Introduction

It is generally accepted that Work Related Musculoskeletal Disorders (WMSD) cover a range of disorders characterised by pain and/or other sensations in muscles, tendons, nerves and joints with evidence of clinical signs. Much controversy exists regarding the actual causes and remedies for WMSD. It is generally accepted, however, that biomechanical factors such as repetitive actions, forceful movements and constrained postures cause or at least contribute to the condition especially when these are sustained or of sufficient intensity as to exceed the usual ability of the body to recover [1]. There is still ongoing debate about even the appropriate term/acronym to use for the family of disorders. As an example, in New Zealand the accepted term until recently was Occupational Overuse Syndrome (OOS). However, the Accident Rehabilitation and Compensation Insurance Corporation (ACC) of New Zealand recently decided that OOS was no longer an adequate diagnosis, largely as a result of the deliberations of its Task Force for Treatment Providers [2]. Instead medical practitioners have been advised to provide a specific diagnosis from 3 classification groups comprising local inflammations, compression syndromes and pain syndromes.

Local inflammations

Compression syndromes

Pain syndromes

trigger finger de Quervains tenosynovitis epicondylitis rotator cuff syndrome bursitis cervicothoracic dysfunction postural syndromes, muscle strain.

carpal tunnel syndrome, thoracic outlet syndrome, ulnar nerve compression, radial nerve compression.

chronic pain syndrome, myofascial syndromes, fibromyalgia, Complex regional pain syndromes [reflex sympathetic dystrophy].

This classification is often unhelpful to the treating practitioner, as pain is frequently present in the absence of clinical tissue inflammation. Furthermore there may be symptoms of compression neuropathy eg tingling, numbness and weakness, but scant clinical signs of nerve entrapment. Attempts at electrodiagnosis using nerve conduction studies are often unhelpful. Frequently more than one peripheral nerve would seem to be involved and the pain syndromes are difficult to distinguish one from the other.

Clinical Presentation Sub Types

It is more helpful and indeed logical to classify WMSD according to its common clinical presentation pattern in the workplace based on the predominant tissue affected. Each sub type presents with a typical presentation, each pattern often arising through different causes.

1. Tendon or Tendon Attachment Disorders

These usually present acutely as localised regional pain involving a tendon [tendonitis], its sheath [tenosynovitis] or its attachment [epicondylitis/enthesitis] to bone. The affected muscle belly may manifest trigger point tenderness. Inflammation manifesting as heat, swelling and crepitus may be present in the acute phase. The involved part is tender to palpation. These types of conditions occur usually in association with unaccustomed forceful cumulative trauma and/or returning to work after an extended period of absence, eg. holidays, sickness. Heavy unaccustomed work eg factory process work may induce tendonitis, tenosynovitis and enthesitis through the influences of frictional forces. Clinical findings of acute inflammation are present on examination.

2. Myofascial Dysfunction Disorders

Myofascial dysfunction presents sub acutely as the myofascial pain syndrome affecting specific overloaded muscles in related muscle groups, eg. the wrist and finger extensors in the forearm. The tendons themselves are not inflamed but may be non-specifically tender to palpation. Clinical findings present on examination include muscle tension or tightness with or without co-contraction, primary hyperalgesia (an increased pain response) at specific trigger point sites which usually conform to acupressure points [3] and a reduced range of motion. The diagnosis is confirmed by five major criteria and at least one of three minor criteria:

Major criteria

1. localised spontaneous pain
2. spontaneous pain or altered sensations in expected referred pain area for given trigger point
3. taut, palpable band in accessible muscle
4. exquisite, localised tenderness in precise point along taut band
5. some measurable degree of reduced range of movement

Minor criteria

1. reproduction of spontaneously perceived pain and alleviated sensations by pressure on trigger point
2. elicitation of a local twitch response of muscular fibres by transverse "snapping" palpation or by needle insertion into trigger point
3. pain relief obtained by muscle stretching or injection of trigger point

3. Neuropathic Disorders Through Poor Posture and Muscle Imbalance

These patients present with diffuse upper limb and shoulder pain accompanied by neural compression and/or neural tension symptoms of tingling, numbness, burning or shooting pains. The symptoms are of gradual onset, are initially confined to the work cycle but this association is rapidly lost with symptomatic progression. Abnormal or prolonged static postures that may be assumed during work activities or repetitive movements may result in a muscle imbalance [4]. This may include forward drawn shoulders, a poking chin posture and poor muscular stability. This may lead to neural tension and signs of chronic neural compression [5]. Clinically, these patients may also manifest signs and symptoms of the myofascial form of thoracic outlet syndrome.

