Maladaptive movement and motor control impairments as underlying mechanism

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Manual Therapy 10 (2005) 242–255
Masterclass
www.elsevier.com/locate/math
Diagnosis and classification of chronic low backpain disorders:
Maladaptive movement and motor control impairments as
underlying mechanism
Peter O’Sullivana,b,
aBody-logic Physiotherapy, 146 Salvado Rd, Wembley, WA 6014, Australia
bSchool of Physiotherapy, Curtin University of Technology, Perth, Western Australia
Received 3 April 2005; accepted 9 July 2005
Abstract
Low backpain (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 backpain (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 backpa in (LBP) is common with up to 80% of
people reporting LBP over their life time (Dillingham,
1995). The majority of acute LBP disorders resolve
within a 4 weekperiod 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 backpa in, 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
Corresponding author at: Body-logic Physiotherapy, 146 Salvado
Rd, Wembley, WA 6014, Australia.
E-mail address: POSullivan@curtin.edu.au.
1356-689X/$ - see front matter r 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.math.2005.07.001

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P. O’Sullivan / Manual Therapy 10 (2005) 242–255 243
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 backpa in (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, neurophysiolo-gical,
physical and psychosocial factors (Waddell, 2004).
To date, the majority of studies that relate to the
classification of backpa in 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 mechan-ism(
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 steno-sis
with associated nerve pain are commonly assumed to
be related to backpa in (and in some cases associated
neurogenic pain), with interventions provided on the
basis of this assumption (Nachemson, 1999).
However, the problem with pathoanatomical diag-noses
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
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 backpain 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, blockor 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 under-lying
mechanism or cause of the pain generation,
and these approaches frequently only result in short
term pain relief and lackbroad 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 psychoso-cial
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 inter-ventions
to reduce the forebrain facilitation of pain
(Woby et al., 2004).

244 P. O’Sullivan / Manual Therapy 10 (2005) 242–255
2.4. Psychosocial model
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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 abnor-mal
anxiety regarding pain, avoidant behaviour, cata-strophizing
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, workpla ce disputes,
workand 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 regard-ing
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 cogni-tive
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 psycho-social
driven due to a lackof 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 riskfact ors 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 exacerba-tion
of CLBP. These factors include; sustained low load
postures and movements (such as sitting, standing,
bending and twisting), exposure to whole body vibra-tion,
high loading tasks (such as repeated lifting and
bending), as well as sudden and repeated spinal loading
in sports specific and manual worksitu ations (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, workplace design and
sporting equipment. Individual physical factors such as
where in its range a spinal articulation is loaded (neutral
zone vs. elastic zone), reduced trunkmuscl e 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 sensi-tization
(Adams et al. 1999; Nachemson, 1999; Aben-haim
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 classify-ing
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 dis-orders
(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 impair-ments
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’’ move-ment
or motor control impairments or treat dysfunction
in the spinal muscles in many of these disorders would
be inappropriate and ineffective due to the non-mechanical
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 backpa in (when tissue healing would have normally
occurred), ongoing mal-adaptive motor control beha-viour
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 neuromuscu-losketetal
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 taskforce classification system provides a
logical approach for the diagnosis and classification of
LBP disorders within a biopsychosocial framework
(Spitzer, 1987; Abenhaim et al., 2000; Waddell, 2004).
Under this frameworkred 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 impair-ments
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 backmuscle 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 lordo-sis)
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 manage-ment
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 sensitisa-tion,
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 (Aben-haim
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 under-lying
mechanism driving the pain disorder, and conse-quently
there is no clear direction for specific
management (Padfield and Butler, 2002).

3.2. Classification of CLBP
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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 under-lying
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 clin-ical
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, worken vironment, lifestyle factors
and beliefs regarding their disorder is also critical
(Waddell, 2004). Whether the patient has active or
Patho-anatomical factors
- structural pathology
- identify peripheral pain generator
(IVD / Zt joint / SI Jt / neural tissue / myo-fascial /
connective tissue)
Physical factors
- ‘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
passive coping strategies in managing their disorder, and
whether they pace themselves is important in under-standing
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 pathoanatomi-cal
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 disor-ders,
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 patholo-gical
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
Social factors
- relationships – family, friends, work
- work structure
- medical advice
- support structures
- compensation – emotional, financial
- cultural factors
- socio-economic factors
Psychological factors
- personality type
- beliefs attitudes
- hypervigilance
- coping strategies – confronter vs
avoider
- pacing
- emotions - fear / anxiety / depression
/ anger
- iIlness behaviour
Genetic factors
- potentially influencing all
other domains
Pain
Neuro-physiological factors
- peripheral sensitisation
- central sensitisation
- sympathetic nervous system activity
- somatic complaints
Fig. 1. Factors that need consideration within a biopsychosocial framework, for the diagnosis and classification of CLBP disorders.

