Specifically targeted therapy management may be
indicated for some of these disorders in conjunction with
other primary medical interventions with full knowledge
of the non-mechanical underlying basis of the disorder
(Elvey and O’Sullivan, 2004). These disorders represent
a small but severely disabled group within the CLBP
population.
(2) A second small sub-group exists where the drive of
the pain disorder is from the forebrain, secondary to a
dominance of psychological and/or social (non-organic)
factors. Although psychological and social impact
occurs with all chronic disabling pain disorders, it
appears that for a small group of patients it represents
the dominant central drive of their disorder. This results
in high levels of disability, altered central pain processing, amplified non-remitting pain, and resultant disordered movement and motor control impairments.
These disorders commonly present with dominant
psycho-social features, including pathological anxiety,
fear, anger, depression, negative beliefs, un-resolved
emotional issues, poor coping strategies (lack of pacing
resulting in pain provocation or excessive avoidance of
activity as means of controlling pain) as well as negative
social and inter-personal circumstances (Linton, 2000;
Bergstrom et al., 2001; Waddell, 2004). These psychological and social stresses present as dominant coexisting, precipitating and primary aggravating factors
for the disorder (Linton, 2000).
The key feature of these disorders is the absence of an
organic basis to the disorder, and lack of clear and
consistent mechanical provocation or relieving patterns
(absence of peripheral nociceptor drive). When mechanical factors are provocative they are inconsistent and tend
to result in abnormal and disproportionate pain, disability
and emotional responses. These patients commonly
present with high levels of dependence on strong analgesic
medication and passive forms of health care provision by
multiple practitioners, even though they report a poor
response to these interventions (Waddell, 2004). It is
important to note that a therapist should not arrive at this
classification without consultation and confirmation by
either a treating clinical psychologist or psychiatrist.
In this sub-group, attempts to simply treat the ‘signs
and symptoms’ of the disorder directly (e.g. movement
and control impairments) does not result in their
resolution, as the underlying mechanism driving the
pain is not addressed. Management of these disorders
requires multi-disciplinary management with a primary
focus on cognitive behavioural therapy (Bergstrom
et al., 2001) and psychiatric management. Physiotherapy
management can play a specialized role in reinforcing
graded functional recovery while reducing the focus on
pain, however it cannot be seen as the primary treatment
for these disorders (Elvey and O’Sullivan, 2004).
247
(3) It is proposed that a large third sub-group exists
where mal-adaptive movement or control impairments
and associated faulty coping strategies result in chronic
abnormal tissue loading (associated with either excessive
or reduced spinal stability), pain, disability and distress.
This group is classified on the basis that the ‘movement’
impairments (characterized by pain avoidance behaviour) or ‘control’ impairments (characterized by pain
provocation behaviour) act as the underlying mechanism that drives the CLBP state. Normalisation of the
movement or control impairments based on a cognitive
behavioural approach results in resolution and/or
control of these disorders. Disorders with a ‘movement’
and ‘control’ impairment classification present commonly in clinical practice, and they appear to have
different underlying pain mechanisms from each other
and therefore their management is distinctly different
(Figs. 2 and 3). These disorders may present as specific
(associated with a pathoanatomical diagnosis) or nonspecific CLBP disorders, and are commonly associated
with psychological, social, neurophysiological (central
sensitisation) factors, that may contribute to but do not
dominate or drive the disorder. The classification of
these disorders leaves them amenable to therapy
intervention directed at the primary physical (movement
and control) impairments while addressing the secondary cognitive aspects of the disorder (see Fig. 4).
3.2.1. Movement impairment classification
CLBP disorders classified as ‘movement impairment’
present with a painful loss or impairment of normal
(active and passive) physiological movement in one or
more directions (Figs. 2, 3 and 5a). These disorders are
associated with abnormally high levels of muscle
guarding and co-contraction of lumbo-pelvic muscles
when moving into the painful and impaired range. This
appears to be driven by an exaggerated withdrawal
motor response to pain. This leads to high levels of
compressive loading across articulations, movement
restriction and rigidity (excessive stability), resulting in
a mechanism for tissue strain and ongoing peripheral
nociceptor sensitisation. These patients are usually
acutely aware of their pain and are fearful of moving
into the painful movement direction as they perceive
that pain provocation is damaging. The fear of movement appears to develop from the patients’ initial
experience of severe acute pain, as well as their beliefs
(reinforced by sympathetic family members and treatment providers) that pain is harmful. Movement related
fear, hyper-vigilance and anxiety associated with the
pain reinforces the faulty cognitive coping strategies and
beliefs, further amplifying the pain centrally and
reinforcing their muscle guarding. This represents a
mal-adaptive response to the pain disorder, as the
compensations for the pain in turn becomes the
mechanism that drives the disorder. These disorders
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248
(A) Movement impairment classification
Nature and mechanism of pain:
Localised pain +/- referral
Severe pain of rapid onset
Movement impairment in direction of pain
Hyper-awareness of pain
Exaggerated reflex withdrawal motor
response
Muscle guarding and abnormal tissue
loading (↑spinal stability)
Avoidance of movement into painful range
Disability
Directional (flexion, extension, rotation,
lateral shift, loading)
Multi-directional
Result: Peripheral pain sensitisation
(B) Control impairment classification
Nature and mechanism of pain:
Localised pain +/- referral
Gradual onset of pain from repeated or sustained
strain
No impaired movement in direction of pain
Lack of awareness of pain triggers
Poor lumbo-pelvic position sense
Absence of reflex withdrawal motor response
Ongoing tissue strain (↑or↓ spinal stability)
Provocation into painful range
Avoidance of painful activity
Disability
Directional (flexion, extension, rotation, lateral
shift, loading)
Multi-directional
Result: Peripheral pain sensitisation
Anxiety related to movement pain
Fear avoidance when moving in direction
of pain (pathological)
Hyper-vigilence
Belief that pain is damaging (pathological)
Anxiety related to chronic disabling pain
Fear of activity (non-pathological)
Lack of control and awareness of disorder
Belief that activity is damaging (non-pathological)
Result: Central pain sensitisation
Result: Central pain sensitisation
Normalisation of movement impairment
leads to resolution / control of disorder
Normalisation of control impairment leads to
resolution / control of disorder
Fig. 2. The nature and mechanism associated with mal-adaptive motor control disorders with: (A) Movement impairment classification and (B)
control impairment classification (italics represent common features of the disorders / normal text highlights differences between the disorders).
may present in a directional manner (flexion, extension,
side bending and rotational impairments) as well as
combinations of these movements (multi-directional
movement impairments).
Management of this patient sub-group is directed at
both the dominant physical and associated cognitive
factors that underlie the disorder. The aim is first to
educate the patient that their pain is not damaging and
they have developed faulty compensations to their pain,
which now act to maintain their disorder. Restoration of
the painful impaired movement is critical for the
resolution of the disorder. The aim of the intervention
is to desensitize the nervous system by restoring normal
movement, reducing the fear of movement into pain and
associated muscle guarding. This is facilitated by graded
movement exposure into the painful range in a relaxed
and normal manner based on the individual patient
presentation. The cognitive strategies of reducing fear
and changing beliefs regarding pain is augmented by
manual therapy ‘treatment’ to restore the movement
impairment (articular mobilisation/manipulation and
soft tissue techniques). This is combined with active
‘management’ approaches directed to restore the movement impairment (muscle relaxation, breathing control,
postural adjustments, graded movement exposure ex-
ercises, cardio-vascular exercise and most importantly
graded functional restoration to normalize motor
control). As the movement impairment and associated
movement-based fear reduces, so too does the disability
and pain related to the disorder. Stabilising exercise
programs and treatment approaches that focus on pain
and reinforce the avoidance behaviour usually exacerbate these disorders and are contra-indicated.
3.2.1.1. Case study 1. A 28-year-old woman reported a
3 year history of disabling non-specific CLBP (central
lower lumbar) that had developed following a lifting
injury while working as a nurse. She was placed off work
for three weeks and was told by her physiotherapist that
she had injured her disc, should do ‘McKenzie extension
exercises’, avoid flexion and maintain her lumbar
lordosis at all times. She reported becoming disabled
with pain and very fearful of bending her back which she
avoided doing from that time.
Her treatment history consisted of McKenzie extension exercises, Pilates, stabilisation training (with a focus
on pelvic floor, transverse abdominal wall and lumbar
multifidus co-activation) and swimming. She had seen
an orthopaedic surgeon, pain specialist, clinical psychologist, a number of physiotherapists and was taking
ARTICLE IN PRESS
Mal-adaptive CLBP disorders -where ‘movement’ and ‘control’ impairments ….
dominate and represent underlying mechanism for pain
Tissue injury / localised pain
Motor response
Movement impairment
classification
Factors that may influence pain and motor
response
physical
patho-anatomical
genetic
neuro-physiological
motor control
psycho-social
coping strategies
beliefs
fear avoidance
compensation
- segmental spinal
- directional / multi-directional
Management
Non resolution
mal-adaptive patterns adopted
poor coping strategies
NMS response prolonged
excessive↔reduced spinal stability
abnormal tissue loading
peripheral / central sensitisation
Resolution of the disorder
- education – regarding pain mechanism
- reduce fear
- cognitive behavioural approach
- restore movement impairment
- graded movement restoration
- graded pain exposure
- functional restoration
- normalise movement behaviour
Control impairment
classification
- segmental spinal
- directional / multi-directional
Management
- cognitive behavioural motor control
intervention
- pain control (avoid provocation)
- retrain faulty postures and movements
- self control of pain
Fig. 3. Mal-adaptive motor control impairment CLBP disorders.
CLBP disorders associated
with altered motor control
Adaptive / protective altered
motor response to an
underlying disorder
- inflammatory disorders
- centrally mediated pain
- sympathetically maintained pain
- neurogenic pain
- neuropathic pain
Altered motor response and
centrally mediated pain
secondary to dominant
psychosocial factors
Mal-adaptive motor control
patterns that drive the pain
disorder
- movement impairments
- control impairments
(may result in an excess or loss
of spinal stability)
Fig. 4. Altered motor responses in the presence of CLBP (3 groups).
249
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250
8/10, her disability index (Oswestry disability index) was
40% and she had high levels of kinesiophobia (Tampa
scale of Kinesiaphobia).
Investigations:
Physical examination
Observation
X-rays/MRI Lumbar spine—
NAD
she sat and walked with a
rigid erect thoraco-lumbar
spine posture
she sat forward on the chair
with a lordotic spinal posture
she maintained
thoracolumbar lordosis and
avoided flexion when moving
from sitting to standing and
while undressing
AROM
Fig. 5. (a) Patient with classification of movement impairment into
flexion (note the pain provocation into flexion is associated with an
impairment of lumbar spine flexion). (b) Patient with classification of
control impairment into flexion (note the pain provocation into flexion
is not associated with an impairment of lumbar spinal flexion).
anti-depressants, strong analgesic and muscle relaxant
medication.
She was only able to work 2 days per week doing light
duties because of her CLBP disorder.
She reported that her symptoms were exacerbated by
all flexion postures and movements such as slump
sitting, bending, dressing and lifting activities. Extension
related spinal movements such as standing and walking
were pain free. She gained relief from her pain with heat
and rest.
She reported high levels of anxiety relating to pain,
disability and an inability to work full time. She
constantly worried about her back pain and believed
that she would not get better as she had a disc injury
that had not resolved. She coped with her back pain by
avoiding provoking it and restricting her activities
involving spinal flexion. Her pain intensity level was
Flexion—hip flexion 501, no
thoraco-lumbar flexion with use
of hands to support her and
assist her return to upright
(Fig. 5a)
Extension—301 no pain
Side bending—full ROM and
pain free
Repeated flexion increased
guarding and report of pain
Motion palpation
L5/S1—hypo-mobile in flexion
Provocation palpation of L4 and L5 centrally—
reproduced pain (highly sensitized)
SIJ
NAD
Neural provocation NAD
tests
Motor control
1. Functional movement tests—stated under
observation
2. Specific movement testing—attempts to posteriorly
rotate pelvis in sitting, supine and four point kneeling
were associated with pain and muscle guarding.
3. Specific muscle testing—able to isolate co-activation
of the transverse abdominal wall and lower lumbar
multifidus in neutral lordosis (difficulty observed
relaxing them).
Diagnosis
Classification
non-specific CLBP
Movement impairment
disorder–flexion pattern L5/S1
The disorder diagnosis of non-specific CLBP was
based upon the non-resolution of a flexion back sprain
and the absence of a specific diagnosis.
The disorder classification of this patient was a
movement impairment disorder (into flexion with localized pain at L5/S1).
ARTICLE IN PRESS
The mechanism underlying the pain is a movement
impairment with a loss of normal physiological movement into flexion, with associated muscle guarding and
fear of forward bending. This movement impairment
and associated fear was initiated in the acute phase and
was reinforced by her beliefs that pain associated with
flexion of her spine was damaging for her. This patient
avoided bending due to the knowledge that flexion will
provoke pain and the belief (reinforced by treatment
providers) that this movement causes ‘further damage’
and that by not moving into this painful direction will
prevent damage. The basis of this pain disorder is linked
to both dominant peripheral and secondary central pain
mechanisms.
Management of this patient was directed at both the
dominant peripheral and secondary central mechanisms
of the pain disorder over a 12 week period. Management
first focussed on educating the patient regarding the
basis and mechanism of her disorder. It was critical to
change the patient’s beliefs, so that she understood that
to relax the spinal muscles and restore normal movement in the direction of her pain was essential for
resolution of the pain disorder. The patient was assured
that her movement-provoked pain into flexion was not
dangerous or damaging.
The restoration of normal tissue compliance and
reduction of muscle guarding was facilitated by ‘passive’
treatment techniques directed to restore flexion mobility
to the lower lumbar spine (L5/S1 flexion articular
mobilisation techniques and soft tissue inhibitory
techniques directed to her back extensor and psoas
muscles). This was combined with graded active movement into the restored range. This involved the patient
initially being taught to posteriorly tilt her pelvis in a
relaxed manner without trunk muscle guarding and
breath holding (initially in supine and four point
kneeling progressed to sitting and standing). She was
instructed to cease cognitively contracting her
spinal ‘stabilising muscles’ but rather to relax her
upright postures so to reduce her thoracolumbar hyper-lordosis to a neutral spine posture. Finally
the patient was trained to flex her spine in upright
postures (sitting and standing) in a normal physiological
manner without guarding. As the movement impairment
was restored, the pain, disability and fear of bending
also reduced. At this stage the patient reported that
she had the capacity to control her pain. This new
control was then introduced into previously provocative
functional tasks such as dressing and housework.
She reported that she could work longer and increase
her general activity levels. She was encouraged to
carry out regular cardio-vascular exercise and join a
yoga class to maintain her spine mobility in a
relaxed manner. The resolution of her CLBP disorder
supported the classification and management approach
taken.
251
3.3.1. Control impairment classification
CLBP disorders classified as ‘control impairment’
appear to be most common in clinical practice. These
disorders are associated with impairment or deficits in
the control of the symptomatic spinal segment in the
primary direction of pain. In these disorders there is no
movement impairment in the direction of pain (Figs. 3
and 5b). Pain in these disorders is associated with a loss
of functional control around the neutral zone of the
spinal motion segment due to specific motor control
deficits (and muscle guarding in some situations) of the
spinal stabilising muscles. This is manifest during
dynamic and/or static tasks as
1. ‘through range movement pain’ due to non-physiological motion of the spinal segment observed during
dynamic tasks,
2. ‘loading pain’ due to non-physiological loading of the
spinal segment (not end range) observed during static
loading tasks and
3. ‘end of range pain’ or ‘overstrain’ due to repetitive
strain of the spinal motion segment at the end of
range observed during static and dynamic functional
tasks.
