Volume 17, Issue 1 , Pages 1-15, February 2003
Clinical examination as a tool for identifying the origin of regional musculoskeletal pain
Article Outline
- Abstract
- 1. The physiology of pain
- 2. Clinical evaluation of RMP
- 3. Physical evaluation
- 4. Conclusions
- 5. Summary
- References
- Copyright
Abstract
A knowledge of the physiopathology of the processing of noxious stimuli in regional musculoskeletal disorders is useful for an understanding of the clinical history.
In regional musculoskeletal pain (RMP) the physiopathology of the pain may be separated into two main features. First, the nociceptive pain which results from the activation of nociceptors diffusely distributed among the anatomical structures in and around the joint, apart from the cartilage; the nociceptive pain has a protective role. Second, the abnormal impulses from a nervous tissue lesion give rise to a neuropathic pain which offers no biological advantage and is a maladaptive pain. This chapter describes the main physiological characteristics of these two kinds of pain. From these, in the majority of cases, the clinical history and the physical examination must specify the diagnosis of the RMP and localize the source of pain. Furthermore, the clinical characteristics permit diagnosis of different complex situations where these two types of pain are associated.
Keywords: regional musculoskeletal pain, clinical diagnosis, physiopathology, neuropathic pain, joint pain, soft-tissue pain, musculoskeletal pain
The common definition of pain is ‘an unpleasant sensory and emotional experience, associated with actual or potential tissue damage or described in terms of such damage’ (International Association for the Study of Pain, 1979). Nociception refers to the reception of signals by the central nervous system (CNS) induced by activation of specialized receptors or nociceptors of various types, under noxious stimuli. A noxious stimulus is one which potentially or actually damages a body tissue. Pain is always an individual and subjective experience.
Not all pain experienced results from a noxious stimuli or an injury, nor do all noxious stimuli lead to the experience of pain through the neurological process.1., 2. So, the first medical approach is to understand that the painful condition is a complex individual state that can be influenced by several psychological and physiological factors. Some painful conditions are ‘just a window on the predicament of life’.3
Musculoskeletal pain is one of the most common causes of visits to the primary care office. Regional musculoskeletal pain (RMP), mainly from the back, shoulder, neck, knee, hip, foot or hand, is a major cause of morbidity in both the community and workplace.4
RMP may be analysed in two ways. First, an actual or potential lesion of the musculoskeletal system: the nociceptive pain. Second, an aberrant somatosensory processing in the peripheral or CNS: the neuropathic pain. These two features of pain may be associated. RMP has many causes (Table 1). Appropriate history and clinical examination assist in the differentiation of such causes of RMP.
Table 1. The causes of RMP
| Joint or soft-tissue pain | Neuropathic pain | |
|---|---|---|
| Localizations | Capsule | Nerve |
| Ligaments | Radicular pain | |
| Muscle | Central nervous system | |
| Vascular components | ||
| Tendon | ||
| Peritendon | ||
| Bursa | ||
| Enthesis | ||
| Synovium | ||
Aetiologies | ||
| Soft-tissue diseases | Nerve | |
 Tendinitis | Nerve entrapment | |
| Tendinosis | Mononeuritis | |
| Enthesopathy | Multineuritis | |
| Paratendon inflammation | Radiculopathy | |
| Tendon rupture | Disc herniation | |
| Tendon sheath diseases | Spine osteoarthritis | |
| Bursal inflammation | Radiculitis | |
| Capsulitis | Polyneuritis | |
| Muscle strain | ||
| Delayed muscle soreness | ||
| Muscle cramps | ||
| Myopathies | ||
| Fatigue | Central nervous system | |
| Degenerative diseases | ||
| Joint diseases | Vascular diseases | |
| Osteoarthritis | Syringomyelia | |
| Infectious monoarthritis | Myelitis | |
| Non-infectious arthritis | Spinal cord compression | |
| Metabolic diseases of the spinal cord |
RMP must not be separated from the cognitive, behavioural components of pain. For example, in the workplace, organizational factors and economic factors (i.e. downsizing) interact with the sick leave resulting from musculoskeletal pain.5., 6. The observed increase in musculoskeletal disorders, particularly those localized to the back, neck and shoulders, in association with these economic factors, may be explained by the increase in physical demands, the reduction of job latitude, and job insecurity.7 Furthermore, in workplaces with a high proportion of older employees, major (compared to minor) downsizing may lead to a tenfold increase in the risk of an individual developing musculoskeletal disorders.5 Women have musculoskeletal problems more frequently than do men. Women seem to be vulnerable to the development and maintenance of musculoskeletal pain conditions due to a state of increased pain sensitivity from peripheral or central origin; biological and psychosocial factors might account for these differences.8 Compared with men, women with mental distress have more primary care consultations in the workplace.9
Genetic factors (race, ethnicity) may influence the experience of acute pain.10 These genetic factors may be associated with the molecular biology of pain but also with the ways of coping with pain, the meaning of pain and disparities in socioeconomic status. These appraisals of pain, in turn, can have a major influence on pain-related emotional responses (e.g. depression, guilt, anxiety).
