Apelt and Telstra Corporation Limited
[2005] AATA 602
•24 June 2005
Administrative
Appeals
Tribunal
DECISION AND REASONS FOR DECISION [2005] AATA 602
ADMINISTRATIVE APPEALS TRIBUNAL )
) No Q2002/601
GENERAL ADMINISTRATIVE DIVISION )
Re RONALD JAMES APELT Applicant
And
TELSTRA CORPORATION LIMITED
Respondent
DECISION
Tribunal Dr EK Christie, Member Date24 June 2005
PlaceBrisbane
Decision The Tribunal affirms the decision under review. This means Mr Apelt’s application for review is unsuccessful. ...................[Sgd]......................
EK Christie
Member
CATCHWORDS
COMPENSATION – Commonwealth employees – spondylolisthesis - progression of deformity following spinal fusion – spinal malalignment – nerve root compression – low back pain –expert evidence: proof of causation and workers’ compensation legislation – expert evidence: accepted body of knowledge
Safety, Rehabilitation and Compensation Act 1988 ss 4, 14, 16, 39
Briginshaw v Briginshaw (1938) 60 CLR 336
Dahl v Grice [1981] VR 513
EMI (Australia) Ltd v Bes (1970) 2 NSW 238
O’Neill v Commonwealth Banking Corporation (1987) 13 ALD 234
Clark v Ryan (1960) 103 CLR 486
R v Lucas [1992] 2 VR 109
R v Runjanjic (1991) 56 SASR 45
Casley-Smith and Ors v FS Evans & Sons Pty Ltd and Anor (No 1) (1988) 49 SASR 314
Caswell v Powell Duffryn Associated Collieries Ltd (1939) 3 All ER 722
R v C (1993) 60 SASR 467REASONS FOR DECISION
24 June 2005 Dr EK Christie, Member 1. This is an application by Ronald Apelt for a review of the decision made by Paul Johnston, Senior Claims Officer on 16 May 2002 who found that liability to pay compensation in respect of the L5/S1 spondylolisthesis claimed on 7 March 2002 did not exist. In addition, that there was no liability, pursuant to the provisions of section 39 of the Safety, Rehabilitation and Compensation Act 1988 (“the SRC Act”), to pay compensation in respect of the provision of a special bed and frame.
2. The evidence before the Tribunal comprised the documents filed pursuant to section 37 of the Administrative Appeals Tribunal Act 1975 (the “T” Documents) [Exhibits R1, R2] and the various exhibits lodged by the parties.
3. The applicant was represented at the hearing by Mr A Harding of Counsel. The respondent was represented by Mr C Clark of Counsel.
4. The non-disputed facts before the Tribunal were that Mr Apelt commenced employment with Telstra on 12 January 1976 and resigned from Telstra on 23 November 1987. Mr Apelt had posterior L5/S1 lower back orthopaedic surgery in January 1977. In September 2004 he had further orthopaedic surgery in relation to the lumbosacral spinal fusion at L5/S1 that had been performed in January 1977. The surgery in September 2004 was performed by Dr P McCombe, the Orthopaedic Surgeon called to give expert evidence in relation to the applicant’s case.
Issues Before The Tribunal
5. The only issues for the Tribunal to decide were whether the respondent was liable to pay compensation to Mr Apelt under the provisions of the SRC Act in respect of lower back/spondylolisthesis; and an ancillary issue, whether the compensation would include provision of a Queen Size Sealy Bed and nexus frame.
§ Expert Evidence: Dr Peter McCombe (Orthopaedic Surgeon)
6. Dr McCombe provided the following explanation for the issue of development of nerve root compression in Mr Apelt (Exhibit A14, p.2):
“In attempting to identify why Mr Apelt’s symptoms of nerve root compression should develop many years after his fusion I considered the possibility that the deformity of the spondylolisthesis had increased ‘despite his fusion’. I could not conceive of any other reason for him to develop late stage L5 nerve root compression apart from increasing deformity. Another factor which led me to consider this possibility was the end stage disc degeneration at the L5/S1 disc. The disc was exceptionally narrowed with almost bone on bone contact. It is not my experience that disc degeneration of this rarity is present in adolescents at aged 19 years who present with symptomatic spondylolisthesis. Disc space degeneration usually occurs with this condition (in the absence of fusion) in middle age with the disc degenerating prematurely sometimes in the thirties or forties. Furthermore, it is well known that when progression of deformity occurs due to disc space degeneration in this age group, the L5 nerve root compression frequently becomes symptomatic. Dr Licina, in his report dated 4th November 2004, acknowledges that, ‘further slip can occur throughout adulthood, the primary cause being loss of disc height at L5/S1’.
I therefore considered on the basis of the development of L5 nerve root symptoms later in life and, given the presence of L5/S1 loss of disc height that further deformity occurring at the site of the spondylolisthesis had probably occurred. The only way to really refute this argument would be the presence of an x-ray report, or x-rays, that suggested that he had a similar degenerative disc at the time of his spinal fusion.
If one accepts the notion that further deformity of the spondylolisthesis has occurred despite the presence of a postero-lateral fusion, one has to accept that there was plastic deformation of the fusion. Whilst this is not necessarily likely it has been reported and I consider this a possible explanation. When looking for further evidence to support the theory that further deformation, despite his spinal fusion, occurred, I was led to the conclusion that the development of his abnormal posture with flexed hips and knees, and a loss of lumbar lordosis was also consistent with this theory. In other words, I formed the view that on my first examination, he had evidence of a subtle form of fixed sagittal malalignment and L5 nerve root compression. The only theory that I could think of that explained the late development of both of these conditions would be an increase in the deformity at his spondylolisthesis.” [Tribunal emphasis]
7. In relation to his methodology for evaluating and the measurement of sagittal malalignment, Dr McCombe stated (Exhibit A14, p.3):
“Dr McPhee states in his report that the measurements I have used should be taken from the upper end plate of L5 rather than the endplate of the sacrum on the basis that, with the presence of a deformity of spondylolisthesis, it is no longer valid to use the baseline measurements at the top of the sacrum. It is quite clear that by changing the reference points that the various angular measurements can be seen to be quite different. If one measures from the top of L5 the various parameters can become normal. If one measures from the top of the sacrum various parameters are abnormal. I believe that Dr McPhee, in his report, is quoting a consensus statement from the scoliosis research society about the reference line to measure sagittal balance in patients with spondylolisthesis.
I am not certain that Dr McPhee and myself are in fact disagreeing. In fact we may be talking about the same condition from a different perspective for the following reasons.
Proper understanding of sagittal balance, and subsequently imbalance, has only recently become clear. The main reason for this is poor understanding of what represents a normal lumbar lordosis. There is a quite a large range in the normal population of lumbar and thoracic lordosis. The problem when one sees a patient with a small lumbar lordosis is to decide whether this is the lower end of the normal range, or whether this is truly an acquired condition that can cause pain. A significant breakthrough in this regard has been made by various French authors including Beaupere, and more recently Jackson. The important finding was that there was a good correlation between lumbar lordosis and a line drawn between the midpoint of the hips and, either the posterior portion of the sacrum (Jackson), or the perpendicular bisector of the upper portion of the sacrum (Beaupere).
The importance of this finding is that this angle is present at birth and is not changed by any degeneration or deformity because the angle is measured within the pelvis.”
8. Dr McCombe then offered the following conclusions that had largely been used to justify the surgical management of Mr Apelt’s condition (Exhibit A14, p.4):
“In conclusion, I offer the following theory in Mr Apelt’s case which has largely been used to justify surgical management of his condition. This theory may or may not have value in the management of his legal case.
I believe Mr Apelt, at the time of his spinal fusion at L5/S1, had a reasonably normal or only partly abnormal disc height. Following a postero-lateral fusion further deformity has occurred at the spondylolisthesis and this has caused two conditions:
- compression of both L5 nerve roots
- subtle sagittal imbalance
Both of the above mechanisms have been responsible for causing pain. I believe to some extent this theory has proved to be correct by the fact that his symptoms have improved following decompression of the L5 nerve roots by partial restoration of the deformity of the spondylolisthesis.”
9. In his final report (Exhibit A16), Dr McCombe expressed the following opinion:
§ that Mr Apelt had a low grade spondylolisthesis treated as a young man by postero-lateral fusion;
§ that there was reasonable evidence to suggest that the deformity of the spondylolisthesis had increased by plastic deformation of the fusion mass;
§ that the plastic deformation had led to chronic back pain and bilateral leg pain caused by compression of the L5 nerve root;
§ that for the deformity to develop, a load (or force) must be applied to the L5/S1 level;
§ that performing heavy manual work, as described by Mr Apelt in his employment with Telstra, would increase the load across his spine;
§ that it was reasonable to assume that Mr Apelt’s work activities with Telstra have ultimately been partly responsible in producing the final deformity;
§ an acknowledgement that there were alternative explanations for Mr Apelt’s observed deterioration with respect to pain; that there has been pain originating from the disc above his fusion (the L4/5 level); or from damaged muscles by scarring produced by the original operation. However, the fact that deformity appears to have occurred led him to have a significant preference for the “deformity theory”, rather than the alternative explanation.
