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Teen V Acc (244/2002) W-r gradual process.. - physical injury?

#1 User is offline   ernie 

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Posted 27 September 2004 - 01:09 PM


District Court, Wellington (244/2002)
Judge M J Beattie

Mr J A Wilton, Counsel for Appellant
Mr B A Corkill, Counsel for First Respondent
Mr J Haigh Q C and Ms J A Kean, Counsel for Second Respondent

  • The issue in this appeal is whether the first respondent, by its agent CRM Risk Managers, was correct by its decision of 5 June 1998 to revoke cover for the appellant which had been granted to her on 29 October 1996 for a gradual process injury to her right shoulder arising from her employment with the second respondent.

  • This appeal results from the decision of the High Court delivered on 28 June 2001 whereby it quashed the previous decision of this Court (335/99) and directed that the issue in this appeal be reheard.

  • The relevant background facts in this appeal are not in dispute and may be stated as follows:
    • In March 1996 the appellant, then aged 47 years, commenced employment with Telecom as a Credit Service Representative.

    • Her duties involved use of telephone and computer, including data input using a keyboard.

    • On 1 October 1996 the appellant consulted her GP, Dr O’Connor complaining of pain in her neck, shoulders, back and arms and the appellant and Dr O’Connor completed an ACC claim form at that time.

    • The ARC18 Claim Form gave as the diagnosis of injury “possible OOS of R shoulder, arm, back, neck, L neck and upper arm”. The date of the injury was said to be 29 July 1996.

    • The appellant was certified as unfit for work and the form noted that she was to see Dr W Turner.

    • CRM as agent for Telecom, an Accredited Employer, received the claim and thereupon sent out gradual process questionnaires to the appellant, her medical practitioner and her employer.

    • The claimant questionnaire completed by the appellant stated that her condition was sore neck, shoulders, back, arms. The appellant went on to state that she was not sure how this condition developed but possibly the way I use a particular function. She said that she first noticed her condition in July and although advising of her previous employment stated that she had not suffered from a similar condition in the past.

    • The medical practitioner questionnaire was completed by Dr Ross Fountain, of the Medical Practice at which the appellant attended. He gave as his diagnosis OOS ESP of rhomboids and R supra spinature extending in R shoulder and down arm. Dr Fountain stated that the cause of the condition was working as a computer operator with mouse, changed mouse to left hand usage no improvement.

    • In the Employer Questionnaire it ticked yes to the question whether it considered the injury to be work related and noted that the appellant had first complained about the condition in July.

    • By letter dated 29 October 1996 CRM advised the appellant, inter alia

      “I have considered your application for cover which was submitted by your doctor on your behalf. The injury that you received on 7/10/96 has been accepted for cover. This means that you are covered under the Accident Rehabilitation & Compensation Insurance Act 1992”

    • The appellant was seen by Dr W E D Turner, Specialist in Occupational Medicine, on 4 November 1996 and he reported to the second respondent. It was Dr Turner’s opinion that the cause of the appellant’s condition was her work environment in respect of her long repetitive mouse and key board use with the adoption of constrained statically loaded postures inducing tension and lactic acid overload in the muscles. Dr Turner then went on to advise on further management of the appellant’s condition and of her work place.

    • A work place assessment was undertaken on 22 January 1997 and certain modifications were recommended. The appellant was seen again by Dr Turner following that work place assessment and he made a further report to CRM on a return to work programme for the appellant.

    • The appellant continued in her employment at Telecom until September 1997 when her condition caused her to be certified as unfit again and she began to receive weekly compensation.

    • In early 1998 CRM sought specialist opinion from Dr John Alchin, Specialist Occupational Physician and Professor Des Gorman, Head of Occupational Medicine at the Faculty of Medicine, Auckland University.

    • On receipt of reports from Dr Alchin and Professor Gorman, CRM advised the appellant by letter dated 5 June 1998 that on the basis of advice it had received her claim was not acceptable under the Act as there was no demonstrated personal injury, that the claim did not satisfy the criteria of section 7 of the Act and that therefore her cover was being cancelled and entitlements withdrawn.

    • The appellant sought a review of that decision and a review hearing took place on 8 February 1999. For the purposes of that review, the appellant introduced a report from Dr R D Wigley, Consultant Rheumatologist who had examined the appellant on 30 July 1998 and whose advice and opinion disagreed with that of Dr Alchin, Dr Turner and Professor Gorman. The review hearing also received further evidence from Dr Alchin, Dr Turner and Professor Gorman.

    • In his decision dated 1 March 1999 the Reviewer found on the evidence that the appellant had not suffered a physical injury within the meaning of the Act and therefore could not satisfy the criteria required of section 7 of the Act and he therefore confirmed CRM’s decision to revoke cover and cancel entitlements.

  • For the purposes of the appeal to this Court no party has sought to introduce any further specialist medical evidence and therefore the evidence to which this Court can refer is that which was available and presented to the Reviewer at the review hearing.

  • The matter which is at the heart of the issue in this appeal is whether the appellant has suffered a personal injury, that is a physical injury, arising in circumstances which satisfy the criteria set out in section 7 (a) (b) and © of the Act. Whilst the determination of the issue is one of mixed fact and law the factual aspect of it is very much a medical matter and I therefore set out the medical evidence to which the parties have referred and which each contends supports their respective positions. In chronological order that medical evidence is as follows:

    (1)Report from Dr W E D Turner dated 4 November 1996 to Telecom (CRM)

    Telecom had requested Dr Turner to provide an occupational musculoskeletal assessment on the appellant. He was asked to provide a diagnosis of her condition, recommend treatment and rehabilitation and advice as to return to work. Dr Turner gives a helpful description of the nature of the appellant’s employment with Telecom as she related it to him.

    “Mrs Teen informs me that she has been employed with Telecom for some 14 months as a credit representative. This work involves the organisation of payment plans to help customers pay their accounts. The physical activity she undertakes in this regard consists of spending some 7½ hours per day on a keyboard answering telephone calls, typing in information via a keyboard into a computerised customer data base. She uses a headset in the process spending approximately 60% of her 7½-hour day using the mouse, the remaining 40% spent on the keyboard.

