Thurling and Comcare
[2008] AATA 270
•4 April 2008
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2008] AATA 270
ADMINISTRATIVE APPEALS TRIBUNAL )
) No A2007/1099
GENERAL ADMINISTRATIVE DIVISION ) Re LEANNE THURLING Applicant
And
COMCARE
Respondent
DECISION
Tribunal Mr S. Webb, Member
Dr P. Wilkins, MemberDate4 April 2008
PlaceCanberra
Decision The decision under review is affirmed. ...........signed...................................
Mr S. Webb, Presiding Member
CATCHWORDS
COMPENSATION - right shoulder and lumbar spine injuries accepted - permanent impairment - degree of whole person impairment - right shoulder claim not pressed - 2nd Edition of the Comcare Guide - clinical findings - degree of impairment less than 10 percent - decision affirmed
Safety, Rehabilitation and Compensation Act 1986 ss 4, 24, 25, 27, 67
Canute v Comcare [2006] HCA 47
Comcare v Amorbieta [1996] FCA 312 (3 May 1996)
Martin v Australian Postal Corporation [1999] FCA 655
Jordan v Australian Postal Corporation [2007] FCA 2028 (19 December 2007)
Brennan v Comcare (1994) 50 FCR 555
REASONS FOR DECISION
4 April 2008 Mr S. Webb, Member
Dr P. Wilkins, Member1. Leanne Thurling injured her right shoulder and her lower back in the course of employment as a Corrections Officer by the ACT Department of Correctional Services. She claimed and was paid compensation. Subsequently, she claimed compensation for permanent impairment.[1] Her claim was rejected by primary determination[2] and on reconsideration.[3]
[1] T27.
[2] T37.
[3] T39.
2. These decisions concerning compensation for permanent impairment as a result of the injuries to Ms Thurling’s right shoulder and her lower back are before the Tribunal for review. Prior to the hearing Ms Thurling informed the Tribunal that she did not press her claim in relation to the right shoulder injury. At the hearing Mr P. Stockley, counsel for Ms Thurling, informed us that the part of the reconsideration decision concerning the right shoulder was not under challenge. Without hearing that aspect of Ms Thurling’s claim, but considering the relevant evidence, we are satisfied that Ms Thurling’s right shoulder injury does not give rise to a permanent impairment of at least 10 percent under the Guide to the Assessment of the Degree of Permanent Impairment (2nd Edition) (the Comcare Guide).[4] Thus, that aspect of the reconsideration decision is affirmed.
[4] See
3. The remaining issue for determination is whether or not Ms Thurling is entitled to compensation for permanent impairment as a result of the injury to her lower back. We note in passing that Comcare did not dispute that such an injury occurred in compensable circumstances.[5] We are satisfied that it did- Ms Thurling fell at work and suffered a lower back injury on 12 September 2004 in the course of her employment. The specific nature of the injury is a matter to which we will return. For the compensation claim to be made out we must be satisfied that:
(a)the lower back injury resulted in a permanent impairment, and
(b)the degree of the permanent impairment is at least 10 percent under the Comcare Guide.
[5] T4, T5, T6, T7 and T8 refer.
4. Ms Thurling asserts that her lower back injury has resulted in a diagnosis-based 13 percent whole person permanent impairment under Table 9.17 of the Comcare Guide. She relies on the reports by Dr G. Eaton, an occupational physician,[6] and his oral evidence concerning clinical findings of radiculopathy, especially in relation to the absence of left ankle reflex. In her submission, these findings indicate significant signs of radiculopathy on 22 October 2007. Ms Thurling says that the radiculopathy is the result of a torsional injury simpliciter at the L5/S1 level in her lumbar spine, even though no such injury is apparent on the MRI scan taken on 15 November 2005.[7] In the alternative, Ms Thurling asserts that the injury in September 2004 caused swelling and inflammation in her lumbar spine that subsequently impinged upon a nerve root or nerve roots to cause the radiculopathy. Ms Thurling asserts that the evidence of Dr Eaton and Dr I. Kelman, a surgeon, support such a conclusion. In Ms Thurling’s submission, Dr V. Pascall, an occupational physician, did not give evidence that is inconsistent with a diagnosis-based estimate of a 13 percent whole person impairment of her lumbar spine. Thus, she says, the evidence supports her case and the aspect of the reconsideration decision concerning the lumbar spine injury should be set aside.
[6] Exhibit A2.
[7] T19 folio 80.