10. In his oral evidence, Dr McCombe expressed the following opinion:
(a)That there was both clinical and radiological evidence to support his conclusion that Mr Apelt suffered from L5 nerve root compression. Whilst there was a large quantity of fat behind and in front of the nerve, on the MRI images he could not see any fat above and below the nerve.
(b)That he was “not suggesting that [Mr Apelt’s] employment has caused his spondylolisthesis”;
(c)An acknowledgement that his opinion, in relation to “further deformity”, was a “supposition” on his part as there was no starting point upon which to determine the loss of disc height over time: “[without] an x-ray, it is a bit hard to know”. In expressing an opinion about loss in disc height over time, he conceded that he had been “absolutely hypothesising”. Dr McCombe stated:
“Just my theory suggests that, at some stage, this deformity has occurred. We are a little unclear about when it has occurred. In formulating this theory, I’ve based it on my understanding of his history, which has probably occurred at roughly at the time he developed the increasing symptoms which I felt was before ’98, but I could accept that if the facts of the matter are different, but, my understanding was that it was somewhat before then. So how this deformity occurred, whether it was rampant and then stopped, or whether it was progressive, I don’t know.
And secondly, the loss of disc height in that period of time goes to accuracy of measurement, so if you were to produce those x-rays, it would suggest within the limits of accuracy of measurement that deformity hadn’t much occurred in that time.”
11. Dr McCombe was asked by the Tribunal about the objective basis for his opinion that, at the time of his spinal fusion at L5/S1, Mr Apelt had a “reasonably normal or only partly abnormal disc height” at the time of his spinal fusion; also, as to his further opinion that “further deformity at the [L5] site had probably occurred”. Dr McCombe conceded that a plain x-ray would help in looking at this question of disc height. He agreed that an x-ray would “absolutely clarify the situation” stating that “if we had an x-ray in 1977 after the fusion then … it would absolutely either refute or support this argument 100 per cent”. However, he stated that the x-rays from August 1976, March 1978 and March 1979 were not available as far as he was aware.
12. Under further re-examination by Mr Clark, Dr McCombe conceded that it was only a theory on his part that Mr Apelt had a reasonably normal or only partly abnormal disc height at the time of his spinal fusion. This was the case because of the absence of x-ray images of this time as the x-rays were the essential starting point for his opinion of a loss in disc height over time.
§ Expert Evidence: Dr Paul Licina (Spinal Surgeon)
13. In his first report (Exhibit R8(b), 8 April 2003), Dr Licina states:
“I understand that he had an isthmic spondylolisthesis at L5/S1, a developmental condition which occurs before age ten and a slip occurs in teenage years. It seems that an injury caused some sort of disruption to the area with pain and was treated appropriately with a fusion.
I understand now he has increasing back pain which is worse on sitting. He described to me the exercises he performs. I looked at the x-rays and saw that he had normal age-related changes at the discs above the level of fusion and there was no evidence of any accelerated degeneration. I told him that people with his condition, whether they have a fusion or not, are pre-disposed to back pain…
I also told him that the bulk of evidence suggests that a spinal fusion does not lead to accelerated degeneration at the levels above and in those who do have this, it is a multi-level problem due to constitutional factors rather than increased biomechanical stressors on any one particular level.”
14. In a further report (Exhibit R8(a), 4 November 2004), Dr Licina concluded that his diagnosis for Mr Apelt was of a non-specific low back pain in the presence of pre-existing L5/S1 spondylolisthesis treated with spinal fusion. Dr Licina then expressed the following opinion:
“Mr Apelt suffered an aggravation of a pre-existing back condition, namely L5/S1 spondylolisthesis. He underwent spinal fusion, with good results. He has continued to have low back pain, which has increased in severity without obvious cause. The most likely explanation is age-related low back pain, possibly associated with degeneration of the lumbar spine. I can find no evidence that the surgery has negatively influenced the natural history of Mr Apelt’s back condition. With regard to background, isthmic spondylolisthesis is a condition that is relatively well understood. The most common form is associated with pars defects. These are thought to be stress fractures in part of the L5 vertebra. These are due to a combination of factors, of varying significance, depending on the individual. The first is a congenital variation where the bone is weak or the biomechanical forces through the area are increased.
The second is repeated activities, especially hyperextension, which load the spine in the susceptible area, leading to a stress fracture. These fractures usually occur between age five and ten years. They are often not associated with any symptoms at the time. During adolescence the L5 vertebra slips forward on S1. This is because the normal supporting structure of the posterior elements has been disrupted. The majority of this slip occurs by the end of spinal growth at about age 18 years but further slip can occur throughout adulthood, the primary cause being loss of disc height at L5/S1. The L5/S1 disc in the majority of people with this condition degenerates more rapidly than usual because of the increased load on the disc. The incidence of back pain is increased in people with a significant spondylolisthesis as would have been the case with Mr Apelt. The onset of back pain is often due to a trivial event, or, it can be due to a more major force on the spine. Usually however it is considered that this event has bought to light the problem rather than causing it in the first place. There are a number of mechanisms by which this can occur. The first possibility is that the spine has undergone a fibrous union of the pars defect and has stabilised. The event that causes pain may disrupt this fibrous union. The second possibility is that there is an annular tear to the intervening L5/S1 disc which has already undergone some premature degeneration. There are other possibilities, but in Mr Apelt’s case it is likely that either there was a disruption of the fibrous union or an annular tear.”
and:
“I would also agree with Dr McPhee’s report. I would agree with his subsequent reports regarding ‘flatback syndrome’ and spinal alignment. I would not entirely agree with Dr Pentis’ report. He states that it is common to find aggravation of the discs above a fusion. The literature is contradictory but there are certainly well designed studies that show that a fusion does not pre-dispose to further degeneration. Conversely it is believed that the process that caused the degeneration in the first disc continues and this is why the subsequent discs degenerate. I would also not agree with the fact that if there is degeneration in the spine that long term problems are likely to continue. As previously stated, degeneration does not correlate well with back pain. I would also not agree with the statement that the treatment (the fusion) has resulted in subsequent degeneration.
I am unable to agree with Dr McCombe’s report. However, I did not have the benefit of having reviewed the patient to have observed them standing, nor to have reviewed the imaging. I accept the point that it is possible that Mr Apelt has an altered posture and that this could be seen as contributing to his back pain, however I cannot agree that he has ‘flatback syndrome’. ‘Flatback syndrome’ is a condition which is mainly seen after treatment of scoliosis with first generation instrumentation, namely Harrington rods. This distraction in instrumentation would often cause the loss of the normal lumbar lordosis with subsequent degeneration below the fusion and pain. An L5/S1 fusion is normally not associated with ‘flatback syndrome’. When one looks at the x-ray of the spine, the degree of kyphosis at the L5/S1 slip is minimal. I would also not agree that the erect x-rays can be interpreted using normal controls, as Dr McCombe has, as the sagittal balance has been compromised by the original slip. I would not agree with his surgical suggestion of performing a posterior lumbar interbody fusion. I am unable to see how this would significantly alter the overall lumbar alignment nor how it will significantly improve Mr Apelt’s pain.” [Tribunal emphasis]
15. In his final report (Exhibit R11, 12 January 2005), Dr Licina states:
“Overall, my opinion has not changed. Dr McCombe in his report outlines the concepts of flat back deformity and lumbar sagittal alignment. These are complex issues that are incompletely understood, not agreed upon and are still evolving. Overall I could not convince myself that Mr Apelt’s spinal fusion could have changed enough to make his spine mal-aligned to the point where he developed symptoms as a result of this that required corrective surgery. It is much more likely that his back pain is associated with the normal ageing process.”
16. In his oral evidence, Dr Licina gave the following answers to questions:
(a)In terms of whether further deformity had occurred following posterior lateral fusion, Dr Licina was not familiar with any medical literature that would support this.
(b)In terms of the proposition that further progression of the deformity would be caused by workplace activities in Telstra from 1978 to 1987, compared with 1987 to 2003, he stated that “things happening to the current time would have a greater effect than that which occurred back then”.
(c)On examining the diagnostic radiology he stated that “I don’t know that the [further] deformity could occur” and “I didn’t see one”.
(d)That the issue of saggital imbalance was an evolving field of study and a concept which was “not mainstream thinking where everyone accepts its validity”.
