J.berh.2006.10.001 - Manjemen Pain

You might also like

Download as pdf or txt
Download as pdf or txt
You are on page 1of 14

Best Practice & Research Clinical Rheumatology

Vol. 21, No. 1, pp. 153e166, 2007


doi:10.1016/j.berh.2006.10.001
available online at http://www.sciencedirect.com

10

Management of musculoskeletal pain

Stefan Bergman* MD, PhD


GP and Research Director
Spenshult Hospital, SE 313 92 Oskarström, Sweden

Chronic musculoskeletal pain is a major public health problem affecting about one third of the
adult population. Pain is often present without any specific findings in the musculoskeletal system
and a strictly biomedical approach could be inadequate. A biopsychosocial model could give a bet-
ter understanding of symptoms and new targets for management. Identification of risk factors for
chronicity is important for prevention and early intervention. The cornerstones in management
of chronic non-specific, and often widespread, musculoskeletal pain are non-pharmacological.
Physical exercise and cognitive behavioral therapy, ideally in combination, are first line treatments
in e.g. chronic low back pain and fibromyalgia. Analgesics are useful when there is a specific
nociceptive component, but are often of limited usefulness in non-specific or chronic widespread
pain (including fibromyalgia). Antidepressants and anticonvulsants could be of value in some
patients but there is a need for more knowledge in order to give general recommendations.

Key words: biopsychosocial; management; musculoskeletal; non-specific; pain.

INTRODUCTION

Chronic musculoskeletal pain is a major health problem in most industrialised coun-


tries with a prevalence of around 35% in the general population.1,2 It can be the con-
sequence of a pathological process in the musculoskeletal system, but often presents
as a clinical problem when pain persists beyond the expected time of healing and with
no specific pathological findings in bones, joints or muscles. In the latter situation a tra-
ditional biomedical management approach is often inadequate. Failure in the under-
standing and treatment of the condition can lead to both frustration for the health
care provider and mistrust from the patient.3 Also in cases with a well defined cause,
such as osteoarthritis (OA) or rheumatoid arthritis (RA), pain can be more intense
and generalised than expected from pathological findings or persist despite good
management of the underlying disorder.4 A recent large population study, involving

* Tel.: þ46 35 263 5253; Fax: þ46 35 263 5255.


E-mail address: stefan.bergman@spenshult.se
1521-6942/$ - see front matter ª 2006 Elsevier Ltd. All rights reserved.
154 S. Bergman

15 European countries, pointed out that 40% of those suffering from chronic pain re-
ported inadequate management of their pain problem.5 It is thus important to develop
and implement management strategies for subjects with, or at risk for developing,
chronic musculoskeletal pain.
The aim of this article is to give a biopsychosocial model of specific and non-specific
musculoskeletal pain, review options for pharmacological and non-pharmacological
treatment and, finally, suggest an evidence-based management strategy for prevention
and treatment. The focus is on both pain with no obvious specific cause and pain with
a specific cause where that pain persists beyond the expected time of healing or has
a greater impact than expected.

SPECIFIC VERSUS NON-SPECIFIC PAIN

Musculoskeletal pain is the most common feature in various musculoskeletal disor-


ders, such as OA and RA, but also a common complaint in the absence of an obvious
specific pathological process. There could be both specific and non-specific compo-
nents of pain in the same individual and the balance and expression of these compo-
nents of pain is highly individual. Also, pain without any tissue damage must be viewed
as ‘real’ pain, otherwise the patient’s experience is being denied.6
Although pain may be considered non-specific from the musculoskeletal point of
view, it is important to identify, and take into account, specific processes such as cen-
tral sensitisation7, cognitive beliefs and/or inadequate coping strategies8 in a structured
management of the pain problem. There are often also concomitant problems, e.g. de-
pression, that have to be properly managed.9
Musculoskeletal pain is often described in terms that give an impression of a specific
cause or specific localisation of tissue damage, such as low back pain or hip pain.
Chronic pain in a specific region is, however, often associated with a non-specific wide-
spread pain. The high prevalence, around 11%1,2, of chronic widespread pain (CWP) is,
thus, reflected in reports of pain from different bodily regions. In patients reporting
apparently localized pain, CWP may form part of that pain in 52e74% of women,
but occurs to a lesser extent, 32e51%, in men (Table 1). When pain is part of

Table 1. The prevalence of chronic musculoskeletal pain in different body regions by gender.
Prevalence of chronic pain Proportion with CWP
Women % Men % Women % Men %
Anterior chest 5.6 3.8 73.6 51.2
Neck 22.9 14.5 56.4 42.1
Dorsal chest 12.0 7.1 60.6 40.7
Low back 26.4 19.0 51.6 32.4
Shoulder/upper arm 23.8 15.4 55.7 45.1
Elbow/lower arm/hand 21.4 11.4 58.0 48.1
Hip/upper leg 15.3 10.7 67.2 48.8
Knee 14.6 12.9 67.7 39.0
Lower leg/foot 14.9 9.5 66.7 48.1
n ¼ 2425.
The proportion that may be part of a concurrent chronic widespread pain (CWP) is also given. Based on
data from Bergman et al. (2001).1
Management of musculoskeletal pain 155

a widespread pain problem, it is not surprising that e.g. X-ray of the hip is normal.10
However, when there is a specific hip disorder such as OA, it is crucial to identify
and adequately treat that specific cause, even when the patient suffers from a wide-
spread pain. This may improve the overall pain problem11 or otherwise, if not attended
to, lead to a worsening of the problem.12