5. As will appear, we do not agree.
6. Under the Safety, Rehabilitation and Compensation Act 1986, where an injury to an employee results in a permanent impairment, Comcare is liable to pay compensation (s 24). The words ‘permanent’ and ‘impairment’ are defined at subs 4(1). The amount of compensation is to be worked out on the basis of the degree of permanent impairment expressed as a percentage, which is to be determined by application of the Comcare Guide. If the degree of permanent impairment is less than 10 percent, no compensation is payable (subs 24(7)).
7. The Comcare Guide is to be approached in order to determine the degree of permanent impairment resulting from each injury (Canute v Comcare [2006][8]). The parties agreed, correctly in our view, that the degrees of permanent impairment arising from Ms Thurling’s right shoulder and lumbar spine injuries cannot be combined.
[8] HCA 47, at [14].
8. We are reasonably satisfied that Ms Thurling suffered from a degenerative lumbar spine condition at the L2/3 and L4/5 levels and an arthritic congenital abnormality at the L5 level (the L5 vertebra is articulating through an abnormal joint with the sacrum on the left side) prior to the injury on 9 September 2004.[9] These conditions were permanent and not amendable to curative treatment.
[9] Exhibit A1.
9. In Ms Thurling’s submission, these lumbar spine conditions were asymptomatic in the months and years prior to the injury in 2004, but the conditions were susceptible to aggravation. She says that she undertook physical activities such as abseiling and caving without difficulty before the injury, but was not so able after the injury. Ms Thurling says that the lower back injury in September 2004 caused a frank injury simpliciter at the L5/S1 level in her lumbar spine, aggravating her previously asymptomatic lumbar spine conditions.
10. We accept that Ms Thurling was forced to reduce the level and extent of her physical activities after the injury in September 2004. However, this was primarily as a result of her shoulder injury. Simply put, there is no radiological evidence or other compelling evidence that she suffered any frank injury to the L5/S1 disc or associated structures or nerves on 12 September 2004. We are reasonably satisfied that she did not. We note that Ms Thurling consulted Dr Reddy, a general practitioner, on 13 September 2004, but the Doctor did not note any complaint of low back pain on that day. On 17 September 2004, Dr Reddy noted “Now has pain at lower back”.[10]
[10] Exhibit R2.
11. It is more likely than not that Ms Thurling’s low back injury has two elements: a contusion and a strain. By Ms Thurling’s own account of the incident on 12 September 2004, she fell to her knees and then fell twisting to the right while weight bearing and wearing an air tank in a harness on her back. Her evidence is that the pain she experienced in her back was “at the belt line” and not in the lower levels of her lumbar region. That is consistent with Dr Pascall’s report of an upper lumbar contusion at the L3/4 level on the midline and pain in the right lumbar region. We accept that evidence and so find. We are reasonably satisfied that the pain in the right lumbar region about which Ms Thurling complained after the injury in June 2005, as reported by Dr Pascall, was the result of a twisting strain injury affecting the paravertebral musculature in that region. It is moot whether these injuries aggravated the previously existing lumbar conditions reported by Dr Ashman in 1995. We will return to this point.
12. The question is whether or not these injuries resulted in a diagnosis-based permanent impairment of 10 or more percent. The words ‘results in’ that are used in s 24 of the Act import a concept of causation that is well understood, in which the injured person is taken as found (Comcare v Amorbieta [1996][11]). We accept that Ms Thurling’s previously existing lumbar spine condition may have been susceptible to aggravation and that any such susceptibility, in the present circumstances, does not disentitle her to the compensation she has claimed.
[11] FCA 312, at [7].
13. However, if there is a previously existing condition, in the form of a degenerative spinal disease for example, and that previously existing condition has been aggravated by an injury, where the degree of impairment resulting from the previously existing condition can be assessed accurately, the determination of the degree of permanent impairment under the Comcare Guide must only relate to permanent impairment that is the result of the aggravation.[12] Thus, it is necessary to isolate the compensable effects of an injury from the effects of any previously existing condition if it is possible to do so on the available evidence (Martin v Australian Postal Corporation [1999][13]; Jordan v Australian Postal Corporation [2007][14]). As Burchett J said in Martin’s case, that task may be very difficult if the previously existing condition is of fluctuating severity. If there is ambiguity applying the principle of assessment to which we have referred, the remedial nature of the legislation requires a liberal rather than a restrictive interpretation (Brennan v Comcare (1994)[15]).
[12] Comcare Guide, above n 4, ‘Principles of Assessment’, Part 1, p12.