(e)That the methods for the measurement of sagittal imbalance in a normal person were “not quite agreed upon” and in Mr Apelt’s case there were two factors (vertebrae slip and inclination of his pelvis) that made measurement imprecise and difficult to interpret.
(f)That his assessment of Mr Apelt was inconsistent because the clinical picture did not specifically point to L5 nerve root compression. There was no firm proof that a “specific nerve root” was involved and that he would need more evidence to make a specific diagnosis of L5 pain.
(g)He qualified the above conclusion with the following statement:
“It [the proposition of a degree of entrapment at the L5 nerve roots bilaterally] certainly is possible, according to the description of the symptoms and the x-rays, that L5 is responsible with regard to compression for the symptom. However, the fact that there is narrowing of the foramen in a fused spine often means – and I would say more often than not means that the nerves aren’t causing the pain, as well as the symptoms described. So if I were to be deciding on whether to operate or treat this man on the basis of his L5 symptoms, I wouldn’t say that there is enough evidence to be confident that the L5 nerve root compression is the cause of his symptoms.”
(h)That he could not accept the applicant’s proposition that “it would not be unexpected for the [L5/S1] disc to be somewhat narrowed at age 19” without seeing x-rays of an earlier time at age 19.
(i)That he agreed that the only real way to know if there had been further degeneration of the disc at L5/S1 leading to it becoming narrower would be to view an x-ray around the time of the spinal fusion.
(j)That a discogram was a test that was a source of controversy amongst surgeons – specifically, the fact that it was subjective and the findings were based on the response by the patient i.e. responses that could not be measured.
(k)That in the absence of a “complete discogram” he could not place “complete confidence” in the findings to clearly say that the L4/5 disc was – or was not, the main source of pain for Mr Apelt.
(l)That there was no correlation between the degree of back pain and the degree of degeneration found in Mr Apelt. “Whilst the MRI suggests that there is degeneration” the “discogram [suggests] that the degeneration isn’t severe or painful. So the two don’t go together….the two pieces of evidence do not match”.
(m)That the progression of degeneration in the spine is “something we know for a fact and we certainly understand degeneration well”. There is no evidence that the natural progression of degeneration in the spine is significantly affected by one’s occupation. Moreover,
“If we then wish to extrapolate that to this theory of plastic deformation, which I don’t agree with, and look at what work may have done to that, then it’s reasonable to assume that, similarly, the loads placed on the spine from – from one’s occupation wouldn’t have a significant effect on those bio-mechanical loads either.”
(n)That he disagreed with the proposition that when Mr Apelt was performing his workplace activities with Telstra that caused him back pain, the extra load had an impact on Mr Apelt’s back. Dr Licina provided the following explanation:
“It is known that in manual workers the episodes of back pain are more common than those who are sedentary but there is no increase in the measurable amount of degeneration or other ill effects of load on the spine. In other words, I accept that his work would have caused the symptoms of back pain but I cannot accept that his work would have caused any structural change to his spine over a period of time, be it to the discs that aren’t in the fusion or even less so to the fusion itself.”
§ Expert Evidence of Associate Professor Bruce McPhee (Spinal Surgeon)
17. Dr McPhee provided a number of expert reports in this application for review over the period August 2003 to January 2005 (Exhibits R4, R5, R7 and R10). The latter report (Exhibit R10, 28 January 2005) consolidates much of the earlier reports together with further conclusions made in relation to Dr McCombe’s final report (Exhibit A16, 18 February 2005).
18. It was Dr McPhee’s opinion that Mr Apelt’s spondylolisthesis was developmental in origin and predated the onset of any back pain in the 1970s. Aggravation of the spondylolisthesis may have arisen either from heavy physical work or from an injury whilst employed with Telstra.
19. He referred to the specific propositions of the applicant: that some 20 years after his posterolateral fusion for a spondylolisthesis of L5/S1 in 1977, Mr Apelt had presented with low back pain and leg pain which the applicant claims to be causally related to the spondylolisthesis; and that the pain Mr Apelt now suffers arose as a consequence of his spinal fusion. That is, because of a malalignment resulting in saggital imbalance of the trunk.
20. Dr McPhee’s reviewed the literature in relation to the assessment and measurement of sagittal balance (i.e. as a radiological determination) and concluded:
(a)“Sagittal balance is measured as a relationship of the C7 plumb line to the pelvis in the standing position. It is most commonly measured in relationship to the sacrum. This line is not the axis of gravity which probably lies a little more anterior. There are a number of pelvic and spinal perimeters which relate to spinal balance such as pelvic incidence (PI), sacral slope (SS), pelvic tilt (PT) and lumbar lordosis (LL) which can be measured to quantify posture and its relationship to sagittal balance (Appendix 1).
(b)Pelvic incidence and the other associated perimeters (sacral slope, pelvic tilt and lumbar lordosis) are radiological research tools for quantifying posture. They have not been used as a factor in determining the treatment of a patient with low back pain. The range of normal has been defined for people with no structural abnormality of the spine.
(c)Where structural abnormality exists, these radiological perimeters differ from a normal population. In the case of spondylolisthesis, the pelvic incidence angle is greater than normal and corresponding, apparently abnormal changes occur in the other radiological parameters. All radiological parameters in a patient with spondylolisthesis differ from the ‘normal’ range.
(d)At the other end of the age spectrum, it has been shown that with aging comes an anterior shift of the C7 plumb line (loss of sagittal balance) and a loss of lordosis.
(e)Care must be taken in interpreting the C7 plumb line and its relationship to the sacrum as a measure of sagittal balance. These radiological parameters vary with age and spinal abnormalities. A number of researchers have questioned the accuracy of these radiological parameters which can vary with change in arm position. The accuracy and relevance of the vertical axis as a measurement of sagittal balance in spinal deformity therefore remains questionable.
(f)Once a lumbosacral fusion has been done the fused segments constitute part of the sacrum. The first motion segment above the fusion is now the new lumbosacral junction because spinal adjustment to restore balance occurs at this point. Hence in a lumbosacral fusion, all measurements should be made from the centre of the upper end plate of a fused lumbosacral spine. By my estimation when the upper end plate is used in the determination of pelvic incidence, sacral slope and pelvic tilt, the measurements are within the limits of the ‘normal’ population indicating balance has been restored.” (Exhibit R10)
21. In relation to his analysis of the medical evidence, as well as his review and analysis of the literature, Dr McPhee expressed the following opinion with respect to two key issues relating to the question of saggital balance:
(a)Whether Mr Apelt’s lumbosacral fusion resulted in malalignment and sagittal imbalance:
“Mr Apelt is now at an age where the C7 plumb line would normally be moving forward into a position which by comparison with young norms would be regarded as outside the normal range.
Secondly, a forward displacement of the C7 plumb line and changes in all the radiological parameters of balance is ubiquitous in spondylolisthesis and probably should not be compared with the normal spine.”
(b)Whether Mr Apelt’s spinal fusion has caused significant sagittal balance leading to secondary consequences:
“If Mr Apelt has been fused in a flexed position then his spine should have compensated by extending above the fusion. This would result in adjacent segment degeneration and retrolisthesis. While the MRI shows signal changes consistent with degeneration, [the literature indicates] this finding is unreliable and cannot be definitely correlated with his low back pain….Despite Dr McCombe stating that there is retrolisthesis at L4/5 which could be concordant with spinal imbalance induced degeneration at the adjacent segment, I have viewed these x-rays and would consider that the alignment was within normal limits. The conclusive evidence however is that Mr Apelt underwent L4/5 discography. While a nucleogram was morphologically abnormal, there was no pain response. One can only conclude that despite some degeneration in the L4/5 disc, this disc was not the source of the claimant’s pain.” (Exhibit R10)
22. Dr McPhee concluded that from the evidence available, and having examined Mr Apelt, there was no evidence to support the hypothesis that symptomatic degeneration had occurred at L4-5 due to abnormal stresses arising from spinal malalignment secondary to the lumbosacral fusion.
23. Dr McPhee then considered the applicant’s proposition that Mr Apelt’s leg symptoms and back pain were due to a compression of the L5 nerve roots as they emerged through the lumbosacral invertebral foramen.
24. On his examination of the MRI scan, Dr McPhee stated that there was a halo of fat around the nerve root, although the dimensions of the foramen were less than normal. He concluded that this was entirely in keeping with a spondylolisthesis. However, the presence of the halo of fat was not consistent with nerve root compression.
25. Furthermore, Dr McPhee stated that the radiological evidence of compression was lacking. In addition, no nerve conduction studies had been undertaken notwithstanding that they may have confirmed some nerve root compression.