    She dates the onset of her symptoms back to early July 1996 at which time she first began to notice discomfort over the lateral aspect of her right neck initially describing that she was tender to touch in the region. She related the onset of the symptoms to work at a time when she was undertaking her usual activities of mousing and keyboarding. Shortly after she also began to notice symptoms over the anterior aspect of her right shoulder having some difficulty lying on her right hand side in bed. In the early stages of her symptom history she described a tendency for the symptoms to crescendo through the working week and to resolve over the weekends. At the end of July on the advice of the occupational health nurse she removed the mouse from the right hand to the left, she was provided with a mouse pad and a footstool, there being a minor improvement of her symptoms. In mid August however she suffered a further recurrence of right neck and shoulder pain together with interscapular discomfort. Her back symptoms tended to exacerbate at a time when she was undertaking “CTI” which involves extended mouse use. As a result she consulted her general practitioner again who completed the standardised employee report form diagnosing her as having possible OOS, recommending anti-inflammatory medication as the treatment and a return to work programme of avoiding keyboards altogether and undertaking filing duties, faxing, photocopying, filling coffee/milo dispenser for 8 hours a day.”

    Dr Turner advised the results of his examination as follows:

    “Examination of her upper limbs revealed no evidence of deformity, joint enlargement, scarring untoward colour change of the skin nor was there any wasting or fasciculation of the muscles. Palpation of the hands revealed tenderness over the right thenar eminence and first finger web musculature particularly adductor pollicis. In the forearms she was tender over the extensor carpi radialis and extensor digitorum bilaterally. There was a levido reticularis-like appearance of the skin over the flexor forearms and upper arms. At the elbows there was common extensor, common flexor origin and supinator tenderness. In her upper arms she had tender points diffusely placed in the triceps and biceps. In the chest wall there was tenderness at the pectoralis minor attachment at the coracoid process particularly on the right. There was also tenderness in the second and third interspaces. In the supraclavicular fossa she was tender over the scaleni particularly on the right. In the shoulders she was tender over the subscapularis insertion onto the lesser trochanter. She had trigger points in the middle aspect of the upper trapezius muscle bellies. Examination of the scapular musculature revealed bilateral infranspinatus muscle belly and there was rhomboids major and minor trigger point tenderness. In the neck there are suboccipital and C5/6 paraspinal tenderness. She also manifested bilateral gluteus maximus, greater trochanter and medial knee fat pad tenderness.”

    Dr Turner then gave as his opinion and causation as follows:

    “In my opinion Mrs Teen has developed a diffuse myofascial pain syndrome affecting predominantly the postural and phasic muscles of her neck, shoulders and shoulder blades. Clinically on examination she manifested hypertonicity with the presence of trigger points in the levator scapulae, upper trapezius, infraspinatus, rhomboids, subscapularis and in the cervical musculature paraspinally. In addition she manifested the likelihood of an early fibromyalgia pain syndrome with diffuse tender points below the diaphragm associated with fatigue, lack of energy, paraesthesia and general muscle stiffness. Thirdly there is the presence of brachial plexus tension particularly on the right undoubtedly related to myofascial shortening in the scaleni. Fourthly, as a result of persistent discomfort she has become deconditioned lacking aerobic fitness, strength and endurance in her muscles. Fifthly, there was evidence of the so called cubital tunnel syndrome with entrapment of the ulnar nerve at the medial elbow bilaterally. This is most likely as a result of adverse neural tension than any specific entrapment. Finally she had forward drawn shoulders no doubt exacerbated by tension within the pectorales and posterior muscular weakness of the scapular stabilisers.

    I think the basis of this condition in terms of causation is the ergonomics [in a wider sense] of her work environment in respect of prolonged repetitive mouse and keyboard use with the adoption of constrained statically loaded postures inducing tension and lactic acid overload in the muscles. Clearly with persistent discomfort and an inability to undertake her usual tasks there has been an overlay of occupational stress and deteriorating staff relationships which has had an additional influence in terms of increased muscle tension and the development of chronic diffuse pain in the form of fibromyalgia”.

    (2)Report from Dr W E D Turner dated 23 January 1997 to CRM

    This was a report from Dr Turner following a work place assessment that had been carried out on 22 January 1997. Dr Turner noted that various modifications were needed to the appellant’s work station. He advised that the wrist rest required modification and her chair needed to be readjusted and he noted it was important that she changed her postural techniques.

    (3)Report from Dr W E D Turner dated 18 February 1997 to CRM

    This was a follow-up report advising progress on the appellant’s rehabilitation. He also advised the results of the appellant’s initial status outcome measurement from which he diagnosed:

    (1)“Diffuse myofascial pain syndrome affecting the neck, shoulders and shoulder blades [levator scapular, upper trapezius, infraspinatus, rhomboids and neck].
    (2)Right brachial plexus tension.
    (3)Early fibromyalgia syndrome.
    (4)Bilateral cubital tunnel syndrome secondary to adverse mechanical neural tension.”

    Dr Turner also noted that the appellant was experiencing occupational stress and that she was being transferred into a new team which was a relief to her.

    (4)Report from Dr John Alchin dated 10 February 1998 to CRM

    Dr Alchin was requested to report giving advice of diagnosis and any contributing causative factors and a prognosis. Dr Alchin examined the appellant on 14 January 1998 and he had the reports from Dr Turner for reference. On the question of diagnosis Dr Alchin stated as follows:

    “You correctly note that “OOS” is not an acceptable diagnosis, either medically, or for ACC. Mrs Teen had the gradual and spontaneous onset of neck and right shoulder pain 18 months ago, which has persisted ever since, with some subsequent but less severe and intermittent pain elsewhere through her upper body. The right neck/shoulder girdle pain is a burning almost constant pain which worsens spontaneously, with normal and customary activity, and cold weather. There is associated typical sleep disturbance with non-restorative sleep, lethargy, low mood, loss of interest, and frustration. She has right hand weakness, occasional tingling in her hands, and previously had some swelling of the right hand and forearm. Examination findings are of pain with active neck shoulder movement, and tenderness, particularly of her upper spine. She had a ganglion on the dorsum of her right wrist. Although she had a painful arc with right shoulder abduction, and positive Tinel’s tests over the ulna nerve at both elbows, there was no supportive evidence for significant right rotator cuff tendonitis, or of ulnar entrapment neuropathy at the elbows. She has failed to recover after several periods of time off work, including a recent 4 month period. Thus the diagnosis is regional pain syndrome of her upper body, primarily her neck and right shoulder girdle. Other diagnoses include ganglion over the dorsum of the right wrist, previous left lateral epicondylitis with successful surgery in 1995, and treated depression.”

