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Accident Compensation Cases

Cochrane v Accident Compensation Corporation (DC, 14/06/07)

Judgment Text

Judge D A Ongley
This appeal concerns a decision by the respondent dated 27 April 1999 under s 73 of the Accident Rehabilitation and Compensation Insurance Act 1992. The decision stated that in view of the presence of degenerative process now causing the appellant's difficulties, the Corporation decided that the effects of the covered injury have passed, and ongoing incapacity is caused by age related degenerative disease. 
The decision was confirmed on review and on appeal to this Court. Leave was granted to appeal to the High Court on the ground that the causative test for continuing cover under the Accident Compensation Act 1982 had not been applied. The appellant maintained that the application of the test to the evidence would establish that entitlements should be continued. On 2 June 2004, Miller J delivered a judgment in the High Court reported as Cochrane v ACC [2005] NZAR] 193. He allowed the appeal but accepted that further evidence directed to the correct test might lead the Court to confirm the Corporation's 1999 decision so he ordered a rehearing in the District Court. 
When aged 54, Mr Cochrane injured his back when he was helping to lift a 6 cylinder valiant motor off a low trailer when he stepped into a 6 inch sump hole and slipped. He lurched and twisted his back while holding part of the weight of the motor. When examined in 1984 he said he did not notice trouble with his back until the following morning when he felt moderately severe low lumbar backache radiating across the right side of the back of his pelvis. When examined in 2000 he said that he felt the pain immediately. There are discrepancies in the manner in which the accident has been described or recorded in medical reports from time to time, but Mr Cochrane's credibility has been accepted. 
Despite his moderately severe low lumbar backache he carried on at his heavy work as a truck driver and general labourer. As the pain became worse, he consulted his General Practitioner who put him off work. As a result, he lost his job. 
Mr B S McMillan, orthopaedic surgeon at Dunedin Hospital and Senior Lecturer in Orthopaedic Surgery, examined Mr Cochrane on 30 November 1984, eight or nine weeks after the accident. He accepted that the pain had persisted despite physiotherapy treatment and Mr Cochrane was then looking for lighter work. Mr McMillan also recorded that Mr Cochrane had first developed backache at about the age of eighteen, connected with accidents at that time. At the time of examination he had not experienced back trouble for about 10 years. Mr McMillan found no reason to disbelieve his statement that for the past ten years, he had no bother. He wrote: 
“Although, as far as I could tell, that when he slipped and gave his back a sudden jerk, and forced flexion, that no great strain from the engine he was carrying fell upon him, but such an unguarded movement, in my opinion, could be expected to aggravate his pre-existing abnormality and produce symptoms where none had previously been present, ie. that had it not been for this episode he may well have remained asymptomatic for many years if not forever. Notwithstanding this, it can also be argued that this strain was no greater than one might expect in the course of normal everyday activities. It is my view that it is the unexpectedness of such incidents that cause the problem rather than necessarily their severity. ”
Mr McMillan noted that x-rays of the lumbar spine taken on 5 November 1984 showed narrowing of the fifth lumbar disc space but with no associated degenerative changes. He noted that there were well marked degenerative changes in the posterior joints between L4/5. The pain was in the lower lumbar spine and was described as mechanical back pain probably coming from the posterior joints at L4/5 “where there are longstanding degenerative changes”. Mr McMillan said that “the presence of degenerative change on x-ray does not imply that the patient will be experiencing symptoms from this”, and he concluded: 
“In summary therefore, I think that he has significant, quite severe, genuine mechanical problems which arose after an unexpected although not severe twist to his back, the twist, however, being within the range of what one would expect from normal everyday activity. Although it is impossible to state with certainty as to whether his present complaints are of the same cause as those he complained of in his teens and twenties, I think that this is unlikely as I am in little doubt that his present troubles have an origin in degenerative changes in the posterior joints at the lumbo sacral level, such changes would almost certainly not have been present in his late teens. ”
The present significance of this report is that continuing pain is now associated with degenerative changes at L4/5 and the respondent maintains that the pain is produced by ongoing age related degenerative changes and not by any injury associated with the 1984 twisting accident. Mr Beck for the appellant notes that Mr McMillan's opinion of degenerative change did not concern the disc itself, but only the posterior joints. The appellant's argument is that the accident caused emerging degeneration of the disc and associated pain, consistent with Mr McMillan's opinion that the pain was not necessarily caused by the posterior joint degeneration. 