A BIOPSYCHOSOCIAL MODEL FOR PAIN PERCEPTION


AND THE TARGETS FOR PAIN MANAGEMENT

Acute musculoskeletal pain is often nociceptive in its origin and the pain is aimed at pro-
tecting the individual, giving an early warning when there is a harmful or potentially
harmful process in the body. Neuropathic pain, where there is an injury or dysfunction
in the nervous system, is another common cause for pain perceived as coming from
the musculoskeletal system. Pain is considered to be idiopathic when there is no specific
or obvious known cause. This does not mean that the non-specific pain is any less real
but calls for an analysis of how the nociceptive system interacts with the patient’s whole
situation. The same basic structures and processes in pain perception have to be
considered in both acute and chronic pain, although the importance of each part
depends on the musculoskeletal disorder and the affected individual. The following
model of pain perception focuses on processes that are of interest for the management
options presented in this paper or are relevant for the prevention of chonicity.
A pain generating process in the musculoskeletal system is typically present in acute
nociceptive pain but should also be considered in chronic, widespread and, apparently,
non-specific pain. The disorder could be minor with respect to the experienced pain
and therefore easily ignored. It could also be part of the patient’s medical history. Fur-
thermore, muscle tension with ischaemia or a local ‘energy crisis’ have been proposed
to generate nociceptive pain.13 Nociceptors are specialised nerve endings on primary
afferent sensory neurons found throughout the body. In a normal situation, the stim-
ulus has to be potentially noxious (tissue damaging) in order to evoke a response in
the nociceptors. A peripheral sensitisation gives a lower threshold for activation of
the nociceptors and a stimulus no longer needs to be noxious to trigger the nocicep-
tor and eventually be perceived as pain in the brain.7 This phenomenon, where a nor-
mally non-painful stimulus is perceived as pain, is known as allodynia. Normally painful
events can be perceived as even more painful and this is termed hyperalgesia. This in-
creased sensitivity is normally seen when there is a traumatic or inflammatory process
in the tissue, but has also been proposed as one factor behind increased pain sensitivity
in situations where no inflammatory process is present.14
Central sensitisation is the result of repeated or prolonged activity in primary afferent
neurons leading to an increased response in the secondary sensory neurons, emanat-
ing from synapses in the spinal cord’s dorsal horns.7 The increased response can
contribute to allodynia, hyperalgesia and a referred pain outside the injured area.
One factor behind this hyper-excitability is activation of N-methyl D-aspartate (NMDA)
receptors and these receptors could be important targets for future pharmacological
interventions. Recent studies have also proposed an important role for glia cells in
the amplification and spread of pain.7,15 The sensory transmission in the spinal cord is
regulated by inhibitory pathways within the spinal cord or descending from the brainstem
to the synapses in the dorsal horns. Regulation of pain transmission at this level was
suggested as far back as 1965, in the famous gate-control theory.16 Important neuro-
transmitters in central inhibition are gamma-amino butyric-acid (GABA), serotonin
156 S. Bergman

and endorphins.7 Disturbances in this central regulation of pain processing is proposed


to be one factor behind the increased sensitivity for pain that is found in patients with
neuropathic pain and fibromyalgia and is an interesting target for treatment.
Cognitive and emotional factors (thoughts, memories, beliefs, expectations, fears, anx-
iety and depression) interact with how the sensory input is handled by the individual.
This involves attention, interpretation, coping strategies and behavioral responses. Cog-
nitive and emotional factors have been shown to interact with the ascending regulation
of pain transmission in the spinal cord.7 The complex nature of how these factors
modulate pain transmission and perception is not fully understood but the neuromatrix
theory suggests an interaction between brain activities and pain processing in neural
networks.17 Depression is common in association with chronic musculoskeletal
pain18 and could be a factor that promotes the development of chronic pain, but it
could also be a consequence of the situation. Longstanding stress and the psychosocial
situation interact with pain perception and add to the vulnerability for developing
chronic musculoskeletal pain.19,20 Sleep problems have been reported, not only as a con-
sequence of pain but also as preceeding or being an early feature in chronic pain
development.

PREVENTING CHRONICITY e PREDICTORS AND INTERVENTIONS

Predictors of chronicity can be related both to the clinical disorder and to the affected
individual’s personal lifestyle or psychosocial risk factors. Patients with factors indicat-
ing a risk for chronicity should be considered for an intervention equalling that for
those with established chronic musculoskeletal pain. These factors are often referred
to as ‘yellow flags’.
In the clinical situation special attention should be paid to previous pain episodes, pain
reports from other locations, tender points, distress, somatisation, fatigue and sleep distur-
bances, predicting possible development towards chronic pain.21e23 The development
and persistence of chronic musculoskeletal pain is also predicted by several sociode-
mographic, lifestyle and psychosocial risk factors.19 Chronic pain is more prevalent
with increasing age up to a plateau at around 60e69 years of age. Several potentially
painful musculoskeletal disorders are more prevalent in women (RA, fibromyalgia, oste-
oporosis) and women more often have persistent and widespread pain. Family history of
chronic pain, low educational level, low socio-economic group and lack of social support are
other common risk factors. Some ethnic groups and immigrants to western countries
have also been shown to have an increased risk.22,24 Smoking, sedentary lifestyle and obe-
sity are predictive factors that could be targets for intervention.25,26 The work situation
can result in harmful physical load to body structures, but also work with high de-
mands and little control over the work situation have been shown to be predictive
for musculoskeletal pain.20,27,28
It is important to treat acute pain and potentially painful chronic diseases adequately.
This includes realistic and confident information about what the patient can expect during
the healing period. Studies on back-pain and whip-lash injuries suggest that chronicity
might be prevented by encouraging the patient to continue or return to normal activities
as soon as possible.29,30 It is important, early on, to identify yellow flags that indicate
psychosocial factors predicting chronicity and barriers to recovery.19 Good practice
can also be to refrain from doing some diagnostic procedures, as they may inflict/introduce
fear and negative experiences. One example is radiography of the spine in sub-acute
low back pain.31
Management of musculoskeletal pain 157

The high prevalence of musculoskeletal disorders and risk factors in the pop-
ulation justifies a public health perspective with community-based prevention pro-
grammes.32 Such programmes need to address the biological and psychosocial
aspects of musculoskeletal pain to change beliefs and behaviours in order to re-
duce the impact of musculoskeletal disorders.33,34 Part of this strategy is also to
identify subjects in the population with a higher risk for a more intensive man-
agement approach.

