Nicholls v Accident Compensation Corporation

IN THE DISTRICT COURT AT WELLINGTON DECISION No. 217/2005 UNDER The Injury Prevention, Rehabilitation and Compensation Act 2001 IN THE MATTER OF an appeal pursuant to section 149 of the Act (Appeal No. AI 102/04) BETWEEN GENEVIEVE NICHOLLS Appellant AND ACCIDENT COMPENSATION CORPORATION Respondent Hearing: 6 April 2005 Appearances: Hazel Armstrong for appellant Bruce Corkill for respondent Judgment: 18 July 2005 RESERVED JUDGMENT OF JUDGE D A ONGLEY [1] The appellant originally lodged a claim with the ACC on 2 July 1996 for an occupational overuse Injury. Cover was given initially for the left arm only but later extended for both arms. [2] Mrs Nicholls was employed as an Operational Advisor for Community Corrections. The ACC claim for cover form (M46) completed by GP Dr Palmer on 2 July 1996 stated: “Increased use of the keyboard to my computer at work. OOS in arm.” In an ACC gradual process disease or infection questionnaire on 11 July 1996 Mrs Nicholls wrote: “Pain stiffness, numbness, tingling in both lower arms neck and shoulders. Pain from right elbow down outside of arm to little fingers when using keyboard and tingling. Numbness in hands. Lack of accuracy and speed when typing also increase in clumsiness with hands.” [3] The Corporation issued a decision on 28 July 2003 revoking its earlier decision to accept cover. The decision was confirmed on review on 3 February 2004. Physical injury [4] It is agreed that Mrs Nicholls now suffers a general pain syndrome classified as fibromyalgia. The symptoms began with paraesthesia and elbow pain following intensive computer use with long hours working under stress. Such symptoms were classified at the time as occupational overuse syndrome, but more recently that description has been found inadequate to describe an injury. In reliance on the weight of medical opinion, ACC ceased to extend cover to a pain syndrome caused by occupational overuse without evidence of a specific injury such as tendonitis or epicondylitis as a cause of the pain syndrome. [5] Mr Corkill for the respondent submits that the symptoms in this case are typical of the kind of diffuse pain syndrome caused by circumstances such as those affecting Mrs Nicholls, and that there is no evidence in this case of an injury for which cover could be given. Therefore, it is submitted that cover was granted in error and must be revoked. [6] The Reviewer found that Mrs Nicholls first experienced pain in her fingers and wrist of her right hand in June 1995. In June 1996, she went to her GP about pain in her arms and hands and in July 1996 her right arm was swollen above and below the elbow, along with pain in her arms, shoulder and back. [7] In August 1996 she saw Dr Lissa Judd, occupation medicine specialist. Dr Judd recorded that the pain which caused Mrs Nicholls to see her doctor in June 1996 occurred after she had spent much of the weekend typing a large document and was incapacitated on Monday morning. She had been put off work for two weeks, then returned for two weeks and was then put off for 12 weeks. Dr Judd said that the picture was consistent with fibromyalgia following excessive workload and awkward postures secondary to poor ergonomics. It has since been suggested that the symptoms at that stage would have been consistent with a regional pain syndrome rather than fibromyalgia. Dr Judd recommended modifications to her work environment and activities. [8] The claim that there was an initial physical injury was based on the notes of Mrs Nicholls’ general practitioner, Dr Palmer. An analysis of Dr Palmer’s notes was done by Dr Judd in a much later letter on 12 June 2004 after Mrs Nicholls had asked for her opinion on progression of the condition from an initial tendonitis injury. The general practitioner’s notes were as follows: “RX: Diclofenac Tabs 25mg 1 bd pc 50. Pain R arm 4 weeks. Uses computer several hours per day. Unable to straighten R elbow. Also present on L. Paraesthesiae 4th & 5th fingers (R). OE swelling and tenderness around elbow. Imp: OOS. For rest and P/T.” [9] Dr Judd said that, assuming the notes were quoted in full, they are so inexact that it is difficult to extract any meaning from them at all. She wrote: “Strain of what muscle? Tendonitis of which tendon? How can one infer such a diagnosis from notes such as this? How can one recall what one intended several years after the consultation? The only physical signs are swelling and tenderness but it is not stated where these are, except to say that they are ‘around the elbow’. If a particular structure in the elbow or the vicinity of the elbow was injured one would expect tenderness to occur at that point. Identifying the precise location of tenderness is part of the business of making a diagnosis – of deciding which structure or structures is injured or damaged”. After further observations on the lack of any detail in the notes that might suggest injury, Dr Judd said: “If Dr Palmer had considered that a tendonosis was the diagnosis then there is insufficient information in the notes to corroborate this, or even to suggest which tendon she was thinking of, and it does not account for physical signs (such as the paraesthesia) which do not fit with a diagnosis of tendonosis (or a diagnosis of muscle strain). The symptoms and signs referred to in Dr Palmer’s notes do not suggest a diagnosis of tendonosis, any more than they suggest a diagnosis of ulnar nerve entrapment or pronator syndrome. The information provided in Dr Palmer’s notes is insufficient to make a diagnosis of any kind.” [10] There are other medical opinions which lead to the same conclusion and it is not necessary to set them out here. There is no