Medical opinions 
On 11 June 1986, Mr McMillan examined Mr Cochrane again and reported that there was essentially no change in his complaints of low lumbar backache which did not radiate to his legs. X-rays in 1986 showed marked degenerative changes at the fifth lumbar disc with almost complete loss of disc space, adjacent sclerosis and osteophyte formation. This indicated significant degenerative change in the fifth lumber disc space since the examination in 1984. The ongoing degenerative changes include the posterior joints at L4/L5 and L5/S1. Mr McMillan said that there was unlikely to be improvement or deterioration in the future and that the problems arose from the degenerative changes in the lower spine which had shown progression since his earlier report. He said “it would have to be accepted that the strain that he suffered would be likely to have caused such progression”. This opinion as to causation did not consider the further question whether the strain caused in injury as distinct from aggravating a condition that was previously asymptomatic. 
Mr J C Theis, Orthopaedic Surgeon and Associate Professor of Orthopaedic Surgery examined Mr Cochrane and reported on 7 April 1999. He noted Mr McMillan's 1986 report of almost complete loss of disc space between L4 and L5 with adjacent scelerosis and osteophyte formation and degeneration in the posterior facet joints between L4/L5 and L5/S1 with progression in the degenerative changes between L4 and L5 as compared with x-rays taken in 1984. A CT scan in 1995 had shown degenerative changes with loss of height of the L4/L5 and L5/S1 discs accompanied by degenerative changes in the facet joints at both levels but no significant prolapse or nerve root compression was identified. 
In describing the injury, Mr Theis noted that the appellant claimed that his right foot slipped into a drain hole while he was assisting the lift of a six cylinder motor onto the back of a trailer. The unexpected drop of his right foot into a drain hole was not a point reported by Mr McMillan. It has since been accepted in assessing the probable degree of force or twisting affecting the appellant's spine. The specific question put to Mr Theis was “Is the claimant's incapacity mainly related to his original injury or to non-accident problems?”. This was a question relevant to the assessment of cover in 1999, but was not a precisely directed question for cover under the 1982 Act. Mr Theis answered by saying 
“I personally feel that the claimant's ongoing incapacity is mainly related to his degenerative disease of the lumbar spine which cannot be entirely attributed to the injury he suffered in 1984. A single event like that is unlikely to result in degenerative changes as seen in this claimant's case …  ”
Mr Hlavac for the respondent submitted that Mr Theis answered in terms of the question and he was not asked to state whether he thought the ongoing incapacity was wholly related to degenerative disease. Mr Theis added: 
“I don't think that there are any other physical or anatomical problems other than the degenerative process that would account for his ongoing problems at the moment. ”
Mr Cochrane was examined by Dr Hugh Burry, Consultant Rheumatologist, who reported on 20 March 2000. In relation to the continuity of symptoms, Dr Burry wrote: 
“He does not seem to have had any very structured treatment programme and made various attempts to return to work which proved unsuccessful and ultimately he was laid off by management. Some time later, perhaps 18 months, although his back pain was still quite severe, he obtained part time work at a service station, four hours per day, working on the forecourt and doing tyre repairs. ACC paid make up pay during this time. This arrangement continued for a number of years, with Mr Cochrane's pain slowly becoming more pronounced and he finally resigned his job because of the pain. He tried repeatedly to find part time work, but his history of back injury and ACC claim made it much more difficult for him. He does not seem to have had much assistance ”
Mr Cochrane told Dr Burry that he did not suffer from any back problems prior to 1984, although he had rolled a grader down a bank a number of years before and emerged with general bruising but no particular back problems and was only off work, he thought, for a day. Dr Burry commented that it did not appear that any rehabilitation had been offered after the 1984 accident that might have restored the strength and elasticity of the appellant's trunk musculature and its function in supporting posture and movement to normal. Instead the focus of medical attention was the condition of his intervertebral discs. Dr Burry wrote: 
“Mr Theis has apparently assumed that the presence of degenerative changes in the intervertebral discs will be accompanied by pain and dysfunction. It is now recognised that this is far from the case. The so-called degenerative changes are really the process of maturation that goes on in the spinal column commencing in early adult life and progressing throughout life with the intervertebral discs altering in their physicochemical and structural characteristics with the passage of time. ”
I do not think that Mr Theis necessarily made that assumption, rather he weighed the nature of the degenerative changes, the pre-accident history and the nature of the accidental trauma. Dr Burry went on to say: 
“The literature related to this matter has recently been reviewed in the New Zealand Medical Journal (ref 1) and if there were to be any doubt as to whether ‘degenerative changes’ were inevitably accompanied by symptoms one would only have to look at Mr Cochrane's situation prior to the accident in 1984. At this time it is clear that he had well developed ‘degenerative changes’ in his lumbar spine and yet had never been incapacitated by back pain. In other words he had x-ray changes at a time that he continued to function normally in his chosen occupations. Since that time, the radiological signs of intervertebral disc and other changes in the spine have progressed as could normally be expected with the passage of time, but this does not mean that his function is compromised by this process. It could be anticipated that his spine would become stiffer as has been demonstrated when the ranges of movement of the spine were quantified but there is no reason to suppose that he would have pain from this cause. 