PHARMACOLOGICAL METHODS OF PAIN MANAGEMENT

It is important to have adequate management of any underlying specific musculoskel-


etal disorders. Such management could include disease modifying drugs and pharma-
cological treatment of nociceptive and neuropathic pain. Pharmacological treatment
is often of lower value than non-pharmacological intervention when pain is non-
specific, chronic or widespread.

Analgesics

The three-step WHO analgesic ladder (non-opioids, weak opioids, strong opioids),
originally presented for the treatment of cancer pain, has evolved to be a framework
for the treatment of musculoskeletal pain as well.35 Analgesics are useful when there
is a specific nociceptive component, but have often limited usefulness in non-specific
or CWP (including fibromyalgia).36,37 It is important to carefully monitor the effect
on pain and side-effects when analgesics are used for chronic musculoskeletal
conditions.
The first step is represented by paracetamol (acetaminophen) and cyclo-oxygenase
(COX) inhibitors, including acetylsalicylic acid (aspirin) and non-steroidal anti-
inflammatory drugs (NSAIDs). Specific COX-2-inhibitors were launched with a
proposed better safety profile, with regard to gastrointestinal bleeding, than that of
non-specific COX-inhibitors (traditional NSAIDs). Long term studies have, however,
revealed a risk for fatal and non-fatal ischaemic heart disease and stroke for at least
some of these compounds and it is now recommended that their clinical use be re-
stricted.38 The choice between paracetamol and NSAIDs in the treatment of painful
musculoskeletal disorders such as OA and RA is under debate and evidence from re-
views are not conclusive.39e41 Paracetalamol is often suggested as the drug of choice
due to safety reasons, mainly with regard to the risk for gastrointestinal bleeding, and
has been shown to have the same or nearly the same efficacy as NSAIDs. NSAIDs have
been shown to have a better effect than paracetamol on OA pain and also to be pre-
ferred by patients with RA. There is no clear cut recommendation and the choice is
probably more an issue of individual factors with regard to safety and preferences due
to previous experience. The combination of paracetamol and NSAIDs has been sug-
gested as an alternative to opioid treatment.42 The additional effect of a combination
may, however, be small and there could be additional side effects.43
When non-opioids have insufficient effect or are badly tolerated, the next step to
consider is weak opioids, such as tramadol, codeine and dextropropoxyphene, either
alone or in combination with non-opioids. Tramadol is proposed to be the better
choice due to its pharmacological profile and effect on pain in several musculoskeletal
disorders.35,44,45 Strong opioids could be considered in musculoskeletal pain when
other treatment options have failed, and if they are part of an active treatment
158 S. Bergman

plan.45,46 It has been reported that patients with strong pain, despite having continued
or elevated opioid medication, could benefit from a withdrawal of the opioid and, in-
stead, be enrolled onto a pain coping programme.47 This is also supported by studies
that suggest that opioid action could contribute to the central sensitisation process
and, thus, an aggravation of the pain problem.48

Antidepressants

Tricyclic antidepressants (TCA), especially amitryptiline, have been found to be useful in


the treatment of neuropathic pain49 and also beneficial for patients with chronic mus-
culoskeletal pain problems, such as fibromyalgia and low back pain.50 They are supposed
to interact with the pain pathways in several ways and the effect is separated from the
anti-depressive action.51 Similar positive effects have been reported in studies on
chronic musculoskeletal pain and serotonin and noradrenaline reuptake inhibitors (SNRIs),
but not selective serotonin reuptake inhibitors (SSRI)51e53, The anti-nociceptive effect
seems to be more effective for antidepressants that act on both the noradrenaline and
serotonin systems than those working on the serotonin system alone.50,54 The role of
SNRIs in the treatment of chronic musculoskeletal pain is still under debate and more
studies should be on the research agenda.55

Anticonvulsants

Anticonvulsants such as karbamazepin, phenytoin, gabapentin and pregabalin, primarily


developed for treatment of epilepsy, also have a long therapeutic tradition in the treat-
ment of specific neuropathic pain conditions, such as trigeminal neuralgia, diabetic neu-
ropathy and post-herpetic neuropathy.56,57 Such specific conditions could be an
important part of a chronic pain problem perceived as coming from musculoskeletal
structures. The use of anticonvulsants has been suggested for the treatment of condi-
tions where central sensitisation is believed to be part of the mechanism. Studies on
the treatment of fibromyalgia with more recently developed compounds such as gaba-
pentin and pregabalin are reported to be promising, but more research is needed to
establish their role in the treatment strategy.50,58