26. By reference to “well documented” published studies, Dr McPhee further stated that Dr McCombe’s assertions that foraminal compression of the nerve roots was not associated with the physical sign of restricted straight leg raising, were incorrect. He referred to a number of published studies that found the straight leg raising test was positive in a significant number of patients with spinal/foraminal stenosis (Exhibit R10, References n.30, n.31, n.33).
27. Dr McPhee then referred to Dr McCombe’s hypothesis that the foraminal stenosis was the result of progressive degeneration of the lumbosacral disc over time. In his report (Exhibit R10), Dr McPhee states:
“It is misquoted that in spondylolisthesis ‘further slip can occur throughout adulthood, the primary cause being loss of disc height at L5/S1’. This statement is incorrect. What is missing from this statement is the important fact that the ‘natural history of untreated (unfused) spondylolisthesis’ is one of progressive disc degeneration and possible increase in slip. Once a solid fusion has been achieved, the relationship of L5 to the sacrum remains unchanged for the rest of the patient’s life.”
28. It was Dr McPhee’s opinion that, in adults –
“the deformity of spondylolisthesis does not increase once solidly fused. Slip may increase in the few months after doing a fusion before fusion has been achieved (at which time the relationship becomes stable) or in the presence of the non-union. The latter was excluded at the recent operation. Slip progression can increase in children who have had a solid spinal fusion because of plastic deformity. This is a phenomenon peculiar to continuing growth and ceases at maturity.” (Exhibit R10)
29. Dr McPhee acknowledged that Mr Apelt has low back pain. He stated that a fusion of a spondylolisthesis, at the age of 20 years, would not guarantee freedom from low back pain for the rest of Mr Apelt’s life. However, it was his opinion that there was no evidence that Mr Apelt’s low back pain symptoms –
“were due to a junctional degeneration secondary to sagittal malalignment arising from the fusion of the spondylolisthesis over twenty years ago or due to changes in the spondylolisthesis over time and the presence of a fusion is lacking. The low back pain is frequently multi-factorial. Once infection, tumour and fracture have been excluded, there is no certainty of a diagnosis based on radiological findings. Furthermore a favourable response to treatment may be due to a placebo effect rather than successfully treating the cause of the low back pain.” (Exhibit R10)
30. Dr McPhee gave the following answers to questions raised during the examination of his oral evidence:
(a)In terms of whether spinal fusion has caused significant changes to sagittal balance leading to secondary consequences, he stated that the clinician would look at radiological tests for retrothesis and degeneration of that disc. In Mr Apelt’s case, he could find no evidence of retrothesis or degeneration in that disc [L4/5]; this was subsequently confirmed by a discogram which was negative.
(b)Dr McPhee considered the relationship between foraminal compression of the nerve roots and the physical sign of restricted leg raising. His physical examination of Mr Apelt, in this regard, indicated that straight leg raising was 70% bilateral without nerve root tension signs. It was his opinion that it would be “more than likely” for a L5 nerve root compression to be reflected in a positive straight leg raising test. Whilst conceding that “no test on its own” will definitively determine the end result, Dr McPhee stated that a significant number of patients with L5 nerve root compression would have a positive straight leg raising test. Whilst acknowledging that a negative straight leg raising test may be associated with nerve root compression, he qualified his response with the statement that in such a case, other signs would be present.
(c)The medical evidence that occupational hazards caused back pain was not strong. Studies indicated that the “genetic side” [inheritance] associated for at least 70-75% of the problem; back pain arising from work was not strong at all and was around 10-12%.
(d)In relation to nerve root compression at the L5/S1 in Mr Apelt, Dr McPhee’s opinion was that for “true compression and stenosis there should be no fat…the nerve root is not a rigid structure. It’s a plastic structure and you can squash it, you can change its shape”. Furthermore, he disagreed with Dr McCombe’s proposition that the absence of fat on the top and bottom of the root, was indicative of nerve root compression. In addition, “to get compression you have to constrict … you can change shape as long as it doesn’t compress it flat like a strap. Even then, these nerves, a lot of them will continue to function…you have got to be very careful when you start to draw clinical conclusions based on radiological studies that don’t really support the evidence”.
(e)In relation to changes in disc height in Mr Apelt, Dr McPhee opined that once the fusion had occurred at age 19, there would be no change in disc height thereafter. That is, the relationship between L5 and S1, in terms of disc height, today would have been the same as at the time of the fusion.
(f)Dr McPhee rejected the alternative hypothesis of progressive deformity because this could only occur in an adult in two ways: not having a fusion or having an unsuccessful fusion [i.e. a non-union]. Neither of these alternatives existed for Mr Apelt.
(g)Dr McPhee was referred to Dr McCombe’s opinion, that notwithstanding it would be rare for a disc to continue to degenerate in the presence of a fusion - this in fact did occur in Mr Apelt’s case. Dr McPhee did not accept this view stating “You are talking about a hypothesis that I can’t agree with” and If you had told me he had a non-union, yes, I could accept it”.
(h)The opinion of Dr McCombe in relating to saggital (postural) balance was considered. Dr McPhee expressed the view that two established authorities in this area defined imbalance [malalignment] as 5cm shift and “there’s no way in the world [Mr Apelt] is anything like that”.
(i)The correlation between the cause of Mr Apelt’s back pain and posture was “highly theoretical”. Dr McPhee stated that “I didn’t think there’s any published work that’s going to show this”.
§ Expert Evidence of Dr Tony Blue (Orthopaedic Surgeon)
31. Dr Blue’s report (Exhibit R3) was prepared in November 2002. In his report, Dr Blue expressed the following opinion:
(a)the opinion that liability for long-term pre-existing spondylolisthesis at the L5/S1 level be not admitted; this condition would have dated from his early years, probably under the age of 5;
(b)that the spinal fusion performed in 1977 had been highly successful in stabilising the unstable L5/S1 articulation that has existed for many years and that the subsequent transference of stress into levels above has simply allowed normal aging degeneration to occur at these levels.
§ Evidence of Applicant – Ronald James Apelt
32. Mr Apelt was employed by Telstra from 12 January 1976 until 23 November 1987, initially employed as a linesman and later promoted to a line serviceman.
33. During this period he was required to do both technical and physical labour which included – but was not limited to – hand-digging, jack-hammering, carrying ladders, above and on ground work jointing, repairing cables and telephone faults. In addition, the installation of telephone and facsimile services and some storeman duties such as lifting and unloading building materials e.g. cement bags, concrete pits, cable drums, tools, cartons of telephones and other miscellaneous articles. Clerical duties were also involved.
34. Mr Apelt described his work duties as a linesman as involving the installation and repair of telephone services, requiring him to undertake a lot of squatting and back flexion due to the requirement for climbing into ceilings, under houses and carrying heavy timber ladders on site – including through bushland.
35. Mr Apelt further described his work duties from 1978 onwards as duties requiring him to sit for long periods, to crawl within ceiling spaces and under low set houses as well as to manoeuvre himself within very cramped locations. The need to work at ground level often involved jointing or pulling cables through conduits. Another work situation required him to stand on ladder rungs with a safety belt strapped around his lower back whilst jointing cables for extended periods. The rope safety belt was positioned across his L5/S1 transverse scar.
36. Mr Apelt described the events that were associated with injuries to his lower back (see Exhibit A17)
37. Prior to commencing employment with Telstra he sustained a “muscular back strain” on 29 October 1972 whilst using a “Bullworker” exercise device.
38. During his employment with Telstra, he sustained the following injuries to his lower back:
(a)22 March 1976: Muscular strain to the lower back whilst loading wet clay spoil on to the back of a truck. Compensation was received for this condition.
(b)9 August 1976: Lower back injury sustained during heavy labouring work, including jack-hammering and using manual hand tools for excavation.
(c)December 1979: Further difficulties associated with his back when undertaking work duties within a cramped ceiling environment.
(d)August 1980: Bruising to lower back and extensive bruising to other parts of the body after being knocked off his bicycle on his way home from work.
(e)26 March 1986: A lower back strain injury but the actual event that caused the injury could not be recalled. No time was lost from work.
39. After leaving Telstra he sustained an injury on 30 August 1998 when he fell off a ladder whilst removing leaves from a gutter at his home. The vertical height to the gutter was 490 cm. His knee joint hit a handrail (vertical height 300 cm) when he fell.
40. Mr Apelt had a bilateral spinal fusion (L5/S1) on 27 January 1977. Dr Sugars performed this surgery at the Prince Charles Hospital. On 20 September 2004, Mr Apelt had further surgical treatment for his lower back (“revision surgery”) performed by Dr McCombe.
41. During cross-examination, Mr Apelt was asked a number of questions in relation to the frequency of his backache whilst employed with Telstra from April/May 1978 until November 1987.
“What symptoms did you suffer?---Backache.