A much more probable explanation for his continuing low back pain is damage to the soft tissues of the lumbo-sacral junction causing a lumbo-sacral strain syndrome. (ref 2). The precise cause of the pain cannot be identified with confidence but the presence of well localised tenderness at the site of attachment of the paravertebral lumbar musculature and its investing fascia and supporting structures such as the iliolumbar ligament suggests that there is some chronic disorder of the soft tissue. 
Mr Cochrane has had continuous pain and reduced functional capacity since his accident in 1984. He had x-ray signs of degeneration in his spine at that time which were asymptomatic and there is no reason to suppose that his present pain is related to this abnormality. He damaged the soft tissues of his spine in 1984, has not received (as far as I can determine) appropriate treatment, and has been assured that his spine is degenerate. I believe that his current reduced work capacity can only be attributed to the acute strain to the spine which occurred in 1984 and which has obviously never resolved. ”
The appellant does not pursue the point that pain was caused by muscular or ligamentous soft tissue damage. It is generally accepted that soft tissue injury resolves in about 6 months in all but a small proportion of cases. As I understand the appellant's position, he continues to rely on Dr Burry's opinion as one of the possible injury causes of chronic back pain, but the appeal is based principally on orthopaedic opinion concerning damage to the disc at L4/5. The appellant also relies on Dr Burry's report that despite well developed degenerative changes in his lumbar spine he had never been incapacitated by back pain. 
Dr Burry was then furnished with Mr McMillan's opinion stating that Mr Cochrane had in fact experience repeated episodes of low back pain requiring short periods off work after the accident when he was aged 18. The history remained that until the 1984 episode he had had no bother from his back for about ten years. After reading that opinion, Dr Burry's views were unaltered. In relation to emergence of symptoms, he said: 
“Mr McMillan's opinion expressed in 1986 with respect to the significance of degenerative changes of the spine and their correlation with symptomatology was the accepted view at that time and it is only in recent years that more critical appraisal of the correlation between the appearance of x-ray visible degenerative changes and symptoms of spinal dysfunction such as pain and disordered movement has been critically evaluated. As noted in my original report we now know that little or no correlation exists. ”
The main support for the appellant's claim is from Mr M R Fosbender, orthopaedic surgeon at Invercargill, who examined Mr Cochrane and wrote a report on 15 September 2000. He wrote: 
“My view of the CT scan is that the facet joints show marginal change at best, the discs do not show any real impingement or compression. Review of the scout film of the CT scan demonstrates perhaps a hint of narrowing at L4/5. The thoraco-lumbar junction demonstrates a very slight degree of wedging and not to the extent to diagnose Schuermann's disease. ”
His opinion was that the appellant's current incapacity is directly linked to injury sustained in 1984. Part of this report is set out at length as follows: 
“Annular tear 
This man has ongoing discogenic low back pain. This is mechanical in character associated with activity and tending to settle with rest, but with certain postures of rest promoting pain such as sitting. The pain is confined to the low back. It does not radiate in to the lower limbs. The onset of his symptoms is dated from the time of his injury which was severe. He was lifting with other men a very heavy engine and he stepped into a hole, lurched and took much of the weight of the engine himself. This especially while lifting in a bent fashion would have provided considerable force onto the low lumbar spine to provide a tear and disruption of the annular ligament of one or more discs. The ongoing pain from this injury has become chronic and thus, the very nature of this pain suggests it to be discogenic. 