4. Regional Pain Syndrome With Spinal Dysfunction

This is a gradual onset pain syndrome characterised by severe regional pain with spinal dysfunction, eg neck, shoulder and arm involvement, also termed cervicobrachial disorder. The pain is associated with dysaesthesia (a change in the sensation of pain); pins and needles, numbness, shooting and burning pain. Symptoms wax and wane with activity and the adoption of statically loaded postures. Patients who work in pain may need to take time off or undertake alternative duties when the pain crescendos. Many may need to work shortened hours. There may be a past history of cervical strain. There is a direct correlation between the degree of spinal motion restriction and the intensity of symptoms. Clinically, patients have motion restriction in the cervical and thoracic spine and there is diffuse muscle tension with hyperalgesia at tender points [can be in excess of ten], allodynia [a painful response to a non-noxious stimulus] and spontaneous pain. Some authors regard this condition as a form of localised fibromyalgia syndrome [6]. The author's experience suggests that there is often a mixed fibromyalgia and myofascial pain syndrome present.

5. Fibromyalgia Pain Syndrome [FMS]

This is a condition that can arise out of overuse or de novo. It is a common chronic pain disorder characterised by diffuse musculoskeletal soreness and stiffness, a decreased pain threshold, non restorative disturbed sleep, fatigue and psychological disturbance [7]. Patients have diffuse spontaneous pain made worse by activity and associated with hyperalgesia and allodynia. There is chronic fatigue, sleep deprivation, dysaesthesia and significant levels of past and present emotional stress with anxiety and depression. Patients may manifest constitutional factors such as irritable bowel syndrome, migraine, Raynauds phenomenon and sicca symptoms (symptomatic dry eyes and mouth). On examination, patients exhibit diffuse tender points [as opposed to trigger points] above and below the diaphragm in a typical distribution, a reduced range of motion in the shoulders and neck, grip strength weakness, poor posture, lack of cardio-vascular fitness and deconditioning. Patients have clinically positive nerve tension tests in the upper limbs and invariably have an elevated body mass index. There is work incapacity and invariably the condition is treatment resistant to the usual physical therapy modalities.

6. Normal Aches and Pains Exacerbated by the Work Process.

Here the patient manifests symptoms only of mild aching and/or pain that is confined to the work cycle. There are no clinical signs on examination; there is normal joint mobility and no muscle tenderness present.

Causation

Whilst the biomechanical causes of WMSD are fairly obvious the exact pathophysiology of the pain symptoms have yet to be clarified. The possible mechanisms by which overuse symptoms may arise have been reviewed by Edwards [8]. Compression of capillaries induced by sustained muscle tension and repetitive movements leads to local ischaemia and an accumulation of metabolites in the static muscle. These metabolites irritate nerve endings which themselves become sensitised, the most likely primary source of fatigue and discomfort. With intense and prolonged stimulus discomfort gives way to pain through a central facilitation component with reflex neural discharge causing tension through a splinting response. This may explain the basis of the myofascial pain syndromes. The ischaemic process entails biochemical changes without evidence of permanent muscle damage.

Quintner et al [9] have argued that the primary site of abnormality is at the emergence of the nerve roots from the cervical spine and focus attention on the aetiological role of posture and muscle imbalance. This may explain the neuropathic model.

Cohen et al [10] have expanded the Melzac and Wall gate-control theory of pain [11] and proposed a chronic pain paradigm which identifies three levels of contributing factors namely nociceptive, spinal cord and psychogenic. Nociceptor stimulation from peripheral nerve endings in anatomically relevant sites such as muscles, tendons and spinal facet joints, influences the spinal cord dorsal horn wide dynamic range [WDR] interneurones inducing central sensitisation such that previously sub threshold stimuli now produce neural impulses. Impulse traffic via the mechanoreceptive system in the dorsal horn is falsely processed as nociceptive to the extent that routine movement or postures become painful. Coghill et al [12] have demonstrated that non painful stimulation within the receptive field of a WDR neurone can be misinterpreted as pain in the presence of C fibre activity. The misinterpretation of touch and mechanical sensation as pain provides a cogent explanation of the observed phenomenon of allodynia so frequently seen in FMS.