evidence of a specific injury accompanying the onset of Mrs Nicholls’ initial symptoms [11] The medical questions in this case are similar to those considered before in the District Court in the case of Teen (244/2002); refer also the judgment of Wild J refusing leave to appeal in Teen v Arcic (unrep. High Court, Wellington CIV 2003- 485-1478, 11 November 2003). In the first place it is essential to show that the condition for which cover is sought is a physical injury or caused by a physical injury. Secondly, there have been a number of cases in which a disorder of the peripheral nervous system has been put forward as evidence of a possible injury but in the absence of reasonably persuasive medical opinion it has not been enough to establish actual injury. Each case depends on its own medical evidence, but it has been consistently difficult to show that a pain syndrome, developing from repetitive work under stress in an office situation, has involved an injury to nerve cells or nerve fibres. [12] In this appeal, the parties have called expert scientific medical evidence from Dr Evan Dryson and Dr Peter Dodwell, both of whom gave oral evidence at the appeal hearing. There are other opinions in the case material, however the difference in views are encapsulated by the evidence of those two specialists. [13] Dr Dryson is an occupational medical specialist who has been practising as a consultant in Auckland since 1987 and has published original research in the areas of pain syndromes and upper limb pain in the International Journal of Occupational and Environmental health. He examined Mrs Nicholls in October 2004 and confirmed that she had a pain syndrome of the fibromyalgia type with clinical findings of tender points. Dr Dryson said that tender points are objective evidence of a pain syndrome, constituting pain referred to recognised locations in the body. He said: “It is generally recognised that a pain syndrome is accompanied by physical changes, such as alterations in the levels of neurotransmitters at nerve endings in the spinal cord, new and abnormal neural connections in the spinal cord, and changes in regional blood flow in the central nervous system. It has however been argued that these are consequences, and not the cause, of a pain syndrome, and do not therefore constitute a preceding injury as would usually be required for cover under the Act. Regardless of the above it is my opinion that a regional pain syndrome is a physical injury when it occurs in a context of intensive computer work as here. I base this on recent research evidence by Jane Greening and her co- workers, and published in the Journal "Pain" Volume 104 (2003) pages 275- 281.” [14] Dr Dryson referred in particular to an article published in the International Journal Pain Vol. 104 (2003) entitled Sensory and autonomic function in the hands of patients with non-specific arm pain (NSAP) and symptomatic office workers, by Jane Greening, Bruce Lynn and Rachel Leary of University College London. It is not disputed that the publication was in a highly reputable journal published by the International Association for the Study of Pain and that the research was peer reviewed prior to publication, is peer reviewed. [15] It is this article in particular that tends to extend the scope of evidence beyond that considered in the earlier cases in this jurisdiction. While the court must consider all the evidence in this case, there was particular focus on the study by Greening et al, and most of the oral evidence was directed to that research. [16] In the Greening research, a control group and two other groups were selected. One of those other groups consisted of patients who displayed non-specific arm pain (NSAP), and the other consisted of asymtomatic office workers who used display screen equipment (DSE) for at least 40% of their working time. The direction which the study took was to show that there were signs consistent with neuropathy in the group of office workers who did not have pain symptoms. The members of the NSAP group attributed their arm pain to DSE or keyboard use, but there was no analysis of the extent of that activity. [17] A conclusion that may be drawn from the study is that deterioration of peripheral nerve function may occur before symptoms of a pain syndrome are felt by a patient. It is also postulated that the reduced nerve function suggests neuropathy or neural “injury”. [18] The study involved three nerve response tests, namely flare response, sympathetic vasocontrictor effects and vibration threshold testing. The tests involved peripheral nerve and autonomic nerve responses. The study showed that pain syndrome patients displayed reduced peripheral nerve function in comparison with the control group, stating: “There are clear differences between the NSAP patient group and the control group for functions involving small and large sensory fibres (flare and vibration threshold, respectively) and for autonomic reflex amplitude. Overall the patients have a 45% rise in vibration threshold, a 33% fall in axon flare area and a 20% reduction in a sympathetic vasoconstriction reflex. The patients thus show a clear pattern consistent with loss of function affecting all nerve fibre classes. As we have argued previously (Greening and Lynn, 2000) this is consistent with the patients having a minor neuropathy.” [19] Dr Dodwell did not dispute that there was consistency with minor neuropathy, but he was of the opinion that neuropathy was not established. The discussion at the end of the study reported: “Office workers who spend 40% or more their working time using DSE equipment present an interesting contrast. They have a reduced flare, similar to the patients and