He has undergone investigations. Those done at the time of injury demonstrated that there were changes of disc narrowing at the level L5-S1 soon after his injury. There was also suspected to be degenerative changes in the posterior joints of L4-5. The disc itself (L4/5) was intact. Over the years there has been slow, but progressive change in the x-ray investigations done on his back, but the investigations are rather sparse. The Chiropractors x-rays, which are not well penetrated were carried out in 1990 and demonstrated the level L5-S1 to be narrowed and sclerotic. The remainder of the spine appeared normal in these x-rays. There was no obvious or advanced changes at the level L4-5. A CT Scan was carried out in 1995. The salient points of this scan was that he had well established narrowing at L5-S1 and posterior degeneration, that is degeneration of the apophyseal joints at 3/4, 4/5 and L5-S1. These changes are consistent with the aging spine and do not indicate the origin of his pain and nor are they out of the ordinary with an aging spine. The changes therefore cannot predict that there would be chronic and incapacitating pain. 
Severe injury can promote changes and symptoms associated with this when the soft tissue damage is bad enough to provide the biochemical, inflammatory changes and instability which occur at disc and joint level. I would therefore state that the evolution of the degeneration within his spine is not of itself consistent with the prediction of incapacitating pain. 
There is not enough investigative evidence to be accurate with the source of this mans pain. To improve the accuracy an MRI Scan should be carried out. 
This man after his injury had chronic low back pain. He did undergo reasonable rehabilitation, getting back to work that he could cope with although on a part time basis (Reduced hours). It was only when the nature of his employment changed that he was no longer able to cope. His situation is unchanged to this day. He feels that he could cope with work provided similar to his first job as Forecourt Attendant, but without having to be involved in heavy mechanical work. It would have been reasonable for the ACC to have worked with this man to have rehabilitated him into similar work once his previous job had altered conditions and caused him to lose it. 
The current incapacity that this man has is directly linked to the injury sustained in 1984. The process of pain was started with the accident and has continued since. The progress of radiologic degeneration has been slow and the most recent update in 1995 indicates a common finding in a man of his age group and cannot be correlated or predicted to be painful in the absence of injury. In the population age group of 60 years, 40% of those x-rayed for reasons other than spinal pain would have changes of degeneration and have no incapacity or disability from chronic low back pain. This man demonstrated degenerative changes on x-ray at the time of injury and therefore had these changes prior to injury yet had no significant history of back pain which shows that the process as a radiologic finding is not correlative of low back pain. I therefore disagree with the idea that the progressive radiologic change in this man's case resulted in his incapacity and that it is a natural event of age. An extension of such logic would predict that 40% of the population at 60 years of age would have some degree of incapacitating low back pain which simply is not the case. 
The assignment of proportion of incapacity to injury and other factors by prediction of future change is invalid as the events are now set in motion by the injury and incapacity provoked by the injury. 
The prediction has also been made that if this man had a ‘normal’ back at the time of injury then he would have recovered to full work capacity. The statistics on significant back injuries including information published by the ACC in Medical News sheets demonstrates that 3% will go on to have a degree of chronic low back pain with incapacity. I therefore could not support the idea that such an optimistic prediction of recovery in this man's or in other cases of initial significant back injury. ”
The basis of Mr Fosbender's opinion was that spinal degeneration was not a predictor of pain and therefore it could not be counted as the cause of Mr Cochrane's condition without further evidence. I have included his comment on the 3% occurrence of chronic back pain, but the paragraph does not distinguish between injury and non-injury cases. Mr Fosbender noted that the symptoms dated from the time of the injury which he described as severe and involved lurching and taking most of the weight of the engine when stepping into a hole while lifting in a bent fashion so that there would have been considerable force on the low lumbar spine to cause a tear and disruption of the annular ligament of one or more discs. He said that the ongoing pain had become chronic and the nature of the pain suggests it to be discogenic. 