Thus, patients with RMP experience pain that can be intense, persistent and disabling, precociously.
The clinical evaluation of RMP may be, as far as possible, complete at the initial stage. In the first part, we analyse the physiopathology of the two main types of pain (nociceptive and neuropathic pain). In the second part, we describe the main clinical characteristics associated with the two types of pain.
1. The physiology of pain
1.1. Joint and soft-tissue pain
The sensory receptors are diffusely distributed in the joint (capsule, ligaments) and around the joint (tendons, muscles, fascia, skin). Two main types of receptors can be identified: encapsulated and free nerve endings, which are predominantly near the vessels.
Pain arises from nociceptors: a noxious stimulus activates a receptor responding to stimuli which may cause tissue damage. Some receptors respond to mechanical stimuli (unimodal receptors), others to mechanical and thermal stimuli, and yet others to chemical, thermal and mechanical stimuli (polymodal receptors).11 There is a dynamic competence of the sensory receptors which send, or not, a noxious input in function of the intensity of the stimulus. Some receptors do not react to any mechanical stimulus (silent nociceptors).
Three main types of fibre convey the sensory input: heavily myelinated A-Beta fibres with a high conduction velocity and associated with proprioception, thinly myelinated A-Delta fibres with an intermediate conduction velocity, and unmyelinated C-fibres with a slow conduction velocity. Two main types of fibre conduct input to the nociceptors: the A-Delta fibres and the C-fibres.
Different anatomical structures in and around the joint are able to signal nociception. The cartilage is not normally innervated. The human synovium contains free nerve endings (sympathetic efferent fibres and unmyelinated C nociceptive afferents). The ligaments contain A-Delta receptors and the capsule has unmyelinated C afferent fibres. In the tendons and muscles a very wide distribution of receptors is observed, from high-to low-threshold, with A-Beta, A-Delta and free nerve ending receptors.
The cell bodies of all somatic afferent fibres are located in the dorsal root ganglia. All the afferent sensory fibres converge to the dorsal horn where they synapse with spinal neurones in the dorsal grey matter.
Afferents from the nociceptors have synaptic connections with efferents to skeletal ipsilateral or contralateral muscles, from the same spinal segment but also from adjacent levels12, with sympathetic efferents leading to localized vasoconstriction.
After tissue damage, the nociceptors (polymodal and silent nociceptors) are sensitized (decrease in response threshold). This primary sensitization may be provoked or enhanced by: prostaglandins, leucotrienes, a decrease in pH, release of ATP from muscle, bradykinin, different neurotransmitters, substance P (SP), calcitonin gene-related peptide (CGRP), neurokinin, catecholamines, dynorphine, exitatory amino-acids such as N-methyl d-aspartate, and nitric oxide. These neurotransmitters may act directly on the nociceptors (free nerve endings) or indirectly through a sequential process initiated at the spinal level. Some of them (SP, CGRP) can promote hyperexcitability of the dorsal horn neurones and expansion of the receptive fields. This sensitization explains the alteration of sensitivity to light touch13, the extension of the painful area (secondary pain) and, to some extent, explains the referred pain that is a zone of radiation of a perceived pain. This area of radiation is almost never a neurological area.