[13] FCA 655, at [30].
[14] FCA 2028, at [34]-[35].
[15] 50 FCR 555, at 559.
14. There is no contemporaneous medical evidence concerning the state of Ms Thurling’s degenerative lumbar spine condition in the months and years immediately preceding the injury on 9 September 2004.
15. We feel compelled to observe that we have concerns about the reliability of Ms Thurling’s evidence. She did not fully disclose her medical history of low back problems (as evidenced by the materials in Exhibit A1) on her compensation claim form, or to medical experts who examined her for medico-legal purposes in connection with these proceedings. She explained this as an oversight on her part. We find this explanation implausible. However, we do not reject her evidence outright, but will proceed with caution when evaluating her evidence concerning controversial aspects of the case. Thus, it is necessary to carefully assess and weigh Ms Thurling’s evidence with the medical evidence over time, in some detail.
16. Ms Thurling’s oral evidence is that she experienced lower back problems in 1995 as a result of sedentary duties in her employment at that time. She said that she consulted a general practitioner, Dr C. MacDonald, and an X-ray was taken of her lumbar spine.[16] She was referred to Dr B. Ashman, a surgeon. Dr Ashman reported “a 13 year history of intermittent low back pain which has become more frequent and severe over the last few years” and “She has a restricted range of motion with pain reproduction on lateral flexion to the left”. Dr Ashman diagnosed “premature lumbar disc degeneration and a congenital abnormality which has become arthritic”.[17] We note that Ms Thurling denied that she had a 13 year history of intermittent low back pain, as reported by Dr Ashman. The Doctor was not called to give evidence and this aspect of his report was not the subject of further evidence. Nevertheless, Dr Ashman’s diagnosis is consistent with the pathology found on X-ray in 1994, which includes a transitional vertebra with lateral joints between the transverse process and the sacrum (a congenital abnormality) and “quite marked sclerosis around the left sided joint”, as well as degenerative changes at the L4/5 level with some scoliosis of the lumbar spine.[18] There is no evidence to suggest that this pathology was the product of injury or that related symptoms were of sudden onset. Thus we prefer and accept Dr Ashman’s description, assessment and diagnosis of Ms Thurling’s lumbar spine condition at that time.
[16] See X-ray report by Dr K. Cramer dated 12 September 1994, at Exhibit A1.
[17] See Dr Ashman’s report dated 3 May 1995, at Exhibit A1.
[18] X-ray report by Dr K. Cramer, at Exhibit A1.
17. By Ms Thurling’s account, Dr Ashman advised her to undertake physical activities to strengthen her back musculature. She ceased sedentary duties and says that her lower back problems improved with exercise to the extent that she did not experience symptoms in the months and years prior to the injury in September 2004. Thereafter, by her account, she experienced severe low back pain that gradually improved until she undertook a Fit To Manage program in August 2005, which made her symptoms worse. She completed the program in early November 2005. Her evidence was that soon thereafter she first experienced intermittent pain in her right leg from her buttock through the back of her thigh to her knee and intermittent tingling in the balls her feet and in the first three toes when walking up hill. We note in passing that this account is not consistent with Dr Kelman’s report in September 2006, consequent upon examination of Ms Thurling on 23 August 2006, in which the Doctor reports that Ms Thurling complained of “intermittent radiation of pain in a sciatic distribution on the left” with no complaint of parasthaesia in the feet.[19] We prefer and accept Dr Kelman’s account, which was not seriously challenged. We also note that Dr Pascall examined Ms Thurling on 19 July 2006 and there is no indication of any complaint of pain radiating into either leg at that time.[20]
[19] T32 folio 129.
[20] T31.
18. Ms Thurling gave evidence that after surgery on her left shoulder in December 2006, which caused her difficulty sleeping on her left side, she experienced intermittent pain radiating into her left leg from the buttock down the back of the thigh to her knee. Ms Thurling attributes all of these symptoms to the lower back injury in 2004.