Mr Fosbender considered that the degenerative changes are consistent with the ageing spine. Mid-life degenerative changes are more or less normal and they are not associated with pain. Pain is more closely associated with the consequences of tears in the annulus. The onset of pain which developed into chronic pain and which began with a lurching accident capable of producing an annular tear is evidence of discogenic injury caused by the accident. 
Mr Theis wrote another report on 21 November 2000. He acknowledged the literature showing that degenerative changes in the lumbar spine are not inevitably accompanied by symptoms and stated that he agreed. But he went on to link that with the fact that most cases of acute low back pain, whether with or without underlying degenerative changes, settle with minimal intervention within 6-12 weeks. Less than 5% will continue to suffer from ongoing back pain. They are classified under the chronic low back pain group for which it is well recognised that the cause of ongoing back pain is multi-factorial. For that group, no specific localised abnormality in the lumbar spine has been identified which correlates reliably with the back pain. 
He commented that the reported incidence of low back injuries is significantly higher in New Zealand than in other countries without an accident compensation system. A paper by Harry McNaughton in the New Zealand Medical Journal showed that individuals with acute low back pain on earnings related compensation do not recover as well from their low back problem compared to individuals who are not on earnings related compensation. 
Mr Theis went on to distinguish this case from that of somebody suffering acute back and leg pain on the basis of a single level acute disc prolapse with evidence of disc material pressing on the nerve root. That is of course the central problem. The appellant cannot point to an observed change demonstrating injury by accident in 1984. The appellant's case is that the change could not have been observed by plain x-ray. Mr Theis stated the problem in this way: 
“Although I agree with Robertson and Nicholson that degenerative changes will not inevitably be accompanied by symptoms I disagree with the concept that degenerative changes in the presence of a previous back injury are automatically discounted and any ongoing back pain related to the initial injury. As far as I can tell it is very difficult to establish the exact anatomical damage done at the time of the injury except perhaps a fracture or an acute disc prolapse with an MRI showing compression of a nerve root and in all other circumstances the anatomical damage caused by the injury is unclear and to link any ongoing back pain to this unknown anatomical damage is pure speculation. The presence of degenerative changes on x-rays or on MRI demonstrates structural abnormalities in the lumbar spine with a potential source of symptoms and if this correlates with the clinical findings then a link is clearly established. It is also clear that there are degrees of degeneration and the studies of asymptomatic subjects show the radiological changes of degenerative disease to be very localised and minor in nature whereas in cases where there is severe disc degeneration, accompanied by facet joint arthritis and if this is localised at more than one level, then it is much more likely that ongoing back pain following an injury is likely to be caused by degenerative disease. ”
Mr Fosbender in turn considered Mr Theis' opinion and report. He restated that it is incorrect to associate appearances on x-ray with the cause of back pain. He referred to an article mentioned in the exchange of opinions, that an article by Robertson & Nicholson in the New Zealand Medical Journal 28/1/2000 to the effect that there is a normal ageing process within the lumbar spine and that the process of change termed degeneration, is inevitable, and that radiologic change cannot predict symptoms and disability with x-ray abnormalities being equally distributed amongst those with low back pain and asymptomatic individuals. The article accepts that some findings of change within the spine are relevant and can be correlated with symptoms, but this requires careful clinical history and clinical examination of the patient. 
Mr Fosbender noted that from the time of x-rays in 1984 the level L5-S1 hardly changed and the levels above that were normal at the time of the injury, including L4-5. When a CT examination was done in 1995, the level L4-5 had changed to progress to narrowing. That is consistent with post-injury degeneration. He said: 
“It is undoubted that degeneration is causing this man's pain. The degeneration is within the lumbar spine at disc level, mainly the level L4-5 since it involves change since the accident, and the bulk of the pain originates from the disc itself (discogenic pain). The cause is injury. ”
He referred to two prevailing theories in a text The Adult Spine, Principals and Practice, Second Edition, Frymoyer Et al, published 1997. Mr Fosbender summaries those theories as follows: 
“The first being of acute compressive mechanical overloads causing disruption of vertebral end plate going onto accelerate degenerative change to cause pain. 