The irony with these patients is that they adopt
postures and movement patterns that maximally stress
their pain sensitive tissue (Burnett et al., 2004; O’Sullivan et al., 2004; Dankaerts et al., 2005b), and yet they
have no awareness that they do this. One reason for this
may relate to the fact that their pain is often of a gradual
onset and therefore they lack a withdrawal reflex motor
response, coupled with a lack of proprioceptive awareness of the lumbo-pelvic region (Fig. 2) (O’Sullivan
et al., 2003; Burnett et al., 2004). This control deficit is
clearly mal-adaptive and represents a powerful mechanism for ongoing pain (which is both peripherally and
centrally mediated) and disability. These patients present with movement based fear that is real, as their
movement strategies are highly provocative of their pain
disorder, resulting in failure to respond to general
exercise and conditioning interventions. These disorders
frequently present in a directional manner (flexion,
extension (passive or active) and lateral shift control
impairment) as well as combinations of these directions
(multi-directional control impairment). These disorders
may be associated with deficits in the spinal stabilising
muscles (i.e. flexion pattern) or excessive muscle activity
resulting in increased spinal loading (i.e. active extension
pattern). These directional patterns are described in
detail elsewhere (O’Sullivan, 2000, 2004). Clinical
instability of the lumbar spine represents a sub-group
of these disorders (O’Sullivan, 2000, 2004).
Management of this sub-group is based on a cognitive
behavioural motor learning intervention model. This
intervention is based on the premise that mal-adaptive
ARTICLE IN PRESS
252
motor control behaviour provides an ongoing mechanism for tissue strain and peripheral nociceptive drive.
The aim of the intervention is to desensitize the nervous
system by educating the patient to control their pain
provocative postures and movement patterns so as to
avoid repetitive strain on the painful tissue, reduce the
peripheral nociceptive drive and in turn enhance
function. This is not simply an exercise program rather
it follows a motor learning intervention model with the
aim of changing movement behaviour via physical as
well as cognitive learning processes. As the motor
control is enhanced, the repeated stress on the symptomatic tissue reduces, resulting in less peripheral nociceptive drive into the nervous system, allowing the pain
disorder to resolve. This provides the patient with the
capacity to manage their disorder in an effective
manner, which reduces their fear of activity and increase
their levels of function. This intervention directly
impacts on both the dominant peripheral nociceptive
as well as the secondary central drives for the pain
disorder.
The role of manual therapy treatment in control
impairment disorders is limited only to the restoration
of articular movement away from the direction of pain
provocation and only if this movement is impaired and
inhibiting the muscle synergies controlling this movement. These techniques are never used in isolation, but
rather they facilitate movement so as to enhance the
restoration of motor control to dynamically unload the
pain sensitive tissue. For example in a flexion pattern
control impairment disorder, if a loss of segmental
spinal extension prohibits restoring control over the
lower lumbar lordosis, then manual therapy treatment
may be used to facilitate extension. This is immediately
followed by training active control over this movement
so as to reduce the flexion load of the motion segment.
The specifics of this intervention have been reported in
detail previously (O’Sullivan, 2000, 2004).
3.3.1.1. Case study 2. A 42-year-old male reports a
2 year history of non-specific CLBP. He first developed
central LBP while lifting (with a flexed lumbar spine) a
30 kg bag of fertilizer while working as a labourer. His
back pain disorder did not resolve and he had not been
able to return to work.
His previous treatment consisted of physiotherapy,
Pilates, gym based exercise programs, psychological
intervention and medication (strong analgesics and antidepressants).
He reported that his back pain was provoked by static
flexed spinal postures (sitting, driving, semi-inclined
bending) and activities (such as lifting, sit—stand,
dressing). He reported that he avoided all such activities
as they exacerbated his pain and it took days then to
settle. He reported relief with extension or lordotic
postures.
He reported feeling depressed due to the nature of his
disability, his loss of independence and his alienation
with his health providers, work and family and was
tearful when describing this. He was also limited in his
ability to socialize with his friends. He had been told
there was nothing structurally wrong with his back and
that he would have to learn to live with his problem and
he believed that his condition was unlikely to improve.
His pain intensity level was 7/10, his disability index
(Oswestry disability index) was 42% and he had high
levels of kinesiophobia (Tampa scale).
Physical examination
Observation
he sat down to undress, and
used his hands to assist
transferring from sitting to
standing
AROM
Flexion—no lower lumbar
movement impairment (full low
lumbar ROM) into flexion with
report of LBP mid range (Fig.5b)
Extension—301 no pain
Right and left side bending—full
ROM
Repeated and sustained spinal
flexion increased his LBP
PPIVM
L5/S1—hyper-mobile in flexion
Provocation palpation of L5/S1 central—painful with
reproduction of back pain
Neural
NAD
provocation tests
Motor control:
1. Functional movement tests—forward bending,
reaching, lifting, sit to stand and squatting were
associated with increased flexion at the lower lumbar
spine, a loss of anterior pelvic rotation and lordosis in
the upper lumbar and thoracic spine (Fig. 4b). The
use of the arms was observed to support the trunk
with these activities.
2. Specific movement tests—Attempts to initiate
anterior pelvic tilt and extend the lower lumbar spine
in standing, sitting and supine were associated with
upper lumbar and thoracic spine extension
3. Specific muscle testing—Inability to isolate the
activation of the pelvic floor, transverse abdominal
muscles and lumbar multifidus with posterior pelvic
rotation and flexion of the lower lumbar spine, with
bracing of the upper abdominal wall.
Investigations
Diagnosis
Classification
X-rays/MRI lumbar spine—
degenerative disc disease L5/S1
(mild)
non-specific CLBP
control impairment disorder—
flexion pattern at L5/S1
ARTICLE IN PRESS
The diagnosis of non-specific CLBP was based on the
non-resolution of a flexion back sprain beyond normal
healing time and the lack of a specific diagnosis.
The classification of this patient as control impairment
disorder (flexion pattern) is based on the underlying
mechanism of this pain disorder being directly linked to
an ongoing flexion strain of the L5/S1 motion segment
secondary to a loss of functional control of the segment
into flexion. The patients’ sense of alienation, frustration, anger and depression further confounds his
situation resulting in increased central drive of his pain.
Management of this patient was directed on a
cognitive behavioural motor learning frame-work
(O’Sullivan, 2004). The patient was first educated that
subsequent to his initial back sprain he had adopted a
mal-adaptive motor control pattern that exposed the
symptomatic segment to abnormal and repetitive strain
into flexion, which in turn maintained his pain. This was
further reinforced by his anxiety levels related to work
and home, lack of control over his pain disorder and
inactivity.
Management focused on a motor control intervention
to reduce the flexion strain at L5/S1 in a functionally
specific manner with relaxation of the thoraco-lumbar
spine and enhancing control of segmental lordosis at
L5/S1. Initally he was taught to dis-associate lumbo-pelvic
lordosis from thoracic in supine, sitting and standing. This
was in order to develop proprioceptive awareness and
control of this region and so reduce the flexion strain at
L5/S1. Once this was achieved he was then taught to coactivate his lower lumbar multifidus with his transverse
abdominal wall (in a neutral lordosis), with relaxation of
his thoracic erector spinae and upper abdominal muscles
(with normal respiration) in these postures. At this stage
previously aggravating postures and movements into
forward bending were targeted and retrained so that the
patient could perform them (controlling the L5/S1 within a
neutral lordosis), in a pain-free manner thereby enhancing
his functional capacity. This in turn reduced his fear of
movement and activity. His exercise program was then
progressed into a gym setting where he was taught to
integrate his lumbo-pelvic control into a graded cardiovascular exercise program as well as training strength and
endurance with loaded tasks such as squats, lunges and
resistance lifting tasks. As the patient’s functional mobility
increased and pain reduced his coping strategies improved
and he was capable of a graduated return to work. The
resolution of the disorder supports the classification that
the control impairment into flexion represented the
dominant underlying mechanism driving the disorder.
4. Validity of the classification system
There is a growing concensus within the literature that
current diagnostic and classification approaches for
253
CLBP are limited, and a mechanism based classification
of CLBP disorders from a biopsychosocial perspective is
required (McCarthy et al., 2004). Although considerable
research has documented the biopsychosocial nature of
CLBP, further research is required to test the validity of
this approach in management of CLBP disorders to
determine whether it predicts and indeed improves
patient outcomes.
There is growing evidence to support the validity of
the ‘control impairment’ classification system as a
subgroup with CLBP. Recent research has shown that
physiotherapists trained in the classification system can
reliably identify five different subgroups with a classification of control impairment (Dankaerts et al.,
2005a, b). Laboratory evidence for the presence of
specific motor control and postural deficits have been
documented in a series of studies conducted on patients
with CLBP with a classification of ‘control impairments’
(O’Sullivan et al., 1997a–c, 2003; Burnett et al., 2004;
O’Sullivan et al., 2004; Dankaerts et al., 2005b).
Motor learning interventions have been shown
efficacious in patient groups with a classification of
control impairment, with documented reductions in
pain and disability (O’Sullivan et al., 1997a–c, 1998,
2001; Dankaerts et al., 2004).
5. Summary
CLBP disorders must be considered within a biopsychosocial framework. The presence and dominance of
the potential pathoanatomical, physical, neurophysiological, psychological and social factors that may impact
on these disorders is different for each individual with
CLBP. This highlights the enormous complexity and
individual nature of the problem. It is critical that
classification of CLBP pain disorders be based on the
mechanism (s) underlying and driving the disorder. It is
proposed that motor control impairments may be
adaptive or mal-adaptive in nature. The treatment of
the signs and symptoms of a pain disorder cannot be
justified without an understanding of its underlying
mechanism as there are sub-groups of patients for whom
physiotherapy treatment is not indicated. It is proposed
that there is a large sub-group of CLBP disorders where
mal-adaptive movement and control impairments dominate the disorder, resulting in either excessive or
impaired dynamic spinal stability and loading. This in
turn becomes a mechanism for ongoing pain. Physiotherapy interventions that are classification based and
specifically directed to the underlying driving mechanism, have the potential to alter these disorders and
impact on both the primary physical and secondary
cognitive drivers of pain. This approach is not limited
only to the lumbo-pelvic region but can be applied to all
regions of the musculoskeletal system. The evidence to
ARTICLE IN PRESS
254
date supports these proposals although further research
is required to further develop and validate this
approach.
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TITLE:
Diagnosis and classification of pelvic girdle pain disorders Part
1: A mechanism based approach within a biopsychosocial
framework.
AUTHORS:
Ass Prof Peter B. O’Sullivan, PhD
Curtin University of Technology
School of Physiotherapy
Darren J. Beales, Master of Manipulative Therapy
CORRESPONDANCE:
Ass Prof Peter O’Sullivan
GPO Box U1987
Perth WA Australia 6845
Phone: 61 8 9266 3629
Fax: 61 8 9266 3699
E-mail: [email protected]
INSTITUTIONAL ATTRIBUTION:
As above
KEY WORDS:
pelvic girdle pain, sacroiliac joint, classification, pain mechanisms
ABSTRACT:
The diagnosis and classification of pelvic girdle pain (PGP) disorders remains
controversial despite a proliferation of research into this field. The majority of PGP
disorders have no identified pathoanatomical basis leaving a management vacuum.
Diagnostic and treatment paradigms for PGP disorders exist although many of these
approaches have limited validity and are uni-dimensional (ie. biomechanical) in nature.
Furthermore single approaches for the management of PGP fail to benefit all. This
highlights the possibility that ‘non-specific’ PGP disorders are represented by a number
of sub-groups with different underlying pain mechanisms rather a single entity.
This paper examines the current knowledge and challenges some of the common beliefs
regarding the sacroiliac joints and pelvic function. A hypothetical ‘mechanism based’
classification system for PGP, based within a biopsychosocial framework is proposed.
This has developed from a synthesis of the current evidence combined with the clinical
observations of the authors. It recognises the presence of both specific and non-specific
musculoskeletal PGP disorders. It acknowledges the complex and multifactorial nature
of chronic PGP disorders and the potential of both the peripheral and central nervous
system to promote and modulate pain. It is proposed that there is a large group of
predominantly peripherally mediated PGP disorders which are associated with either
‘reduced’ or ‘excessive’ force closure of the pelvis, resulting in abnormal stresses on pain
sensitive pelvic structures. It acknowledges that the interaction of psychosocial factors
(such as passive coping strategies, faulty beliefs, anxiety and depression) in these pain
disorders has the potential to promote pain and disability. It also acknowledges the
complex interaction that hormonal factors may play in these pain disorders. This
classification model is flexible and helps guide appropriate management of these
disorders within a biopsychosocial framework. While the validity of this approach is
emerging, further research is required.
TEXT:
PELVIC GIRDLE PAIN DISORDERS
Pelvic girdle pain (PGP) disorders represent a small group of musculoskeletal pain
disorders. Pain associated with the sacroiliac joints (SIJ’s) and/or the surrounding
musculoskeletal and ligamentous structures represent a sub-group of these disorders.
Specific inflammatory pain disorders of the SIJ’s, such as sacroiliitis, are the most readily
identified PGP disorders (Maksymowych et al., 2005). However PGP disorders more
commonly present as ‘non-specific’ (no identified pathoanatomical basis), often arising
during or shortly after pregnancy (Bastiaanssen et al., 2005; Berg et al., 1988; Ostgaard et
al., 1991) or following traumatic injury to the pelvis (Chou et al., 2004; O'Sullivan et al.,
2002a). Frequently these pain disorders are misdiagnosed and managed as lumbar spine
disorders, as pain originating from lumbar spine commonly refers to the SIJ region.
However there is growing evidence that PGP disorders manifest as a separate sub-group
with a unique clinical presentation and the need for specific management.
A number of PGP disorders do not resolve (Albert et al., 2001; Larsen et al., 1999; Noren
et al., 2002; Ostgaard et al., 1996; To and Wong, 2003), becoming chronic despite the
absence of pathoanatomical abnormalities on radiological examination or signs of a
systemic or inflammatory disorder from blood screening (Hansen et al., 2005). This
leads to a broad diagnosis of a ‘non-specific’ PGP disorder and leaves a diagnostic and
management vacuum. These PGP disorders are commonly associated with signs and
symptoms indicating that the pain originates from the SIJ’s and/or their surrounding
connective tissue and myo-fascial structures (Albert et al., 2000; Berg et al., 1988;
Damen et al., 2001; Kristiansson and Svardsudd, 1996; Laslett et al., 2003; Mens et al.,
1999; O'Sullivan et al., 2002a; Vleeming et al., 2002). However identification of a
painful structure does not provide insight into the underlying mechanism(s) that drives
the pain (O'Sullivan, 2005a).
A number of theoretical models have been proposed with regard to potential underlying
pain mechanisms in PGP. Chiropractic, Osteopathic and Manual Therapy models
commonly propose that the SIJ’s can become ‘fixated’ or ‘displaced’ leading to
positional faults. There are a series of complex clinical procedures proposed to identify
these so called ‘positional faults’ and treatment with manipulation, mobilisation and/or
muscle energy techniques has been suggested to rectify them (Cibulka, 2002; DonTigny,
1990; Kuchera, 1997; Oldreive, 1998; Sandler, 1996). Although manual and
manipulative techniques can result in short term pain modulation (Wright, 1995), there is
little evidence for the long term benefits of SIJ manipulation or other passive treatments
used in isolation for the management of chronic PGP disorders (Stuge et al., 2003). The
selection of these techniques is often directed by treating the signs and symptoms of the
disorder rather than a valid and clear diagnostic and classification paradigm based on the
mechanisms that underlie the pain disorder.