NON-PHARMACOLOGICAL METHODS OF PAIN MANAGEMENT

Non-pharmacological treatment is often more important than pharmacological inter-


vention. The cornerstones of non-pharmacological treatment are physical exercise and
patient education with a cognitive approach, preferably given in combination within
a multi-professional rehabilitation programme.59
Physical exercise includes various interventions such as walking, running, aerobic ex-
ercise, aerobic dancing, cycling and pool exercises. The variety of exercise modes to-
gether with the range of musculoskeletal conditions makes evaluation problematic but
the overall impression is that physical exercise reduces pain and improves function.
Studies are, however, often limited in time and there is little knowledge on long
term effects.60e62 For patients with fibromyalgia it is suggested that physical exercise
should be individualised and of low intensity, such as walking.61 Physical exercise has
been shown to reduce pain and improve function in patients with OA of the knee,
Management of musculoskeletal pain 159

but knowledge is insufficient for hip OA.63 Exercise therapy that includes stretching or
strengthening may improve pain and function in chronic non-specific low back
pain.62,64 In all physical exercise interventions there is a need for strategies to encour-
age adherence.
Physical therapy including mobilisation, body awareness therapy, manipulation and
massage can be beneficial in reducing pain and increasing function. Massage has been
found to be effective in chronic low back pain, but spinal manipulations have only small
benefits.65,66 Body awareness therapy may have a better effect on health status than
traditional physiotherapy in some patients with non-specific musculoskeletal pain.67
Traction is a relatively common treatment for low back pain but a recent review ques-
tions its effectiveness.68
Acupuncture has been shown to be beneficial as an adjuvant therapy in several
musculoskeletal disorders. Pain and joint function can be improved in OA of the
knee.69 For chronic low back pain there is a short term effect only, but it could
be a justified adjuvant to other interventions.70 There is a need for better quality
studies concerning the use of acupuncture in fibromyalgia and non-specific mus-
culoskeletal pain.
Transcutaneous electrical nerve stimulation (TENS) has been used in different pain-
ful musculoskeletal conditions since the 1960s, but the scientific basis for its use is
still weak for several of them. It is proposed that TENS has a short-acting effect
in ‘gate control,’ but there is probably also a more long-lasting effect through the
activation of central descending inhibitory pathways. There is evidence for a posi-
tive effect on pain in knee OA71 but the scientific basis for the treatment of
chronic low back pain is weak and conflicting.72 In chronic widespread pain and
fibromyalgia, TENS is proposed to have an adjuvant role for more localised com-
ponents of musculoskeletal pain.73
Cognitive behavioral therapy (CBT) has become a popular treatment concept for
chronic pain problems. The term is, however, used for different interventions based
on learning and cognitive changes. A cognitive and pedagogic approach would be
a more relevant terminology for the different treatments that are used as well as
‘true’ CBT. Despite this diversity in methodology, CBT has been credited with having
a positive effect on pain and other patient relevant outcomes in chronic pain, including
fibromyalgia, chronic low back pain, OA and RA.8,74e76 The best effect of CBT is seen
when it is used together with physical exercise as part of a multimodal treatment
programme.77,78
Psychosocial and occupational interventions are especially important in the working
population since musculoskeletal pain is associated with several risk factors in social
and working life, and is also a common cause for sickness absence and disability
pensions.
Early workplace interventions have been shown to reduce sick leave and produce
direct cost savings.79,80 The intervention relies on early exercise instructions, advice to
stay active, physiotherapy and educational programmes.81e83 Individual and workplace
psychosocial risk factors must also be taken into account.33,84
Surgery with joint replacement is the ultimate treatment for some patients with
severe musculoskeletal pain or dysfunction due to trauma, OA or RA. It can be
important to carry out this intervention before the patient has developed a more
widespread pain, although patients with fibromyalgia-like pain pre-operatively have
been shown to improve after surgery.11,12 A recent review of surgery for
degenerative lumbar spondylosis found no consistent evidence to support surgical
lumbar fusion.85
160 S. Bergman

A MULTIMODAL STRATEGY FOR THE MANAGEMENT


OF CHRONIC MUSCULOSKELETAL PAIN

Intervention programmes often focus on only one or a few components in pain man-
agement and there is not one single scheme that can be said to give an evidence-based
approach to every patient. In a multimodal approach it is important to note what con-
dition to treat and who the individual is. A practical approach to chronic musculoskel-
etal pain based on the knowledge presented in this article is suggested below. Some of
the points may apply to every patient with, or at risk for the development of, chronic
musculoskeletal pain. Other points should be considered after taking into account in-
dividual needs. The multi-modal strategy should preferably be administered by a multi-
disciplinary team, which also includes the patient as an active member.

Belief in the patient

It is essential to believe in the patient’s experience and description of pain. When pain
is longstanding and widespread there is often no tissue damage found that could ex-
plain all reported pain and the search for a specific cause may well be in vain. The pa-
tient’s pain must, nevertheless, be considered to be true and must be the starting point
for further management.

Carry out a thorough clinical examination

Initially it is important to do a thorough clinical examination as this not only gives the
clinician valuable information but also gives the patient confidence. It is important
to find or rule out potentially dangerous diseases such as malignancies, giant cell arthritis,
endocrine disorders and bacterial infections in the musculoskeletal system. Diagnostic
procedures should be kept to a minimum as they may introduce unnecessary fear and
negative expectations. The case history and the pain drawing provide the first clues
to an understanding of the underlying causes. It is important to have risk factors for
chronicity in mind in order to identify, early on, those patients that are at risk for
the development of a longstanding widespread pain problem. The clinical examination
gives further information on the nature of the pain problem. Peripheral pain generating
processes should be searched for. Swollen or painful joints could indicate the presence
of OA or RA. Muscular tension could be a consequence, but could also be a source of
pain. Diminished sensory modalities of the skin or muscular dysfunction could indicate
neuropathic pain. An exaggerated pain response suggests a situation with peripheral or
central sensitisation.