…All you say there is it caused a lot of discomfort and lower backache. How often?--- Whenever I was sitting for long periods or in squat positions, after long days of sort of heavy work.
All right. So was that every day? This is the detail we’re after. All right. This is not in your statement, is it?---Was it every day? I can’t answer that with total honesty.
All right?---It was basically sort of whenever it was aggravated I was sitting in very cramped positions, I was sitting for a long length of time, I was sitting in the truck.
…..
So was that daily?---As I said before it varied depending on what day it was.
Well, did you get backache every day from doing this sort of work?---I can’t answer that. I had backache on occasions throughout that whole period.
…..
What I’m trying to get from you is how often you had backache?---And I thought I answered the question to you before that I had backache when I was sitting for long uninterrupted periods, in the street.
Well, how often did that happen, you see?---It depended on the work.
All right. Okay. At any given week then how many times would you suffer backache?---Regularly.
Regularly….Does that mean every day?---No it doesn’t mean every day, it means whenever [I was in] situations like climbing up ladders…hanging off the pole…joining wires, leaning back…
Can we establish this much, you would have suffered backache on at least one occasion every working week from March/April ’78 through until 23 November 1987; is that so?---I wouldn’t like to sort of ramp it up that much, no.
Well, that’s not ramping it up that much. How often then? How often did you have backache?---Regularly.
Well, what do you mean by that? You know, is that regularly every month, regularly once every year or whatever?---Whenever I was put in a situation where I was straining my back.
Well, how often did that happen?---It could have been three of the five days, it could have been two of the five days, it could have been – not happen – at all that week because I was sitting in the office doing the plans and sketches.
…..
We’re talking about from 1978 through until 1987?---I had backache on a regular occurrence.
…..
So whenever you did that [replacing cables in street over a week] it caused backache?---It caused aches, yes.
All right. How often would you do that?---Regularly.
All right. So, what, once every week?---Yes.
So we can establish that you had backache at least once every week; is that so?---That’s correct.
All right. Can I just take it a step further? What about within a week, could it be up to every day of the week?---No.
No. All right. Two days a week?---Possibly.
All right. How frequently would that occur?---Regularly.
All right. You can’t give us any indication beyond the word regular?---…it’s quite a long time ago.
And so much turns upon it, Mr Apelt, that’s why I’m asking you. And this is not detail, you haven’t given in your statement, have you?---I’ve just given you the full run of the different duties I did. Now, if I’m to give you a blow by blow for the last wherever that period is, 10 years.
I’m not asking you for a blow by blow, I’m asking you to give us some indication as to how often you got backache?---I’ve given you an indication. If you just want a number, two to three times a week.
I see?---Depending on what I was doing.
All right….I gather that over this … nine year period you had had backache consistently over all that time; is that so?---Yes.
So for argument’s sake, in 1979 you were getting it at the same frequency that you would have been getting it in 1987?...Well, do you accept that or not?---The frequency depended on the work that I was doing.
Yes. I appreciate that but I’m asking you: was the frequency of backache the same in 1979 as what it was in 1987?---No.
It wasn’t. Well, what was happening in 1987? It got less or worse?---It wasn’t as annoying. It depended on what I was actually doing.”
42. During cross-examination, Mr Apelt was referred to Statutory Declarations he had completed over time in relation to injuries he had sustained and which had been described in his oral evidence.
43. A Statutory Declaration he had completed on 20 September 1976 stated that he had “never sustained any back injury or suffered any back complaint prior to 22 March 1976”. In response to a contemporaneous note made by the Royal Brisbane Hospital on 23 August 1976 which stated that “he [Mr Apelt] gave a history of low back pain for years previously following some heavy lifting” Mr Apelt stated he did not believe he had given this history and later, “I can’t recall that detail. I would have told them about the incident with the bullworker [exercise device]”. When asked further as to why the Statutory Declaration referred to the absence of any prior back injury or back complaint, Mr Apelt said that “it slipped my memory”.
44. Mr Clark sought a response from Mr Apelt in relation to a Statutory Declaration he had completed on 22 September 1976 in which he had stated:
“To the best of my knowledge I did not sustain another injury to my back between 22 March and 9 August. On 9 August while I was engaged on heavy shovelling duties the back pain became acute and I notified my party leader who advised me to consult a doctor.”
and a letter he had written six days earlier to the Manager, General Personnel Services, Telecom in which he had stated:
“Prior to 10 August I had been receiving slight intermittent pains to the lower part of my back which I believe extended from my previous injury sustained on 22 March 1976.”
45. Mr Apelt disagreed that both statements were at odds with one another and later, that the Statutory Declaration was incorrect “if you use the term intermittent pains”.
46. Mr Apelt was referred to a Statutory Declaration he had completed on 21 March 1979 [in relation to an Accident Report, lodged on 12 March 1979, of an incident involving sharp pain in the lower back whilst squatting down pouring an epoxy joint] in which he had stated:
“I do solemnly and sincerely declare that I have had previous back complaints, which were incurred during the course of my employment with Telecom Australia. However, the injury, which occurred on 12 March, 1979, is not related to any of the previous back injuries that I have referred to. This can be verified by Dr Sugars, who stated it was probably a strained muscle.”
47. In addition, Mr Apelt was referred to the medical report of Dr W T Sugars, his orthopaedic surgeon (T81, Folio 61) which referred to his consultation three days after the Accident Report was lodged.
“I saw Mr Apelt on 15/3/79. He said that he had had an attack of acute low back pain while at work 3 days previously. He had been resting in bed at home since that time and the pain was settling satisfactorily.
On examination, he had a full range of movement in his back and there were no neurological changes in his lower limbs. X-rays done showed no change from those done 12 months previously and his previously performed lumbo-sacral fusion was quite sound.
He was advised that this was an acute low back pain related to an area of his lumbar spine above the level of his previous fusion and was advised to continue resting until the pain settled sufficiently to allow him to return to work.”
48. When questioned why Dr Sugars’ report made no mention of any back symptoms, other than the event of 12 March 1979, Mr Apelt stated:
“Do you agree with that or not?---It’s not there, yes.
It’s not there because you never told him about any previous history of back pain prior to 12 March 1979. Isn’t that so?---I went to see him because I was concerned about that specific incident and other experiences.
…..
TRIBUNAL: The question was, Mr Apelt, did you tell Dr Sugars any past history of back – symptoms of back complaints at that date?---I think I did.
…..
MR CLARK: You think you did. I’m suggesting to you that you didn’t?---Okay. You suggest that …..
Well, what do you say to that?---No, I don’t believe so.
He doesn’t mention that, does he?---Well, it’s not written there. That doesn’t mean to say it wasn’t discussed.”
49. Mr Clark referred Mr Apelt to the clinical notes of Dr G Wright for the period December 1990 to September 2003 (Exhibit R21). These notes, under Medical History, contain the notation: “Spondylolisthesis” and “Spinal fusion L5 S1 in 1976”. Mr Apelt had previously stated that “it’s quite possible” he commenced to see Dr Wright in December of 1990 and he believed that he had not seen any GP about his back in the intervening period 1987 – 1990.
50. In the final phases of his cross-examination, Mr Apelt was questioned about the reasons for his resignation from Telstra in 1987. He agreed with the proposition that worsening back pain was a principal reasons why he left Telstra and stated later:
“There’s a whole host of reasons and I built up an opportunity to make a move because basically I was in a dead situation of continuous back pain – periodically through those years.”
Contentions And Submissions Of The Parties
51. Mr Harding submitted that the Tribunal should give weight to Dr McCombe’s expert opinion rather than the opinion of the respondent’s medical experts. In particular, that Mr Apelt’s back problems arose from a “progression of the deformity” i.e. a loss in disc height and a progression of the slip.
52. In terms of back pain, Dr McCombe had taken a history from Mr Apelt which included dull backache which had increased over recent years and a more recent onset of leg pain and numbness. A part of his clinical examination he noted altered posture. He also noted the results of diagnostic tests [radiological evidence of compression of the L5/S1 nerve and gross loss of the L5/S1 disc space] that led Dr McCombe to conclude that it was consistent with what he described as “end stage disc degeneration”. This led him to consider what hypotheses might explain these findings. The hypothesis which he considered most likely was that Mr Apelt had experienced a “progression of the deformity [at L5/S1]”.
53. In terms of his physical examination in relation to Mr Apelt’s posture, Dr McCombe’s view was that his altered posture was consistent with, and could be explained by, “saggital imbalance” caused by a “progression of the deformity”.
54. In addition, Mr Harding referred to Dr McCombe’s opinion that the “progression of the deformity had led to the development of the compression of the L5/S1 nerve”.
55. Mr Harding relied on Dr McCombe’s evidence in submitting that the results of the surgery performed by Dr McCombe in September 2004 were “suggestive” that Dr McCombe’s hypothesis was correct.