In the inflammatory rheumatic disorders, pro-inflammatory cytokines (tumour necrosis factors and different interleukins—IL-1β, IL-6, IL-8) augment activity in nociceptive pathways. They may cause sensitization directly or indirectly by triggering other cytokines or classical mediators of hyperalgesia such as prostanoids. Other interleukins (IL-4, IL-10, IL-13) may inhibit release of pro-inflammatory cytokines or the activity/expression of cyclo-oxygenase.
The liberation of SP and CGRP by non-myelinated fibres, closely associated with blood vessels, may induce modifications of the vascular tone, with oedema, redness, heat and pain: neurogenic inflammation.
Subsequently, the nociceptive input, through the nerve cells of the dorsal horn, uses two principal routes of transmission: the spinothalamic tract and a more diffuse polysynaptic tract which projects bilaterally to the brain stem reticular formation (spinoreticular tract) and reaches the lateral thalamic nuclei (Figure 1).
Figure 1.
The pain process.
Different cortical areas, implicated in the motor process, are involved in acute—and particularly chronic—pain states (modifications of the motor memory processing and of the motor anticipation processing). It is only at this stage that the noxious input or stimulus is integrated as pain.
Different descending pathways (diffusely in the spinal cord and the mid brain, as the endogenous opioid system and the noradrenergic system) decrease the nociceptive information at the spinal cord level, particularly at the dorsal horn level, by pre-synaptic inhibition of the release of C-fibre neurotransmitter (SP, SGRP). These descending pathways play a major role in the endogenous control of pain and in the processes of central sensitization to pain. A dysfunction in the descending pathways leads to a decrease in the noxious input by a decrease in the activity of the inhibitory interneurones; this enhances the peripheral sensitization. Box 1
1.2. Neuropathic pain
Unlike nociceptive pain—which initiates protective reflexes to limit further damage—pain from damaged neurological tissues (roots, plexi, nerves or CNS) has no beneficial effect on the organism and is termed neuropathic pain.14 Neuropathic pain is characterized by greatly reduced pain thresholds (mechanohyperalgesia or thermal hyperalgesia) and sometimes by painful sensations through light touch (mechanical allodynia) or by variations in temperature (thermal allodynia)—although it may also occur spontaneously. While a classification of neuropathic pain is frequently made according to the type of underlying pathology, this distinction does not account for the possible mechanisms that may be present: touch-evoked allodynia due to A-Beta fibre sensitization and static mechanoallodynia and hyperalgesia due to C-fibre sensitization which may be associated with sympathetic hyperactivity.15 In fact, despite the multiple lesions giving rise to neuropathic types of pain, many of these conditions associate a paradoxical combination of sensory loss and hyperalgesia in the painful area—paroxysms and a gradual increase of pain following repetitive stimulation.
These pains may be explained by a hyperexcitability of the peripheral and CNS. This hyperexcitability is explained by abnormalities of the ion channels leading to abnormal input (ectopic input or ectopia). These abnormal impulses occur without permanent lesion.
Moreover, it has been observed that an abnormal sensitivity of peripheral nociceptors to catecholamines is associated with an increase in the adrenergic innervation of the dorsal horn ganglia1., 14., leading to an adrenosensitivity and a sympathetically maintained pain. In the dorsal ganglia it has been observed that some neurones with A-Beta fibres begin to express SP/CGRP after a peripheral injury which may be induced by nerve growth factor (NGF). In the dorsal horn, rearrangements may be found: sprouting of A-Beta and A-Delta fibres with post-synaptic structures that normally receive C-fibre input, a sympathetic sprouting that may induce a coupling between sympathetic efferents and sensory neurones. These mechanisms may provoke disinhibition. The release of SP or CGRP may favour local sensitization. These compensatory responses in neuropathic pain evoke a ‘fail-safe mechanisms’.
A reorganization of the cortical areas occurs during neuropathic pain. These changes make it impossible for the diffuse analgesic system to control, endogenously, the rate of inputs, leading to a central disinhibition of pain. Box 2
1.3. Joint and soft-tissue pain: motor alterations
Due to synaptic connections with the motor neurones at different and adjacent spinal levels, motor alterations may occur very early in the course of a musculoskeletal disorder through alterations of myotonic reflexes, modifications of the motor organization, modifications of the proprioceptive innervation of the muscles and tendons, and reorganization of the motor cortex associated, or not, with behaviour processing.