Consider pharmacological treatment

Analgesics often play a minor role when pain is non-specific or has become chronic and
widespread. There is an obvious place for analgesics when a peripheral nociceptive
pain generating process is found to contribute to the pain. It is also important to treat
acute pain adequately. The WHO analgesic ladder (COX-inhibitors/paracetamol, weak
opioids and strong opioids) can be used as a model for treatment strategy. Amongst
the mild opioids, Tramadol has been reported to have benefits. Strong opioids should
be used with great care and are seldom beneficial in the long-term treatment of mus-
culoskeletal pain.
Management of musculoskeletal pain 161

Tricyclic antidepressants (TCA), especially amitryptiline, have been found to be useful


in the treatment of neuropathic pain and also beneficial for patients with chronic mus-
culoskeletal pain problems, such as fibromyalgia and low back pain. They are supposed
to interact with the pain pathways in several ways and the effect is separated from
their anti-depressive action. Similar positive effects have been reported in studies
on chronic musculoskeletal pain and serotonin and noradrenaline reuptake inhibitors
(SNRIs), but not selective serotonin reuptake inhibitors (SSRIs). The role of SNRIs
in the treatment of pain in different musculoskeletal disorders is still under debate
and more studies are needed.
Anticonvulsants have a therapeutic tradition in the treatment of specific neuropathic
pain conditions that can be perceived as coming from musculoskeletal structures.
Studies on the treatment of fibromyalgia with more recently developed compounds
such as gabapentin and pregabalin are reported to be promising, but more research
is needed to establish their role in the overall treatment strategy.

Encourage physical exercise

Physical exercise is one of the cornerstones of chronic musculoskeletal pain manage-


ment. As well as positive effects on the musculoskeletal system, there are also effects
on pain processing that could reduce pain perception. The main problem is that of ad-
herence to the recommendations. Aerobic exercise can be performed on land or in
water, individually or in a group, supervised or self-managed at home. The first step
could be to take a daily walk. To reduce the barrier and minimise the risk of worsening
of pain, the advice should be to start low and go slow, gradually increasing the intensity
of training. Aerobic exercises can be combined with training for muscle flexibility,
strength and endurance under the supervision of a physiotherapist in order to im-
prove pain and function.

Combine physical therapy with other therapeutic interventions


for an adjuvant effect

Mobilisation, body awareness therapy, manipulation and massage can reduce pain and
improve function. Acupuncture and transcutaneous electric nerve stimulation (TENS)
may reduce pain perception and nociceptive flow and could be beneficial in several
musculoskeletal disorders if used together with other therapeutic interventions.

Pay attention to cognitive and emotional aspects

Thoughts, memories and expectations influence pain perception and behaviour. Fears
and earlier experiences should be asked about and discussed. In a cognitive approach
to the patient vicious circles in thought and behaviour should be identified and made
obvious to the patient. Cognitive behavioral therapy (CBT) can be considered for
some patients. Education and motivation of the patient should be an integrated part
of pain management. It is important to make the patients involved in their own recov-
ery and to give realistic and confident information about what the patient can expect dur-
ing the healing or rehabilitation period. The patient should be encouraged to continue
or return to normal activities as soon as possible. Concomitant depressive disorders
must be recognised and treated together with the pain symptoms. SSRIs may be the
162 S. Bergman

drugs of choice if pain is managed in other ways, although SNRIs should also be con-
sidered for a possible positive effect on pain perception.

Pay attention to stress, psychosocial situation, sleep and lifestyle

Chronic stress contributes to an exaggerated transmission and perception of pain, as


well as to symptoms such as fatigue, sleep problems, irritable bowel syndrome and
cognitive dysfunction. Sleep problems are often an early feature in chronic pain devel-
opment and may be part of the pathological process. Barriers for recovery and return
to work can be found in the psychosocial situation at home or at work. Early identi-
fication and attendance to these psychosocial factors are crucial. Individual counselling
at the workplace and worksite physical activity programmes can positively change
physical activity and reduce musculoskeletal disorders. A referral to an occupational
therapist or physiotherapist would be justified and helpful if an adverse ergonomic
work situation is suspected. Lifestyle factors of special importance are smoking, seden-
tary lifestyle and obesity, all being predictors for chronicity that could be targets for
intervention.

SUMMARY

Musculoskeletal disorders interact with the affected individual’s lifestyle and psychoso-
cial situation and the experienced pain is often non-specific with regard to findings in
the musculoskeletal system. As well as specific treatment of peripheral pain generating
disorders, non-pharmacological treatments are often the first line of treatment. The
cornerstones are physical exercise and patient education with a cognitive approach.
Management of chronic musculoskeletal pain calls for a biopsychosocial perspective
and a multimodal management strategy, preferably given within a multi-professional re-
habilitation programme.

Practice points

 Chronic musculoskeletal pain is often present without there being any struc-
tural changes in the musculoskeletal system and this calls for a biopsychosocial
approach to management.
 Chronic widespread pain can account for up to half of the pain present in a par-
ticular body region. If this is the case, then an analysis of the total pain situation
is called for.
 Management of chronic musculoskeletal pain relies on a confident relationship
between the patient and the medical profession.
 Physical exercise and cognitive behavioural therapy, or at least a cognitive ped-
agogic approach, are the cornerstones of the treatment of chronic musculo-
skeletal pain.
 Analgesics are often of less value in a situation without any nociceptive pain
generating pathological process.
 Other pharmacological options, such as antidepressants and anticonvulsants,
can be of value in some patients with chronic musculoskeletal pain.
Management of musculoskeletal pain 163

Research agenda

 Pain experience is the result of a multitude of processes, whereof the sensory in-
put is one, that interact in a proposed neural network, the neuromatrix. There is
a need for more knowledge of how e.g. cognition and chronic stress interact with
pain transmission and perception, in order to tailor management strategies.
 There is a need for better knowledge of how pain and functional limitations
develop in different musculoskeletal disorders, often without any relation to
structural changes or obvious pathological processes in the musculoskeletal
system.
 Treatment studies in musculoskeletal disorders are often unimodal. There is
a need for more studies of a multimodal management scheme that, having a bi-
opsychosocial perspective, will attend to several aspects of pain perception at
the same time.