    Dr Alchin then went on to give his advice regarding causative factors or otherwise and stated:

    “The recognised risk factors for chronic pain syndrome include (as mentioned) “fear-avoidance behaviour”, “catastrophising” beliefs about pain (that the pain has the capacity to be severely disabling), a tendency to low mood and social isolation, and a reliance on passively receiving treatment rather than active self management. Some of these factors are identifiable in this case: she had pre-existing depression, which would be considered to be a predisposing factor. Kirstie Dray noted fear-avoidance behaviour. A desire to have her damaged tissues cured by physiotherapy was evident in my consultation with her. “Catastrophising” beliefs unfortunately are part and parcel of the “OOS” construct, which is of course one of the problems with this notion, as is fear-avoidance behaviour. But, apart from these psychological factors, the only identified pre-existing medical condition is her depression.

    The development of regional pain syndrome is related more to these psychosocial factors than it is to physical factors such as work tasks or environment, or injury factors. Dr Turner notes this in his report, correctly commenting that psychosocial stressors (including work) appear to have exacerbated her pain, and are certainly related to the development of regional pain syndrome (which Dr Turner terms fibromyalgia syndrome, an acceptable alternative term for the same condition)”.

    (*)Report from Professor Des Gorman dated 9 March 1998 to CRM

    Professor Gorman was provided with the medical reports from Dr Turner and Dr Alchin and Professor Gorman advised that he did not need to examine the appellant in order to answer the questions which had been posed.

    Professor Gorman advised that the appellant had a chronic pain syndrome that could probably be sub-classified as fibromyalgia (FMS). Professor Gorman noted that ACC had recognised and compensated claims for post traumatic fibromyalgia but noted as follows in respect of such an injury claim.

    “Cover in this context requires that the following conditions are met.

    The pain syndrome is, at least in part, a response to a discrete injury. Many pain syndromes such as FMS onset with local pain – this is not indicative of any injury and just represents the first phase of the evolution of the syndrome. Despite the previous history of a tennis elbow, this does not appear to be related to her current invalidity; there is no clinical description here of a discrete injury prior to the onset of her pain syndrome and no record of recovery once the assumed “causative” process was avoided. The onset of her wrist ganglion is after the onset of her generalised pain. It follows that an acute antecedent injury has not been established.

    The discrete injury is the result of either an accident or a biomechanical process at work. This is, of course, somewhat academic, if no discrete injury has been established. The insistence on a biomechanical process is due to mental trauma being excluded from cover under the ARCI Act 1992. The insistence on any gradual process being at work is due to the requirement that the “property or characteristic” responsible for the injury is essentially restricted to the work environment. There is no history here of an “accident” and Barbara’s work process can not explain her current invalidity in the absence of a pain syndrome such as FMS. Her work process could be responsible for some local injury to her upper limbs, but no such injury has been recorded. Non-work factors have been considered and include depression. I also note the important role of workplace psychosocial stressors in the progress of her pain.

    Overall then, Barbara’s entitlement to cover under the ARCI Act 1992 has not been established as there is no description of a discrete injury to substantiate a post-traumatic FMS”.

    (*)Report from Dr John Alchin dated 21 May 1998 to CRM

    Following receipt of his first report CRM posed several questions to Dr Alchin and those questions and answers are as follows:

    “Q Is there evidence of a work-related injury? Is there an Injury?
    A The diagnosis was Regional Pain Syndrome (RPS), predominantly of the right neck and shoulder girdle. As discussed in my previous report this is a pain syndrome due to altered pain processes and perception in the central nervous system, but it is not due to persisting tissue damage or injury. In the normal sense of the word “injury” (eg fracture, bruise, cut, inflammation) there is therefore no injury present. Whether the altered function and physiology in the central nervous system in these states is classified as an injury is perhaps a legal question. Her painful arms, neck and shoulders is not an “injury” in the usual or medical sense of the term.

    Q Is the RPS “work-related”?
    A I have addressed this question at the bottom of page 6 of my previous report (“Any other factors, or pre-existing conditions”), and at the top of page 7 (“Contributing causative factors”), to which I refer you. I pointed out that the recognised risk factors for chronic pain syndromes are predominantly psychosocial, which I understand are not acceptable for cover in terms of the ACC Act, even if there are psychosocial factors at work. Work may well cause muscular discomfort; I am sure we have all experienced a sore neck from sustained neck flexion, or holding a telephone between one ear and hunched shoulder while talking on the phone and writing. This however is quite distinct from RPS, and it has never been shown that it is physical ergonomic factors at work which cause an acute localised pain to develop into a chronic pain syndrome. We do not in fact know why some people develop chronic pain such as RPS. We do know what the risk factors are, and that there is no good evidence relating it to ergonomic factors at work. So she has a pain syndrome rather than any tissue damage. This pain syndrome has an unknown relationship to her work.

    Q Is there evidence of any injury?
    A See 1) above. I assume this question relates to whether there was any initial injury when she first developed pain in mid 1996, and when she first saw Dr Fountain in August 1996. I cannot comment with certainty as I did not see her until 18 months later. But I obtained no evidence, either written or from Mrs Teen, to suggest that there was any initial acute injury, or specific diagnosable lesion. It is not correct to believe that all pain is due to injury, it is possible to have a headache, or muscular neck discomfort, for example, with no actual injury.

    Q Is there evidence of any injury now?
    A See 1) above.”

    (*)Report from Dr R D Wigley dated 30 July 1998
    Dr Wigley was instructed by counsel for the appellant and for the purposes of his examination and report he was provided with the reports of Dr Turner, Dr Alchin and Professor Gorman. He was also provided with the work place assessment report which had been carried out in November 1996.