56. Mr Harding relied on Dr McCombe’s conclusion that the only explanation for Mr Apelt’s “progression of deformity”, in the context of all the circumstances, was that it had increased, despite the fusion surgery in 1977.
57. Mr Harding contended that the principal alternative hypothesis to account for Mr Apelt’s back pain advanced by the respondent’s medical experts, namely “age related degenerative changes at the discs”, did not explain Mr Apelt’s other symptoms – in particular his posture and radicular signs.
58. Mr Harding challenged the proposition that Mr Apelt did not have a compressed nerve based on the presence of a halo of fat on the radiographs. There was divergent expert opinion on this point. Mr Harding submitted that the Tribunal should give weight to the radiologist opinion in this regard.
59. It was Mr Harding’s contention that Dr McCombe’s hypothesis had not been disproven based on the results of straight leg raising tests performed during physical examination undertaken by Dr McPhee and Dr McCombe; it was his submission that the evidence before the Tribunal indicated some patients with a compressed L5 nerve did not have a positive straight leg raising test.
60. In terms of the extent of further disc degeneration, leading to a narrowing of the disc, Mr Harding conceded that some form of diagnostic radiological test taken around the time of the spinal fusion in January 1977 was required for verification. However, in the absence of such radiological evidence, Mr Harding contended that an inference could be drawn that there had been a progression of the deformity from the following facts:
(a) the recent development of L5 nerve root symptoms; and
(b)unexpected extent of degeneration at L5/S1.
61. Mr Harding contended that the Tribunal should give little weight to the hypothesis advanced by the respondent’s medical specialists that the source of Mr Apelt’s back pain was degeneration of the discs above the fusion. In making this submission, Mr Harding referred to the expert evidence of Dr McPhee and Dr Licina and contended:
(i)there was no evidence of accelerated degeneration of the discs apart from the fusion but there was normal age-related degeneration [Dr Licina]; there was an acknowledgement of a possibility of disc degeneration of a constitutional nature [Dr McPhee];
(ii) that degeneration changes at L4/5 may be asymptomatic [Dr McPhee];
(iii)that there is little correlation between the degree of degeneration seen and the degree of pain [Dr Licina]; and
(iv)an acknowledgment by Dr McPhee that Mr Apelt has back pain. His final report contains the comment that he “cannot adequately explain what is causing it from the information available”.
62. Mr Harding submitted that Mr Apelt’s spine was subjected to load in the course of his employment with Telstra. This load was in the form of repeated activities resulting in hyper-extension. This load placed stress on the vertebra and the discs and were a cause of the deformity. The activities that Mr Apelt was engaged in, especially between May 1978 and 1987, placed moderate to heavy loads on his spine and were a regular component of his work; Mr Apelt experienced back pain at any time he performed these activities.
63. Mr Harding relied on Dr McCombe’s opinion that the carrying out of these workplace activities over a 9 year period would, in all probability, have been at least a moderate cause of the deformity progressing.
64. Mr Harding challenged assertions as to the credibility and reliability of Mr Apelt’s evidence. He contended that answers given by Mr Apelt about specific incidents must be viewed in the context of him answering questions about relatively minor incidents which occurred approaching 30 years ago.
65. It was Mr Harding’s further contention that when examining the contemporaneous documents there were no occasions when any statements were made by Mr Apelt which significantly conflicted with documents. Furthermore, that the history as recorded in the medical records was non-controversial and entirely consistent with Mr Apelt’s evidence given to the Tribunal both in his oral evidence and in his statement.
66. Mr Clark referred to the initial acceptance of liability by the respondent. It was his contention that the medical opinion evidence supported the conclusion that Mr Apelt’s isthmic spondylolisthesis was a naturally occurring condition that could be aggravated by work. However, contemporaneous medical opinion evidence (T65, September 1977) concluded that the effects were of a temporary nature and that it was reasonable to assume that the effects had ceased.
67. As a “measure of theorisation” contained in Dr McCombe’s expert opinion, he referred to the following statement in a report of Dr McCombe (Exhibit A14, p.2) as an example:
“If one accepts the notion that further deformity of the spondylolisthesis has occurred despite the presence of a posteriolateral fusion, one has to accept that there has been plastic deformation of the fusion. Whilst this is not necessary likely to have been reported, I consider this a possible explanation.”
68. It was Mr Clark’s further contention that this example of “theorisation” by Dr McCombe was supported by other statements made by Dr McCombe in respect of his expert opinion. Specifically, Dr McCombe’s oral evidence before the Tribunal that it was only a theory on his part that Mr Apelt had a “reasonably normal” or “partly abnormal” disc height at the time of his spinal fusion. In turn, that this theory was the basis for his opinion in relation to further deformity of the L5 site.
69. Mr Clark then referred to the cross-examination of Dr McCombe to support his submission that the “theory” relied on by Dr McCombe was not supported by the medical literature at the time.
70. Mr Clark submitted that Dr McCombe’s theory relating to continuing deformity was a matter of conjecture – given that a vital piece of medical evidence was missing that might lead to some weight to be given to the acceptance of this theory. Specifically, the absence of radiological tests taken after the fusion that might show the state of the disc space at that time. Mr Clark referred to the concession made by Dr McCombe that the existence of this radiological evidence would have assisted him in this regard.
71. Mr Clark submitted that the Tribunal should prefer the expert opinion evidence of the respondent’s medical specialists to Dr McCombe. The respondent’s medical expert’s conclusions gave no support whatsoever to Dr McCombe’s opinion with respect to the methodology he had relied upon to arrive at his conclusions. In particular, the aetiology of spondylolisthesis, diagnostic tests relied upon and their interpretation (e.g. radiology), the measurement of saggital balance and quantification of posture, the analysis of the pattern of radiation of pain and lumbosacral nerve root compression and conclusions being consistent with the published medical literature.
72. Mr Clark submitted that it was particularly relevant that Dr McPhee provided extensive published articles to support the conclusions contained in his report. In contrast, this was not the case for the reports prepared by Dr McCombe. It was Mr Clark’s submission that the issue raised in these circumstances was whether any weight could be attached to Dr McCombe’s “theory”.
73. Mr Clark submitted that the credibility of Mr Apelt was a key aspect of the weight to be given to his evidence. In particular, factual evidence relating to Mr Apelt’s current complaint, past symptoms – especially any corroboration or other evidence to support the reporting of those symptoms at the relevant time. If there had been a history of recurrent ongoing low back, over time, as stated by Mr Apelt in his oral evidence, then he submitted that it would have been reasonable to have expected Mr Apelt to have raised this fact during his medical consultations, at some stage, over time.
74. Mr Clark submitted that the evidence before the Tribunal indicated that Mr Apelt was a person willing to stand up for, and to enforce, his rights in relation to workplace injuries. There were many incidents during his employment with Telstra from 1977 – 1987 where he sustained injuries to his back, resulting in low back pain, from workplace injuries. However, there was no mention made to his treating doctors (either workers’ compensation doctors or his GP), or in statutory declarations that he had completed which dealt with reporting of the incidents, where he had made reference to his recurrent, periodic back pain over the entire period that he was employed with Telstra.
75. Moreover, it was Mr Clark’s contention that if Mr Apelt’s back condition had been as important as he maintained, it would have been mentioned in his letter of resignation.
76. Mr Clark submitted that any analysis of what is being asserted now by Mr Apelt as to his low back pain, and what was stated and recorded in the past was inconsistent; that there was no contemporaneous evidence to support Mr Apelt’s claims that he made in relation to his back symptoms during the period he was employed with Telstra.
77. Mr Clark further submitted that the history taken by Dr McCombe from Mr Apelt could not be supported. In particular, the increased pain arising from workplace activities.
78. Mr Clark concluded with the submission that any analysis of Mr Apelt’s evidence would lead to one inevitable conclusion: that the credit and reliability of Mr Apelt was such that little weight should be given to it. Moreover, the expert medical evidence before the Tribunal totally rejected Dr McCombe’s claims – and Dr McCombe’s expert opinion was the very foundation of Mr Apelt’s case.