More recently emphasis has been placed on enhancing motor control deficits in PGP
disorders. This is based on the premise that deficits in lumbo-pelvic motor control result
in impaired load transference through the pelvis and thereby contribute to a peripheral
nociceptive drive of symptoms (Mens et al., 1996; O'Sullivan and Beales, 2007;
O'Sullivan et al., 2002a; Vleeming et al., 1996; Vleeming et al., 1990b). There is
growing evidence based on outcome studies that some PGP disorders do indeed respond
well to specifically targeted motor training interventions (O'Sullivan and Beales, 2007;
Stuge et al., 2004a; Stuge et al., 2004b). However not all PGP disorders respond to these
interventions (Stuge et al., 2006). Relevant to this inconsistency in outcome, is the
existence of different patterns of motor control impairments in PGP subjects. For
instance increased pelvic floor activation has been documented in subjects with
peripartum PGP consistent with SIJ involvement (Pool-Goudzwaard et al., 2005), while
another group of subjects with SIJ pain (with a positive active straight leg raise test
(ASLR)) demonstrate compromised control of the pelvic floor (O'Sullivan and Beales,
2007; O'Sullivan et al., 2002a). These findings highlight that; (i) there may be various
underlying mechanisms that drive different PGP disorders, and (ii) the need for a
classification based approach which guides targeted interventions for sub-groups of
subjects with PGP, which is based upon the underlying pain mechanism(s) that drives the
disorder.
CHALLENGING THE BELIEFS REGARDING
THE SACROILIAC JOINTS AND THE PELVIS
The SIJ perhaps more than any other joint complex in the body has been shrouded by an
enormous amount of mystique within the field of Manual Therapy – with complex,
poorly validated and often confusing theories and treatment approaches associated with
it. Beliefs of the clinician (that the pelvis is ‘displaced’ or ‘unstable’) commonly become
the beliefs of the patients. For many patients these clinical labels can be detrimental with
the potential to render the patient passively dependent on someone to ‘fix them’,
elevating anxiety levels, reinforcing avoidance behaviours and promoting disability.
Increased passive dependence and fear/anxiety has the potential to further increase the
central drive of pain, contributing to disability and the chronic pain cycle. It is therefore
important to be clear on the ‘facts’ regarding the SIJ’s and put them into the context of
current knowledge. The basic anatomy, biomechanics and stability models proposed for
the SIJ are documented elsewhere and as such wont be reviewed in full here (Lee and
Vleeming, 2000; Pool-Goudzwaard et al., 1998; Vleeming et al., 2006).
The facts regarding the SIJ’s
•
The SIJ’s are inherently stable (Snijders et al., 1993a; Vleeming et al., 1990a;
Vleeming et al., 1990b).
•
The joints are designed for load transfer (Gray and Williams, 1989; Kapandji,
1982) and can safely transfer enormous compressive loading forces under normal
conditions (Snijders et al., 1993a).
•
The SIJ has little movement in non-weight bearing (average 2.5 degrees rotation)
(Brunner et al., 1991; Jacob and Kissling, 1995; Sturesson et al., 1989; Vleeming
et al., 1992a; Vleeming et al., 1992b), and even less in weight bearing (average
0.2 degrees rotation) (Sturesson et al., 2000).
•
Movement of the SIJ cannot be reliably assessed by manual palpation, particularly
in weight bearing (Sturesson et al., 2000; van der Wurff et al., 2000a; van der
Wurff et al., 2000b).
•
Due to its anatomical makeup, intra-articular displacements within the SIJ’s are
unlikely to occur. No study utilising a valid measurement instrument has
identified positional faults of the SIJ – in fact the converse is true (Tullberg et al.,
1998).
•
Distortions of the pelvis observed clinically are likely to occur secondary to
changes in pelvic and trunk muscle activity, resulting in directional strain and not
positional changes within the SIJ’s themselves (Tullberg et al., 1998).
•
No study utilising a valid measurement tool has demonstrated that pelvic
manipulation alters the position of the pelvic joints (Tullberg et al., 1998) – pain
relief from these procedures is likely to result from nociceptive inhibition based
on neuro-inhibitory factors and/or altered patterns of motor activity (Pickar, 2002;
Wright, 1995).
•
Asymmetrical laxity of the SIJ’s, as measured with Doppler imaging, has been
shown to correlate with moderate to severe levels of symptoms in subjects with
peripartum PGP (Damen et al., 2001). Generalised SIJ laxity is not associated
with peripartum pelvic pain (Damen et al., 2001).
•
When clinical signs of reduced force closure have been identified (positive
ASLR), the increased movement is identified at the symphysis pubis – not the
SIJ’s (Mens et al., 1999). It is likely that the torsional forces occurring at the
SIJ’s can cause strain across pain sensitised tissue.
•
Pain from the SIJ is located primarily over the joint (inferior sulcus) and may
refer distally, but not to the low back (Dreyfuss et al., 1996; Fortin et al., 1994a;
Fortin et al., 1994b; Maigne et al., 1996; Schwarzer et al., 1995; Slipman et al.,
2000; van der Wurff et al., 2006; Young et al., 2003).
•
SIJP disorders can be diagnosed using clinical examination (Laslett et al., 2005a;
Laslett et al., 2005b; Laslett et al., 2003; Petersen et al., 2004; Young et al., 2003).
This includes the finding of pain primarily located to the inferior sulcus of the
SIJ’s, positive pain provocation tests for the SIJ’s and an absence of painful
lumbar spine impairment.
•
The SIJ has many muscles that act to compress and control it (force closure),
thereby enhancing pelvic stability (creating stiffness) allowing for effective load
transfer via the pelvis during a variety of functional tasks (Damen et al., 2002;
Mens et al., 2006; O'Sullivan et al., 2002a; Pool-Goudzwaard et al., 2004;
Richardson et al., 2002; Snijders et al., 1993a; b; Snijders et al., 2006; Snijders et
al., 1998; van Wingerden et al., 2004; Vleeming et al., 1995; Vleeming et al.,
1990a; Vleeming et al., 1990b).
•
PGP disorders may be associated with ‘excessive’ as well as ‘insufficient’ motor
activation of the lumbopelvic and surrounding musculature (Hungerford et al.,
2003; O'Sullivan and Beales, 2007; O'Sullivan et al., 2002a; Pool-Goudzwaard et
al., 2005).
CLASSIFICATION OF PELVIC GIRDLE PAIN DISORDERS
Chronic pain disorders are complex, multifactorial and need to be considered within a
biopsychosocial framework. A different cluster of potential physical, pathoanatomical,
psychosocial, hormonal and neuro-physiological factors is associated with each disorder
(Figure 1). Needless to say the interactions between these factors are very complex. This
highlights the need for a flexible classification and management approach for each
disorder.
Although the SIJ’s and the surrounding ligamentous and myofascial structures are
potentially nociceptive structures (Fortin et al., 1994a; Fortin et al., 1994b; Vilensky et
al., 2002), from a neurophysiologic perspective it is well known that ongoing pain can be
mediated both peripherally and centrally, and the forebrain can greatly modulate this
process (Woolf, 2004; Zusman, 2002). It is therefore logical that PGP disorders can
potentially be both peripherally or centrally induced/maintained, with a different balance
or dominance of peripheral and central factors associated with each disorder (Elvey and
O'Sullivan, 2005).
Furthermore with PGP there is the potential contributing role of sex hormones. There are
a number of possible pathways by which hormones may influence PGP (Figure 2). There
is some evidence that sex hormones are active in pain modulation (Aloisi and Bonifazi,
2006). Sex hormones are also known to influence the inflammatory process in
inflammatory pain disorders (Schmidt et al., 2006). Furthermore sex hormones may alter
collagen synthesis (Kristiansson et al., 1999), thereby effecting the load capacity of the
pelvis. There is some evidence to support the role of hormones in PGP disorders, with
higher serum levels of progesterone and relaxin in early pregnancy being found in
subjects who develop peripartum PGP compared to those who do not (Kristiansson et al.,
1999). Via these processes sex hormones have the potential to contribute to PGP in
different clinical presentations (Figure 2). Further research is required to clarify how the
role of hormones may differ in these various presentations of PGP.
The proposed classification model for PGP disorders is based on the potential
mechanisms that can drive the PGP. This classification approach is not exhaustive but
rather provides a framework to guide the clinician. Based on the mechanism(s) that
underlie these disorders and operating within a biopsychosocial framework, the
classification model aims to facilitate the diagnosis, classification (Figure 3), and targeted
management of these disorders.
The clinical examination
The clinical examination is critical to the clinical reasoning process that underpins this
diagnosis and classification framework. In the interview process all the following need to
be considered:
•
the pain area (localised versus generalised pain can indicate peripheral from
central pain drive)
•
pain pattern (intermittent versus constant, 24 hour pain pattern, sleep
disturbances)
•
pain intensity
•
pain behaviour (specific movements and postures that provoke and relieve pain)
•
levels of disability and impairment
•
specific pain history (specific and surrounding events that may have contributed
to the development of symptoms)
•
family history of PGP
•
the patients pain coping strategies (active versus passive coping)
•
the patients pain beliefs
•
presence of avoidant behaviours due to fear of movement and other psychosocial
factors including present and past history of anxiety and depression
•
pacing patterns
•
concurrent presence of disorders of continence and/or sexual dysfunction.
Review of radiology if present and screening for specific causes PGP may be indicated
from this process. This allows for a determination as to the area and nature of the pain.
A thorough physical examination is then required to determine the pain source and
behaviour in relationship to the patients’ movement behaviour. Physical tests should
include:
•
palpation of the inferior sulcus of the SIJ and surrounding pelvic ligamentous and
myo-fascial structures
•
provocative tests for the SIJ and surrounding ligamentous and myofascial
structures (Laslett et al., 2005a; Laslett et al., 2005b; Laslett et al., 2003; Petersen
et al., 2004; Young et al., 2003)
•
the ASLR test in supine and prone as a test of load transfer, with a positive test
resulting in normalisation of ASLR with the addition of pelvic compression
(Mens et al., 1999; O'Sullivan and Beales, 2007)
•
careful analysis of the pain provoking and relieving activities and postures
(functional impairments) highlighted from the interview to identify the presence
of impairments of movement and motor control as well as avoidance behaviours
and determine their relationship to the pain disorder. Determining whether altered
motor patterns are adaptive/protective (pain is aggravated when motor control
patterns are normalised) or mal-adaptive (pain is relieved when motor control
deficits are normalised) is essential.
•
tests for specific muscle function for the pelvic floor, the abdominal wall, the
back muscles, iliopsoas, quadratus lumborum, the gluteal muscles and piriformis.
In addition the adjacent areas of the lumbar spine (including neural tissue) and hip joints
should be thoroughly investigated to rule out involvement of these areas or to assess for
coexisting pathology/dysfunction in these regions.
Correlating the patients reported pain behaviour, beliefs and levels of impairment with
their clinical presentation (observing for avoidance behaviours, catastrophising etc) is
important to determine whether cognitive issues such as fear of movement are present
and dominant. On synthesis of this material a diagnosis and classification of the PGP
disorder can be made.
1. Specific pelvic girdle pain disorders:
Pelvic girdle pain disorders associated with specific pathological processes include
inflammatory arthritis, sacroiliitis, infections and fractures. These disorders are amenable
to specific diagnosis with appropriate blood screening and radiological investigation.
They can be associated with altered patterns of motor control behaviour that are
‘adaptive’ and/or protective of the underlying disorder. Treating the signs and symptoms
of these disorders by manual therapy and/or specific exercise interventions is generally
not appropriate as it does not address the underlying pain mechanism of the disorder.
Physiotherapy may be limited to management of the sequelae of the underlying
disease/pathological processes especially in disorders such as ankylosing spondylitis.
2. Non-specific pelvic girdle pain disorders:
2.1 Non-specific inflammatory pelvic girdle pain disorders:
There appears to be a group of PGP disorders that present as being inflammatory in
nature, rather than mechanical. They are characterised by constant, disabling and nonremitting pain, located in the SIJ’s, that is provoked with weight bearing, pelvic
compression (such as a SIJ belt) and with SIJ pain provocation tests. These disorders
may show areas of increased uptake on bone scan but are not linked to a specific
inflammatory disorder diagnosis based on blood screening. They may be relieved with
rest, anti-inflammatory medications and local steroid injections to the SIJ, but are
resistant to physical interventions.
Although the exact underlying mechanism for these PGP disorders is unknown it is
possible that hormonal factors play a role, particularly given their common onset in the
first trimester of pregnancy or pain modulation with hormonal cycles or changes.
Although the role of sex hormones is purely speculative in this group of patients, further
research into their effect is warranted.
2.2 Peripherally mediated (mechanically induced) pelvic girdle pain
disorders:
These disorders are characterised by localised pain that has a defined anatomical location
(SIJ and associated connective tissue and myofascial structures +/- symphysis pubis).
The pain is intermittent in nature and is provoked and relieved by specific postures and
activities related to vertical or directional loading in weight bearing positions. They are
not usually associated with spinal movement related pain and/or spinal movement
impairment. A specific pain source at the SIJ and its surrounding structures can usually
be identified by specific provocative manual tests (Laslett et al., 2005a; Laslett et al.,
2005b; Laslett et al., 2003; Petersen et al., 2004; Young et al., 2003). These disorders are
usually associated with consistent local motor control changes (inhibition or excitation).
These disorders usually have a clear mechanism or time of onset (either repeated strain or
direct trauma to the pelvis or peripartum PGP). It is proposed that these disorders may be
classified into two clinical subgroups (Figure 4).
2.2.1 Reduced force closure
The first group represents disorders where the peripheral pain drive is associated with
excessive strain to the sensitised SIJ’s and/or surrounding connective tissue and
myofascial structures secondary to ligamentous laxity (Damen et al., 2001), coupled with
motor control deficits of muscles that control force closure of the SIJ’s (Hungerford et al.,
2003; O'Sullivan and Beales, 2007; O'Sullivan et al., 2002a). These motor control
deficits may have originally developed secondary to the pain disorder, but now their
presence is mal-adaptive as the resultant ‘reduced forced closure’ leads to impaired load
transfer through the pelvis, acting as a mechanism for ongoing strain and peripheral
nociceptive drive for the pain disorder. Hormonal influences on collagen synthesis may
be an important factor in this group.
These disorders are commonly associated with postpartum PGP and present with a
positive ASLR test (normalised with pelvic compression) (O'Sullivan et al., 2002a; Stuge
et al., 2004a). The motor control deficits that present in these disorders are variable and
are linked to a loss of functional patterns of co-contraction of the local force closure
muscles of the pelvis (such as the pelvic floor, the transverse abdominal wall, the lumbar
multifidus, iliopsoas and the gluteal muscles). This is commonly associated with
attempts to stabilise the lumbopelvic region via co-activation of other trunk muscles
(quadratus lumborum, thoracic erector spinae, diaphragm, external oblique, rectus
abdominis and vertical fibres of internal oblique). Their primary functional impairments
are associated with pain in weight bearing postures such as sitting, standing and walking,
or loaded activities inducing rotational pelvic strain associated with coupled spine / hip
loading activities (ie. cycling and rowing resulting in posterior rotational strain on ilium).
These patients commonly assume postures that are associated with inhibition of the local
pelvic muscles (pelvic floor, transverse abdominal wall, lumbar multifidus and the gluteal
muscles) such as ‘sway’ standing, ‘hanging off one leg’, ‘slump’ sitting or ‘thoracic
upright’ sitting (Dankaerts et al., 2006; O'Sullivan et al., 2006; O'Sullivan et al., 2002b;
Sapsford et al., 2006) and present with a loss of lumbopelvic control (inability to
disassociate pelvic from thoracic movement). These disorders may be relieved with a SIJ
belt (Mens et al., 2006; Ostgaard et al., 1994), training optimal alignment of their spinopelvic posture and functional enhancement of local co-contraction strategies across the
pelvis with relaxation of the thoraco-pelvic musculature (O'Sullivan and Beales, 2007).
These disorders may gain short term relief from mobilisation, muscle energy techniques,
soft tissue massage and manipulation of the SIJ’s (clinical observation) although these in
isolation tend not to benefit the long term outcome of the disorder. There is evidence that
long lever exercise regimes may aggravate these disorders (Mens et al., 2000). These
disorders can be further sub-grouped based on their pattern of motor control dysfunction.