19. Unfortunately there is almost no contemporaneous medical evidence concerning Ms Thurling’s low back symptoms or pathology in the weeks and months following the injury. Dr Pascall examined Ms Thurling on 16 June 2005 and reported “a notable disparity in the skin folds of the lower thoracic and upper lumbar area on the right compared with the left”; “some slight rotation of the right hip posteriorly”; “her back is less painful than it used to be”; and “there was no tenderness of the lumbar vertebrae or the paravertebral muscles”.[21] Dr Pascall concluded that Ms Thurling’s “low back strain appears at this time to be more a problem of mechanics and posture than anything else. Whatever bruising occurred as a result of the tank hitting her back is not causing a problem at this time. The low back pain has resulted from posture, most likely to protect the right shoulder.”[22] Ms Thurling did not inform Dr Pascall about her previous lumbar spine condition. On 22 August 2006 Dr Pascall provided a second report in which she reported that Ms Thurling “says that her back pain is quite manageable if she does a lot of walking”, “the more she walked, the better her back felt. She managed [the Kokoda Trail] without difficulty but says that she can irritate her back with just a sneeze”.[23] This is to be contrasted with Dr Kelman’s report on 4 September 2006, that Ms Thurling suffered from mechanical back pain that would be exacerbated by activity and Ms Thurling’s assertion that the symptoms in her legs and feet are intermittent and related to activity. Doctor Pascall examined Ms Thurling on 19 July 2006, with particular focus on her right shoulder problem and reported that Ms Thurling “was tender in her lower back at the L4/5 region in the midline and there was no muscle guarding or spasm on palpation. However, with lateral flexion to the right there was evidence of some muscle spasm on the right side and flexion on the right was reduced and less than it was to the left.”[24] The Doctor concluded at that time that Ms Thurling’s “lower back condition remains the problem of degenerative spines” and “her symptoms are consistent with the degenerative nature of the spine”.[25]
[21] T15 folio 66.
[22] T15 folio 68.
[23] T31 folio 116.
[24] T31 folio 118.
[25] T31 folio 119.
20. Further information concerning Ms Thurling’s medical history of low back problems, including the materials in Exhibit A1, was provided to Dr Pascall with a request to provide a supplementary report for the purposes of these proceedings. On 3 February 2008 Dr Pascall provided a third report in which she discussed the nature of any aggravation of Ms Thurling’s previously existing lumbar spine condition and the injury she suffered on 9 September 2004:
…in the immediate period after the incident [in September 2004], there was soreness of the upper lumbar region that is consistent with contusion caused by the breathing apparatus hitting her.
There was ongoing pain in the right lumbar region (paravertebral muscles) caused by an aggravation of the pre-existing postural problem [1994 X-ray showing lumbar scoliosis concave to the right]. She would not have had as much flexibility and muscular support in the lumbar region as might be required to sustain a twisting fall without injury.
Over the ensuing months after the accident and with massage treatment and adequate mobilisation, the aggravation subsided to minimal levels and possibly to pre-injury levels.[26]
[26] Exhibit R3, pp3 and 4.
21. Dr Pascall did not accept that Ms Thurling was free of lumbar spine symptoms in the period prior to her injury and reported “I suspect that her level of complaint in mid 2005 for the lumbrosacral spine is her background level of complaint, that is, if she bent over in one specific direction she felt tightness and possibly even some pain.”[27]
[27] Exhibit R3, p4
22. Thus, it appears on Dr Pascall’s evidence that Ms Thurling’s low back strain injury had resolved by July 2006 and that her symptoms at that time were the result of her degenerative spinal conditions. We note that Dr Pascall’s findings and conclusions at that time were made without knowledge of Ms Thurling’s medical history of degenerative disease and abnormality in her lumbar spine. Dr Pascall’s evidence is supported by all other contemporaneous evidence in the period to July 2006, including the reports of Mr S. Andrews and Dr J. May, both of whom treated Ms Thurling but were not called to give evidence.
23. On 22 August 2005 Mr S. Andrews, a masseur conducting ‘Fit To Manage’ programs, reported that “Ms Thurling’s continued discomfort in her lumbar spine seemed to be more a factor of having tight hamstrings and gluteus muscle groups and this is in my opinion responsible for her symptoms not abating”.[28] On 18 November 2005 Mr Andrews reported that Ms Thurling completed an 8 week physical rehabilitation program and, with regard to Ms Thurling’s lumbar strain “in my opinion this was a result of having tight calves, hamstrings and gluteus muscle groups as outlined in FTM’s initial report. This has since been rectified, as Ms Thurling is now able to touch her toes with no sign of pain or discomfort. Ms Thurling is also able to regularly leg press in excess of 120 kg again with no sign of pain and discomfort as well as performing advanced floor based exercises which demonstrate that Ms Thurling’s lower back can tolerate dynamic movements whilst focusing on the transverse abdominal muscles as a means of moving excessive loads off the lower back. Once again in all these above mentioned exercises Ms Thurling has excelled.”[29]
[28] T17 folio 73.