    Dr Wigley examined the appellant and agreed with the diagnosis described by Dr Turner but preferred to call it regional pain syndrome due to occupation. He noted the symptoms and stated:

    “Her symptoms arose while she was engaged in a type of employment well known to induce the type of symptoms that she has. She was working without breaks in an unsatisfactory position that was somewhat improved after the modifications recommended by Dr Turner. Computer rate monitoring practiced by Telecom is an undesirable feature in inducing the type of symptoms that she has, as also is the somewhat Draconian management attitude. This improved when she was transferred to another team, doing the same work.”

    To the question, “is there an injury”, he stated as follows:

    “Dr Alchin is of the opinion that there is no injury, and likewise, Dr Gorman. Obviously there is no injury in the sense that there is no recognisable bruising or abnormality of tissue disclosable by macroscopic examination. Professor Schug (Ref) has produced evidence that there may be damage to the sensory cell, leading to the general increase in sensitivity. He even states that the sensory cell may die. In my view this supports the contention that there is injury. I also consider that the complex biochemical abnormalities detailed by Prof Schug should be considered injury unless one excludes them by definition. The dictionary definition of injury is much wider than this. I enclose a summary of the evidence of the occurrence of injury in overuse pain syndromes (encl.).

    Section 6.1 in defining injury omits the word “physical” so that chemical or physiological disruption would satisfy this requirement for this gradual process disorder.”

    Dr Wigley then makes comment on points made by Professor Gorman stating as follows:

    “It is important to note that he has not examined Mrs Teen. He prefers the term “diffuse chronic pain syndrome” to occupational overuse syndrome and suggests that the term fibromyalgia could be used. She does not currently satisfy the criteria for a diagnosis of fibromyalgia, having only two tender points. When Dr Turner saw her, he describes trigger points, rather than tender points, suggesting that the diagnosis then was myofascial pain syndrome. Dr Gorman evidently does not regard these as being different complaints but rather different distributions and degrees of basically the same problem and I agree on this.

    Paragraph 3, page 1: “Many authorities do not accept that either an injury or a work process can ever cause pain syndrome, especially those suggestive of FMS”. Many authorities do strongly support an association and this position is detailed in the enclosed reports from Silverstein et al and Armstrong et al. (encl.)”

    Dr Wigley then goes on to refer to various legal aspects of ACC legislation to which I will refer later.

    (8)Letter from Dr Ross Fountain dated 14 August 1998 to CRM

    Dr Fountain was asked to clarify his diagnosis as contained in the questionnaire. He enclosed a copy of his medical notes of his consultation with her in October 1996. These have not been produced in evidence. His letter then stated as follows:

    “Your second question re: an explanation of the diagnostic criteria for the diagnosis for probable OOS is included in those notes. At the time in 1996, OOS was an acceptable diagnosis for Accident compensation. I understood that pain syndrome occurred in situations where it was ongoing despite rest. At that stage, rest from doing her office work and using the computer and the mouse eased and settled symptoms, as indicated in my notes. It was probably more at that stage a fibromyalgia or myofascial syndrome which has progressed to a regional pain syndrome over time.

    Your final question asks about pre-existing conditions. You will note on my notes of 14th October, I made comment regarding the right shoulder from July 1996. What I wrote there was symptoms in the right arm, right shoulder and wrist needs OOS assessment”.

  • In addition to the medical evidence pertaining to the appellant in particular, the Court also received evidence from the various specialists on the nature of the condition known as fibromyalgia and its causes. I now set out the passages from the evidence of the specialists which I set out their respective views on this matter.

    Dr Alchin:

    “The question of the nature of Regional Pain Syndrome arises. This condition goes by a number of different names, including “Localised Fibromyalgia Syndrome”. It is called “localised” because Fibromyalgia Syndrome itself implies widespread pain throughout the body. If the pain is restricted to a region of the body, but with the other typical features of fibromyalgia (hand symptoms, sleep disturbance, lethargy), then it is called Regional Pain Syndrome or localised Fibromyalgia Syndrome.

    There are in fact about 60 different names for Fibromyalgia Syndrome used in the medical literature. This condition is one of abnormal pain and tenderness of normal tissue. That is, there is no evidence of tissue damage or injury in these cases, either clinically or on investigation (eg blood tests, imaging techniques, or microscopically) as the cause of the pain. Instead, the ongoing pain, tenderness and difficulty performing normal activities is due to changes in central nervous system function, in particular to sensitisation of nerves in the spinal cord which carry pain messages to the brain. These sensitised nerve fibres now respond abnormally, so that non-painful messages from the body, such as normal light touch and arm movement, are interpreted as painful messages. That is, although the pain and tenderness is in Mrs Teen’s neck and shoulder girdle, they are normal; the problem rather is of abnormal pain perception in her central nervous system.

    This explains why treatment directed at (non-existent) tissue damage in the arms, such as physiotherapy, rest and anti-inflammatory medication, fails to effect a cure. This understanding also explains why recovery does not occur in the expected timeframe, as there is no damaged tissue to recover. Instead, rather than recovering, her symptoms had persisted. Thus other names for this condition include “Delayed Recovery Syndrome”, and “Pain Amplification Syndrome”. It is a disorder of pain perception rather than a disease or injury in her arms.

    As far as the cause(s) of Regional Pain Syndrome is concerned, the following can be stated. Firstly, the exact causes are unknown. Secondly, it has never been established that physical factors at work (such as abnormal posture or unaccustomed overuse resulting in pain or even strain) are the cause of this condition. This is in marked contrast to the popular perception that this is the case; it is not. Thirdly, most people who develop acute muscular discomfort or even injury due to abnormal posture, unaccustomed overuse, or minor trauma, recover quickly and predictably, and their symptoms are proportional to the cause.

    Regional Pain Syndrome is the condition where a very small minority of people with such acute muscular pain do not recover as predicted, but instead the pain persists and in fact worsens in intensity and spreads in extent, and other features develop (hand symptoms, sleep and mood disturbance). In these cases, rather than symptoms being proportional to the apparent cause, the symptoms becomes quite disproportionate, so that severe pain and incapacity may result from minor apparent causes.