slightly elevated vibration threshold but no reduction in the sympathetic reflex. As a group they show similar alteration in sensory nerve function as the NSAP patients. It is clearly possible that some reduction in sensory, but not autonomic nerve function, can precede symptom onset. In conclusion, NSAP patients demonstrate clear indications of changed peripheral nerve function involving small and large sensory and autonomic fibres. Office workers who intensively used DSE show early signs of changed sensory nerve function, but no change in autonomic responses.” [20] It is to be noted that the study concluded that it was “clearly possible” that some reduction in sensory nerve function can precede symptom onset. The study did not make a positive conclusion. Dr Dryson put it in this way: “16. The authors found that the nerve function of the control group was normal. This was to be expected. 17. The results also showed that the computer users who suffered arm symptoms showed significant impairment of nerve function. This finding is of some importance as it confirms peripheral nerve damage in the computer users suffering arm symptoms. 18. However, the most important finding was that the group of computer users who did not suffer arm symptoms showed an intermediate impairment of nerve function, termed by the researchers a ‘neuropathy’. 19. A neuropathy can be described as a disorder of a peripheral nerve. 20. A neuropathy can be termed a physical injury as it involves damage to function. It could be the result of either damage to the axon or myelin sheath. Whereas it may be possible that a biopsy would show these changes, such research has never been reported in medical literature, and consequently carrying out biopsies on individuals would be of little value. It would be invasive, and would not be diagnostic. 21. The significance of this finding is that it proves peripheral nerve damage occurs before the onset of pain. Since the neuropathic changes occur before the onset of pain, it is clear that there is a physical injury leading to the pain syndrome. 22. Based on this finding, it is my opinion that Ms Nicholls’ regional pain syndrome was preceded by a physical injury, namely a neuropathy, as it occurred in a context of intensive computer work over long hours. [21] In relation to Mrs Nicholls’ diagnosis he said that she developed pain, swelling, sensory disturbances in her right arm after a period of intensive computer use up to 50 hours a week. The symptoms later extended to involve the rest of the body. Dr Dryson regarded that as the classical presentation of what used to be called occupational overuse syndrome, a pain syndrome which has developed because of excessive repetitive activity on a computer in the context of long hours and poor ergonomics. He said: “ .. the Greening paper suggests that there is damage occurring to peripheral nerves in people who are in the process of developing pain syndromes. … this is called a neuropathy and it was my opinion that it was most likely that this was how it had started in Mrs Nicholls’ case. And that - whatever anyone might think about pain and the objectivity of it, a neuropathy is in my opinion an objective physical injury. ... it’s usually considered that work which involves tightening of the muscles such as sitting in fixed postures for lengthy periods without moving, or without changing the task and repetitive activities such as very fast contraction and relaxation of the muscles, is likely to increase the traffic in the nerves which supply the muscles so that there is in a sense a sensory overload in the nerves sending signals to the brain. This is - conjectural in the sense that it is not possible to conclusively prove it but there certainly is a fair amount of evidence that people who do unduly repetitive work or fixed constrained postures are the ones that seem to get these pain syndromes and in Mrs Nicholls’ case she certainly was doing highly repetitive tasks and long hours sitting at a computer, which is a fixed posture.” [22] Dr Dodwell disputed Dr Dryson’s interpretation of the results. He said that the study did not show that nerve deterioration was progressive and leading to onset of pain. It showed only that the asymptomatic users group exhibited a deterioration in nerve function. The study did not show that they would go on to experience pain. He disputed Dr Dryson’s view that the study proved peripheral nerve damage occurs before the onset of pain. Rather it showed only that peripheral nerve damage occurred without pain symptoms. [23] Dr Dodwell’s report is of considerable value to the Court in assisting to analyse the conclusions of the Greening study and the difficulty in establishing a causal connection between intensive computer use and injury to nerve cells. It is worth setting out his discussion of the concept of damage, as follows (original emphasis): “10.15.1 Damage and injury are not always synonymous. Unfortunately, it is extremely common in the medical world for ‘damage’ to be used either in a very general way to encompass the effects of either disease or external forces; or to be used with the assumption that only an external force has been involved. This results in unnecessary confusion. If the latter more restrictive use were to be generally adopted, the term damage would have to be restricted to situations where the external force had been clearly identified. 10.15.2 A more useful general term would be deterioration rather than damage. Genuine neuropathy may well involve deterioration of nerves, but such deterioration can be the result of disease processes such as endocrine disorders, genetic disorders, toxic exposure and infections as well as damage resulting from external forces. 