[29] T20 folio 81.
24. Dr J. May, a doctor practising in sports medicine, first examined Ms Thurling on 29 September 2005. On 4 November 2005 Dr May did not report any complaint of low back pain by Ms Thurling prior to 31 October 2005, on which day it appears that Ms Thurling “felt that her low back pain was increasing”.[30] On examination of her lumbar spine, Dr May reported that Ms Thurling “had forward flexion to the mid-shins. She had painful extension. She had pain in her back with a straight leg raise at 90º and with slump but had normal neurological examination. She was tender over the para-vertebral muscles to the right of L5”.[31] Dr May reported that Ms Thurling had “no past history of low back pain”.[32] Subsequently on 2 December 2005 Dr May reported that she had evaluated Ms Thurling’s MRI results from 21 November 2005[33] and that the scan “shows that she does have lateral recess stenosis of the left L5 nerve root and degenerative change through L4/5 and L5/S1. I feel these changes were likely to be present prior to injury but the fall she had at work has exacerbated this and she is continuing to complain of pain related to her low back”.[34] On 30 March 2006 Ms B. Nairn, an occupational therapist, reported that Ms Thurling was managing her back pain with exercise.[35] On 24 April 2006 Dr May again reported and described the cause of Ms Thurling’s low back pain as “Lumbar spine spondylosis” but did not relate that condition to any injury.[36] It is likely that Dr May was not aware of Ms Thurling’s history of low back problems when she wrote these reports. Dr May was not called to give evidence and that point could not be tested.
[30] T18 folio 76.
[31] T18 folio 77.
[32] T18 folio 78.
[33] See T19.
[34] T22 folio 84.
[35] T25 folio 89.
[36] T29 folio 103.
25. We note that Dr May does not report any complaint of pain radiating into either of Ms Thurling’s legs or parasthaesia of any kind. On that basis, and with an eye to Dr Pascall’s clinical findings in July 2006, significant doubt attaches to Ms Thurling’s assertions concerning the onset of such symptoms in or about October 2005. We do not accept her evidence in this regard. The first reliable report of any such symptoms is found in Dr Kelman’s report in September 2006. Thus, we find that it is more likely than not that if Ms Thurling truly suffered any such symptoms in 2006, they commenced in her left leg in or about August of that year.
26. On 4 September 2006 Dr Kelman reported that Ms Thurling complained of “intermittent pain in the lumbar region” and “intermittent radiation in a sciatic distribution on the left side” without parasthaesia in her feet or any weakness.[37] On examination of her lumbar spine, Dr Kelman reported “reduced lumbar lordosis”; “no scoliosis”; “Forward flexion was 50º (lumbar flexion 0-60º), extension 20º (lumbar extension 0-30º), lateral flexion 20º to the left and right”; “straight leg raising test was 60º bilaterally”; “sciatic stretch test was negative bilaterally”; “reflexes in her knees and ankles were present, but only after augmentation”; “sensation to light touch was assessed from L1 to S1 and found to be normal”.[38] Dr Kelman diagnosed “mechanical backache caused by bending and lifting”[39] and reported that:
…there is age-related degenerative disease in her lumbar spine, demonstrated by facet joint arthritis and narrowing of the L4/5 and L5/S1 discs. However, the injury has resulted in an aggravation of this condition, which has not resolved and she still has symptoms of pain in her lumbar spine, which date from the injury.[40]
[37] T32 folio 129.
[38] T32 folio 130.
[39] T32 folio 131.
[40] T32 folio 132.
Dr Kelman was not informed by Ms Thurling about her previous history of low back problems. On 31 January 2008 Dr Kelman, having been provided with materials in Exhibit A1, provided a supplementary report.[41] The Doctor reported that his previous “clinical examination [of Ms Thurling’s lumbar spine] demonstrates that there is no true radicular pain” and explained that Ms Thurling did not demonstrate any findings consistent with ‘true’ radicular pain.[42]
[41] Exhibit R4.
[42] Exhibit R4, p2.
27. On 27 November 2007 Dr Eaton reported that “Ms Thurling said she continues to experience a painful and tender lower spine. She continued to experience posterior thigh pain extending to knee level and also left hip pain” and that “the anti-inflammatory medication Celebrex helps control her various aches and pains”[43]; “said she was not experiencing any major back pain on the day of the assessment”[44]; and “she said she is able to mobilise reasonably well and had no problem climbing stairs”, “she can experience some leg pain walking up slopes and hills”[45]. On examination of Ms Thurling’s lumbar spine, Dr Eaton reported that:
[43] Exhibit A2, report dated 27 November 2007, p3.