In states of neuropathic pain, a lipid atrophy of the muscular fibres may be observed which may be related to modifications of motoneurone tone, to the sympathetic system, to modifications of vascular tone or genetic factors.
Aberrant movement patterns and postures are obvious in patients with nociceptive musculoskeletal pain: increases and decreases in muscle activity have both been shown, along with alterations in neuronal mechanisms, proprioception and local muscle morphology. Muscle activation and recruitment are altered in the presence of noxious stimuli (neuromuscular activation model). These changes affect the ability of muscles to perform synergistic functions related to maintaining joint stability and control.16
Tonic muscle pain can inhibit the motor system. Motor cortex inhibition is followed by a reduction in the excitability of both cortical and spinal motoneurones.17
Fatigue is another important manifestation frequently associated with musculoskeletal pain. In RMP, fatigue is often localized but may be described as generalized. Muscular fatigue is a failure to maintain force at an expected level. Fatigue is perceived both physically and mentally.18 It is generated from three systems: the muscle at several sites (accumulation of byproducts such as hydrogen ions, phosphate and lactic acid), the anterior horn cell performance (slowing of the anterior horn cell discharges, sensory feedback from muscle spindles, abnormalities in the neuromuscular junction), the CNS pathways (feeling from the cortical and somatosensory cortical areas that increased effort is required to maintain the same force). Modifications leading to fatigue can arise from noxious input or from neuropathic disorders. Box 3
2. Clinical evaluation of RMP
Obtaining details of the patient's history of pain and associated conditions is the first fundamental step in diagnosis. The patient's past history permits us to find diseases that may be associated with lesions in the nervous system (traumatic, spinal surgery, radiotherapy, metabolic as diabetus mellitus, alcoholism…).
In the acute setting, the words used to describe pain allow us to separate nociceptive pain from neuropathic pain (Table 2).
Table 2. The words used to refer to pain
| Joint or soft tissue-pain | Neuropathic pain | |
|---|---|---|
| Functional terms | Deep pain | Dysesthesia |
| Burning | Neuralgia | |
| Cramps | Spontaneous | |
| Localized | Diffused | |
| Fasciculations | ||
Physical terms | Hyperalgesia | Hyperpathia |
| Analgesia | ||
| Causalgia | ||
| Hypoalgesia | ||
| Hypoesthesia |
2.1. Nociceptive pain
A nociceptive pain, arising from tendons, ligaments or capsular structures, is fairly well localized.19 Others signs may coexist: stiffness, swelling, cracking (Figure 2). A pain that arises in the morning or during the second part of the night is suggestive of an inflammatory component (including neurogenic inflammation) as a pain occurring without any activity or movement. Even in a referred pain, a nociceptive pain does not affect an entire limb.20
Figure 2.
Clinical diagnosis of RMP.
In non-inflammatory RMP, noxious stimuli occur during physical activity or 1–3hours after the activity. Periarticular pain from tendons is often induced by a specific type of activity, particularly by leisure or occupational activities. A pain arising from the ligament is associated with a traumatic event. A post-exertional muscle pain may occur 1 or 2 days after an activity and is described as fatigue, weakness, stiffness or tightness in the area of the muscle.18
2.2. Neuropathic pain
Many patients exhibit persistent or paroxysmal pains that are independent of any mechanical stimulus. A neuropathic pain, is more diffuse than a nociceptive pain and is characterized by paraesthesia distally to the neurological lesion and in the sensitive field of the nerve or root or plexus. The dysfunction of the nervous system gives rise to spontaneous excitation of burning or ‘pins and needles’ types or numbness, typically in a neurological systematization, sometimes without any systematization.
Paraesthesia are often at the second place and masked by more severe sensations, such as ‘electric shock’, ‘shooting’ type or ‘burning’ pain. Some sensations are typical; for example, a sensation of ‘wrist bracelet’ is typical of a median nerve lesion, and a sensation of ‘ankle bracelet’ evokes a lesion of the L5 root. Paraesthesia is the main typical subjective sensation of a neuropathic pain and must be carefully searched for.