10.15.3 I avoid using the word ‘damage’ since some consider it synonymous with ‘injury’ and misinterpret the term when used in its more general - or legal - sense. To avoid confusion I use the terms deterioration or dysfunction as generic terms which may indicate effects of either a disease process or the result of an external force. 10.15.4 His claim that neuropathy ‘involves damage to either the axon or the myelin sheath’ demonstrates this assumption on Dr Dryson's part. If his statement is revised to read as ‘involves deterioration in either the axon or the myelin sheath’ the statement is less susceptible to misinterpretation. Alternatively he could have correctly stated that neuropathy ‘sometimes involves damage to either the axon or the myelin sheath’. The Greening study hypothesised something similar, but merely indicated that this ‘remains a possibility’ when discussing the results. 10.16 In paragraph 21, Dr Dryson claims that the Greening study ‘proves peripheral nerve damage occurs before the onset of pain’. This is a factual error; the Greening study does not find nor conclude this at all. Stripped of exaggeration, the paper has demonstrated that peripheral nerve dysfunction can exist without pain. The paper does not demonstrate a time sequence of development of a pain syndrome, starting with no abnormality, progressing with time to mild neuropathy without pain, and then to more severe neuropathy with pain. This study may just demonstrate that our understanding of what is normal needs further exploration; one group of high computer users in this study seemed to display abnormal nerve functions but had no pain whatsoever. 10.17 In paragraph 22, Dr Dryson concludes with an opinion that ‘her regional pain syndrome was preceded by a physical injury, namely a neuropathy, as it occurred in a context of intensive computer work over long hours’. This conclusion expresses unwarranted certainty. In the absence of tests confirming neuropathy in Ms Nicholls, it cannot just be assumed to be true. Even if the Greening study had supported the hypothesis that every person with neuropathy will develop regional pain syndrome (which it clearly doesn’t), this argument would be faulty for the exact same reason as the following: ‘people who drink and drive have accidents; this person has had an accident; therefore this person has been drinking and driving’. There are other factors in road accidents, and similarly neuropathy may not be a prerequisite for a pain syndrome.” [24] The last paragraph deals with the central fact question in this appeal, namely whether Mrs Nicholls sustained a work related physical injury. Dr Dodwell’s view is that there is still no evidence of any physical injury. If the case for physical injury is to be based on the Greening study there are two objections, first that the study does not establish neuropathy in the subjects, but only deterioration in nerve function consistent with neuropathy. Secondly the test results for the Greening study cannot be automatically applied to Mrs Nicholls who has not been tested in the same way. The appeal [25] The appeal is presented on alternative grounds, that either there was a physical injury precipitating a chain of events leading to fibromyalgia, or that pain syndrome involved neuropathy which was itself a physical injury. [26] I find that the appeal must fail on both grounds. There is no evidence of a precipitating injury such as tendonitis. Dr Palmer made notes that could tenuously be regarded as a description consistent with tendonitis, but in the light of Dr Judd’s criticism in particular, I do not consider that the observations can be so regarded. While it is true that practitioners with an accident compensation claim in mind may not have needed, in 1996, to describe a specific soft tissue injury, that does not provide a licence to find in Dr Palmer’s notes something which is not there. [27] In relation to the postulated neuropathy leading to a pain syndrome, I find that the evidence is not sufficient to show that Mrs Nicholls suffered an injury. In the past, this Court has failed to be persuaded by evidence that an occupational pain syndrome must involve physical injury to nerve cells. The study by Greening et al tends to show that a deterioration in nerve response can be caused by intensive DSE use independently of a pain syndrome. The responses in NSAP patients are similar to responses of asymptomatic subjects. The modified nerve function may be a precursor to a pain syndrome. There is also the possibility that reduced nerve function could occur in large numbers of DSE users without a consequent pain syndrome developing, or even that pain syndromes have some other cause. I accept the logic of Dr Dodwell’s view that the study does not show that pain syndrome is caused by occupational related neuropathy. [28] Certainly the subjective experience of patients tells them that repetitive occupational tasks with intensity and stress cause an intractable pain syndrome, and that seems to be an acceptable intuitive conclusion. It was in fact the conclusion broadly accepted in the medical profession until about ten years ago. The reasons for abandoning it were perhaps nurtured in the interests of compensation providers, but that does not detract from the validity of modern opinion. The evidence before the Court is that mainstream medical opinion now rejects the postulate that occupation related pain syndrome in DSE users is caused through a physical injury, unless an independent diagnosis of soft tissue injury can be reached on valid clinical grounds. [29] For those reasons the appeal is dismissed. Signed at Wellington on 18 July 2005 Judge D A Ongley District Court Judge