Legal Principles
§ Proof of Causation
79. The reasoning of Dixon J (as he then was) in Briginshaw v Briginshaw (1938) 60 CLR 336 at 361-362 as to the legal standard of proof in civil litigation, the balance of probabilities, is particularly relevant:
“The truth is that, when the law requires the proof of any fact, the tribunal must feel an actual persuasion of its occurrence or existence before it can be found. It cannot be found as a result of a mere mechanical comparison of probabilities independently of any belief in its reality…it is enough that the affirmative of an allegation is made out to the reasonable satisfaction of the tribunal. But reasonable satisfaction is not a state of mind that is attained or established independently of the nature and consequence of the fact or facts to be proved. The seriousness of an allegation made, the inherent unlikelihood of an occurrence of a given description, or the gravity of the consequences flowing from a particular finding are considerations which must affect the answer to the question whether the issue has been proved to the reasonable satisfaction of the tribunal. In such matters ‘reasonable satisfaction’ should not be produced by inexact proofs, indefinite testimony, or indirect inferences.” (Tribunal emphasis)
80. The approach taken by our Courts to scientific evidence and the question of causation under “workers’ compensation” legislation is well illustrated in O’Neill v Commonwealth Banking Corporation (1987) 13 ALD 234, a case dealing with section 29(1) of the Compensation (Commonwealth Government Employees’) Act 1971. In this case, Pincus FCJ stated (at 235,236):
“…To ask the question whether a particular employment was a contributing factor to the contraction of a disease or to its aggravation, acceleration or recurrence is not to use language of a technical character.
A similar point was made by Mason JA (as he then was) in Midge v Wormed Bros Industries Ltd [1972] 2 NSWLR 29, in a judgment relied on by the Full Court of this court in Kirkpatrick v Commonwealth of Australia (1985) 62 ALR 533 at 537. His Honour said, at 44, in effect, that questions of causation in the application of workers’ compensation legislation ‘are to be resolved by the application to the facts of the case of common sense, rather than scientific or logical theories of causation’. At 47 he referred to a decision of the New South Wales Court of Appeal as emphasising ‘that the question of causation is essentially one of fact’. In Kirkpatrick’s case, after referring to these passages, the Full court said at 527: ‘Eschewing metaphysics, the decision of the Tribunal is in this case fundamentally a finding of fact upon a commonsense consideration of the factors which led to the applicant’s condition’…” (Tribunal emphasis)
81. A further element for expert medical opinion and the question of proof of causation with respect to possibility/probability was recognised by the Full Court of the Supreme Court of Victoria in Dahl v Grice [1981] VR 513 where Gobbo J stated (at 522):
“A third consideration is that there is inevitably much difference in the views of expert witnesses as to what constitutes a probability as opposed to a possibility, whether in terms of a particular case or simply as a matter of logic. There is the obvious danger that an expert when asked to provide an opinion as to whether a causal link exists may do so in terms of scientific proof that may be altogether too exacting for the degree of satisfaction necessary in a legal proceeding.”
82. The reasoning of Herron CJ in EMI (Australia) Ltd v Bes [1970] 2 NSWR 238 (Court of Appeals NSW) is significant with respect to the evaluation of medical evidence by our Courts. At 242, Herron CJ stated:
“But if medical science is prepared to say that it is a possible view, then, in my opinion, the judge after examining the lay evidence may decide that it is probable. It is only when medical science denies that there is any such connexion that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try.”
83. The opinion of Dr McCombe has relied on the scientific method of “inference” to provide the basis for his conclusions on causation viz. progressive deformity. The common law of evidence that is relevant in any consideration of the weight to be placed on an inference is contained in the decision of LJ Wright in Caswell v Powell Duffryn Associated Collieries Ltd (1939) 3 All ER 722 at 733:
“There can be no inference unless there are objective facts from which to infer the other facts which it is sought to establish…But if there are no positive proved facts, from which any inference can be made, the method of inference fails and what is left is mere speculation or conjecture.”
§ Analysis of Competing Medical Opinions
84. Orthopaedic opinion evidence is central to determining this application for review. In this case, as is commonly the situation where expert medical evidence is before the Tribunal, divergent opinion existed. Accordingly, the question for the Tribunal is to determine the weight to attach to the competing medical opinions.
85. Clark v Ryan (1960) 103 CLR 486 is conventionally seen as a leading authority on expert evidence:
“[T]he opinion of witnesses possessing peculiar skill is admissible whenever the subject matter of the inquiry is such that inexperienced persons are unlikely to prove capable of forming a correct judgement without such assistance, in other words, when it so far partakes of the nature of a science as ton require a course of previous habit, or study, in order to obtain a knowledge of it (at 491)”.
86. Analysis of the following authorities provides some underlying legal principles that may be applied to address this question of the weight to attach to competing expert opinions:
(a)That for specialist scientific evidence to be admitted, it must have a basis in a body of recognised scientific theory. Its value and effect need not be subject to complete unanimity by all experts in the field: R v Lucas [1992] 2 VR 109 at 115;
(b)An essential pre-requisite to the admission of expert medical evidence is that it be accepted by experts competent in the appropriate field as a scientifically established facet of this area of medicine. This must be established by appropriate evidence: R v Runjanjic (1991) 56 SASR 45 at 47;
(c)An assumption that a topic is a fit subject of expert evidence if it is proved that there is a scientifically accepted body of knowledge concerning the subject area of the expert opinion: R v C (1993) 60 SASR 467 at 473; and
(d)In Casley-Smith and Ors v FS Evans & Sons Pty Ltd and Anor (No 1) (1988) 49 SASR 314, Olsson J stated that an analysis of authoritative texts and decided cases established a number of propositions, including whether the opinion evidence “forms part of a body of knowledge…which is …sufficiently organized or recognised to be accepted as a reliable body of knowledge” (at 320). Later, Olsson J made the following observation (at 323) in relation to evaluating scientific principles that could be extracted from the existing body of learning (“at least so far as any relevant published works or research publications were concerned”) :
“…it is useful to bear in mind not only the dictum of King CJ in R v Bonython (supra) but also those of the United States Court of Appeals in the leading case of Frye v United States 293 F 2d 1013 which made the point that:
Just when a scientific principle or discovery crosses the line between the experimental and demonstrable stages is difficult to define. Somewhere in this twilight zone the evidential force of the principle must be recognised, and while the courts will go a long way in admitting expert testimony deduced from a well-recognised scientific principle or discovery, the thing from which the deduction is made must be sufficiently established to have gained general acceptance in the particular field in which it belongs.”
Consideration of the Issues
87. The central issue for the Tribunal to decide is the question of causation: whether there has been a progression of the deformity of L5/S1 of Mr Apelt following his spinal fusion in 1977 – and any attendant consequences: specifically, sagittal imbalance and bilateral foraminal narrowing at L5/S1 with L5 nerve root compression. Should such a finding be made by the Tribunal, the next issue to decide would be whether the progression of the deformity was an ongoing effect of aggravation that had been contributed to by employment with Telstra from 1976 to 1987.
88. Questions of causation in workers’ compensation legislation are essentially one of findings of fact upon a commonsense consideration of the factors that have led, in this case, to Mr Apelt’s condition (O’Neill’s case).
89. There is no dispute that Mr Apelt suffers back pain. The issue in dispute is the cause of the back pain.
90. The evidence and information before the Tribunal indicates that the surgery performed on Mr Apelt in 1977 resulted in a solid fusion i.e. there is no evidence of a “non-union”. For example, see report of Dr W Sugars prepared after a consultation five months after the spinal fusion in 1977 (T7, Folio 25).
91. The expert evidence before the Tribunal involved divergent and competing opinions as to the question of causation. The issue for the Tribunal is to evaluate these opinions in terms as to what constitutes a probability – as opposed to a possibility (see Dahl’s case). In this regard, the Tribunal makes the observation that Dr McCombe has described his opinion as to progressive deformity as a “theory”, a “supposition” or an “hypothesis”.
92. In arriving at its findings of fact in such a factual situation, the Tribunal has applied the following common law principles in order to determine the weight to attach to the competing medical opinions as to causation:
(a)a recognition that divergent opinion exists amongst experts and complete agreement may not exist for a body of recognised scientific theory (Lucas’ case);
(b)that a pre-requisite for expert medical evidence is that it be an accepted body of knowledge by appropriately qualified experts (Runjanjic’s case; R v C);
(c)that the body of knowledge be sufficiently recognised to be accepted as a reliable body of knowledge (Casley-Smith’s case); and
(d)that the scientific principle to have gained acceptance in the particular field to which it belongs (see Casley-Smith’s case) [Emphasis added].
93. The foundation for Dr McCombe’s theory of “progressive deformity” relies on the scientific method of inference. Dr McCombe has acknowledged the limitation imposed by the non-availability of x-rays at the time of the spinal fusion in 1977. As a consequence, there is no starting point to determine any loss of disc height over time. Accordingly, Dr McCombe raises the following possible explanations for his “theory”:
(a)abnormal posture and loss of lordosis i.e. a “subtle sagittal imbalance”; and
(b)compression of both L5 nerve roots.
§ Sagittal Imbalance
94. Dr Licina’s opinion is that lumbar sagittal alignment is a complex issue involving issues that are not agreed upon and are still evolving.