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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 proces-sing,
amplified non-remitting pain, and resultant dis-ordered
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 (lackof 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 psycho-logical
and social stresses present as dominant co-existing,
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 lackof clear and
consistent mechanical provocation or relieving patterns
(absence of peripheral nociceptor drive). When mechan-ical
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).
(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 beha-viour)
or ‘control’ impairments (characterized by pain
provocation behaviour) act as the underlying mechan-ism
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 com-monly
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 non-specific
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 second-ary
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 move-ment
appears to develop from the patients’ initial
experience of severe acute pain, as well as their beliefs
(reinforced by sympathetic family members and treat-ment
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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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 move-ment
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 exacer-bate
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 backwhich she
avoided doing from that time.
Her treatment history consisted of McKenzie exten-sion
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 psychol-ogist,
a number of physiotherapists and was taking
(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
Anxiety related to movement pain
Fear avoidance when moving in direction
of pain (pathological)
Hyper-vigilence
Belief that pain is damaging (pathological)
Result: Central pain sensitisation
Normalisation of movement impairment
leads to resolution / control of disorder
(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 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
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).

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Mal-adaptive CLBP disorders -where ‘movement’ and ‘control’ impairments ….
dominate and represent underlying mechanism for pain
Tissue injury / localised pain
Motor response
Factors that may influence pain and motor
response
Resolution of the disorder
Movement impairment
classification
- segmental spinal
- directional / multi-directional
Non resolution
mal-adaptive patterns adopted
poor coping strategies
NMS response prolonged
excessive↔reduced spinal stability
abnormal tissue loading
peripheral / central sensitisation
Management
- 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
physical
patho-anatomical
genetic
neuro-physiological
motor control
psycho-social
coping strategies
beliefs
fear avoidance
compensation
Management
- education – regarding pain mechanism
- cognitive behavioural motor control
intervention
- pain control (avoid provocation)
- retrain faulty postures and movements
- self control of pain
- functional restoration
- normalise movement behaviour
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).

ARTICLE IN PRESS
anti-depressants, strong analgesic and muscle relaxant
medication.
She was only able to work2 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 workfull time. She
constantly worried about her backpa in and believed
that she would not get better as she had a disc injury
that had not resolved. She coped with her backpa in by
avoiding provoking it and restricting her activities
involving spinal flexion. Her pain intensity level was
8/10, her disability index (Oswestry disability index) was
40% and she had high levels of kinesiophobia (Tampa
scale of Kinesiaphobia).
Investigations: X-rays/MRI Lumbar spine—
NAD
Physical examination
Observation 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 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
tests
NAD
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 non-specific CLBP
Classification 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 loca-lized
pain at L5/S1).
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).

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The mechanism underlying the pain is a movement
impairment with a loss of normal physiological move-ment
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 weekperiod. 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 move-ment
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 backextens or and psoas
muscles). This was combined with graded active move-ment
into the restored range. This involved the patient
initially being taught to posteriorly tilt her pelvis in a
relaxed manner without trunkmuscl e 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 thoraco-lumbar
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 worklonger 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.
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-physio-logical
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’Sulli-van
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 lacka withdrawal reflex motor
response, coupled with a lackof proprioceptive aware-ness
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 mechan-ism
for ongoing pain (which is both peripherally and
centrally mediated) and disability. These patients pre-sent
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

motor control behaviour provides an ongoing mechan-ism
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 sympto-matic
tissue reduces, resulting in less peripheral noci-ceptive
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 move-ment.
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
backpa in 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 anti-depressants).
He reported that his backpa in 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 tookdays 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, workand 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 backan d
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 backpain
Neural
provocation tests
NAD
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
X-rays/MRI lumbar spine—
degenerative disc disease L5/S1
(mild)
Diagnosis non-specific CLBP
Classification control impairment disorder—
flexion pattern at L5/S1
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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 lackof 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, frustra-tion,
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 backsprai n 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, lackof 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 co-activate
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 cardio-vascular
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
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 classi-fication
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 biopsy-chosocial
framework. The presence and dominance of
the potential pathoanatomical, physical, neurophysio-logical,
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 dom-inate
the disorder, resulting in either excessive or
impaired dynamic spinal stability and loading. This in
turn becomes a mechanism for ongoing pain. Phy-siotherapy
interventions that are classification based and
specifically directed to the underlying driving mechan-ism,
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
date supports these proposals although further research
is required to further develop and validate this
approach.
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