Lynn and Greening [13] have recently demonstrated that people with keyboard overuse symptoms and heavy users of keyboards have raised thresholds to vibration in both the median and ulnar nerves consistent with a minor polyneuropathy through fascicular damage to sensory fibres. They concluded that deviated arm and particularly wrist postures may induce minor nerve irritation which when combined with repetitive muscular activity involved with keyboard operation further compromises neural blood flow to an extent that there is fascicular and endoneurial damage. This is supported by Bennett and Xies' research [14] which has shown that minor nerve trauma produced by application of loose ligatures to a peripheral nerve was associated with A fibre loss which has been shown to cause hyperalgesic behaviour in animal models. A modest degree of spontaneous firing of C fibres has also been seen in this model system [15]. The nervi nervorum, small nerve fibres in the sheaths of peripheral nerves, may also contribute to the nociceptive input to the dorsal horn following irritation of nerve trunks. Such aberrant input can lead to changes in dorsal horn sensory processing, changes that may contribute to the hyperalgesic and allodynic pains observed with neuropathic disorders [16].

Wigley et al [17] in an attempt to explain chronic pain of overuse have proposed a working hypothesis. They suggest that muscle spasm is the initial abnormality inducing ischaemia which in turn leads to release of substance P, a neuropeptide, and the nociceptive barrage that is perhaps necessary to produce a self sustaining pain syndrome. Substance P has been cited as the principal mediator of neurogenic information and also may have a role in nociceptive stimulation [18]. In addition to the production of neurotransmitters, sustained muscle contraction leads to anoxia and then anaerobic metabolism with accumulation of the by-products of this process eg lactic acid. Chaffin and Andersson [19] demonstrated that with continuous static muscle contraction blood flow in the muscles ceased at 70% of maximum voluntary contraction [MVC] and is reduced at loads above 30% with diminished endurance. Bystrom and Kilbom [20] found that forearm blood flow was insufficient with continuous isometric contractions as low as 10% MVC. At 25% MVC a 5 second relaxation after a 10 second contraction allowed recovery. This is some of the theory underlying the recommendation that frequent brief relaxation breaks [micropauses] be taken. It may also explain the basis for normal physiological fatigue, aches and pains associated with work, which resolves with rest. Sunderlin and Hagberg reported reduction in discomfort in keyboard operators taking short pauses ten times per hour [21]. Swanson and Sauter have also showed that frequent breaks increased productivity and decreased musculoskeletal stress [22].

Prevention

Accepting that WMSD arises from sustained muscle contraction, which in turn gives rise to central neural sensitisation and self-sustained chronic pain outlasting the initial stimulus, offers a practical approach to prevention and control.

The key to prevention of overuse pain syndromes is through mutual ownership of problems where employer and employee accept a shared responsibility. The employer owns his/her work environment and therefore has greatest control over task design and organisational changes within it. The employee is responsible for his/her own personal health as well as fitness, strength and endurance to do the job. These will directly influence ones ability to cope with day to day stressors. WMSD should be seen neither as an "all in the head" nor "all in the workplace" problem. The middle ground position presents the largest therapeutic window for effective intervention where there is a consensus towards shared responsibility through self-management and hazard identification and control.

Employers responsibility

The employer has a responsibility to modify ergonomics to at least minimal standards in compliance with the Health and Safety in Employment legislation of their country. Emphasis should be placed on ergonomic modifications such as equipment design for maximum comfort, appropriate education and training for at risk employees, appropriate task design and organisational procedures eg work rates, job rotation and rest breaks.

Micropauses

These are short breaks every 3-6 minutes for 5-15 seconds. They are easy to implement, inexpensive and can make up for a wide range of human factor and work station deficiencies. Instituting micropausing may reduce discomfort and pain by reducing muscle and nerve tension. Micropausing to prevent fatigue is more effective than resting than to recover from it. Micropauses may be passive where the employee rests and active where the employee undertakes a range of stretching type exercises.

Stress Management

Littlejohn [6,7] contends that emotional stress, when intense, translates easily into central sensitisation which is the core pathophysiological event in chronic pain syndrome development. He further contends that there is usually no physical cause for the chronic pain syndrome that can be directly linked to a traumatic injurious event in the workplace and that the emotional response and distress of the individual is the important link between workplace events and symptom evolution. Clearly, therefore stress management through, for example, learning relaxation techniques and breathing exercises may have a central role. Spence [23] in a controlled intervention study showed an advantage to those who had cognitive behavioural therapy including instruction in relaxation.

Employees Responsibility

In terms of individual employees responsibility to maintain fitness for work he/she must consider the following:

1. Daily [at least 4 times] stretching of muscles and nerves.
2. A warm up routine.
3. Working the muscles aerobically [aerobics, swimming, brisk walking, jogging] for half an hour three times a week.
4. Increase strength and improve posture, perhaps join a gym.
5. Become more relaxed, reduce anxiety and stress levels

• start an exercise programme
• learn abdominal breathing techniques
• consider stress and/or anger management
• consider counselling
• control weight at an ideal level
• keep fit [become a working athlete].