Different combinations of motor control deficits may be found within the local
lumbopelvic muscles such as is observed in low back pain disorders that result in
different directional (vertical, rotational) strain patterns within the pelvis (O'Sullivan,
2005b).
Management of these disorders focuses on functionally enhancing force closure across
the pelvic structures based on the specific motor control deficits present. The aim of the
intervention is to provide functional activation of the motor system in order to control
pain and restore functional capacity (Figure 4). There is good evidence to support the
efficacy of this type of approach in these disorders (O'Sullivan and Beales, 2007; Stuge et
al., 2004a; Stuge et al., 2004b).
2.2.2 Excessive force closure
The second group is defined by a group of PGP disorders where the peripheral
nociceptive drive is based on excessive, abnormal and sustained loading of sensitised
pelvic structures (SIJ’s and surrounding connective tissue and or myofascial structures)
from the excessive activation of the motor system local to the pelvis (excessive force
closure). This patient group presents with localised pain to the SIJ’s and commonly also
the surrounding connective tissue and myo-fascial structures (such as the pelvic floor and
piriformis muscles) as well as positive pain provocation tests. However this group of
patients has a negative ASLR (no feeling of heaviness). Compression (manual or using a
SIJ belt), is often provocative, as is local muscle activation (pelvic floor, transverse
abdominal wall, back muscles, iliopsoas, gluteal muscles). They commonly hold habitual
erect lordotic lumbopelvic postures associated with high levels of co-contraction across
various muscles such as the abdominal wall, pelvic floor, local spinal muscles (lumbar
multifidus, psoas major) and in some cases the gluteal and piriformis muscles which may
become pain sensitised. These motor control responses often become habitual secondary
to excessive cognitive muscle training and/or muscle guarding of the lumbopelvic
muscles, and are themselves mal-adaptive (provocative). These patients report pain relief
from cardiovascular exercise, relaxation, assuming passive spinal postures (which they
seldom do), as well as short term relief with stretching, soft tissue massage, manipulation,
muscle energy techniques and cessation of stabilisation exercises. These disorders are
commonly associated with the patients belief that their pelvis is ‘unstable’ or ‘displaced’
and that more muscle contraction or ‘pelvic re-alignment’ is beneficial. This is
commonly reinforced by the treating therapists’ beliefs. These disorders may be induced
by intensive ‘stabilisation exercises’, Pilates, ball exercise, and cognitive muscle exercise
training of the abdominal wall, lumbar multifidus and pelvic floor. Patients with these
disorders are commonly anxious, under high levels of stress, highly active and seldom
rest.
Management of these disorders focuses on reducing force closure across the pelvic
structures (Figure 4). This is carried out with a combination of approaches such as:
general as well as targeted relaxation strategies, breathing control, muscle inhibitory
techniques, enhancing passive/relaxed spinal postures, pacing strategies, hydrotherapy,
cessation of stabilisation exercise training, and a focus on cardiovascular exercise.
Anecdotally this approach appears very effective although clinical studies are required to
validate this.
2.2.3 Psychosocial influences on peripherally mediated pelvic girdle pain
It is known that chronic pain and PGP disorders are commonly associated with not only
physical but also psychosocial and cognitive impairments (Bastiaenen et al., 2004;
Bastiaenen et al., 2006; Linton, 2000; 2005; Main and Watson, 1999) (Figure 1). Even in
the presence of a dominant peripheral nociceptive drive to PGP (such as described
above), cognitive and psychosocial factors are invariably linked to these disorders
influencing pain amplification and disability levels to varying degrees. This highlights
the need for a biopsychosocial (behavioural) approach to understanding and managing
chronic PGP disorders even when they are peripherally mediated in nature.
Psychosocial factors have the potential to both ‘up’ regulate or ‘down’ regulate pain. For
example, a classification of ‘reduced force closure’ may be associated with associated
cognitive impairments such as faulty beliefs, elevated anxiety levels and passive coping
strategies that amplifies pain via the central nervous system and promotes high levels of
disability associated with the pain disorder. In this case the intervention must address the
cognitive impairments associated with the disorder within the motor learning intervention
such as by promoting accurate beliefs, relaxation techniques and active coping strategies.
On the other hand, if the same ‘reduced force closure’ classification is associated with
positive beliefs, active coping strategies and limited functional impairments, then the
primary focus can be placed more on the physical impairments of the disorder to establish
pain control.
Similarly a classification of ‘excessive force closure’ may be associated with underlying
stress and anxiety. In this case dealing with these cognitive factors with relaxation,
breathing strategies, pacing and cardiovascular exercise is a critical adjunct to the motor
learning management of these disorders. Where the psychosocial/cognitive components
of the disorders are resistant to change, complementary psychological and/or medical
intervention may be essential.
2.4 Central nervous system driven pelvic girdle pain disorders:
The mechanisms of central nervous system sensitisation and/or glial cell activation and
their involvement in the maintenance of chronic pain states are well known (Hansson,
2006; Woolf, 2004), and may persist even once a peripheral nociceptive drive is removed
or has resolved. In this way chronic PGP can be potentially mediated largely or entirely
via the central nervous system. In these disorders, the pain may have initially presented
as a peripherally driven disorder, but once chronic, the pain does not have a presentation
consistent with a peripheral pain source. These pain disorders are commonly associated
with widespread, severe, and constant pain that is non-mechanical in nature. They lack a
specific detectable peripheral nociceptive drive or pathological basis and are commonly
associated with widespread allodynia. These disorders are associated with high levels of
physical impairment and social impact, and may be associated with widespread and
inconsistent motor control disturbances and abnormal pain behaviours that are secondary
to the pain state and do not clearly drive the pain disorder. These disorders are often
associated with dominant psychosocial factors (somatisation, catastrophising,
pathological fear and/or elevated anxiety, depression, as well as significant social factors
such as past history of sexual abuse etc).
Although these disorders appear to represent a small sub-group of chronic PGP disorders,
they are highly disabling and resistant to physical interventions. Management of these
disorders must be multidisciplinary involving medical and psychological management as
a primary approach. Functional rehabilitation should aim to enhance normal general
body function and address abnormal pain behaviours without a focus on pain. Passive
treatments and rehabilitation that focuses on specific muscle control strategies may
simply act to reinforce abnormal pain behaviours and hyper-vigilance in these patients.
2.5 Genetics and pelvic girdle pain:
The role that genetics play with non-specific PGP disorders is largely unknown although
its potential must be recognised. Subjects with PGP are more likely to have a mother or
sister who also has PGP (Larsen et al., 1999; Mogren and Pohjanen, 2005) which may
implicate a genetic link although social influences may also mediate this effect. A
genetic predisposition in PGP patients related to changes in action of relaxin is a
proposed as one mechanism of genetic influence on PGP (MacLennan and MacLennan,
1997). Clearly further research into genetic influences is required.
SUMMARY
This paper provides a broad clinical classification model for the management of chronic
PGP disorders. It is a flexible, mechanism-based approach within a multifactorial
biopsychosocial framework. The classification model directs appropriate management
based on the underlying mechanism/s that drives the pain. Although there is growing
support for the validity of this approach, further research is required into this area.
ACKNOWLEDGEMENTS:
Many thanks to Dr Britt Stuge and Dr Wim Dankaerts for their clinical insights and
advice in the final stages of writing this manuscript.
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CAPTIONS TO ILLUSTRATIONS:
FIGURE 1: Factors that need consideration within a biopsychosocial framework for the
diagnosis and classification of chronic pelvic girdle pain disorders.
FIGURE 1:
Genetic factors
- potentially influencing all other domains
Patho-anatomical factors
- structural pathology
- ligamentous laxity
- identification of peripheral pain generator
(sacroiliac joint / pubic symphysis,
myofascial / connective tissue)
Social factors
- relationships – family, friends, work
- caring for children
- work issues
- medical advice and treatment
- support structures
- compensation – emotional, financial
- cultural factors
- socio-economic factors
- stress
Psychological factors
- personality type
- beliefs & attitudes towards pain disorder
- coping strategies – passive vs active
- hyper-vigilance
- pacing
- fear avoidance behaviour
- emotions - fear / anxiety / depression / anger / helplessness
- illness behaviour
Pelvic
Girdle
Pain
Neuro-physiological factors
- peripheral sensitisation
- hormonal factors
- central sensitisation
- sympathetic nervous system activity
- somatic complaints
- glial cell activation
Physical factors
- mechanism of injury if present
- disorder history (pregnancy related)
- disorder stage – acute, sub-acute, chronic
- area of pain – local / generalised / referred
- pain behaviour – intermittent vs constant
– provocative and relieving factors
- mechanical vs non-mechanical provocation
- +ve active straight leg raise
- SIJ provocation tests
- adaptive vs mal-adaptive movement behaviours
- motor control impairments (↑ or ↓ motor activation)
- disability levels
- activity levels / conditioning / strength / muscle endurance
- work / home environment / lifestyle
- ergonomic factors
FIGURE 2: Possible actions of hormones in the development and maintenance of pelvic
girdle pain. Factor affecting hormone levels are also presented.
FIGURE 2:
Medications
Altered
Collagen
Synthesis
Physical
Stressors
Altered Load
Tolerance of
Pelvic
Ligamentous
Structures
Direct
Modulation of
Inflammatory
Mediators
Toxins
Inflammatory
Pain
Pregnancy
Age
HORMONE
LEVELS
Central
and/or
Peripheral
Sensitisation
Direct
Modulation
of Neural
Excitability
Psychological
Stressors
Menstrual
Cycle
Genetics
Developmental
Organisation of
Central Nervous
System
Structural
Basis
Behavioural
Basis
Synthesis
Psychosocial
Mechanisms
FIGURE 3: Mechanism based classification and management of chronic pelvic girdle
pain disorders.
FIGURE 3:
CHRONIC PELVIC GIRDLE PAIN DISORDERS
Specific pelvic pain disorders
- Specific inflammatory pain
disorders (sacroiliitis)
- Infections
- Fractures
Non-specific
inflammatory
pain disorder
Non-specific pelvic pain disorders
Centrally mediated pelvic girdle
pain
Non-dominant
psycho-social
factors
Dominant
psycho-social
factors
Peripherally mediated pelvic girdle
pain
(+/- cognitive / psychosocial factors
resulting in central pain amplification)
Reduced force
closure
Excessive force
closure
- Medical management
- Management advice
- Medical management
- Functional rehabilitation
- Multi-disciplinary management
Psychological (cognitive
behavioural therapy), medical,
functional rehabilitation
- Motor learning
within cognitive
framework
(enhance force
closure)
- Functional
restoration
- Motor learning
within cognitive
framework
(reduce force closure
/ relaxation)
- Functional
restoration
FIGURE 4: Sub-classification of pelvic girdle pain disorders with a primary peripheral
nociceptive drive. Peripheral drive is perpetuated by mal-adaptive motor control
dysfunctions.
FIGURE 4:
Mal-adaptive chronic pelvic girdle pain disorders where motor control impairments
represent dominant underlying driving mechanism for pain
Tissue injury / localised pain
Motor response
Excessive force closure
classification
- hyper-activity of pelvic muscles
with excessive joint compression
Factors that may influence pain and motor
response
pathoanatomical
ligamentous laxity
physical
motor control
neurophysiological
hormonal
psychosocial
coping strategies
beliefs
fear avoidance
compensation
genetic
Resolution of the disorder
Non resolution
mal-adaptive patterns adopted
poor coping strategies
prolonged neuromuscular response
excessive ↔ reduced spinal stability
abnormal tissue loading
Management
- identify factors that drive motor system
- cognitive behavioural approach
- relaxation of motor system
- relaxation strategies
- graded movement restoration
Reduced force closure
classification
- motor control deficit of pelvic
stabilising muscles with loss of force
closure
Management
- cognitive behavioural motor control
intervention
- pain control (avoid provocation)
- specific motor activation
- retrain faulty postures and movements
ARTICLE IN PRESS
Manual Therapy ] (]]]]) ]]]–]]]
The inter-examiner reliability of a classification method
for non-specific chronic low back pain patients
with motor control impairment
W. Dankaertsa,b,, P.B. O’Sullivana, L.M. Strakera, A.F. Burnetta, J.S. Skouenc,d
a
School of Physiotherapy, Curtin University, Bentley 6102, WA, Australia
Department of Rehabilitation Sciences and Physiotherapy, Ghent University, Ghent, Belgium
c
The Outpatient Spine Clinic, Haukeland University Hospital, Bergen, Norway
d
Section of Physiotherapy Science, Department of Public Health and Primary Health Care, Faculty of Medicine, University of Bergen, Norway
b
Received 15 June 2004; received in revised form 23 December 2004; accepted 16 February 2005
Abstract
The importance of classifying chronic low back pain (LBP) patients into homogeneous sub-groups has recently been emphasized.
This paper reports on two studies examining clinicians ability to agree independently on patients’ chronic LBP classification, using a
novel classification system (CS) proposed by O’Sullivan. In the first study, a sub-group of 35 patients with non-specific chronic LBP
were independently classified by two ‘expert’ clinicians. Almost perfect agreement (kappa-coefficient 0.96; %-of-agreement 97%)
was demonstrated. In the second study, 13 clinicians from Australia and Norway were given 25 cases (patients’ subjective
information and videotaped functional tests) to classify. Kappa-coefficients (mean 0.61, range 0.47–0.80) and %-of-agreement
(mean 70%, range 60–84%) indicated substantial reliability. Increased familiarity with the CS improved reliability. These studies
demonstrate the reliability of this multi-dimensional mechanism-based CS and provide essential evidence in a multi-step validation
process. A fully validated CS will have significant research and clinical application.
Keywords: Agreement; Classification; Chronic low back pain; Motor control impairment; Reliability
1. Introduction
Low back pain (LBP) is one of the most common and
costly musculo-skeletal pain syndromes, affecting up to
80% of people at some point during their lifetime (Katz,
2002; van Tulder et al., 2002; Ehrlich, 2003; Woolf and
Pfleger, 2003). The re-occurrence rate for LBP is high
and these disorders often develop into a chronic
fluctuating problem with intermittent flares (Croft
et al., 1998; Burton et al., 2004). It has been stated that
Corresponding author. School of Physiotherapy Building 408,
Curtin University of Technology, GPO Box U1987, Perth, WA 6845,
Australia. Tel.: +61 08 9266 3667; fax: +61 08 9266 3699.
E-mail address: [email protected]
(W. Dankaerts).
doi:10.1016/j.math.2005.02.001
caring for chronic LBP (CLBP), is one of the most
difficult and unrewarding problems in clinical medicine
(Leclere et al., 1990) as no approach to diagnosis or
treatment has been shown to be clearly definitive or
effective.
One explanation offered for the inability to identify
effective treatments is the lack of success in defining subgroups of patients who are most likely to respond to a
specific treatment approach (Leboeuf-Yde et al., 1997;
Bouter et al., 1998). Indeed, it has been proposed that
the ‘LBP-group’ conceals a large heterogeneous group
of patients (McKenzie, 1981; Delitto et al., 1995; Spitzer
et al., 1995; Borkan et al., 1998; Bouter et al., 1998;
O’Sullivan, 2000; Leboeuf-Yde & Manniche, 2001). Any
specific treatment applied to a falsely assumed homogenous sample may result in either failure to respond or
ARTICLE IN PRESS
2
W. Dankaerts et al. / Manual Therapy ] (]]]]) ]]]–]]]
aggravation of the disorder (Binkley et al., 1993; Fritz
et al., 2000; Leboeuf-Yde & Manniche, 2001; Fritz et al.,
2003).
The perceived need to accurately classify LBP into
homogenous sub-groups to facilitate treatment to be
tailored for specific disorders, led to an international
forum on LBP ranking the accurate and reproducible
characterization of sub-groups of patients with LBP as
the top research priority (Borkan et al., 1998).