Typically, there is no ‘time signal’ in neuropathic pain but emotions, fatigue, and physical activity may enhance the supervention of neuropathic symptoms. Pain that radiates distally below the elbow in cases of shoulder pain suggests a neurological aetiology.21 In cases where a neurological lesion is associated with musculoskeletal disorders, the neuropathic pain occurs at the same time as the musculoskeletal pain. In an entrapment neuropathy, patients may notice a worsening of symptoms at night, in relation to sleep position, related to a postural ischaemia of the neural structures (Figure 2).
A constant and severe pain, without any variation with activity, is more likely to be of a neuropathic or a psychogenic origin than a nociceptive origin.
Some descriptive words are not specific: weakness, fatigue, ‘sensation of swelling’ could be associated with rheumatic or neuropathic pains.
2.3. General evaluation
The history of pain must specify the ‘red flags’: fever, loss of weight, sweats, previous history of cancer, infection and systemic diseases, loss of control of the sphincters, severe motor loss.
RMP may be associated with neurological disorders.22 This does not mean that a pain is neuropathic but that a neurological disorder may have provoked a musculoskeletal disorder. Hence, one must search with particular care for the following disorders: Parkinson's disease, multiple sclerosis and lateral amyotrophic sclerosis.
The psychological background of the patient must be evaluated (emotional distress, anxiety, past history of depression). This background must be systematically evaluated, in typical nociceptive (inflammatory or non-inflammatory disorders) and neuropathic pains (‘yellow flags’). In RMP associated with occupational activities, a rapid screening of work-related satisfaction must be done. Box 4
3. Physical evaluation
The purpose of this part of the chapter is not to compile all the tests for each rheumatological condition observed in RMP but to check the fundamental keys of the physical examination available in all the RMPs.23
3.1. Inspection
The physical examination of a subject with RMP starts with the entry of the patient (the walk, the posture of the trunk and of the head in case of occipito-cervical pain, the automatic movements of the cervical spine during interview, the posture of the upper limb in a pain from the upper limb…). These modifications are associated mainly with nociceptive pain and are associated with either motor and proprioception changes related to the nociceptive pain, or with a fear-inhibition of movement from the cognitive and behaviour components of pain (either nociceptive or neuropathic pain).
In musculoskeletal disorders, different abnormalities may be found by inspection: a bony swelling due to osteophytes for all the superficial joints, a deformity, an effusion, a pitting oedema or overlying skin changes. A periarticular oedema near a joint may evoke neurogenic inflammation. In superficial areas (olecrane, patella), a localized periarticular oedema may evoke a bursitis tenderness.
Fasciculations can be seen in a radiculopathy, in tense, under-rested stressed-out patients. When fasciculations are well-limited, confined to the territory of a peripheral nerve or a nerve root, they evoke neuropathic pain.18
3.2. Palpation
Warmth, tenderness and crepitus are always signs of a nociceptive pain and of inflammation.
The precise palpation of the anatomical sites is of great importance, especially for pain arising from the bursae, the tendons and the articular zone of a superficial joint.
In superficial joints, palpation allows us to find a hydrarthrosis.
The threshold by which palpation induces pain is important to note. Pressure on an anatomical site is potentially noxious, and different zones are very sensitive (trapezius, long portion of the biceps, lateral epicondyle tendons). A light touch or brush is not potentially noxious.
Joint structures are covered by the skin, and primary and secondary sensitizations of the neurological structures create a superficial hyperpathic sensitivity that is observed in both nociceptive and neuropathic pain. This may occur in inflammatory disorders of the joint but also in inflammatory disorders of soft tissues (bursa, tendonitis, tendon sheath inflammation).