The second theory is based on the occurrence of back pain after incidents involving flexion and torsion injury, it places the posterior annulus (the ligament confining the disc within the spine posteriorly) under stress. It is stated that there is evidence suggesting that the peripheral annular tear to be of prime importance in the development of discogenic pain following this trauma. It has been demonstrated in an animal model that the tear of this ligament leads to further failure and nuclear degeneration. 
It is thus stated that discrete peripheral tears of this ligament will have a role in the formation of further tears and accelerating degenerative processes within the disc. This demonstrates that trauma is indeed very significant in the evolution of degeneration within the disc within the lumbar spine and the process on going is similar in radiologic appearance in every way to the asymptomatic changes of age related degeneration. The process after injury evolves with break down of the annular ligament, nuclear degeneration, end plate changes and secondary facette degeneration. All these will contribute to the process of pain to some degree. This is the process that Mr Cochrane has undergone to evolve to the current situation. 
I would therefore state that Mr Cochrane indeed had a significant accident with sudden heavy loading of his spine in a lifting posture and that the whole process evolved to give on-going pain to present day. Mr Theis is not correct when he states ‘that the most common cause at his age of low back pain is degenerative disease’ if he is stating it is in the absence of injury or insult. 
It is clear from the publication by Robertson & Nicholson, who have surveyed the literature to give this opinion, that with increasing years radiologic changes of aging is universally increased, yet symptoms become less prevalent after middle age. ”
Mr Fosbender stated that plain x-rays could not have shown evidence of an annular tear. He said: 
“Degeneration is the final common pathway of progressive soft tissue injury within the lumbar spine. Degeneration whether caused by injury or has progressed purely on relationship of age cannot be identified separately in its advanced form using plain x-ray. Yet it is correlative that injury will promote the symptoms and merely age related change will not. 
I would therefore state that this man has the evidence of his injury, had the evidence of no symptoms prior to his injury and that the process has progressed since, and the only progress on x-ray correlation is that of the level L4-5 which has gone onto narrow, where as the level changed previously has progressed very little in the way of change. The underlying process is of annular tear has promoted degeneration causing his on-going symptoms, the basis of which is trauma, and this is differentiated from the age related changes which cannot be correlated as being predictive of pain and disability. ”
Mr Fosbender provided two further reports. The first, in response to the respondent's written submissions in the first District Court appeal, was dated 9 April 2001 in which he said “the desire of the Legal Officers to seek absolute evidence of injury in any such situation of low back pain is impossible to satisfy. It simply cannot be done and therefore the inference has to be taken from evidence in the literature that I have supplied.” The second was date 10 October 2005 and in which he restated his opinion and wrote: 
“The changes that accumulate with age are not predictive of pain. The changes of injury cannot be differentiated from the changes of age unless there is some associated fracture, soft tissue usually not being seen on plain x-ray, therefore mere x-rays are not predictive of the origins of pain simply because of the appearance of degenerative change. The predictors are taking careful clinical history and examination, and correlating the radiographic changes with that and backing them up with MRI scan in modern day. 
The changes of inflammation are generally different and can be diagnosed as to the cause. 
Mr Cochrane falls into the category of having low back pain from injury in which he has had changes on x-ray, which would be termed degeneration, and this is caused by injury. His condition is obviously painful. ”
Mr Theis responded in a report on 27 February 2006 and leave was granted for Mr Theis to give evidence at the hearing of the appeal. Mr Theis reiterated that the appellant's back was not normal at the time of the accident. His view that the Mr Fosbender's opinion of an annular tear was simply based on Mr Cochrane's symptoms without any other support. He said that if MRI imaging had been available in 1984 it might have shown chronic L4/L5 disc changes indicating pre-injury disc disease. He said: 
“Degenerative or age related disc disease results in structural failure of the disc by loss of hydration and annular incompetence leading to a generalised disc bulge which is well demonstrated on CT or MRI. This was certainly a feature of Mr Cochrane's CT scan carried out in 1995. 
As Mr Cochrane did not have any leg pain or neurological abnormalities of nerve root pressure it is clear that he did not have a disc prolapse as a result of the 1984 injury. There was also no evidence of a fracture as seen on plain x-rays. ”

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