    The current best and widely accepted understanding of why this happens in a few people is as follows. It is accepted by most experts that there is no direct causal link between the initially precipitating painful event and the subsequent clinical features of Regional Pain Syndrome. Instead, the important factor linking these two is the emotional response and distress of the individual. There is always an emotional response to pain or an injury. In some people this emotional distress is more significant, and this emotional distress is a key cause of the sensitisation of the central nervous system, such as of the pain transmission nerve cells in the spinal cord. This emotional distress is influenced by many factors including individual susceptibility, past history of pain experience, gender, age, ethnic and social background, the psychosocial environment at home, their mood and beliefs.

    The emotional response to pain and minor trauma is also influenced by the patient’s interaction with employers, workmates, and workers’ compensation systems. It is obviously compounded if there is anger towards the employer, disputes about entitlement to cover, and anxiety about their future. In this way, these factors decisively affect the spinal cord sensitisation process, and combine in ways which are not completely understood to turn what would be normally a minor and self-limitating problem into chronic pain, tenderness and resulting disability.

    There is no evidence of an injury in RPS such as Mrs Teen has, in the sense of damaged tissue which is visible with the naked eye clinically or at operation, or with imaging techniques such as ultrasound, MRI scans, or under any form of microscope. In that sense there is no injury. However, there is certainly central nervous system dysfunction, e.g. of the pain transmission neurones in the spinal cord. It is probably a question of legal definition whether this altered function (sensitisation) in the spinal cord is an “injury”. There are certainly altered neural processes there which explain the clinical features, such as changes in concentrations of chemicals that transmit nerve impulses. It is not however an injury in the normal sense of that term, such as burn, fracture, or hearing loss due to loud noise (which damages nerve cells in the inner ear, which damage is clearly visible by an electron microscope): in which cases there is significant tissue damage”.

    Dr W E D Turner:

    “Fibromyalgia is a complex systemic musculoskeletal disorder arising from multifactorial causation. There is no one particular cause for fibromyalgia indeed, it is thought to arise from many causes through neuro-endocrine dysfunction. Many patients appear to have a genetic susceptibility to the condition and I think the figure of 10%-15% of the population is conservative. Other factors that suggest a genetic susceptibility include previous history of migraine, past anxiety and depression, irritable bowel syndrome, painful periods, sicca symptoms, Raynauds phenomenon and chronic fatigue.

    Workers involved in jobs which are monotonous, repetitive, involving the adoption of statically loaded postures giving rise to chronic muscle and nerve tension are predisposed to the condition particularly where there is an associated lack of fitness, musculoskeletal deconditioning and psychological factors. Where workers are fit, their muscles are conditioned, they do not suffer from occupational stress and enjoy their jobs symptoms, they are unlikely to arise. Invariably workers who develop symptoms are self-driven, over-conscientious, compulsive, having little or no perception of relaxation or pacing for muscle comfort. In terms of aetiology the association with work is controversial, the evidence from the literature suggesting anecdotal relationships only emphasising aggravating factors rather than direct causation.

    There is no evidence of true injury to the tissues, rather the tissues themselves exhibit pathophysiological changes through accumulation of waste products and oxygen depletion resulting in chronic muscle and nerve tension. Thus the condition is one of abnormal pain and tenderness of normal tissue. The ongoing pain, tenderness and difficulty performing normal activities is due to changes in central nervous system function in particular to sensitisation of nerves in the spinal cord which carry pain messages to the brain. These nerve fibres in becoming sensitised now respond abnormally so that non painful messages from the body such as normal light touch, body position and posture, arm movement are interpreted as painful messages”.

    Dr Turner also commented that the statements he had made in his first report of 4 November 1996 when he stated as follows:

    “Mrs Teen’s condition initially came on as a result of word processing and mouse use on 30/07/96 as a consequence of carrying out her normal tasks there being no evidence of any antecedent physical injury or trauma. Although I did identify that her pain was triggered by the adoption of constrained statically loaded postures [which induce tension in the overloaded muscles] when interfacing with her computer this is in essence low-grade trauma unlikely to cause a disruption of tissue architecture.

    In my view in retrospect, taking into account the clinical findings present on examination, Mrs Teen’s pain is in fact pain without tissue injury as is the case with headaches where there is pain in the head in the absence of physical trauma or head injury. It follows that if gradual process activities such as keyboarding, handwriting or merely sitting at a desk in a sedentary posture as is so frequently the experience of keyboard operators at work give rise to aches and pains in the muscles and these aches and pains are not reflective of any actual disruption of tissue architecture but more a reflection [as the literature would suggest] of muscle and nerve tension with abnormal pain transmission in the central and peripheral nervous system then the chronic pain syndrome in fibromyalgia that develops from non noxious stimuli such as keyboarding, handwriting or adopting sedentary postures could not be said to have followed from a physical injury”.

    Professor Des Gorman:

    Professor Gorman noted that fibromyalgia is influenced by many different factors including trauma, but he stated that it was not known whether those various factors were causes or simply matters which acted to precipitate or aggravate or ameliorate symptoms. He went on to state:

    “Fibromyalgia syndrome can first occur after trauma, but there are no data from well controlled studies to show that trauma can cause FMS. It follows that a diagnosis of FMS after trauma (so-called “post-traumatic” FMS) establishes a casual and not a causal relationship between the trauma and the pain syndrome.

    Not only do I consider the cause of FMS to be unknown, but there are also many reasons why a post-traumatic basis for even some patients is difficult to accept.

    a)The only clinical data that suggest a relationship between trauma and FMS is cited above. However, such cervical injuries are rarely the proposed cause of “post-traumatic” FMS. Instead, most are suggested to be consequent to some gradual work process and especially keyboard work. In the context of the latter, there are no supportive data. Similarly, while trauma is considered to be causal of a very rare chronic pain syndrome, reflex sympathetic dystrophy (RSD), even RSD has never been linked to any gradual work process.

    b)The great majority of people who are severely injured and/or exposed to high levels of acute pain do not progress to any form of chronic pain syndrome. Certainly, there is no correlation between acute injury severity and likelihood of chronic pain.

    c)Most people for whom keyboard work is blamed for their FMS have a long history of such work under worse ergonomic conditions and under greater workloads without health consequences. In this context, there has never been a good correlation shown between workload and likelihood of FMS or other chronic pain syndromes. That is, there is no demonstrable dose-response relationship. This factor was observed in the original descriptions of a “RSI-type injuries” almost 300 years ago.

    d)The great majority of people with any form of chronic pain syndrome have no history even suggestive of an antecedent sensitizing injury and or an injurious work process. Instead, there is often a history of earlier episodes of chronic pain and associated phenomena such as migraine headaches, Raynaud’s Phenomenon and irritable bowel syndromes.

    e)The data that suggest that trauma can have a role in the cause of FMS in some patients is not as sound as that which shows that FMS is inherited as an autosomal dominant trait.