In general, criteria to classify can be defined as
belonging to specific theoretical constructs or dimensions of the domain being classified (Bailey 1994; Ford
et al., 2003). The shift from thinking about LBP as a
patho-anatomical disorder, to viewing LBP as a multifactorial bio-psycho-social disorder is now well accepted
(Borkan et al., 2002). As a consequence of this, the
different dimensions relevant to classifying the domain
of LBP are patho-antomical, signs and symptoms,
psychological and social (Waddell, 1987; Ford et al.,
2003). For LBP, several classification systems (CSs)
from a multitude of perspectives have been proposed.
Recent systematic reviews highlight that the multidimensional nature of LBP is not reflected in most CS
(Ford et al., 2003; McCarthy et al., 2004).
The authors propose that for non-specific CLBP,
there is a special need for a mechanism-based CS
acknowledging the bio-psycho-social dimensions of this
disorder (Woolf et al., 1998; Ford et al., 2003;
O’Sullivan, 2004a). When the mechanism or cause of a
disorder is known, as long as it is amenable for
treatment, treatment of the cause is usually considered
more effective than treating its individual signs and
symptoms (Zimny, 2004).
Table 1 gives an overview of the more commonly used
categories and dimensions used to classify LBP patients
and their limitations. It is increasingly clear that
unidimensional CS’s have limited clinical utility as do
not adequately reflect the nature of LBP nor lead to its
effective management. For CLBP there is no validated
mechanism-based multi-dimensional CS. The development and testing of new CSs based on a multidimensional construct has been recommended (Riddle,
1998; Borkan et al., 2002; O’Sullivan, 2004a).
Recently, O’Sullivan (2000, 2004b) proposed a novel
CS based on multiple dimensions for a sub-group of
patients with NS-CLBP and clinical signs of motor
control impairment (MCI). There is indeed considerable
evidence documenting the presence of MCI in subjects
with NS-CLBP, although, the nature of the impairment
is highly variable (Hodges & Richardson, 1997; O’Sullivan et al., 1997; Hodges and Richardson, 1998;
O’Sullivan et al., 1998; Hodges and Richardson, 1999;
O’Sullivan, 2000; Sahrmann, 2001) and many mechanisms have been postulated for how pain may alter motor
planning (Biedermann et al., 1991; Luoto et al., 1999;
Hodges, 2001). O’Sullivan’s (2000, 2004b) CS has been
described in detail elsewhere but in brief it proposes
(based on very strict inclusion and exclusion criteria)
that a sub-group of patients with NS-CLBP exists
(Table 2). These patients have impairments in the
control of their lumbar spine that expose them to
repeated stress and strain, thereby providing a basis for
ongoing pain. Five distinct clinical patterns were
proposed (Appendix A) based on a specific direction
of MCI and the hypothesized mechanism underlying the
pain disorder (O’Sullivan 2000, 2004b).
Whilst O’Sullivan’s CS appears conceptually coherent, its reliability and validity should be established
before its widespread use in clinical practice and
research. The validation of a CS is a multi-step process
(Woolf et al., 1998; Ford et al., 2003; Fritz et al., 2003;
Dankaerts et al., 2004; O’Sullivan, 2004a) within which
establishing the inter-examiner reliability is a crucial
step. Therefore, the aim of the studies reported in this
paper was to determine the inter-examiner reliability of
this clinical method of classification for NS-CLBP
patients with signs of MCI. The first study aimed to
determine the level of agreement between ‘expert’
clinicians. The second study aimed to determine the
level of agreement between clinicians from Australia and
Norway against the ‘expert’ clinicians and to determine
the effect of the level of clinician familiarity with the
system on their reliability.
2. Methods
Since this paper reports on two studies, the methods
are outlined separately. Fig. 1 provides a flow-chart of
the overall study design. The studies were conducted
from January 2002 till December 2003. Approval to
conduct both studies was obtained from the Curtin
University of Technology, Human Research Ethics
Committee, Perth, Western Australia.
2.1. Study 1
Patients with NS-CLBP were independently assessed
by two ‘expert’ clinicians and agreement between their
diagnoses determined, based on comprehensive subjective and physical examination.
2.1.1. Patients
Patients with a classification of NS-CLBP and MCI
seeking physiotherapy treatment were recruited from a
private multi-disciplinary orthopaedic clinic in the Perth
metropolitan area. After screening and further clinical
assessment using strict criteria for inclusion and exclusion (Table 2), 35 patients were selected (17 males and 18
females; mean age 37712.73 years; duration of LBP
5.676.0 years; Revised-Oswestry disability score
37711%; Body Mass Index 23.172.2 kg/m2). All
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3
Table 1
Different approaches commonly used to classify low back pain (LBP) patients and their limitations
Dimension/category
Uni-dimensional classification systems
Patho-anatomical
Approach
Limitation for NS-CLBP population
Radiological diagnosis (Bernard and
Kirkaldy-Willis, 1987)
Majority (up to 85%) is classified ‘non-specific’ as
no diagnostic imaging procedure is correlated with
LBP (Dillingham, 1995; Deyo and Phillips, 1996;
Nachemson, 1999; Pearce, 2000)
Abnormal findings in asymptomatic individuals are
common (Jensen et al., 1994; Boos and Hodler,
1998; Stadnik et al., 1998; Pfirrmann et al., 1999;
Borenstein et al., 2001; Humphreys et al., 2002)
No insight into the underlying mechanism
responsible for the LBP disorder (may be driven by
neurophysiological, bio-mechanical and/or psychosocial factors)
Identify nociceptive source based on
diagnostic injections (Bernard and KirkaldyWillis, 1987; Bogduk, 1995; Young et al.,
2003)
Signs and Symptoms
‘Treatment based’ approach, using a cluster
of signs and symptoms to classify LBP
(Delitto et al., 1995)
For acute LBP only, a similar approach for chronic
LBP has not yet been reported
Uni-dimensional approach based only on signs and
symptoms has limitations as the basis of a
mechanism-based CS
Prognosis
Based on the future outcome of the patient
(Engel and von Korff MKaton, 1996;
Dionne et al., 1997; Krause et al., 1998)
Of limited use for selection of treatment or
management
Poor prognosis might simply arise because an
appropriate treatment addressing the underlying
mechanism behind the pain disorder has not yet
been identified or tested
Mechanism-based
Hypothesized mechanism behind the
disorder is one of disc derangement
(McKenzie, 1981)
Sahrmann (2001): a classification approach
for LBP consisting of five different categories
based on signs and symptoms and the
premise that ‘impairments’ in the way people
move are the underlying factor of the
musculo-skeletal pain and dysfunction
The validity of this approach for NS-CLBP is
limited
Quebec Task Force Classification (Spitzer,
1987): based on stage of the disorder (acute,
sub-acute or chronic), patho-anatomical
diagnosis (specific or non-specific, ‘red’
flags), signs and symptoms (area of pain
referral), ‘yellow’ flags and work status
(psycho-social)
Designed to assist in making clinical decisions (e.g.
surgery or conservative treatment), establishing a
prognosis, and evaluating the quality of care for
patients with LBP
Of limited use in physiotherapy assessment or
treatment planning (Padfield et al., 2002).
Does not consider the underlying mechanism
behind NS-LBP disorders (apart from
differentiating somatic referred from radicular
pain)
Multi-dimensional classification systems
Stage patho-anatomical signs and
symptoms psychosocial
patients had the protocol explained to them and
provided signed consent prior to entering the study.
2.1.2. Examiners
The two examiners were musculo-skeletal physiotherapists. One clinician (PO’S) was the developer
of the CS and had 18 years experience with patients with
LBP. The other clinician (WD) had 12 years of clinical
experience with patients with LBP and extensive training
by the developer.
No consideration is given to the stage of the
disorder, area of pain, specific versus non-specific
LBP, or yellow flags
Classification model assumes that all LBP disorders
lie within this classification, ignoring the several
other dimensions of LBP within the biopsychosocial framework
2.1.3. Procedure
Prior to conducting this study, 20 patients participating in a different study conducted by the authors were
independently examined and a clinical diagnosis determined by the ‘expert’ clinicians. The aim of this pilot
study was to refine the specific criteria for assignment to
each of the five sub-categories and to further train WD
(O’Sullivan, 2000, 2004b) (Appendix A). With the aid of
videotapes of subjects’ postures and movements, the
clinicians’ diagnoses were compared and discussed, and
operational definitions were refined.
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4
Table 2
Inclusion and exclusion criteria for NSLBP patients with Motor Control Impairmenta
Inclusion criteria
A history of chronic (43 months) LBP
Pain only located to the lower lumbar spine (L4/5 or L5/S1) with minimal radiation
Absence of impaired movement of the symptomatic segment in the painful direction of movement or loading (based on clinical joint motion
palpation examination)
Associated impairments in the control of the motion segment(s) in the provocative movement direction(s)
Clear mechanical basis of disorder: specific postural and functional movements that aggravate and ease symptoms; relief of symptoms when reducing
the strain to the symptomatic spinal segment in the provocation direction
Exclusion criteria
More generalized low back pain (beyond L4-5, L5-S1 region) and/or radiating pain
Dominant non-organic features (yellow flags)
Impaired movement of the symptomatic segment in the painful direction of movement or loading (based on clinical joint motion palpation
examination)
Based on medical assessment (by general practitioner and/or specialist, including radiological imaging): specific diagnoses for LBP disorder (disc
prolapse with radicular pain, severe scoliosis, spondylo-arthrosis, spondylolisthesis, inflammatory or other specific disorders), previous back surgery,
and serious causes of LBP (red flag pathology)
a
All features within the inclusion criteria had to be present; based on O’Sullivan (2000, 2004b).
Following informed consent, patients were allocated
to one of two examiners. The order of testing by the two
examiners varied but for practical reasons could not be
randomized. A full clinical examination was performed
by the first examiner to identify patients with NS-CLBP
who had a classification of MCI based on strict
inclusion and exclusion criteria (Table 1). The comprehensive history of the disorder involved: screening for
yellow and red flags, reviewing medical imaging,
questioning the patient regarding symptom provocation
and relief. The full physical examination consisted of a
series of active and functional movement tests, articular
tests to determine mobility and level of symptom
provocation, neural tissue examination, and tests for
spinal motor control (O’Sullivan, 2000, 2004b). Patients
were then sub-classified into one of the five patterns as
per O’Sullivan (O’Sullivan, 2000, 2004b). Within a
maximum of 1 week (most patients were evaluated by
the second examiner within 24 h) the second examiner
performed a similar full examination and nominated a
classification.
The two examiners acted entirely independently and
were blind to the other’s classification of the disorder.
Assessment sheets were placed in sealed opaque
envelopes and filed for later analysis. Patients were
asked not to provide the second examiner with any
information regarding the first examination process.
2.2. Analysis study 1
Kappa-coefficient and %-of-agreement were calculated to determine the level of agreement between the
‘expert’ clinicians (Portney and Watkins, 2000). The
Kappa-coefficient is a reliability statistic that corrects
for agreement due to chance (Altman, 1991). Data were
analysed using SPSS Version 10.0.
2.3. Study 2
2.3.1. Examiners
Thirteen clinicians (physiotherapists and medical
doctors) of two geographically separate regions (seven
from Western Australia and six from Norway) were
invited to participate based on familiarity with the CS.
Examiners’ characteristics are displayed in Table 3.
The examiners were classified into two sub-groups
based on their level of specific training and clinical
experience with the CS. All examiners were required to
sign a consent form.
2.3.2. Procedure
Patients who participated in Study 1 were asked to
consent to be videotaped and to complete a self-reported
pain questionnaire. If consent was obtained, they were
videotaped performing a series of postures and functional movements that represented commonly reported
aggravating postures and movements of these patients
(O’Sullivan, 2000, 2004b). This included usual posture in
standing, forward bending and return, backward bending and return, single leg standing, usual sitting posture,
slump posture, erect upright posture and sit-to-stand to
sit. Thirty patients classified identically by the two
‘expert’ clinicians (Study 1) gave consent to be
videotaped. Of these, 25 patients were randomly selected
to fill the previously determined numbers (based on
statistical advice) for each of the five patterns. For each
of these 25 patients, a case report was written and
videotapes were edited in a standard manner.
Approximately 1 month prior to the testing day each
participating examiner received an instruction package
consisting of a synopsis of the study methodology and a
comprehensive summary of the study procedure. Three
weeks prior to the testing day a clinical seminar was held
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5
Fig. 1. Flow-chart of study design; MCI ¼ motor control impairment.
by the developer of the CS for all the Western
Australian examiners. One week prior to the testing
day a revision session was held. For logistical reasons
the training for the Norwegian examiners was slightly
different. All Norwegian examiners had previously
undertaken two clinical workshops based on the CS
conducted by the developer. The same instruction
package was sent to Norway 3 weeks prior to the
testing. A 2-day workshop was held prior to testing.
The blinded examiners had to initially determine the
classification for each patient based on the case reports
only. In addition, examiners were given the video
presentation and were asked to classify the patient
based on the combined information. Each examiner
placed their assessment booklet in an opaque envelope,
which was then sealed prior to further analysis.
2.4. Analysis study 2
Kappa-coefficient and %-of-agreement (Portney and
Watkins, 2000) was calculated to determine the level of
agreement between the ‘gold standard’ (as determined
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6
Table 3
Characteristics of examiners (Study 2) as per level of familiarity with Classification System (CS)
Specific training in CS
Age (years)
Clinical experience (years)
Speciality
‘Moderate’ familiar (n ¼ 8)
‘Very’ familiar (n ¼ 5)
Clinical education sessions and/or workshops
regarding the CS with the developer of the CS
45 (range: 40–54; SD: 7)
20 (range: 10–29; SD: 7)
1 GP/physical medicine
1 MD/clinical neurologist
3 Musculo-skeletal physiotherapists
2 Physiotherapists
Postgraduate training under direct
supervision of developer of CS
32 (range: 30–33; SD: 1)
9 (range: 7–11; SD: 2)
4 Musculo-skeletal physiotherapists
1 Sports physiotherapist
Table 4
Results of Studies 1 and 2
Study 1
Study 2
‘Expert’ clinicians (n ¼ 2)
All clinicians (n ¼ 13)
‘Moderate familiar’ clinicians (n ¼ 8)
‘Very familiar’ clinicians (n ¼ 5)
SE+PE
S
S+V
S
S+V
S
S+V
Kappa
%-of-agreement
0.96
0.32
0.61
0.28
0.55
0.40
0.71
97%
48%
70%
44%
65%
54%
78%
(0.13–0.54)
(0.47–0.80)
(0.13–0.37)
(0.47–0.64)
(0.39–0.54)
(0.58–0.80)
(32%–64%).
(60%–84%)
(32%–52%)
(60%–72%)
(48%–64%)
(68%–84%)
Average Kappa-scores (range) and average %-of-agreement (range) SE+PE ¼ based on a comprehensive subjective and physical examination,
S ¼ based on subjective information only (case notes), S+V ¼ based on subjective and video. Guidelines for interpreting the strength of the Kappa
statistic: o0: poor; 0.00–0.20: slight; 0.21–0.40: fair; 0.41–0.60: moderate; 0.61–0.80: substantial; 0.81–1.00: almost perfect (based on Altman, 1991).
by the ‘expert’ clinicians) and the other examiners.
Agreement was also analysed based on the level of
familiarity with the CS, based on subjective information
only, and based on subjective information plus the
videotaped recordings. Descriptive statistics were used
for the analysis of correct classification for each pattern.
Data were analysed using SPSS Version 10.0.
3. Results
3.1. Study 1
Based on independent patient examinations ‘expert’
clinicians demonstrated almost perfect agreement (Kappa-coefficient 0.96; %-of-agreement 97%) (Table 4).