REFERENCES

1. Bergman S, Herrström P, Högström K et al. Chronic musculoskeletal pain, prevalence rates, and sociode-
mographic associations in a Swedish population study. The Journal of Rheumatology 2001; 28(6): 1369e1377.
2. Croft P, Rigby AS, Boswell R et al. The prevalence of chronic widespread pain in the general population.
The Journal of Rheumatology 1993; 20(4): 710e713.
3. Foster NE, Pincus T, Underwood M et al. Treatment and the process of care in musculoskeletal con-
ditions. A multidisciplinary perspective and integration. The Orthopedic Clinics of North America 2003;
34(2): 239e244.
*4. Dieppe PA & Lohmander LS. Pathogenesis and management of pain in osteoarthritis. Lancet 2005;
365(9463): 965e973.
5. Breivik H, Collett B, Ventafridda V et al. Survey of chronic pain in Europe: prevalence, impact on daily
life, and treatment. European Journal of Pain 2006; 10(4): 287e333.
6. Merskey H. Logic, truth and language in concepts of pain. Quality of Life Research 1994; 3(supplement 1):
S69eS76.
*7. Woolf CJ. Pain: moving from symptom control toward mechanism-specific pharmacologic management.
Annals of Internal Medicine 2004; 140(6): 441e451.
8. Morley S, Eccleston C & Williams A. Systematic review and meta-analysis of randomized controlled tri-
als of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache.
Pain 1999; 80(1e2): 1e13.
9. Stahl S & Briley M. Understanding pain in depression. Human Psychopharmacology 2004; 19(supplement 1):
S9eS13.
10. Birrell F, Croft P, Cooper C et al. Health impact of pain in the hip region with and without radiographic
evidence of osteoarthritis: a study of new attenders to primary care. The PCR Hip Study Group. Annals
of the Rheumatic Diseases 2000; 59(11): 857e863.
11. Kosek E & Ordeberg G. Abnormalities of somatosensory perception in patients with painful osteoar-
thritis normalize following successful treatment. European Journal of Pain 2000; 4(3): 229e238.
12. Nilsdotter AK, Petersson IF, Roos EM & Lohmander LS. Predictors of patient relevant outcome after
total hip replacement for osteoarthritis: a prospective study. Annals of the Rheumatic Diseases 2003;
62(10): 923e930.
13. Henriksson KG. Is fibromyalgia a distinct clinical entity? Pain mechanisms in fibromyalgia syndrome. A
myologist’s view. Baillière’s Best Practice and Research. Clinical Rheumatology 1999; 13(3): 455e461.
14. Scholz J & Woolf CJ. Can we conquer pain? Nature Neuroscience 2002; 5(supplement): 1062e1067.
15. Watkins LR, Milligan ED & Maier SF. Glial proinflammatory cytokines mediate exaggerated pain states:
implications for clinical pain. Advances in Experimental Medicine and Biology 2003; 521: 1e21.
164 S. Bergman

16. Melzack R & Wall PD. Pain mechanisms: a new theory. Science 1965; 150(699): 971e979.
17. Melzack R. From the gate to the neuromatrix. Pain 1999;(supplement 6): S121eS126.
18. Rethelyi JM, Berghammer R, Ittzes A et al. Comorbidity of pain problems and depressive symptoms in
young women: results from a cross-sectional survey among women aged 15e24 in Hungary. European
Journal of Pain 2004; 8(1): 63e69.
19. Kendall NA. Psychosocial approaches to the prevention of chronic pain: the low back paradigm. Bail-
lière’s Best Practice and Research. Clinical Rheumatology 1999; 13(3): 545e554.
20. Theorell T, Harms-Ringdahl K, Ahlberg-Hulten G & Westin B. Psychosocial job factors and symptoms
from the locomotor system e a multicausal analysis. Scandinavian Journal of Rehabilitation Medicine 1991;
23(3): 165e173.
21. McBeth J, Macfarlane GJ, Hunt IM & Silman AJ. Risk factors for persistent chronic widespread pain:
a community-based study. Rheumatology (Oxford) 2001; 40(1): 95e101.
22. Bergman S, Herrström P, Jacobsson LT & Petersson IF. Chronic widespread pain: a three year follow-up
of pain distribution and risk factors. The Journal of Rheumatology 2002; 29(4): 818e825.
23. van der Waal JM, Bot SD, Terwee CB et al. Course and prognosis of knee complaints in general prac-
tice. Arthritis and Rheumatism 2005; 53(6): 920e930.
24. Allison TR, Symmons DP, Brammah T et al. Musculoskeletal pain is more generalised among people
from ethnic minorities than among white people in Greater Manchester. Annals of the Rheumatic Dis-
eases 2002; 61(2): 151e156.
25. Goldberg MS, Scott SC & Mayo NE. A review of the association between cigarette smoking and the
development of nonspecific back pain and related outcomes. Spine 2000; 25(8): 995e1014.
26. Webb R, Brammah T, Lunt M et al. Prevalence and predictors of intense, chronic, and disabling neck and
back pain in the UK general population. Spine 2003; 28(11): 1195e1202.
27. Rugulies R & Krause N. Job strain, iso-strain, and the incidence of low back and neck injuries. A 7.5-year
prospective study of San Francisco transit operators. Social Science and Medicine 2005; 61(1): 27e39.
28. Walker-Bone K & Cooper C. Hard work never hurt anyone: or did it? A review of occupational asso-
ciations with soft tissue musculoskeletal disorders of the neck and upper limb. Annals of the Rheumatic
Diseases 2005; 64(10): 1391e1396.
29. Hagen KB, Jamtvedt G, Hilde G & Winnem MF. The updated Cochrane review of bed rest for low back
pain and sciatica. Spine 2005; 30(5): 542e546.
30. Bogduk N. Regional musculoskeletal pain. The neck. Baillière’s Best Practice and Research. Clinical Rheu-
matology 1999; 13(2): 261e285.
31. Kendrick D, Fielding K, Bentley E et al. Radiography of the lumbar spine in primary care patients with
low back pain: randomised controlled trial. British Medical Journal 2001; 322(7283): 400e405.
32. Muirden KD. Community oriented program for the control of rheumatic diseases: studies of rheumatic
diseases in the developing world. Current Opinion in Rheumatology 2005; 17(2): 153e156.
33. Sullivan MJ, Feuerstein M, Gatchel R et al. Integrating psychosocial and behavioral interventions to
achieve optimal rehabilitation outcomes. Journal of Occupational Rehabilitation 2005; 15(4): 475e489.
34. Sullivan MJ, Ward LC, Tripp D et al. Secondary prevention of work disability: community-based psycho-
social intervention for musculoskeletal disorders. Journal of Occupational Rehabilitation 2005; 15(3):
377e392.
35. Reig E. Tramadol in musculoskeletal pain e a survey. Clinical Rheumatology 2002; 21(supplement 1):
S9eS11 [discussion S11eS12].
*36. Curatolo M & Bogduk N. Pharmacologic pain treatment of musculoskeletal disorders: current perspec-
tives and future prospects. The Clinical Journal of Pain 2001; 17(1): 25e32.
37. Moulin DE. Systemic drug treatment for chronic musculoskeletal pain. The Clinical Journal of Pain 2001;
17(4 supplement): S86eS93.
38. Nielsen OH, Ainsworth M, Csillag C & Rask-Madsen J. Systematic review: coxibs, non-steroidal anti-
inflammatory drugs or no cyclooxygenase inhibitors in gastroenterological high-risk patients? Alimentary
Pharmacology and Therapeutics 2006; 23(1): 27e33.
39. Towheed T, Maxwell L, Judd M et al. Acetaminophen for osteoarthritis. Cochrane Database of Systematic
Reviews 2006; 1: CD004257.
*40. Wegman A, van der Windt D, van Tulder M et al. Nonsteroidal antiinflammatory drugs or acetamino-
phen for osteoarthritis of the hip or knee? A systematic review of evidence and guidelines. The Journal of
Rheumatology 2004; 31(2): 344e354.
Management of musculoskeletal pain 165