    Assuming an acceptance of compensability, which FMS sufferers are entitled to cover under the ARCI Act 1992?

    The consensus or majority statements from the New Zealand Consensus Meeting well summarise the issue of which patients with FMS could be compensable under the ARCI Act 1992 and are cited below.

    Fibromyalgia syndrome arising after anything other than a physical injury or occupational disease or infection can not be compensable under the ARCI Act 1992. Patients whose symptoms of FMS first arose after mental trauma are specifically excluded from cover unless the mental trauma is a consequence of a physical injury or occupational disease or infection.

    ·Fibromyalgia syndrome arising after a physical injury or occupational disease or infection can only be compensable if such conditions are politically accepted to be a cause of FMS and if the following clinical criteria are met.

    a)The pain syndrome must be appropriately temporally related to the physical injury or occupational disease or infection. None of the medical practitioners who have seen Barbara have obtained a history even suggestive of a discrete physical injury.

    b)The physical injury or occupational disease or infection should be antecedent to the pain syndrome and the clinical findings that relate to this initial condition should satisfy appropriate diagnostic criteria. To substantiate this compliance and to enable ongoing audit, the clinical findings would need to be recorded along with the original diagnosis of the antecedent condition.

    c)If the pain syndrome is consequent to a physical injury, then that injury should either be the result of an accident or a plausible consequence of a biomechanical work process (providing that there are no factors away from work that could also explain the injury and the type of injury is more prevalent in that worker group). Barbara was not the victim of an accident and, as stated above, none of the many objective assessments of Telecom workplaces have shown these to violate the Department of Labour’s VDU Code.

    d)If the pain syndrome is consequent to a physical injury, then the symptoms and signs attributed to the antecedent injury should resolve within an acceptable time appropriately modified".

    Dr R D Wigley:

    Dr Wigley submitted a paper which he and a colleague Dr Kenneth Couchman had compiled under the heading:

    Currently available evidence of injury in overuse syndromes and fibromyalgia
    (chronic pain syndrome).

    Dr Wigley then set out a number of propositions which he contended had been established from various research and which he stated as follows:

    “To establish that there is personal injury in the individual case it is necessary to show that the complaint arose out of and in the course of employment and also to establish that there is tissue abnormality.

    1.The pain which results from overwork in an unsatisfactory work environment and/or an substandard work station initially may be transient signaling corrective action. Sustained over a period of time sustained bad posture (implying sustained muscle contraction) will lead to continuing pain and a self sustaining pain cycle with local tenderness which can be measured with a dolorimeter. This measurement is partly objective in that the observer controls the pressure applied and observes involuntary flinching in addition to the subjects verbal response.

    2.There is now clear evidence that the level of substance P in CSF is raised in fibromyalgia. There is a considerable body of evidence reviewed by Wigley, Darby and Brown (unpublished) that sustained contraction of muscle causes interruption to capillary circulation in loaded muscle. This leads to release of pain stimulating substances such as substance P. If this is repeated and sustained the plastic nerve cell change can be induced. The pain then persists after the noxious agent has gone. The lowered pain threshold may continue for a very long time leading to a lowered pain threshold and then widespread tender points leading to use of the label, fibromyalgia.

    3.Recent work from University College London has shown that the threshold to vibration sense is raised in keyboard operators with arm symptoms and that this threshold rises further with keyboard use. This potential clinical test separates cases from controls not working at keyboards. There is also a decrease in tolerance of maximal stimulation. This has not yet been tested in fibromyalgia.

    4.There is now evidence from Israel that the serum level of Hyaluronate is raised in fibromyalgia. Levels are clearly higher than in normal and rheumatoid arthritis controls. If confirmed this will provide an objective test for the diagnosis and monitoring treatment of this disorder. It also provides further evidence of a biochemical abnormality in pain syndromes. Possibly this is a manifestation of injury but the mechanism is not yet explained. Evidence that fibromyalgia can be an extension of arm pain and that both may be the result of occupation is available so this test may also be positive in arm pain. It has not yet been tested in the arm pain syndromes but a study is currently planned.

    5.In fibromyalgia electron microscopic examination of collagen fibres show decreased cross-linkage indicating anatomical abnormality at an ultramicroscopic level. This is not likely to be of value in diagnosis but is further evidence of tissue abnormality which could be the result of injury.

    6.A study from Cambridge University shows that skin temperature drops after keyboard use in chronic forearm pain.

    7.Several studies have shown that blood flow in the caudate nucleus is reduced in fibromyalgia. This may result from rather than being a cause of fibromyalgia. This has not been tested in forearm pain.

    8.Fibromyalgia may also occur without apparent occupational or other cause as sequel of whiplash type neck injury.

    9.There is also controversial evidence that psychological factors such as psychosocial stresses can cause fibromyalgia. Against this a recent detailed study failed to show an association between previous stressful life events and fibromyalgia.

    10.Pierre et al have shown thickening of the median nerve and decreased conduction in cleaners. This reference is included as Hadler claimed that failure to show an association between work and carpal tunnel syndrome could be generalised as evidence that occupation does not cause symptoms.

    11.There is one paper suggesting an autosomal dominant predisposition to fibromyalgia. To what extent environmental factors contribute to this apparently hereditary pattern is not clear.

    At present the pattern is incomplete. Research proceeds rapidly so that the missing pieces in the jig saw puzzle should soon be available to allow us to fit them together. Multi factorial causation is almost certainly responsible. There is little evidence to support a single cause hypothesis.

    I believe that presently available evidence is consistent with the view that there is injury in those cases in which there is good evidence that the symptoms result from occupational factors. To say now that “there is no injury” cannot now be justified by the available evidence”.