3.2. Study 2
The agreement between examiners and ‘expert’
clinicians based on subjective information and video
was substantial (Table 3). Agreement was reduced when
examiners made a classification decision based only on
subjective information, and among those examiners who
had less familiarization with the CS (Table 3). Fig. 2a–e
shows the correct classification (%) by all examiners for
each pattern. All five patterns could be reliably
identified, with the Flexion Shifting pattern best
identified (82%), and the Active Extension pattern least
correctly identified (62%).
4. Discussion
The objective of Studies 1 and 2 was to assess the
inter-examiner reliability of a CS for NS-CLBP with
MCI as proposed by O’Sullivan (2000, 2004b). Results
of Study 1 revealed that there was almost perfect
agreement between ‘expert’ clinicians, in identifying and
classifying patients with NS-CLBP into specific subgroups of MCI based on a comprehensive clinical
examination (Table 4). Results of Study 2 indicate
substantial clinical agreement across all five patterns
based on combined subjective case reports and video
observation of postures and movements. Good interexaminer reliability is an essential first step for a CS to
be valid and to be of use, clinically and in research
settings (Delitto et al., 1995).
The poor reliability when classification was based
only on subjective findings was expected. This finding
supports that the CS is highly dependent on the
assimilation of both the subjective and physical examination (O’Sullivan, 2000, 2004b).
Study 2 also aimed to evaluate the importance of
specific training in the CS, relative to the ability to
accurately apply the CS. The results of this study
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100
80
(a)
Classification per pattern (%)
correct
Flexion Pattern
incorrect
n=104
68
60
40
20
9
8
11
4
100
(b)
correct
incorrect
82
80
Flexion Shifting
Pattern n=39
60
40
20
18
0
0
0
0
0
Flexion
Active
Passive
MultiShifting Extension Extension directional
100
(c)
80
Active Extension
Pattern n =78
correct
incorrect
62
60
40
20
20
5
9
4
Flexion
100
Flexion
7
(d)
80
Flexion
Active
Passive
Passive Extension correct
incorrect
Pattern n =39
77
60
40
20
20
0
0
0
3
0
Flexion
Active
Passive
Flexion
Flexion
100
(e)
80
Multi-directional
Pattern n =65
Flexion
Active
Passive
correct
incorrect
68
60
40
20
14
12
0
6
0
Flexion
Flexion
Active Passive
Fig. 2. (a–e) Classification per different pattern (in %) by all examiners in Study 2; n ¼ total number of that specific pattern included 13 (total
number of examiners).
(Table 4) show a very clear pattern of improved
reliability associated with more specific (postgraduate)
training. This finding is consistent with Strender et al.
(1997) who state that the amount of formal instruction
(i.e. continuing education) and specific clinical experience in examination procedures and classification rules
is a necessary prerequisite to improving reliability.
There appears to be a special need for a mechanismbased CS for NS-CLBP based on a bio-pyscho-social
framework (Woolf et al., 1998; McCarthy et al., 2004;
O’Sullivan, 2004a; O’Sullivan, 2004b). It is acknowledged that to validate this novel CS as a mechanismbased CS, a multi-step process is required and cannot be
based solely on inter-examiner reliability. For this
reason a model for clinical research into classification
of NS-CLBP has been proposed by the authors
(Dankaerts et al., 2004; O’Sullivan, 2004a). This model
consists of different stages, each stage dealing with
different criteria. Fig. 3 presents a flow-chart summary
of the model.
This multi-dimensional mechanism-based CS is not
an alternative to existing CSs but can be seen as a new
development for a sub-group within the NS-CLBP,
integrating different aspects of established CSs. For
example, the CS proposed by O’Sullivan fits within the
QTFC as it uses several criteria set forward by the
QTFC: the patient sample consists of ‘non-specific’,
‘chronic’, ‘LBP patients without radiation below the
gluteal folds’, absence of ‘red and dominant yellow flags’
and absence of ‘neurological signs’. The proposed CS by
O’Sullivan can be seen as a further sub-classification of
Category 1 of the QTFC. Similar to McKenzie’s method
(McKenzie, 1981; Donelson, 2001), O’Sullivan’s CS is
based on a comprehensive patient assessment. Like
Delitto’s (1995) treatment-based CS or McKenzie’s
method (McKenzie, 1981), O’Sullivan links a very
specific intervention to each of the five patterns.
Of particular interest for direct comparison with the
proposed multi-dimensional CS is the CS developed by
Sahrmann (2001) which appears to be more unidimensional in nature. Both classification models
assume MCIs as a possible underlying factor in LBP
disorders. But there are some substantial differences in
the proposed ways to validate the CS and in the method
used to classify the patients. Van Dillen et al. (1998)
investigated the reliability (among trained therapists) of
the individual tests used in criteria for classification
according to Sahrmann (2001). The nature of their study
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8
Fig. 3. Flow-chart of proposed new model for validation of mechanism-based classification system (CS) for NS-CLBP with Motor Control
Impairment (MCI). Current study shaded.
design assessed reliability based on individual physical
examination items and did not give any insight into the
ability of the clinicians to classify the patients into the
proposed categories. This reliability study served as a
pilot study for a validation study on the CS proposed by
Sahrmann (Van Dillen et al., 2003b). According to
Bailey (1994), a principal aim of classification is
ordering entities into groups with maximum between
group heterogeneity and within group homogeneity. In
Van Dillen et al. (2003b), the location of symptoms
varied from low back only to all kinds of referred
locations. All three different stages of LBP disorder were
included, without consideration for patho-anatomical
findings nor the presence of non-organic signs. The fact
that these inclusion criteria consist of several different
QTFC categories might have led to a heterogeneous
sample.
Rather than relying purely on signs and symptoms
(Van Dillen et al., 1998, 2003a, b), the current studies
used a process of diagnostics to make a clinical
determination as to whether the MCI is the driving
mechanism behind the disorder or is simply a secondary
effect of another process (O’Sullivan, 2004a, b). This
process of diagnostics is described in detail elsewhere
(Elvey and O’Sullivan, 2004). In contrast with Van
Dillen et al. (1998, 2003b), the authors of the current
study place a strong emphasis on the subjective history
and pain behaviour. Within the CS it is critical in
interpreting how the symptoms (as described by the
patient during subjective examination) are influenced by
changes in postural alignment and movement. Another
purpose of taking and integrating history findings is to
determine the presence of dominant non-organic features. Strong evidence exists to suggest that psychosocial
factors can be an important component of certain NSLBP disorders (Linton, 2000). Psychological processes
(cognition, stress, fear, anxiety and depression) are also
known to alter motor behaviour (Hodges and Moseley,
2003) influencing patient’s posture and movement
(Hodges and Moseley, 2003). Attempts to ‘normalize’
the movement or MCI in many of these disorders would
be inappropriate and ineffective (Elvey and O’Sullivan,
2004; O’Sullivan, 2004a). In Van Dillen et al. (1998,
2003b), no other physical examination was performed to
identify other underlying mechanisms of pain response.
In contrast, in the current study the patients were firstly
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identified as having an MCI based on a set of
characteristics (Table 2). We found it essential to include
‘joint motion palpation’ in Study 1. Firstly, because it
was deemed important to identify whether the observed control impairment was linked to the symptomatic
level of the patient. Secondly, to identify if the pain
disorder is linked to an impairment of ‘movement’ or
‘control’ (Elvey and O’Sullivan, 2004). According to the
present authors, in the case of a painful impairment of
movement, a treatment (such as manipulative techniques) aiming to promote movement into the painful
range is the treatment of choice (Elvey and O’Sullivan,
2004).
4.1. Limitations and recommendations for further studies
A limitation of this study was the fact that only the
clinicians in Study 1 had to agree on identifying MCI
patients from the larger LBP population. Patients in
Study 2 must therefore be seen as a selected group that
does not fully represent the general population of NSCLBP patients which may be more difficult to classify.
Further studies are required to test the ability of
clinicians to identify patients with MCI within this
NS-CLBP population.
The use of ‘expert’ clinicians’ classification as ‘gold
standard’ is another limitation of this study. But in the
absence of a true criterion standard for MCI diagnosis,
this method was justified and has been used by others
(Gracovetsky et al., 1995).
Because of practical and logistic issues, it was decided
to use videotaped recordings of the patients in Study 2.
Videotaping has been previously used during reliability
studies on visual analysis of gait (Krebs et al., 1985;
Eastlack et al., 1991), scapular dysfunction (Kibler et
al., 2002) and spinal movements (Fritz et al., 2000).
Videotaping has been recommended as an alternative to
a test–retest design for assessing inter-examiner reliability with patients who have LBP (Delitto et al., 1992).
Both limitations and advantages of videotaping are
recognized by the authors. The lack of an actual clinical
examination for Study 2 is a limitation and may account
for some of the discrepancy in the results between
Studies 1 and 2. The advantages of videotaping include:
not having to place undue stress on the patient,
potentially altering his or her clinical status, while
allowing a greater number of participants from geographically distinct regions.
In spite of these limitations, the current results
support good to high level-of-agreement across all
categories based on the methods used.
As mentioned above, a multi-step process is required
to validate this novel multi-dimensional CS as a
mechanism-based classification model. Based on the
new proposed model (Fig. 3), several studies have been
undertaken to add laboratory and outcome validity to
9
the CS. A laboratory-based test battery, including EMG
and 3D-motion analysis, is currently being employed to
further validate the clinical diagnosis, determine motor
control differences in pain sub-groups with normative
data, and ultimately, provide outcome measures for
specific interventions.
5. Conclusions
The main aim of these two studies was to investigate
the inter-examiner reliability of a CS for NS-CLBP
patients with MCI. Substantial to excellent reliability was found depending on the level of familiarity.
Further research is required to further validate the
proposed CS as a mechanism-based CS. The authors
believe that the acceptance and integration of a multidimensional mechanism-based CS for NS-CLBP with
MCI could have profound implications leading to the
application of specific ‘targeted’ interventions for
identified sub-groups, and subsequently enhanced
treatment efficacy as suggested by Leboeuf-Yde et al.
(1997, 2001).
Acknowledgment
This study was carried out whilst the first author
(WD) was an International Postgraduate Research
Scholar in Australia and was supported financially by
the Head of School of Physiotherapy Scholarship,
Curtin University of Technology Western Australia.
The authors would also like to acknowledge all
examiners (CP, DB, LP, LG, JW, RY, MK, JS, KH,
LL, KO, KF, AT) who participated in this study.
Special thanks to the administrative staff at ‘Body
Logic’ for their help in co-ordinating the appointments
for patients, Dr. Ritu Gupta for her statistical advice
and Marina Wise for the linguistic corrections.
Appendix A
The different sub-groups of MCI Patterns and their
clinical presentation are briefly described below. Based
on O’Sullivan (2000, 2004b)
Flexion pattern
Definition: MCI of the lumbar spine with a tendency to
flexion strain (loss of segmental lordosis) at the
symptomatic segment. Flexion pain disorders are
associated with functional loss of motor control into
flexion resulting in an excessive abnormal flexion strain.
Provocative postures/activities: all flexion-related
postures (e.g. slouched sitting) and functional activities
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10
(forward bending, cycling) are commonly reported as
being painful.
Easing postures/activities: extension postures/activities
where the lumbar spine is lordosed (e.g. standing, sitting
with a lumbar roll, walking).
Posture and movement analysis: tendency to present with
a loss of lumbar lordosis during sitting and standing
postures. The pelvis is often positioned in posterior
pelvic tilt. During all functional tasks the same tendency to have a loss of lordosis at the ‘symptomatic
level’ is noted. Forward bending movements commonly reveal a tendency of an early ‘loss of lower
lumbar lordosis’ (lumbar curve reversal). Similar loss of
lordosis is accentuated in other functional tasks like sitto-stand, squatting and gait. This is associated with an
increased lordosis in the upper lumbar and lower
thoracic spine.
Specific posture and movement control tests: inability/
lack of motor control to anterior rotate pelvis and
extend lower lumbar spine independent from thorax
during above-mentioned aggravating postures/
movements.
Flexion/lateral shifting pattern
Definition: MCI around the lumbar spine with a
tendency to flex and laterally shift at the symptomatic
segment.
Provocative postures/activities: reaching and rotating in
one direction in association with flexion postures and /
or movements.
Easing postures/activities: relief in extended or lordotic
postures, stretching to the opposite side from the shift,
shift correction (contra-lateral glide from pelvis).
Posture and movement analysis: similar to the flexion
pattern there is a loss of lumbar segmental lordosis at
the affected level with the key feature here an associated
lateral shift at the lower lumbar spine level. Minimal
precipitation of their spine might deviate into a lateral
shift position. E.g.: the lateral shift is accentuated when
standing on the foot ipsi-lateral to the shift. Sagittal
spinal movements reveal a tendency to laterally deviate
during flexion and this is commonly associated with an
arc of pain. Tests like ‘sit to stand’ usually reveal a
typical flexion pattern presentation (see above) plus a
tendency towards lateral trunk shift during the
movement with increased weight bearing on the lower
limb on the side of the shift.
lack of motor control to anterior rotate pelvis
and extend lower lumbar spine independent from
thorax during above-mentioned aggravating
postures/movements with an associated lateral
deviation
Active extension pattern
tendency to hold the lumbar spine actively into
extension.
Provocative postures/activities: all extension-related
postures (standing, erect sitting) and functional activities
(carrying out overhead activities, fast walking, running
and swimming) are commonly reported as being painful.
Also commonly reported as a provocative activity is
forward bending (with the key feature here being the
tendency to hold the lumbar spine into segmental
hyperextension).
Easing postures/activities: flexion postures/activities
where the lumbar spine is flexed (e.g. crook lying,
slouched sitting).
Posture and movement analysis: tendency for the
lumbar spine to be actively held into segmental
hyper-lordosis at the symptomatic segment during
upright sitting and standing postures. During all
functional tasks such as sit to stand, squatting and
forward bending the same tendency to hyper-lordose
at the ‘symptomatic segment’ is noted. Forward
bending movements commonly reveal increased hip
flexion and a tendency of a late ‘loss of lordosis’
(beyond mid range of flexion) or no lumbar curve
reversal. Return to neutral from a forward bended
position reveals an early hyper-lordosing of the spine
at the symptomatic segment.
lack of motor control to initiate a posterior pelvic
during above-mentioned aggravating postures/
movements.
Passive extension pattern
tendency to passively over-extend at the symptomatic
segment of the lumbar spine.
Provocative postures/activities: similar to the active
extension pattern all extension-related postures
(standing, erect sitting) and functional activities
(carrying out overhead activities, fast walking, running
and swimming) are commonly reported as being painful.
Easing postures/activities: flexion postures/activities
where the lumbar spine is de-lordosed (e.g. crook lying,
slouched sitting).
Posture and movement analysis: tendency for patients
to stand into a sway-back posture (thorax posterior to
the pelvis) with a segmental hinging at the symptomatic
level. Forward bending is often pain free, but on
return to neutral they tend to over-extend at the
symptomatic level (hinge into extension) and sway
pelvis anterior.
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lack of motor control to extend the thoraco-lumbar
spine above the symptomatic segment with a tendency
to hinge into extension at this segment.
Multi-directional pattern
Definition: multi-directional MCI around the lumbar
spine
Provocative postures/activities: multi-directional nature
of this pattern often reveals pain all weight bearing
postures and functional activities.
Easing postures/activities: difficulty to find relieving
positions during weight bearing
Posture and movement analysis: patient may assume a
flexed, extended or laterally shifted spinal posture, and
may frequently have to alternate them. Excessive
segmental shifting and hinging may be observed in all
directions, with associated ‘jerky’ movement patterns
and reports of ‘stabbing’ pain on movement in all
directions with observable lumbar erector spinae muscle
spasm.
Specific posture and movement control tests: patients
have great difficulty assuming neutral lordotic spinal
postures, with over shooting into flexion, extension or
lateral shifting postures.