41. Wienecke T & Gotzsche PC. Paracetamol versus nonsteroidal anti-inflammatory drugs for rheumatoid
arthritis. Cochrane Database of Systematic Reviews 2004; 1: CD003789.
42. Romundstad L, Stubhaug A, Niemi G et al. Adding propacetamol to ketorolac increases the tolerance
to painful pressure. European Journal of Pain 2006; 10(3): 177e183.
43. Woo WW, Man SY, Lam PK & Rainer TH. Randomized double-blind trial comparing oral paracetamol
and oral nonsteroidal antiinflammatory drugs for treating pain after musculoskeletal injury. Annals of
Emergency Medicine 2005; 46(4): 352e361.
44. Mattia C & Coluzzi F. Tramadol. Focus on musculoskeletal and neuropathic pain. Minerva Anestesiologica
2005; 71(10): 565e584.
45. Bertin P. Current use of analgesics for rheumatological pain. European Journal of Pain 2000; 4(supplement
A): 9e13.
*46. Kalso E, Allan L, Dobrogowski J et al. Do strong opioids have a role in the early management of back
pain? Recommendations from a European expert panel. Current Medical Research and Opinion 2005;
21(11): 1819e1828.
47. Gartner CM & Schiltenwolf M. Limited efficacy of opioids in chronic musculoskeletal pain (in German).
Schmerz 2004; 18(6): 506e514.
48. Mao J. Opioid-induced abnormal pain sensitivity: implications in clinical opioid therapy. Pain 2002;
100(3): 213e217.
*49. Saarto T & Wiffen PJ. Antidepressants for neuropathic pain. Cochrane Database of Systematic Reviews
2005; 3: CD005454.
50. Maizels M & McCarberg B. Antidepressants and antiepileptic drugs for chronic non-cancer pain. Amer-
ican Family Physician 2005; 71(3): 483e490.
51. Arnold LM, Rosen A, Pritchett YL et al. A randomized, double-blind, placebo-controlled trial of dulox-
etine in the treatment of women with fibromyalgia with or without major depressive disorder. Pain
2005; 119(1e3): 5e15.
52. Briley M. Clinical experience with dual action antidepressants in different chronic pain syndromes.
Human Psychopharmacology 2004; 19(supplement 1): S21eS25.
53. Stahl SM, Grady MM, Moret C & Briley M. SNRIs: their pharmacology, clinical efficacy, and tolerability in
comparison with other classes of antidepressants. CNS Spectrums 2005; 10(9): 732e747.
54. Wise TN, Arnold LM & Maletic V. Management of painful physical symptoms associated with depression
and mood disorders. CNS Spectrums 2005; 10(12 supplement 19): 1e13.
55. Leo RJ & Barkin RL. Antidepressant use in chronic pain management: is there evidence of a role for
duloxetine? Primary Care Companion to the Journal of Clinical Psychiatry 2003; 5(3): 118e123.
56. Vinik A. Clinical review: use of antiepileptic drugs in the treatment of chronic painful diabetic neurop-
athy. The Journal of Clinical Endocrinology and Metabolism 2005; 90(8): 4936e4945.
*57. Wiffen P, Collins S, McQuay H et al. Anticonvulsant drugs for acute and chronic pain. Cochrane Database
of Systematic Reviews 2005; 3: CD001133.
58. Crofford LJ, Rowbotham MC, Mease PJ et al. Pregabalin for the treatment of fibromyalgia syndrome:
results of a randomized, double-blind, placebo-controlled trial. Arthritis and Rheumatism 2005; 52(4):
1264e1273.
*59. Nielson WR & Weir R. Biopsychosocial approaches to the treatment of chronic pain. The Clinical Journal
of Pain 2001; 17(4 supplement): S114eS127.
60. Hunt A. Musculoskeletal fitness: the keystone in overall well-being and injury prevention. Clinical Ortho-
paedics and Related Research 2003; 409: 96e105.
61. Mannerkorpi K & Iversen MD. Physical exercise in fibromyalgia and related syndromes. Best Practice and
Research. Clinical Rheumatology 2003; 17(4): 629e647.
*62. Hayden JA, van Tulder MW & Tomlinson G. Systematic review: strategies for using exercise ther-
apy to improve outcomes in chronic low back pain. Annals of Internal Medicine 2005; 142(9):
776e785.
63. Fransen M, McConnell S & Bell M. Exercise for osteoarthritis of the hip or knee. Cochrane Database of
Systematic Reviews 2003; 3: CD004286.
64. Quittan M. Management of back pain. Disability and Rehabilitation 2002; 24(8): 423e434.
65. Furlan AD, Brosseau L, Imamura M & Irvin E. Massage for low-back pain: a systematic review with-
in the framework of the Cochrane Collaboration Back Review Group. Spine 2002; 27(17):
1896e1910.
166 S. Bergman