95. Dr McCombe challenges Dr McPhee’s opinion as to the reference points that should be used for angular measurements and expresses a “belief” that Dr McPhee is “quoting a consenus statement before the Scoliosis Research Society about the reference points to measure sagittal balance in patients with spondylolisthesis”. Dr McCombe refers to two uncited sources (“Beaupere”, “Jackson”) as to what represents a normal lumbar lordosis.
96. The Tribunal considers that in order to avoid any subjectivity in resolving divergent medical opinion on the issue of the measurement and assessment of sagittal imbalance, the application of the legal principles associated with acceptance and reliability of this body of knowledge is paramount.
97. In this regard, the Tribunal prefers Dr McPhee’s opinion to that of Dr McCombe because of its much greater objectivity; Dr McPhee has counter-balanced the conclusions contained in his opinion against an extensive review of the literature (“body of knowledge”). Accordingly:
(i)the Tribunal considers that the “body of knowledge” Dr McPhee has relied on is sufficiently recognised to be accepted as a reliable body of knowledge with respect to the measurement and assessment of sagittal imbalance; and
(ii)that the “body of knowledge” reviewed by Dr McPhee provides the accepted principles and underlying assumptions for quantifying posture generally – and specifically for patients who have had a lumbosacral fusion.
98. Accordingly, the Tribunal can make no other finding than to conclude that, on the balance of probabilities (the Briginshaw test), the theory of Dr McCombe that progressive degeneration has occurred at L4/5 due to abnormal stresses arising from spinal malalignment, secondary to the lumbosacral fusion, cannot be supported.
§ Nerve Root Compression
99. Dr Licina’s opinion was that Mr Apelt’s clinical picture did not specifically point to L5 nerve root compression: there was no firm proof that a “specific nerve root” was involved; and that more evidence was required to make a specific diagnosis that L5 nerve root compression was the cause of Mr Apelt’s pain.
100. In this regard, the Tribunal makes the observation that the accepted, sequential, approach to diagnosis was reflected in the evidence of Dr McPhee in response to a Tribunal question. That is, sequential steps of taking the patient’s history followed by a clinical examination, then a review of any prior diagnostic tests undertaken (e.g. radiology) and ordering of further diagnostic tests - if considered appropriate at this stage, to confirm the diagnosis. Moreover, that further diagnostic tests, alone, were not relied on as the sole basis for diagnosis and opinion.
101. A CT Scan of Mr Apelt’s lumbar spine was performed on 21 July 2003. The radiologist’s report (Dr J Reasbeck, Exhibit A4) refers to no “obvious nerval compromise at the L5/S1 level”. In contrast, an MRI of Mr Apelt’s lumbar spine was performed on 24 November 2003. The radiologist’s report (Dr D Lisle, Exhibit A6) refers to “evidence of a degree of entrapment at L5 nerve roots bilaterally”.
102. Dr McPhee’s expert opinion refers to two published studies (Exhibit R10, References n.28, n.29) that investigated the correlation between MRI images and back pain. One significant research finding was that “abnormalities on MR images must be strictly correlated with age and any clinical signs and symptoms”. The Tribunal considers that such a research finding is consistent with the sequential procedures for diagnosis and opinion described by Dr McPhee as well as the expert opinion of Dr Licina’s on the need for more evidence to make a specific diagnosis of L5 pain. Accordingly, the Tribunal gives little weight to the contrasting observations contained in the reports of the CT Scan and MR image performed in 2003 i.e. by considering the radiology reports alone, independently of the sequential procedures for diagnosis.
103. Dr McCombe’s opinion was that his theory for nerve root compression could be supported by both clinical and radiological evidence.
104. In terms of the clinical evidence in relation to the examination of Mr Apelt, the Tribunal has had the opportunity to consider the notes and observations of Dr McCombe (Exhibit R17) and Dr McPhee [Exhibit R4(c)] and finds the clinical examination undertaken by Dr McPhee to be more extensive and objective compared with Dr McCombe. In addition, Dr McPhee and Dr McCombe have differing expert opinions as to the association between foraminal compression of the nerve roots and the physical sign of restricted straight leg raising. However, Dr McPhee has referred to published studies (Exhibit R10, Reference n.30, n.31 and n.33) which provide a “body of knowledge” that accepts that the straight leg raising test was positive in a significant number of patients with spinal/foraminal stenosis. Accordingly, with respect to the clinical examination, the Tribunal prefers the opinion of Dr McPhee compared with Dr McCombe, because of its greater objectivity, as well as its linkage to an accepted body of knowledge in this particular field.
105. In terms of the radiological evidence in relation to nerve root compression, Dr McCombe and Dr McPhee have both reviewed the MRI Scans and identified the presence of fat [as a “halo” of fat] around the nerve root. Their opinion diverges as to the distribution, or continuity, of the fat around the nerve root and its consequences for nerve root compression.
106. Dr McCombe’s opinion was based on “my experience” and “there is no doubt in my mind that he’s [Mr Apelt] suffering from L5 nerve root compression”. Dr McPhee’s opinion was that, for true nerve root compression and stenosis, there should be no fat around the nerve root. In addition, that the nerve root was a plastic structure capable of changing its shape. Moreover, Dr McPhee’s opinion reflected “[his] teaching that you determine the cause of the pain clinically and then prove it radiologically”.
107. The Tribunal prefers Dr McPhee’s opinion in this regard, not only because of the sequential steps pursued in formulating his opinion – but, in particular, his greater objectivity in his examination in evaluating the cause of the pain clinically.
108. In terms of the weight to attach to the results of the discogram, the Tribunal accepts Dr Licina’s evidence that uncertainty was associated with the test given the fact that it is subjective and that the findings are based on responses by the patient that cannot be measured. Moreover, and of significance in this case, the absence of a “complete discogram” had led to a situation where it could not clearly be said that the L4/5 disc was the source of pain for Mr Apelt.
109. Given these findings the Tribunal concludes that, on the balance of probabilities (the Briginshaw test), the theory of Dr McCombe that progressive degeneration has occurred at L4/5 has been associated with L5 nerve root compression, cannot be supported.
110. Given the Tribunal findings as to sagittal balance and nerve root compression, the Tribunal concludes that there are no objective facts to support Dr McCombe’s theory on progressive deformity i.e. by relying on the scientific method of inference. As there are no positive proved facts from which such an inference can be made, the Tribunal concludes that Dr McCombe’s theory of progressive deformity is conjecture (Caswell’s case).
111. Given this finding, there is no need for the Tribunal to consider the applicant’s contention that Mr Apelt’s employment with Telstra contributed to the progression of the deformity at L5/S1 in a material degree. Similarly, there is no need for the Tribunal to consider the contention that Mr Apelt’s spinal fusion operation in 1976 was a cause of the deformity by failing to stop the progression of the deformity.
112. The Tribunal had some concerns with Mr Apelt’s evidence. There were a number of instances where his oral testimony could be described as “indefinite testimony” (see Briginshaw’s case), e.g. inconsistencies in relation to past documents completed by Mr Apelt (Statutory Declarations, accident reports). This “indefinite testimony” may reflect Mr Apelt as a poor historian. Accordingly, the Tribunal had some difficulty identifying the weight that could be attached to Mr Apelt’s evidence. These limitations, in some aspects of his oral evidence, created difficulties for the Tribunal in identifying the boundary where Mr Apelt’s evidence could be separated between reliable and unreliable. However, notwithstanding the limitations in Mr Apelt’s evidence, the question of aggravation and employment, ultimately, did not become an issue for the Tribunal to decide.
113. For all of the above reasons, and considering all of the expert and lay evidence, the Tribunal finds that it is more probable than not that symptomatic degeneration has not occurred at L4/5 due to abnormal stresses arising from spinal malalignment arising as a secondary consequence of lumbosacral fusion in 1977: see E.M.I (Australia) Ltd v Bes’ case.
114. The Tribunal prefers the opinion of Dr McPhee and Dr Licina as to the question of causation of Mr Apelt’s symptoms. Accordingly, the Tribunal concludes, on the balance of probabilities, that the source of Mr Apelt’s back pain is normal age-related changes at the discs above the level of fusion that are unrelated to the spinal fusion in 1977.
115. The Tribunal makes the observation that the “body of knowledge” related to isthmic spondylolisthesis is sufficiently recognised to be an accepted body of knowledge.
116. The Tribunal affirms the decision under review.
I certify that the 116 preceding paragraphs are a true copy of the reasons for the decision herein of Dr EK Christie, Member
Signed: Jenny Tran
AssociateDate/s of Hearing 7 and 8 March and 14 April 2005
Date of Decision 24 June 2005
Counsel for the Applicant Mr A Harding
Solicitor for the Applicant Gilshenan and Luton
Counsel for the Respondent Mr C Clark
Solicitor for the Respondent Sparkes Helmore
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