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Case study
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The use of a mechanism-based classification system to evaluate and
direct management of a patient with non-specific chronic low back
pain and motor control impairment—A case report
W. Dankaertsa,b,, P.B. O’Sullivana, A.F. Burnetta, L.M. Strakera
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a
School of Physiotherapy, Curtin University, Bentley 6102, WA, Australia
Department of Rehabilitation Sciences and Physiotherapy, Ghent University, Ghent, Belgium
b
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F
Received 20 September 2005; received in revised form 17 March 2006; accepted 16 May 2006
Abstract
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Keywords: ’; ’; ’
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1. Introduction
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Low back pain (LBP) is one of the most common and
costly musculoskeletal pain syndromes, affecting up to
80% of people at some point during their lifetime (Katz,
2002; van Tulder, et al., 2002; Ehrlich, 2003; Woolf and
Pfleger, 2003). It is reported that in spite of the large
number of pathological conditions that can give rise to
LBP, 85% of these are without a detected pathoanatomical/radiological abnormality. This population is
classified as having ‘non-specific’ (NS) LBP (Waddell,
1987, 2004; Dillingham, 1995) which often develops into
a chronic fluctuating problem with intermittent flares
(Croft et al., 1998; Burton et al., 2004).
Optimal treatment for patients with NS-CLBP
remains largely enigmatic. Randomized controlled
Trials (RCTs) have failed to find consistent evidence
for improved outcomes (Goldby, 2000; Cairns et al.,
2002; Assendelft et al., 2004; Frost et al., 2004). One
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Corresponding author. WD, School of Physiotherapy Bld 408,
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explanation offered for the inability to identify effective
treatments is the lack of success in defining sub-groups
of patients who are most likely to respond to a specific
treatment approach (Leboeuf-Yde et al., 1997; Borkan
et al., 1998; Bouter et al., 1998). Indeed, it has been
proposed that the ‘LBP-group’ conceals a large heterogeneous group of patients (McKenzie, 1981; Spitzer,
1987; Borkan et al., 1998; Bouter et al., 1998; LeboeufYde and Manniche, 2001). Any specific treatment
applied to a falsely assumed homogenous sample may
result in improvement, failure to respond or aggravation
of the disorder (Binkley et al., 1993; Fritz et al., 2000;
Leboeuf-Yde and Manniche, 2001; Fritz et al., 2003).
The shift from thinking about LBP as a pathoanatomical disorder, to viewing LBP as a multi-factorial
bio-psycho-social disorder is now well accepted (Borkan
et al., 2002; McCarthy et al., 2004; Waddell, 2004).
Consequently, the different dimensions relevant to
classifying the domain of LBP include patho-anatomical, signs and symptoms, psychological and social
(Waddell, 1987; Ford et al., 2003). For LBP, several
classification systems (CSs) from a multitude of perspectives have been proposed. A recent review highlights
that the multi-dimensional nature of LBP is not reflected
in most CSs (Ford et al., 2003; McCarthy et al., 2004).
TE
29
Curtin University of Technology, GPO Box U1987, Perth WA 6845,
Australia. Tel.: +61 08 9266 3667; fax: +61 08 9266 3699.
E-mail address: [email protected] (W. Dankaerts).
doi:10.1016/j.math.2006.05.004
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A comprehensive subjective and physical examination
was first performed on the patient in order to classify her
disorder. This information is summarized in Tables 2
and 3, respectively.
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Definition
Flexion
Pain disorder resulting from a loss of motor control of the lumbar segment into flexion (associated loss of segmental
lordosis)
Pain disorder resulting from a loss of motor control of the lumbar segment in the frontal plane (lateral shift pattern).
This pattern is also associated with a loss of control into either flexion or extension
Pain disorder resulting from the lumbar segment being ‘actively’ held into extension (increased segmental lordosis)
Pain disorder resulting from a loss of motor control of the lumbar segment into extension. This is associated with a
tendency to passively over extend (hinging) at the symptomatic segment of the lumbar spine
Pain disorder resulting from a multi-directional loss of control of a lumbar spinal segment (combinations of above)
Multi-directional
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Pattern of MCI
Lateral shift (flexion or
extension)
Active extension
Passive extension
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2. Subjective and physical examination
Table 1
Definition of each pattern of motor control impairment (MCI) based on O’Sullivan (2000, 2004)
U
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N
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57
89
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F
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groups with recent studies revealing altered spinal
repositioning sense (O’Sullivan et al., 2003), different
spinal posture, kinematics and muscle activation patterns among sub-groups consistent with the CS (Burnett
et al., 2004; Dankaerts et al., 2006b, c; O’Sullivan et al.,
2005). Despite this growing evidence, there is a lack of
longitudinal studies documenting outcome on these
specific sub-groups following a targeted intervention.
Synchronized recording of surface electromyography
(sEMG) and spinal kinematics have been reported
frequently in the literature as objective measurement
methods in non-outcome LBP research (McGill et al.,
1997; Callaghan et al., 1998; Peach et al., 1998;
Callaghan and McGill, 2001; Green et al., 2002). This
methodological approach has been shown to be sensitive
to quantify parameters of motor control and to subclassify NS CLBP patients with MCI during sitting
(Dankaerts et al., 2006b, c). An advantage of this form
of measurement is that unlike simple range of motion
(ROM), measures of sEMG and spinal kinematics have
the capacity to quantify the quality and pattern of
movement of the spinal-pelvic region through ROM.
The aim of this case report is to investigate the use of
O’Sullivan’s CS to evaluate and direct management of a
patient with NS-CLBP and MCI. An objective laboratory-based assessment (using sEMG and spinal kinematics) was performed on a LBP patient and a matched
pain-free control subject. The aim of the laboratory
testing was to evaluate its capacity to lend support to the
classification of MCI and to quantify the clinical
changes in motor control secondary to a specific motor
learning intervention.
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While it is well recognized that altered motor control
exists with LBP disorders, the changes in motor control
in this population are highly variable (O’Sullivan et al.,
1997; Hodges and Moseley, 2003; van Dieen et al.,
2003). O’Sullivan reported that in general all disorders
involving pain in the lumbar region are associated with
movement or control impairment. The mere presence of
these impairments does not imply that they represent the
underlying basis for the disorder, or that correcting
these impairments will result in resolving the disorder
(O’Sullivan, 2004, 2005).
O’Sullivan’s approach to classification is based on a
process of ‘diagnostics’ (Elvey and O’Sullivan, 2004) to
make a clinical determination as to whether the patient
presents with a classification of motor control impairment (MCI) or whether the MCI is simply a secondary
effect of another process. This process of diagnostics
places a strong emphasis on the correlation between the
subjective history, radiology, pain behaviour, physical
examination findings and screens for serious pathology
(‘red flags’) and psycho-social factors (‘yellow flags’).
According to O’Sullivan motor responses present with
LBP can be classified into three distinct broad groups
(O’Sullivan, 2005). The first group consists of subjects
whose motor response is secondary (and adaptive) to an
underlying pathological process. The second group
consists of subjects where the motor response is
secondary to a dominance of psychological and/or
social (non-organic) factors. O’Sullivan (O’Sullivan,
2005) proposed that a third group exists where
maladaptive motor responses result in chronic abnormal
tissue loading leading to ongoing pain and distress.
Five distinct (direction based) patterns of MCI have
been previously described in detail (O’Sullivan, 2000,
2004). These sub-groups of MCI consist of the; flexion
pattern, active extension pattern, passive extension
pattern, lateral shifting pattern and a multi-directional
pattern (Table 1).
Recently, Dankaerts et al. (2006a) showed that these
sub-groups could be reliably identified by trained
clinicians (physiotherapists and medical doctors). There
is also growing support for the validity of these sub-
O
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37-year-old female; married; 2- and 4-year-old child
Work: part-time (2/7) nurse; involved minimal lifting
Home: household activities; picking up and carrying children
History: gradual onset of LBP symptoms; starting during the pregnancy of the first child (-4 years); post first pregnancy pain free for 2 years; early in
the second pregnancy (-2 years); progressively deteriorating LBP
Pain: LBP only (occasionally left buttock region)
Aggravating postures: sitting (4 in couch), lying on a hard matrass; sustained forward bending (e.g. doing dishes); sustained backwards bending (e.g.
hanging cloths on the wash-line); standing (carrying children)
Aggravating activities: walking (4 walking up hill), bending; lifting; previous treatment: fit-ball (stabilising) exercises, specific mobilising exercises
(lying flat moving leg)
Easing postures/activities: no symptom relief during weight bearing
Pain-intensity (VAS): 4/10 (day intake examination); 4/10 (average pain week)
Disability-score [Revised-Oswestry (Hudson-Cook, Tomes-Nicholson et al., 1989)]: 34%
Fear avoidance [Tampa Scale of Kinesiophobia(Kori, Miller et al., 1990)]: 34/68
Medical imaging: X-rays and CT-imaging–no abnormalities detected
Psycho-social risk factors (‘yellow’ flags): absent
Serious pathology (‘red’ flags’): absent
Key features
Localised LBP
No signs of neural tissue involvement
No reported impairment of movement
Multi-directional pain pattern mechanical in nature
Absence of radiological abnormality
Absence of dominant non-organic features
Absence of any signs suggesting serious underlying pathology
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Table 2
Subjective examination findings
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4. Laboratory testing
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An objective laboratory-based assessment (surface
EMG and spinal kinematics) was performed on the
patient and a matched control subject. The method of
this laboratory testing has been described in detail
elsewhere (Dankaerts et al., 2006b, c). This case study
reports on the lumbo-sacral kinematics and the sEMG
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activity of superficial Lumbar Multifidus (sLM) and
transverse fibres of Internal Oblique (trIO) during
forward bending. This test was selected since it is
frequently used in the LBP research to investigate the
reduction in back muscle activity at full body flexion
(McGill and Kippers, 1994; Shirado et al., 1995; Kaigle
et al., 1998; Gupta, 2001).
TE
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It is acknowledged that rather than relying on one
test, classification of a disorder should be based on
information of the history taking examination and a
‘cluster of tests’ in combination with a reasoning process
(Elvey and O’Sullivan, 2004). In this way, several key
features of the physical examination findings (not one
single test) consistent with the history, helped to
formulate the hypothesis of a classification of multidirectional pattern of MCI disorder (O’Sullivan, 2004).
The critical factors of the classification were that this
patient had mechanically induced, localized pain that
was multi-directional in nature. She had no impairment
in range of spinal motion but presented rather with MCI
resulting in repeated end range spinal strain and pain.
Normalization of her altered motor control (control of
the spinal neutral zone) reduced her pain.
N
31
3. Classification based on history and physical
examination
U
29
3
59
61
63
65
67
69
71
73
75
77
79
81
83
85
87
89
91
93
5. Intervention
95
The patient’s management consisted of a motor
learning intervention based on a cognitive behavioural
model. It was progressed over a 14-week period (total of
8 visits, the first 3 were spaced 1 week apart, with
subsequent sessions once every 2–3 weeks) to address
the impairments in motor control of this patient in a
functionally specific manner. The choice of this treatment approach was based on the diagnosis and
classification assigned to this patient. Each session
included re-evaluation and review of home exercises.
The specific exercises and progression was linked with
the examination findings and are described in detail by
O’Sullivan (2004). Briefly, this motor learning intervention was divided into stages, based on the model
proposed by Fitts and Posner (1995). This approach to
exercise training focuses on the quality of control of
segmental spinal posture and movement.
97
99
101
103
105
107
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9
11
13
15
17
19
21
23
25
ROM (fingers to floor) with associated pain
Return from forward bending: initiated from the thoraco-lumbar spine by hyper-extending and associated with a lateral shifting pattern and a
painful arc (‘catch of pain’); uses hands to return to neutral
Backwards bending: provoked pain with a lateral shifting pattern present; full ROM
Side bending (R/L): provoked pain with a lateral shifting pattern present; full ROM
Single leg standing: prominent lateral shifting pattern (bilateral)
Sitting posture: flexed at the lower lumbar spine; extended at the thoraco-lumbar spine
Sit to stand: difficulties of shifting load; tendency to hyper-extend and laterally shift the low back
69
Specific movement tests (O’Sullivan, 2004)
Inability to maintain neutral lordosis during trunk flexion and load transfer in sitting and inability to achieve a neutral lordosis in standing
Repositioning sense in sitting (O’Sullivan et al., 2003): inability to reposition the lumbar spine within a neutral lordosis; ‘over-shoot’ into either
flexion (kyphosis) or extension (lordosis)
Specific muscle testing (O’Sullivan, 2004)
Inability to activate the lower transverse abdominal wall (transverse fibres of internal oblique and lower transversus abdominis) in side lying
without breath holding
Screening neurological examination (Hall and Elvey, 1999)
Absence of neurological findings (provocation testing, reflexes sensation and manual muscle testing)
Passive physiological motion segment testing (Maitland, 1986)
Absence of segmental movement restriction; increased segmental motion into both flexion and extension at the two lower lumbar segments
29
Key features
Full ROM with aberrant quality of motion
Through range painful arc with hesitation and lateral movement at midrange of spinal motion
No control of mid-position [‘neutral zone’] (Panjabi, 1992a,b) and rapidly moved from one end range spinal posture to the other
Use of the hands to assist the return from forward bending
Segmental hinging at end of range into extension
Loss of neutral zone control of symptomatic spinal segments during loaded postures and spinal movements
Increased passive segmental motion into both flexion and extension at the two lower lumbar segments
Absence of neurological findings
Absence of a segmental movement impairment
Provocation of pain linked to specific impairments of control
Absence of dominant psycho-social findings (e.g. catastrophizing)
39
TE
EC
R
37
R
35
D
Passive accessory testing (Maitland, 1986)
Posterior/Anterior pressure (PA) at L4/5 and L5/S1 levels highly symptomatic; reproductive of the patient’s symptoms
33
47
49
51
53
55
C
N
45
This approach operates within a cognitive behavioural framework where the mechanism of the ongoing pain
sensitization is explained to the patient. The patient was
educated on the mechanics of the spine, the nature of
ongoing tissue sensitization with habitual adoption of
end range postures and the importance of the muscle
system of the lumbo-sacral region to control spinal
motion segments and minimize strain.
During this cognitive stage the patient was made
aware that the postures and patterns of movements that
she had adopted had in fact resulted in maintaining her
pain. She was made aware she had no control, or sense
of her neutral spine positions, nor an ability to isolate
the activation of specific muscles (transverse abdominal
U
43
O
41
63
67
27
31
61
65
F
7
Standing: hyper-lordotic thoraco-lumbar posture; reduction in tone in the transverse abdominal wall and gluteal muscles
Forward bending: splinting pattern (holding lumbar spine into extension); sudden drop into lumbar flexion (curve reversal) at end range; full
O
5
59
Posture and movement analysis
O
3
57
Table 3
Physical examination findings
PR
1
71
73
75
77
79
81
83
85
87
89
91
93
95
97
wall, superficial fibres of lumbar multifidus/sLM, pelvic
floor and gluteal muscles). She was first instructed to
control her lumbo-pelvic region through the mid-range
independent from the thorax (in supine crook lying). At
the same session she was instructed to co-activate the
pelvic floor, transverse abdominal wall and sLM
(Krause et al., 2000) in side lying. She was also
instructed to change her sitting posture to maintain a
neutral lordosis and relax the thoracolumbar region
with co-contraction of the transverse abdominal (TrA/
trIO) wall. This was then progressed to standing.
Once she had the ability to assume a neutral lordosis
in weight bearing (sitting and standing) with cocontraction of the transverse abdominal wall this was
99
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9
11
13
15
17
19
21
57
7.1. Forward bending: range of motion
59
The patient’s lumbar spine ROM into forward
bending was 481 at the intake examination and 471 at
6-month follow-up. This confirms the clinically observed
absence of any movement impairment into forward
bending being related to her LBP. This is consistent with
the CS.
61
69
Fig. 1 shows the lumbar curvature (L C) in degrees
as measured by the FastrakTM in standing and per
quartile as the subject bends forward. Negative values
represent a lordotic posture. Fig. 1a represents a
matched (age and parity) healthy control subject. A
pattern of gradual change of L C (from being
extended to being flexed) is observed.