In the absence of skin modifications at inspection, a superficial pain may be related to a neuropathic pain (decreased threshold to noxious stimuli, increased pain from suprathreshold stimuli, spontaneous pain, in a typical neurological area). A superficial pain is due to a decreased threshold to noxious stimuli, an increased pain from suprathreshold stimuli spontaneous pain. This superficial pain may be related to a neuropathic pain when the pain is in a typical neurological area or a psychogenic pain, but without any neurological systemization. It is one of the nonorganic signs used from the cervical spine.24
In the case of muscular pain, physical examination may find trigger points in the muscle. Trigger points are discrete focal hyperirritable spots located in a taut band of skeletal muscle. They produce pain locally and in a referred pattern. The palpation of a hypersensitive bundle, or of a nodule of muscle fibre harder than normal consistency, is the physical finding typically associated with a trigger point. It confirms that an abnormal motor response is present. It does not allow us to distinguish between a neuropathic or a nociceptive input.
3.3. Joint movement
Analysis of joint movement allows diagnosis of pain from the joint and from the active structures around the joint (Figure 3). Theoretically, a pain provoked by a passive movement originates from the mobilized joint. This, at the origin of the acute impairment, is associated with joint disease. There is a high correlation between noxious stimuli and the physical impairment during movement in RMP in an acute pain state.25., 26. This is not true in chronic pain, due mainly to the primary and secondary sensitization and to sensitization of the CNS.
Figure 3.
Clinical diagnosis of RMP: physical examination.
A pain provoked only by active movement or during a resistance movement is associated with a noxious stimulus from active structures (muscle, tendon, tendon–osseous junction). This explains why the best tests for disorders of the rotator cuff tendons, and in the subacromial impingement, are active tests27., 28., even if the precise anatomical lesion of the rotator cuff tear is difficult to diagnose only by these active tests.27 To be called a diagnostic test, a clinical test should discriminate between sick and healthy people. More than 20 clinical diagnostic tests exist for subacromial impingement syndrome.28 Compared to findings by magnetic resonance imaging (MRI), the tests with the highest specificity were the drop arm test (97.2%), the Yergason test (86.1%) and the painful arc test (80.5%). In severe MRI findings, the sensitivity and the specificity of the Hawkins and drop arm test were found to be 100%. More clinical tests for rotator cuff diseases are done, more the sensitivity is higher, but less is the specificity of a precise anatomical diagnosis. The active Hawkins' and Neer's tests seem to be positive both in subacromial bursitis and in rotator cuff tears.29
In the upper limb disorders associated with soft-tissue diseases, recommended tests are those associated with a local pain on resisted movements.30 In lateral epicondylitis an elbow tenderness laterally associated with a pain in the lateral elbow on resisted wrist extension had a sensitivity of 73% and a specificity of 97%. In the flexor–extensor peritendinitis or tenosynovitis of the forearm–wrist region, the best test seems to be the self-reported resisted wrist-extension test.30 The occurrence of paraesthesia or of an ‘electric shock’ during the resistance test is suggestive of a neuropathic pain which may be associated with the nociceptive pain.
For the neck, palpation of a facet joint has the highest sensitivity (82%); the upper limb tension test has the highest specificity (94%).31 Pain occurring during a passive rotation of the neck had a sensitivity of 77% and a specificity of 92% and was significantly correlated with the number of sick leave days.32 A trapezius tenderness is associated with a local motor dysfunction but it has a weak specificity in cervical disorders (65%).
A limitation in the passive flexion and internal rotation of the hip is suggestive of an articular lesion of the hip.
Nevertheless, pathological changes remain difficult to diagnose. For example, in the presence of anterior knee pain the diagnosis of chondromalacia is often evoked. Many clinical tests have been described: in a study of 85 knees in which clinical tests were compared with the results of arthroscopical findings, the sensitivity, the specificity, the predictive values and the accuracy of the tests were all low.33
Furthermore, the diagnostic values of the clinical tests in nociceptive pain have been poorly evaluated. For example, a meta-analysis of the accuracy of physical diagnostic tests for assessing meniscal lesions of the knee found 402 identified studies but only 13 met the inclusion criteria; the authors concluded that these tests are of little value for clinical practice.34 In conclusion, in most cases, active and passive joint mobilizations permit us to differentiate the origin of the nociceptive pain from the joint and from the soft tissues but not to diagnose the underlying disease.
3.4. Neurological examination
Physical examination must search systematically for neurological abnormalities—particularly when the history evokes a neuropathic pain. Paresis, sensory loss and reflex loss must be searched for carefully. In general, there is good agreement between observers of neurological signs.