  • Mr Wilton, counsel for the appellant recognised that at the heart of the issue in this appeal was the question of whether or not the appellant had sustained a physical injury. Counsel submitted as follows:
    • A chronic pain syndrome which involves harmful physical changes to the tissues of the nervous system is a physical injury for the purposes of the Act.

    • The Act does not define injury. Its natural and ordinary meaning is broad, with the shorter Oxford dictionary meaning being hurt or loss caused to or sustained by a person … harm detriment damage.

    • A detectable bodily harm or detrimental damage arising from disease, or infection of gradual process will be an injury for the purposes of the Act.

    • Work place causation of the appellant’s injury is established by the Work Place Assessment and the first report from Dr Turner.

    • The apparent turn-around in the opinion of Dr Turner does not effect the opinion he gave on the causative mechanism involved arising from the appellant’s work place.

    • The later contrary opinions expressed by Dr Alchin and Professor Gorman are not sufficiently convincing to displace the contemporaneous evidence upon which cover to the appellant was granted.

  • Mr Corkill, counsel for first respondent submitted that the onus in this appeal was on the appellant to establish an entitlement for cover. He submitted that the evidence did not establish that the appellant had suffered a physical injury caused from any work place circumstances. Counsel further submitted that the condition known as fibromyalgia was not a physical injury and that the evidence established that it was not caused by factors which would bring it within the provisions of section 7 of the Act. Finally, he submitted that the provisions of section 7 (4) must be considered and that the specialists had identified that a probable causative factor was non-physical stress experienced by the appellant during the course of her employment with Telecom.

  • Mr Haigh Q C, counsel for the second respondent, submitted that the circumstances giving rise to this appeal rehearing gave the appellant the opportunity of calling further evidence to test the opinion evidence of the experts that had been presented on behalf of the respondents but that the appellant had chosen not to do so. Counsel submitted that the evidence clearly established that the appellant had not suffered any physical injury and that there was in any event no causative nexus between her condition and her employment. Counsel further submitted that this was not a case where a discrete physical injury had led on to a more generalised condition of a chronic pain syndrome such as would allow for cover in line with a number of authorities established in this Court.


  • As I noted at the outset this appeal concerns the correctness or otherwise of the decision of the first respondent, by its agent CRM, to revoke cover for the appellant on the basis that the grant of cover which had been made to her on 29 October 1996 had been made erroneously.

  • The decision which is the subject of the appeal therefore requires the Court to revisit the circumstances which gave rise to the grant of cover to the appellant in October 1996 and to determine whether such cover was correctly granted or not. It requires the matter to go back to square one and for the appellant to establish on the balance of probabilities that she was entitled to a grant of cover having regard to the circumstances of her claim.

  • The appellant sought cover pursuant to section 7 of the Act, namely that she had suffered a gradual process injury arising from her employment at Telecom. At the heart of a right to cover under section 7 of the Act is the requirement that the claimant must have suffered a personal injury. Section 4 of the Act defines personal injury as meaning the death of or physical injuries to a person, and any mental injuries suffered by that person which is an outcome of those physical injuries to that person.

  • It is clear from that definition that physical injury is clearly distinguished as a separate category of injury from mental injury. Physical in this context I find to be in accordance with the dictionary meaning “of or relating to the body as distinguished from the mind or spirit”. (Using the definition of physical injury in line with the natural and ordinary meaning it must therefore involve) physical damage or hurt, that is bodily harm or damage.

  • It is in that context that the appellant sought cover under the Act and, as noted, the medical evidence that was presented at the time the claim for cover was lodged simply described the injury as possible OOS. That diagnosis was confirmed on by Dr Fountain in the Medical Practitioner Questionnaire as being OOS. The symptoms which were being displayed and which gave rise to that diagnosis he stated as being pain which the appellant was experiencing in her shoulder, neck and arms. In August 1998 Dr Fountain was asked to revisit his notes of October 1996 but he could not elaborate on his diagnosis of OOS, which he simply contended was an acceptable diagnosis for ACC at that time. He was not able to amplify on that diagnosis to give any details of an identifiable physical injury.

  • What is somewhat unusual in this case is that a specialist in Occupational Medicine was consulted within a very short time of the claim for cover being made and the Court therefore has the benefit of that evidence to consider on the question of whether the appellant had suffered a physical injury.

  • To Dr Turner the appellant explained her condition as being pain and discomfort in her neck, shoulders, back and upper limbs together with a weakness of grip and feelings of fatigue, sleep disturbance and general muscle stiffness. Dr Turner’s examination only identified places of tenderness which he described as tender points but he found no evidence of physical injury. His diagnosis at that point in time, which in terms of Section 7 (5) of the Act was approximately one month after the condition was deemed to have arisen, was that the appellant was suffering from a diffuse myofascial pain syndrome affecting her upper body. At that point he identified early fibromyalgia pain syndrome.

  • I consider it pertinent to note that Dr Turner’s opinion was being sought for the purposes of identifying the appellant’s problem and to assist her with treatment and rehabilitation. It was not a situation where his opinion was being sought as to whether or not she was entitled to cover. That matter had already been determined and therefore his evidence is particularly significant. Follow up reports to CRM in early 1997 confirmed the role that he was being asked to play at that time which was wholly treatment orientated.

  • When Dr Turner was subsequently asked to give his opinion for the purposes of the issue which is now the subject of this appeal he was able to refer to his notes and examination made in November 1996 and he confirmed that in his opinion the appellant displayed no symptoms of a physical injury in terms of section 4 of the Act.

  • I find therefore that, having regard to the evidence of the medical practitioners who examined the appellant at or about the time she lodged her claim, the appellant displayed no physical injury in the accepted sense of that word, but rather, displayed symptoms of pain at various points on her upper body. By that finding I say that no discrete physical injury could be seen such as an inflammation of tendons, a sprain or evidence of physical strain.

  • It then therefore requires to be determined whether the condition of regional pain syndrome, chronic pain syndrome or fibromyalgia, which I note are largely interchangeable diagnoses, amounts to a personal injury within the meaning of the Act.

  • At this point I should stress that this is not a case where the Court is called upon to determine whether or not the condition of CPS, RPS or FMS is the follow on consequence of a physical injury suffered. For this reason the line of authorities which this Court has given over the past few years are not relevant as they are addressing an entirely separate and distinct question of law from that which is at the heart of the issue of this appeal.