66. Cherkin DC, Sherman KJ, Deyo RA & Shekelle PG. A review of the evidence for the effectiveness,
safety, and cost of acupuncture, massage therapy, and spinal manipulation for back pain. Annals of Internal
Medicine 2003; 138(11): 898e906.
67. Malmgren-Olsson EB & Branholm IB. A comparison between three physiotherapy approaches with
regard to health-related factors in patients with non-specific musculoskeletal disorders. Disability and
Rehabilitation 2002; 24(6): 308e317.
68. Clarke JA, van Tulder MW, Blomberg SE et al. Traction for low-back pain with or without sciatica.
Cochrane Database of Systematic Reviews 2005; 4: CD003010.
69. Witt C, Brinkhaus B, Jena S et al. Acupuncture in patients with osteoarthritis of the knee: a randomised
trial. Lancet 2005; 366(9480): 136e143.
70. Furlan AD, van Tulder M, Cherkin D et al. Acupuncture and dry-needling for low back pain: an updated
systematic review within the framework of the Cochrane collaboration. Spine 2005; 30(8): 944e963.
71. Osiri M, Welch V, Brosseau L et al. Transcutaneous electrical nerve stimulation for knee osteoarthritis.
Cochrane Database of Systematic Reviews 2000; 4: CD002823.
72. Khadilkar A, Milne S, Brosseau L et al. Transcutaneous electrical nerve stimulation for the treatment of
chronic low back pain: a systematic review. Spine 2005; 30(23): 2657e2666.
73. Offenbacher M & Stucki G. Physical therapy in the treatment of fibromyalgia. Scandinavian Journal of
Rheumatology. Supplement 2000; 113: 78e85.
74. Linton SJ & Ryberg M. A cognitive-behavioral group intervention as prevention for persistent neck and
back pain in a non-patient population: a randomized controlled trial. Pain 2001; 90(1e2): 83e90.
*75. Williams DA. Psychological and behavioural therapies in fibromyalgia and related syndromes. Best Prac-
tice and Research. Clinical Rheumatology 2003; 17(4): 649e665.
76. Keefe FJ & Caldwell DS. Cognitive behavioral control of arthritis pain. The Medical Clinics of North Amer-
ica 1997; 81(1): 277e290.
77. Keefe FJ, Kashikar-Zuck S, Opiteck J et al. Pain in arthritis and musculoskeletal disorders: the role of
coping skills training and exercise interventions. The Journal of Orthopaedic and Sports Physical Therapy
1996; 24(4): 279e290.
78. Williams DA, Cary MA, Groner KH et al. Improving physical functional status in patients with fibro-
myalgia: a brief cognitive behavioral intervention. The Journal of Rheumatology 2002; 29(6): 1280e1286.
79. Arnetz BB, Sjogren B, Rydehn B & Meisel R. Early workplace intervention for employees with
musculoskeletal-related absenteeism: a prospective controlled intervention study. Journal of Occupa-
tional and Environmental Medicine 2003; 45(5): 499e506.
80. Franche RL, Cullen K, Clarke J et al. Workplace-based return-to-work interventions: a systematic re-
view of the quantitative literature. Journal of Occupational Rehabilitation 2005; 15(4): 607e631.
81. Frank J, Sinclair S, Hogg-Johnson S et al. Preventing disability from work-related low-back pain. New
evidence gives new hope e if we can just get all the players onside. CMAJ: Canadian Medical Association
Journal 1998; 158(12): 1625e1631.
82. Heymans MW, van Tulder MW, Esmail R et al. Back schools for nonspecific low back pain: a systematic
review within the framework of the Cochrane Collaboration Back Review Group. Spine 2005; 30(19):
2153e2163.
83. Sinclair SJ, Hogg-Johnson SH, Mondloch MV & Shields SA. The effectiveness of an early active interven-
tion program for workers with soft-tissue injuries. The Early Claimant Cohort Study. Spine 1997;
22(24): 2919e2931.
84. Buckle PW & Devereux JJ. The nature of work-related neck and upper limb musculoskeletal disorders.
Applied Ergonomics 2002; 33(3): 207e217.
85. Gibson JN & Waddell G. Surgery for degenerative lumbar spondylosis: updated Cochrane Review. Spine
2005; 30(20): 2312e2320.

You might also like