In an RMP, the diagnosis of a neurological compression may be evoked when the examination makes a traction on the nervous structure (provocative test)—like the straight raising test of the leg in sciatica. However, the physiology of the neuropathic pain produced by these provocative tests remains unclear. In sciatica due to disc herniation, a meta-analysis found that pain distribution seemed to be the only useful item in the history, and the straight leg raising test the most sensitive.35
Precise tests have been described for upper limb nerve compressions—ulnar nerve and carpal tunnel syndrome (CTS).There are nine tests for CTS. A review of the literature has found 57 clinical studies devoted to analysing the sensitivity and specificity of these tests; of these tests only 21 were found to meet quality criteria for methodology. From these studies, it appears that the carpal compression (Durkan's test) had the best specificity (90–99%) and sensitivity (49–87%), and the Tinel sign a sensitivity of from 45 to 63% and a specificity of from 40 to 67%.36 Unfortunately, Durkan's test has not been kept as a specific test for CTS in the consensus statement from the UK workshop in Southampton.30
In ulnar nerve compression the best test involves the association of a local pressure test with a maximal flexion test of the elbow during a period of 30seconds (sensitivity 91%, specificity 97%); this test provokes the typical troncular paraesthesia.
In radial nerve compression, under the radial head, the best tests are: tenderness in the supinator area on palpation over the radial nerve, 4–7cm distal to the epicondyle, and at least one of the following positive tests: pain provoked by a resisted forearm supination or a resisted middle finger extension30 with a specificity of 96%.
The association of precise palpation with an attentive examination during movement may lead to a precise diagnosis. Box 5
4. Conclusions
The clinical management of RMP depends on the quality of the history of pain and on the past history of the painful patient. Without this simple but fundamental step—and particularly in non-inflammatory diseases of the musculoskeletal system—the orientation for the diagnosis may be hazardous. Differentiation between a nociceptive pain and a neuropathic pain may be easy from typical clinical characteristics (the mode of onset of the pain, the words used to describe the pain, the area of the pain and of the irradiated pain and neurological abnormalities on physical examination); however, such differentiation may be difficult in some circumstances related either to an initial cognitive processing of pain or psychological distress or to a lack of sensitivity and specificity of the physical tests. Unfortunately, physical tests for selected diseases (particularly in painful upper limbs where neuropathic and nociceptive pains may be associated, but also true for the knee or cervical spine) have not been standardized with good methodological criteria of repeatability and validity. The greater the difficulty in diagnosing a disorder physically the greater the need for new tests. Research in this field must be carried out with a modern methodological approach. Box 6
5. Summary
RMP is a very frequent rheumatological entity associated with various diseases of the joint, of anatomical structures around the joint, and of muscles. Pain must be appreciated in a biopsychosocial framework which includes nociceptive, neuropathic, psychogenic (cognitive and behavioural) and socioenvironmental determinants. For the diagnosis of an RMP there are two steps: first the anatomical diagnosis, and second the aetiological diagnosis. This chapter describes the main physiopathological features of nociceptive and neuropathic pains. Knowledge of the physiopathology of these two types of painful condition has a clear impact on the clinical processing of RMP. This allows us to distinguish nociceptive, neuropathic or psychogenic components of pain. This is particularly true in some RMP where a neuropathic pain may coexist with a nociceptive pain (for example, musculoskeletal disorders of the upper limb, pain from the cervical spine and shoulder pain). The patient's present history—and sometimes, past history—assists in differentiating between neuropathic and nociceptive pain from joint or soft tissue. An accurate management of the physical examination of the painful patient allows, in most cases, the anatomical diagnosis of the RMP. Nevertheless, there is a need for standardized assessments of the physical examination; there is also a need to assess clinical studies in order to select the best tests in clinical practice—those with good repeatability and validity—mainly for the aetiological diagnosis of RMP. It would also be useful to develop and evaluate guidelines for diagnostic criteria.
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PII: S1521-6942(02)00098-0
doi:10.1016/S1521-6942(02)00098-0
© 2003 Elsevier Science Ltd. All rights reserved.
Volume 17, Issue 1 , Pages 1-15, February 2003