[44] Exhibit A2, report dated 27 November 2007, p4.
[45] Exhibit A2, report dated 27 November 2007, p5.
Back movements were restricted with flexion reduced to 50 degrees with fingertips reaching the upper shin level. Extension was markedly restricted at 10º only. Rotation, right and left lateral flexion revealed mild restriction.
Lower limb examination revealed reduced straight leg raising at 60 degrees on the left and 60º on the right. The left ankle jerk was absent. Knee jerks were difficult to elicit sensation appeared to be normal at [sic] as was power were [sic] lower limbs.[46]
Dr Eaton diagnosed “Lumbar spine injury, probable lumbar nerve root entrapment at L5 and aggravated lumbar spondylosis” and stated:
I am not aware of any condition which was definitely present and asymptomatic prior to Ms Thurling sustaining her injuries with symptoms being precipitated as a result of the accident.
However it is possible that there was a level of pre-existing degenerative change in the neck, shoulders and back which is difficult to estimate. Ms Thurling denies any symptomatology prior to the accident in question occurring.
It would appear that the main causative factor was a heavy lifting and fall which occurred in September 2004.[47]
[46] Exhibit A2, report dated 27 November 2007, p6.
[47] Exhibit A2, report dated 27 November 2007, p7.
28. Subsequently, on 24 February 2008 Dr Eaton provided a supplementary report in which he reiterated that “Ms Thurling has lost the left ankle reflex due to a probable S1 nerve root lesion which would be consistent with L5/S1 disc prolapse/pathology” and “On the balance of probabilities Ms Thurling sustained S1 nerve root damage due to a previous L5/S1 disc lesion. Her reports of posterior leg/thigh [pain] are consistent with a S1 nerve root lesion/irritation”.[48] It is apparent that Ms Thurling did not disclose any prior history of low back problems to Dr Eaton. We note that there is evidence of herniation and left lateral recess stenosis at the L4/5 level in the MRI on 15 November 2005, which on Dr May’s evidence, was likely to have been present prior to the injury in September 2004. However, at this time there is no contemporaneous or reliable evidence that Ms Thurling suffered from symptoms of pain radiating into her legs.
[48] Exhibit A2, report dated 24 February 2008, p1.
29. Considering all this evidence and the oral evidence given by Doctors Pascall, Kelman and Eaton, we are reasonably satisfied that it is more likely than not that the low back injury aggravated Ms Thurling’s previously existing degenerative lumbar spine condition causing initial pain in the paravertebral musculature on the right side of her lumbar spine. We so find. However, we find that the aggravation resolved in the period to July 2006. We accept Dr Pascall’s evidence that the low level of symptoms at that time were in all likelihood consistent with the level of previously existing symptoms: intermittent stiffness and even pain on lateral flexion to the right. We are not persuaded by the evidence of Dr Kelman and Dr Eaton that the increased symptoms about which Ms Thurling complained from August 2006 were the result of the low back injury she suffered on 12 September 2004. We note that Dr Kelman considered that 50 percent of her low back impairment was due to “the natural process of aging”[49] and Dr Eaton acknowledged the possibility of pre-existing degenerative change in Ms Thurling’s back. At the time, neither Doctor had been provided with a full medical history concerning Ms Thurling’s lumbar spine. On their evidence, it is possible that the injury accelerated the progress of her previously existing lumbar spine conditions to cause this new symptomatology from August 2006, but that is not established as a matter of probability to our reasonable satisfaction on the evidence before us. The causal nexus between the injury on 12 September 2004 and the increased symptomatology from August 2006 is not made out.
[49] T32 folio 134.
30. Furthermore, we do not accept Ms Thurling’s submission that injury-related swelling exerted pressure, over time, on nerve roots in her lumbar spine and ultimately caused symptoms of pain and parasthaesia in her lower limbs. While there is some medical evidence that such a process may be possible (Dr Kelman), there is no objective evidence that any such swelling persisted in Ms Thurling’s lumbar spine for any length of time. Clinical examinations reported by Dr Pascall and Dr May reveal no such finding. Nor is there reliable probative evidence that any swelling caused by the injury was either present or operative in the onset of new symptoms in or about August 2006. We are reasonably satisfied that there was not.