PR
25
6. Clinical outcome
41
43
45
47
49
51
53
55
TE
EC
75
77
79
81
83
85
87
89
R
95
R
39
73
93
97
O
37
71
91
99
C
35
101
N
33
103
U
31
D
27
29
65
67
23
The patient progressed well during the intervention
with a gradual decrease in pain and an increase in
functional ability. At 14 weeks (end of intervention) she
reported to be pain-free with an ability to perform work
and household-related tasks. This was associated with a
normalization of her movement patterns and absence of
pain, improved spinal proprioception, adoption of
neutral zone postures and reduced tissue sensitivity.
The Revised-Oswestry Disability Questionnaire (Hudson-Cook et al., 1989) was used to document functional
progress and disability. The patient’s Revised-Oswestry
score (0–100%) decreased across the study period from
34% (pre-intervention) to 14% post-intervention. In the
three months following discharge, the patient experienced no exacerbation of LBP-related symptoms and
continued to improve functionally (2% at 6-month
follow-up). This status was maintained at 1-year followup (0%). The pain intensity score (average over a week;
0–10) decreased from 4/10 pre-intervention, to 2/10
post-intervention, to 0/10 at 6-month follow-up. This
pain free status was maintained at 12-month follow-up.
The score for fear avoidance (measured by the Tampa
Scale of Kinesophobia) decreased from 34/68 to 17 (the
minimum score that can be recorded) at 6-month
follow-up and was maintained at 12-month follow-up.
These scores reflect an absence of pain, transition in
function from moderate disability (o40) to no disability
and an absence of fear avoidance following the
intervention.
63
7.2. Forward bending: kinematic pattern
F
5
7. Laboratory testing outcome
O
3
incorporated into static holding tasks and dynamic tasks
such as single leg stand, sit–stand, squat and lifting
(associative stage). As she was generally de-conditioned,
she was encouraged to perform gentle aerobic activities
(walking, exercise bike) with low level of co-contraction
of her transverse abdominal wall while maintaining
optimal postural alignment. At the 10-week point she
was trained with loaded exercise (hand weights with
squats and sit to stand) to increase her global strength
and endurance whilst controlling her spinal mid-position.
The final (autonomous) stage was reached when the
patient reported that she could carry out functional
movement tasks with a low degree of attention (Fitts
and Posner, 1995). It should be noted that the patient
had to achieve each stage of the program before it was
progressed.
At the end of the 14-week intervention (8 sessions) she
was asked to be aware of her spinal posture, and
maintain her fitness level by means of regular cardiovascular exercise (alternating between walking and
exercise biking).
O
1
5
105
107
Fig. 1a–c. Forward bending kinematics; lumbar curvature in degrees
(negative values indicate lordosis) as measured by the FastrakTM per
quartile (Q) of full movement (time normalised) for (a) control subject;
(b) case subject pre-intervention and (c) case subject at 6-month
follow-up.
109
111
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7
Fig. 1b represents the case study patient preintervention. Lumbar spine hyperextension was maintained as she progressed into the forward bending range
with a curve reversal at the end (3rd to 4th quartile). At
the 6-month follow-up (Fig. 1c) curve reversal was
observed more central in range (2nd to 3rd quartile) and
this was similar to the control case data (Fig. 1a).
9
7.3. Forward bending: surface EMG findings
11
13
15
17
19
21
7.3.2. Lower transverse fibres of the internal oblique
(trIO)
Surface EMG profile of the control subject (Fig. 3a)
during forward bending and return from forward
bending shows a clear pattern of onset–offset–onset
for trIO similar to that observed in the sLM at the end
of ROM. In contrast the patient pre-intervention (Fig.
3b) showed no clear onset–offset–onset pattern with a
deficit in motor activity. At the six month follow-up an
onset–offset–onset pattern (similar to the control subject) was observed (Fig. 3c).
7.3.1. Superficial lumbar multifidus (sLM)
Fig. 2a shows the raw sEMG activation of the sLM
during forward bending and return from forward
bending of the matched control subject. A burst of
EMG activity, as the subject starts the movement, is
observed followed by a pattern of muscle relaxation at
the end of the forward bending phase and the return is
then associated with a burst in the sLM. This pattern of
onset–offset during forward bending is commonly
referred to as the flexion relaxation phenomena (FRP).
Watson et al. (1997) indicated that this type of dynamic
PR
23
25
D
27
TE
29
31
EC
33
35
R
37
R
39
O
41
49
N
47
U
45
C
43
57
59
61
63
65
F
5
O
3
sEMG activity of the paraspinal muscles can be reliably
measured and is useful in differentiating CLBP patients
from normal controls.
Prior to the intervention, the patient displayed
increased muscle activity with no FRP during forward
bending (Fig. 2b). At the 6-month follow-up, a more
normal sEMG pattern, with an FRP was observed (Fig.
2c).
O
1
67
69
71
73
75
77
79
81
83
85
87
89
91
93
95
97
99
101
103
105
51
107
53
109
55
Fig. 2a–c. Raw surface electromyographic activity of the superficial lumbar multifidus during standing, forward bending and return from forward
bending for (a) control subject; (b) case subject pre-intervention and (c) case subject at 6-month follow-up.
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7
57
3
59
5
61
7
63
9
65
11
67
13
69
15
71
17
73
F
1
O
19
O
21
PR
23
25
D
27
TE
29
31
EC
33
35
Fig. 3a–c. Raw surface electromyographic activity of lower transverse fibres of internal oblique during standing, forward bending and return, for (a)
control subject; (b) case subject pre-intervention and (c) case subject at 6-month follow-up.
R
39
8. Discussion
47
49
51
53
55
C
N
45
The patient described in this case report would be
‘classically’ diagnosed as having NS-CLBP based on the
absence of any abnormal radiological findings linked to
the clinical presentation (Waddell, 1987, 2004; Dillingham, 1995). Based on the CS (O’Sullivan, 2004) this
patient was classified as having a multi-directional
pattern of MCI.
The use of a CS to guide management of patients with
LBP and MCI has been reported previously (Maluf et
al., 2000;Van Dillen et al., 2003). There are several main
differences with the classification approach suggested by
O’Sullivan (and applied on this case subject). Rather
than relying only on signs and symptoms (Van Dillen et
al., 1998, 2003a,b), the proposed CS is based on a
process of ‘diagnostics’ (Elvey and O’Sullivan, 2004) to
U
43
O
41
77
79
81
83
85
87
89
91
R
37
75
93
95
make a clinical determination as to whether the patient
presented with a classification of MCI rather than the
altered motor response being a secondary effect of
another process.
The patient described in this case report presented
with full ROM (no movement impairment) in forward
and backward bending supporting the classification of
MCI. In research and clinical practice, ROM measurements are routinely used to assess patients with LBP.
However, these tests do not quantify control parameters
during the movement itself. Although excellent convergent validity (Saur et al., 1996; Perret et al., 2001) has
been reported for forward bending ROM measurements
(compared to dynamic radiographs), of most clinical
importance is the lack of discriminative validity highlighted by the weak to non-existing relationship between
lumbar ROM measures and functional ability (Parks et
97
99
101
103
105
107
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23
25
27
29
31
33
35
37
39
41
43
45
47
49
51
53
55
F
O
21
O
19
an FRP in the presence of LBP (Ahern et al., 1990;
McGill and Kippers, 1994; Shirado et al., 1995; Kaigle
et al., 1998; Gupta, 2001). Ahern et al., 1990 proposed
that the absence of FRP seen in LBP patients is
associated with guarded movements in response to pain.
Although pain might be a possible mechanism for the
absence of FRP in this case, it is interesting that the
muscle activity near end range did not restrict her
movement (she achieved full range spinal flexion).
Watson et al. (1997) suggested that the assessment of
change in FRP could be used in evaluating treatment
interventions. EMG data at 6-month follow-up clearly
detected a change in motor control pattern during
forward bending with a clear FRP present in the sLM
(Fig. 2c), which was also associated with a similar
pattern in trIO (Fig. 3c).
The sEMG findings from trIO during forward
bending and return highlight a lack of co-contraction
between trIO and sLM prior to the intervention (Fig.
3b). The CLBP literature contains numerous reports on
co-activity and synergistic behaviour of muscle groups
during trunk flexion-extension and it is well accepted
that the trIO muscle increase intra-abdominal pressure
(Cresswell et al., 1992; Cholewicki et al., 1999), and act
in co-contraction with trA, pelvic floor muscles and
back extensors to stabilize the lumbar spine (Panjabi,
1992a,b). Loss of co-contraction between trunk muscles
has been previously reported in LBP populations
(Hodges and Richardson, 1996; O’Sullivan et al., 1997;
Hodges and Richardson, 1999). The absence of cocontraction in combination with the kinematic data, in
this case, lends support to the classification of MCI.
From a review of the literature it seems that the exact
mechanism affecting trunk muscle recruitment in the
presence of LBP is not completely understood with
several mechanisms hypothesized in the literature (see
Hodges and Moseley, 2003 for review). Farfan (1973),
Panjabi (Panjabi, 1992a,b) and Richardson et al. (1999)
amongst others, have presented models that suggest that
deficits in motor control lead to poor control of joint
movement, repeated microtrauma and pain. However,
the opposite (pain leads to changes in motor control)
may also be true. Recent data (e.g. Hodges et al., 2003)
has shown that experimentally induced LBP produced
changes in the motor control of the trunk muscles
similar to that identified in people with LBP. While this
does not exclude the possibility that changes in control
of the trunk muscles may lead to pain, it does argue that,
at least in some cases, pain may cause the changes in
control. Hodges et al. (2003) suggested that it is unlikely
that the simple inhibitory pathways can mediate the
complex changes in motor control of the trunk muscles.
The most likely causes are changes in motor planning
via a direct influence of pain on the motor centres,
factors associated with the attention demand, stressful
PR
17
TE
15
EC
13
R
11
R
9
O
7
C
5
N
3
al., 2003; Zuberbier et al., 2001). Based on clinical
observations it is very unlikely that for patients with
MCI, the lumbar ROM test into forward bending will
have any validity as a sensitive outcome measurement.
Its hypothesized that impaired spinal mobility may be
reflective of a different sub-group of patients with a
classification of movement impairment (O’Sullivan,
2005).
A novel aspect of this case report is the addition of
laboratory-based support to the clinical examination
findings of MCI associated with sagittal spinal movement. Despite having full ROM into forward bending,
the case subject presented clinically with symptoms
through ROM, suggesting a lack of motor control
during this movement. The kinematic quantitative
assessment was capable of identifying patterns of
MCI. Fig. 1b shows that as the patient progressed into
forward bending a substantial lordosis (hyper-extension)
was maintained, with the curve reversal at the end range
(3rd to 4th quartile). This is consistent with O’Sullivan
(O’Sullivan, 2000, 2004) who postulated that patients
with a multi-directional pattern of MCI have a lack of
ability to control a neutral spine posture during
functional movements and have a less gradual transition
from one end range position to the other. At the 6month follow-up, laboratory testing showed the curve
reversal appearing earlier in the range (2nd to 3rd
quartile) (Fig. 1c). This is similar to the control case data
shown in Fig. 1a. This is an important finding in the
search for quantifiable outcome measurements for this
sub-group of CLBP patients. This demonstrates that the
kinematic analyses were sensitive in detecting changes in
motor control following a specific intervention. Further
research is warranted to evaluate these parameters in a
larger population.
For this case report EMG data were also recorded
during the laboratory-based testing. Raw EMG is
frequently used for pattern recognition and onset–offset
EMG detection (Shirado, et al., 1995; Hodges and
Richardson, 1997).
Marked reduction in back muscle activity at full body
flexion, known as FRP, has been investigated in
numerous studies (McGill and Kippers, 1994; Shirado
et al., 1995; Kaigle et al., 1998; Gupta, 2001). Most
studies support that the phenomenon occurs in healthy
subjects before reaching the maximum flexed position.
In contrast, patients with CLBP don’t typically demonstrate FRP (e.g. Shirado et al., 1995; Kippers and
Parker, 1984). These findings are consistent with the
pattern observed in the case subject prior to the
intervention period, a lack of reduction in electrical
activity in sLM (Fig. 2b) during forward bending and
the absence of an onset/offset pattern of EMG activity
in trIO (Fig. 3b).
Several mechanisms have been suggested in the
literature that may be responsible for the absence of
U
1
D
8
57
59
61
63
65
67
69
71
73
75
77
79
81
83
85
87
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13
15
17
19
21
23
25
27
9. Conclusion
29
39
41
43
TE
EC
R
37
R
35
O
33
C
31
This case study illustrates the use of O’Sullivan’s CS
to guide physiotherapy intervention for a patient with a
classification of multi-directional MCI. The kinematic
and EMG data support the classification and demonstrated pre-intervention an impairment in the control of
the spine during functional movement tasks. Following
a motor learning intervention the altered motor control
was normalized and was associated with reductions in
pain disability and movement-based fear. Ultimately,
further research in the form of RCTs is required,
comparing intervention based on the CS to other
approaches. This is an essential final step to validate
this CS-based approach before its widespread use can be
advocated (Dankaerts et al., 2006a).
N
45
49
51
53
55
U
10. Uncited references
47
F
9
O
7
O
5
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manipulative therapy for low back pain. Cochrane Database
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Binkley J, Finch E, Hall J, Black T, Gowland C. Diagnostic
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[discussion 150-5].
Borkan J, Van Tulder M, Reis S, Schoene ML, Croft P, Hermoni D.
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Bouter LM, van Tulder MW, Koes BW. Methodologic issues in low
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Burnett AF, Cornelius MW, Dankaerts W, O’Sullivan PB. Spinal
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Cairns M, Foster N, Wright C. Prospective, pragmatic RCT examining
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Callaghan JP, Gunning J, McGill S. The relationship between lumbar
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Callaghan JP, McGill SM. Low back joint loading and kinematics
during standing and unsupported sitting. Ergonomics
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Cholewicki J, Juluru K, McGill SM. Intra-abdominal pressure
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Cresswell AG, Grundstrom H, Thorstensson A. Observations on intraabdominal pressure and patterns of abdominal intra-muscular
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Croft PR, Macfarlane GJ, Papageorgiou AC, Thomas E, Silman AJ.
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impairment. Manual Therapy 2006a;11(1):28–39.
Dankaerts W, O’Sullivan P, Burnett A, Straker L. Differences in
sitting posture are associated with non-specific chronic low back
pain disorders when patients are sub-classified. Spine, 2006b. In
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superficial trunk muscle activation during sitting in non-specific
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Ehrlich GE. Low back pain. Bulletin of the World Health Organization 2003;81(9):671–6.
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PR
3
and fearful aspects of pain, or due to changes in the
sensory system (Hodges et al., 2003).
For this case subject it is not known whether pain
caused the changes in motor control or whether motor
control changes lead to pain, or both. However, we
hypothesize that the improvement in pain intensity and
disability was primarily due to the improvement in her
spine motor control, which in turn reduced the
peripheral nociceptive drive of pain. It is also acknowledged that cognitive factors such as enhanced patient
awareness, improved coping strategies and increased
functional capacity (which are all powerful cognitive
factors associated with the intervention), are likely to
reduce the central drive of pain. The capacity of this
form of intervention to impact on the physical and
cognitive aspects of the pain disorder is highlighted by
the documented reductions in fear avoidance behaviour
at 6- and 12-month follow-up. Due to the limitations
associated with a case report, the results do not imply a
definite answer to the cause–effect question, nor can the
patient’s outcomes be generalized across a larger
sample. However, the classification of MCI is strengthened by the laboratory-observed changes indicating
more normal spinal kinematics and muscle co-activation
patterns at 6-month follow-up.
D
1
Cairns et al.; Ford et al.; Goldby et al.; O’Sullivan et
al., 2006.
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