6. Establish a work rest break routine in consultation with your work supervisor

• micropauses every 3-6 minutes for relaxation exercises
• macropauses [a longer break] 5 minutes every hour for stretching exercises

7. Avoid the FAT CATS [fat, caffeine, alcohol, tobacco, sugar]

Conclusion

In conclusion it is clear that a paradigm shift from the injury [pathological] model to a more functional cognitive behavioural model is required when dealing with chronic overuse pain syndromes. In the words of Samuel Johnson [Rasselas 1759] on Enterprise "nothing will ever be attempted if all possible objections must be first overcome"

References

1. Kuorinka,I. and Forcier,L. (1995) Work Related Musculoskeletal Disorders.Taylor and Francis, London
2. ACC News.(1996) Issue 16
3. Travell, J.G. and Simons, D.J. (1983) Myofascial Pain and Dysfunction: the Trigger Point Manual, Vol 1, Williams and Wilkins, Baltimore
4. Mackinnon, S.E. and Novak, C.B. (1994) Clinical commentary: pathogenesis of cumulative trauma disorder. The Journal of Hand Surgery 19,5,873-883
5. Higgs P.E. and S.E. MacKinnon. (1995) Repetitive motion injuries. Annual Review of Medicine, 46, 1-16.
6. Littlejohn, G.O.(1994) Repetitive strain syndrome. In: J.H. Klippel and P. Dieppe (Eds), Rheumatology, Year Book Europe, London
7. Littlejohn, G.O.(1998) Management of fibromyalgia syndrome. Current Therapeutics, April
8. Edwards R.H.(1988). Hypotheses of peripheral and central mechanisms underlying occupational muscle pain and injury, European Journal of Applied Physiology and Occupational Physiology, 57, 275-281.
9. Quintner J.L., Elvey R.L. and Thomas A.N. (1987) Regional Pain Syndrome, Medical Journal of Australia, 146,4, 230-231.
10. Cohen M.L., Arroyo,J.F., Champion,G.D. and Browne,C.D. (1992) In search of the pathogenesis of refractory, cervico brachial pain syndrome. Medical Journal of Australia, 156,6, 432-436
11. Melzack,R. and Wall, P.D. (1965) Pain mechanisms: a new theory. Science, 150, 971-979
12. Coghill R.C., Mayer D.J. and Price D.D. (1993) The role of spatial recruitment and discharge frequency in spinal cord coding of pain: a combined electrophysiological and imaging investigation. Pain, 53,294-309.
13. Greening, J. and Lynn, B. (1998) Vibration sense in the upper limb in patients with repetitive strain injury and a group of at-risk workers. International Archives of Occupational and Environmental Health 71,1,29-34
14. Bennett G.J. and Xie Y.K.(1988). A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man. Pain, 33, 87-107.
15. Lang E., Claus D., Neunodorfer .B. and Handwerker H.O. (1995) Parameters of thick and thin nerve fibre function as predictors of pain in carpal tunnel syndrome. Pain, 60,3,295-302.
16. McMahon S.B., Lewin,G.R. and Wall, P.D. (1993) Central hyperexcitability triggered by noxious inputs. Current Opinion in Neurobiology, 3,4, 602-610.
17. Wigley R.D., Darby,F.W and Brown, D. (1997) The Overuse Syndrome: The Role of Muscle in the Generation of Intial Symptoms, unpublished abstract
18. Nakamura-Craig M., Smith T.W. (1989) Substance P and peripheral inflammatory hyperalgesia. Pain,38,1,91-98
19. Chaffin,D.B and Anderson,G.B.J. (1994) Occupational Biomechanics, John Wiley and Sons, New York
20. Bystrom S.E.G.and Kilbom, A. (1990) Physiological response in the forearm during and after isometric intermittent hand grip. European Journal of Applied Physiology,60,6,457-466
21. Hagberg, M. and Sundelin,G. (1986) Discomfort and load on the upper trapezius muscle when operating a wordprocessor. Ergonomics 29,12,1637-1645
22. Sauter,S.L, Swanson, N.G (1992) The effects of frequent rest breaks on performance and wellbeing in repetitive VDT work. In H.Luczak, A.Cakir and G. Cakir (eds) Work with Display Units 92: Proceedings of the third International Scientific Conference on work with Display Units.Technische Universitat Berlin, pp D-52
23. Spence S.H. (1989) Cognitive-behaviour therapy in the management of chronic, occupational pain of the upper limbs. Behaviour Research and Therapy, 27,4, 435-446.

The Author

Dr Bill Turner