31. That being so, we are satisfied that Ms Thurling’s low back injury on 12 September 2004 did not result in a permanent impairment. However, even if the injury did result in the new symptomatology in August 2006, and we make no such finding on the evidence before us, it does not mean the matter would resolve in Ms Thurling’s favour. For completeness we will address this point.
32. In order to qualify for payment of compensation for permanent impairment, it must be determined that Ms Thurling has a permanent impairment of 10 or more percent under the Comcare Guide. It is agreed that Table 9.17 of the Guide applies.
33. Table 9.17 sets out diagnosis-based estimates of whole person impairment in percentage terms and the criteria that apply at each percentage level. Considering the matters agitated by the parties, the percentage levels that have present relevance are 0 percent, 8 percent and 13 percent. Thus it can be seen that Ms Thurling is only entitled to compensation for permanent impairment in her lumbar spine if that impairment is determined to be within the criteria attaching to the 13 percent level.
34. Three criteria are set out at this level. As there is no evidence of fracture, it is not necessary to consider that criterion. The remaining two criteria are as follows:
Significant signs of radiculopathy, such as dermatomal pain and/or in a dermatomal distribution, sensory loss, alteration of relevant reflex(es), loss of muscle strength or measured unilateral atrophy above or below the knee compared to measurements on the contralateral side at the same location (may be verified by electrodiagnostic findings);
or
History of herniated disc at the level and on the side consistent with the objective clinical findings, associated with radiculopathy, or employees who have had surgery for radiculopathy but are now asymptomatic;[50]
[50] Comcare Guide, above n 4,
35. Ms Thurling expressly relied on the first of these criteria and not the second. Nevertheless, we will address both.
36. The term ‘radiculopathy’ is defined in Part III of Chapter 9 of the Comcare Guide, concerning the spine: “Radiculopathy is significant alteration in the function of a nerve root or nerve roots, and is usually caused by pressure on one or more nerve roots.” The definition sets out what is required to diagnose radiculopathy:
The diagnosis requires a dermatomal distribution of pain, numbness and/or parasthaesia in a dermatomal distribution. A root tension sign is usually positive. A diagnosis of herniated disc must be substantiated by an appropriate finding on an imaging study. The presence of findings on an imaging study is insufficient to make the diagnosis of radiculopathy. There must also be clinical evidence as described above.
37. We are not satisfied that there are significant signs of radiculopathy as a result of Ms Thurling’s injury. Dr Eaton found no left ankle reflex in October 2007. We accept that the Doctor applied appropriate augmentation techniques when attempting to elicit the reflex, without success. There are three things to say about this.
38. First, Dr Eaton’s clinical finding concerning his failure to elicit a left ankle reflex in Ms Thurling is not sufficient to satisfy the first criterion attaching to a 13 percent diagnosis-based estimate of whole person impairment. The criterion requires ‘significant signs of radiculopathy’ and sets out a list of what such significant signs may include. Plainly enough ‘alteration of relevant reflexes’ is one of those examples. However, the existence of only one such sign is not sufficient. The criterion is cast in the plural. Thus, more than one significant sign is required. From a medical perspective, that is consistent with Dr Kelman’s evidence that the absence of the left ankle reflex alone is not sufficient to diagnose radiculopathy, although it may indicate pathology at the L5/S1 level. That is consistent with Dr Pascall’s evidence.
39. Second, the signs must be ‘significant signs’ of radiculopathy. Dr Eaton considered that the absence of the left ankle reflex was a significant sign of radiculopathy. The evidence of Dr Kelman and Dr Pascall is that while the absence of an ankle reflex may be a sign of radiculopathy, in the absence of other clinical findings it is not a significant sign of that condition. With reference to the particular criterion, we prefer the evidence of Dr Kelman and Dr Pascall on this point. Dr Eaton diagnosed radiculopathy, but, with respect, we are not persuaded that such a diagnosis is made out. Even though the Doctor made clinical findings in relation to the absence of the left ankle reflex, and it can be accepted that such an absence is a sign of radiculopathy, we do not accept that other findings[51] concerning “S1 nerve root damage” (which is not supported by radiological evidence), “posterior thigh/leg pain” (which, as will appear, we are satisfied is not radicular pain) and “reduced straight leg raising” without a positive tension stretch response are ‘significant signs’ of radiculopathy as defined.
[51] See report dated 24 February 2008.