  • For the sake of brevity I will hereon refer to those various conditions as all being FMS.

  • I have set out in some detail the evidence of specialists as to what is FMS and I distil from those expressions of opinion that FMS is a disorder in the nature of an abnormal pain perception of the central nervous system. The nerve fibres have become dysfunctional and respond abnormally so that painful messages are transmitted to the brain from body positions when in fact a non painful message ought to have been sent. It is the various tender points or trigger points that a person is experiencing which are shown to be where there is no physical injury or damage to the body but yet when that particular point is touched it nevertheless sends a message of pain through the central nervous system.

  • As was stated by Professor Gorman FMS, is a syndrome for which no pathological hypothesis has yet been validated. At best the experts state that it is multi-factorial and does result in changes in both the central and peripheral nervous systems. Professor Gorman advised that the majority at the Consensus meeting found that the origin of the pain and the hypersensitivity in FMS probably lay within the nervous system and was based on the plasticity of that nervous system.

  • I find that in essence the condition involves a disordering of the nervous system in some unknown way, that condition may involve the death of cells or tissue but that the nature of it is not in the way of damage to the nervous system such as would be the case where a person suffered paralysis or loss of feeling because of damage to nerves. Here the nervous system is still in situ but is, for some unexplained but nevertheless complicated reason not sending the right messages.

  • All the specialists indicated that there was a heavy psychological emphasis in the creation of and continuation of the condition and that non-physical stressors were considered to play a major part.

  • In the case of this appellant the Court was referred to various observations made by these specialists about the stress which the appellant felt she was under in her job, that stress being non physical stress in the sense that she was under pressure to perform to at a certain level and that this was impacting upon her and she was unhappy in her work, particularly when working under a particular team leader.

  • For the avoidance of doubt I find that the question of stress, whilst it was certainly present and can be expected to be a feature, nevertheless was not a physical stress. It being of a non physical nature it is excluded from coming within the definition of gradual process injury by virtue of section 7 (4) of the Act.

  • In the final analysis therefore I find that the appellant did not suffer a personal injury in the course of her employment with Telecom. That she suffered harm during the time that she was so employed there is incontrovertible but the fact of the matter is that the Act limits compensability to a physical injury which can be established as having been caused by a particular property or characteristic of a work task performed by the person. In the present case not only do I find that there is no evidence of personal injury within the meaning of the Act, but also there is no evidence to suggest that the appellant’s condition was caused by any property or characteristic of her employment tasks.

  • Dr Wigley stated that in his opinion the appellant’s condition was regional pain syndrome due to occupation. He accepted that there was no injury in the sense of there being any recognisable bruising or abnormality of tissue. However he said there may be damage to the sensory cell leading to the general increased sensitivity. He considered that the complex biochemical abnormalities suggested by Professor Schug should be considered injury. Dr Wigley then suggested that as section 6 (1), which defines work injury did not include the word physical there was somehow no reason for the injury in a gradual process injury to have a physical component. His whole theory then proceeded on the basis that a physical injury was not required to be established for a gradual process injury under section 7 and it was on that basis that Dr Wigley referred to what he understood to be cell change induced as part of the fibromyalgic condition and he also referred to other biochemical abnormality.

  • Having regard to the basic requirement which I have found must be necessary in order to found cover, being that of a personal injury being a physical injury, I find that Dr Wigley’s theory cannot be accepted in terms of Accident Compensation Legislation.

  • Furthermore I take note of the criticism that was made of Dr Wigley’s theories by Professor Gorman which I have not set out herein but which nevertheless I have had regard to and which I find to be preferable as it is based on a wider gathering of research material than that which Dr Wigley relied on.

  • In particular I note Professor Gorman’s response to Dr Wigley’s assertion that the incidence of fibromyalgia involves physical changes which indicate injury where Dr Wigley referred to electromicroscopic examination on the collagen fibres showing decreased cross-linkage, suggesting anatomical damage at an ultra microscopical level. Professor Gorman’s response to this was that the observation that fibromyalgia patients demonstrate changes in collagen biology does not suggest anatomical damage. It suggests nothing other than that there are alterations in collagen biology. He went on to state that similar changes are seen in a wide range of collective tissue diseases. He stated that it was nonsensical to see such physical changes as indicating either damage or an injurious base.

  • Professor Gorman was at pains to state that physical changes such as change in blood flow or changes in nervous system physiology do not imply any particular aetiology and that an argument that such changes are indicative of injury would result in such things as migraine headaches being considered as injury given the significant changes in extra cranial blood flow which occur in this condition.

  • Taken in the whole I find that Dr Wigley’s assertions do not stand close scrutiny from experts and I find that his research, much of it being of his own, lacks the authority which would be necessary for it to carry the day.

  • The situation as I find it therefore is that the appellant was not entitled to cover under the Act for the condition that she presented, firstly to her GP and then to Dr Turner, as it did not have the basic requirement of being a personal injury, that is a physical injury. Furthermore, her condition could not be said to have been the consequence of or the progression from a physical injury, which might have allowed her to obtain cover under one of the recognised precursors of the fibromyalgic condition namely a discrete physical injury.

  • Having found as I have, it is not necessary to consider whether the appellant could satisfy the requirements of section 7 (1) (a) (b) © but it must be clear from the finding that I have made that the appellant could not satisfy the requirements of section 7 (1) (a) which requires a causative link between work place characteristics and the physical injury suffered.

  • Whilst the work place may have contained stressors which may well have impinged on the appellant’s well being and may have been part of the “mix” or factors which caused her to suffer the pain disorder which was a myofascial pain syndrome and which became fibromyalgia, that connection, being non-physical stress, is itself excluded by section 7 (4) of the Act even if the causal connection were to be demonstrated, a circumstance which I find on the expert evidence cannot be sustained to the necessary degree of probability.

  • It follows therefore that on the particular facts of this appellant’s case and her medical condition as it presented at the time she made her claim for cover, she did not have a right to cover under the Act and the first respondent’s decision to subsequently revoke her cover was correct.

  • This appeal is dismissed. In the circumstances I make no orders as to costs. Each party shall bear its own costs.


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Posted 11 March 2013 - 04:06 PM

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