40. Third, as can be seen, more than just the absence of the left ankle reflex is required to satisfy the first criterion at the 13 percent level under Table 9.17. No other significant signs of radiculopathy are established on the evidence before us. We are reasonably satisfied that the intermittent upper leg pain and parasthaesia in the feet about which Ms Thurling complained is not in a dermatomal distribution. Dr Kelman’s evidence is that without symptoms below the knee, the distribution of pain symptoms cannot be said to follow a dermatomal distribution. Dr Pascall gave evidence that the upper leg symptoms were consistent with referred pain or pain in a sciatic distribution as a result of peripheral nerve pressure, but are not radicular. Dr Eaton’s evidence is that the symptoms are in a dermatomal distribution associated with the nerves at the L5/S1 level. We note that Dr Eaton gave evidence that he was unsure whether the abnormality in Ms Thurling’s spine at the L5/S1 level articulating through the transverse process with the sacrum on the left side could explain the absence of her left ankle reflex, and that he would defer to a surgeon or a neurologist on that point. Dr Kelman is an orthopaedic surgeon with relevant expertise, and his evidence is to be preferred.
41. We accept that the dermatomal distribution of pain is a matter that is not amenable to the application of a general standard in all cases, and that variation may be found from one case to another. Nevertheless, in Ms Thurling’s case we are reasonably satisfied that her symptoms are not of radicular origin, but are more likely explained as referred pain or sciatic pain, being pain that in all likelihood results from peripheral nerves rather than from any alteration of nerve root function and in that regard is not a sign of true radiculopathy. Furthermore, if there is alteration of nerve root function or ‘entrapment’ at the L5 level, as suggested by Dr Eaton, it is more likely than not that such alteration is the result of the progressive deterioration of Ms Thurling’s previously existing degenerative disease and facet osteoarthritis at the L4/5 level[52] or pathology associated with the abnormality of her L5 vertebra.
[52] Dr Kelman, T32 folio 129.
42. For these reasons we prefer the evidence of Doctors Kelman and Pascall, that Ms Thurling does not have a diagnosis-based permanent impairment that is consistent with significant signs of radiculopathy. It follows that we are satisfied that the diagnosis-based estimate of Ms Thurling’s impairment is not within the terms of the first criterion of the 13 percent level of whole person impairment under Table 9.17.
43. Turning, finally, to consider the second criterion at the 13 percent level under Table 9.17, some evidence was adduced concerning the existence of “a small left paracentral/foraminal disc protrusion” at the L4/5 level in Ms Thurling’s spine.[53] We accept that this is consistent with a herniated disc. As can be seen the herniation is at the L4/5 level and marginally on the left side. The origin of the herniation is not clear. Dr Eaton gave evidence that the MRI scans from 15 September 2000[54] and 15 November 2005[55] were “about the same” and did not indicate any significant change in Ms Thurling’s lumbar spine during the intervening period. The films of these MRI scans were not provided to any of the expert medical witnesses and were not tendered in evidence. Nevertheless, the second criterion at the 13 percent level under Table 9.17 requires objective clinical findings, associated with radiculopathy. Other than Dr Eaton’s failure to elicit a left ankle reflex, there are no objective clinical findings that are consistent with radiculopathy on the left side as a result of altered nerve function at the L4/5 level. Ms Thurling’s complaints of intermittent symptoms of pain at the rear of her upper left leg with parasthaesia in her left foot are not consistent with radiculopathy as a result of altered nerve function at the L4/5 level. One would expect pain resulting from nerves at the L4/5 level in a dermatomal distribution below the knee.
[53] T19.
[54] Exhibit A1.
[55] T19.
44. Thus, even though Ms Thurling did not press any claim in relation to the second criterion at the 13 percent level, we are satisfied that the requirements of that criterion are not satisfied in her case.
45. It follows that Ms Thurling does not have a permanent impairment of 13 percent under Table 9.17. We so find. As compensation is not payable unless the subject injury results in a permanent impairment of 10 percent or more, even if we found that her injury resulted in the bilateral leg symptoms of which she complained, and we did not, her claim cannot succeed.
46. The decision under review is affirmed.
I certify that the 46 preceding paragraphs are a true copy of the reasons for the decision herein of Mr S. Webb, Member
Signed: (signed)
Jane Gribble
AssociateDate of Hearing 17, 18 March 2008
Date of Decision 4 April 2008
Counsel for the Applicant Paul Stockley
Solicitor for the Applicant Daniel Steiner
Capital Lawyers
Counsel for the Respondent Lorraine Walker
Solicitor for the Respondent Andrew Schofield
Sparke Helmore Lawyers
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