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Ashley and Comcare [2012] AATA 4 (5 January 2012)

Last Updated: 5 January 2012

Administrative Appeals Tribunal

DECISION AND REASONS FOR DECISION [2012] AATA 4

ADMINISTRATIVE APPEALS TRIBUNAL )

) No 2010/1268

GENERAL ADMINISTRATIVE DIVISION
)

Re
LEONIE ASHLEY

Applicant
And
COMCARE

Respondent

DECISION

Tribunal Professor RM Creyke, Senior Member

Miss EA Shanahan, Member

Date 5 January 2012

Place Canberra

Decision
The decision under review is affirmed.

...............................[sgd].......................
Professor RM Creyke, Senior Member

CATCHWORDS

COMPENSATION – Commonwealth employees – permanent impairment - L5 facet joint strain – aggravation of intervertebral disc disorder - degenerative spondyloarthopathy – radiculopathy - sciatica – pain in dermatomal distribution – sensory loss – difference between signs and symptoms - whether suffered in course of employment – whether effects of accepted injury continued to be suffered – degree of whole person impairment according to American Medical Association’s Guides to the Evaluation of Permanent Impairment (5th edition)

Safety, Rehabilitation and Compensation Act 1988 (Cth) s 4, 24, 27

Comcare v Broadhurst [2011] FCAFC 39

Thurling v Comcare [2008] AATA 270

REASONS FOR DECISION

5 January 2012 Professor RM Creyke, Senior Member


  1. Ms Leonie Ashley had been employed as a senior sonographer by The Canberra Hospital since 1990.
  2. She had an accepted claim for aggravation of intervertebral disc disorder, lumbar region, with a date of injury of 21 May 2001.
  3. On 19 October 2009, Comcare made a determination denying liability for compensation for permanent impairment for the condition under sections 24 and 27 of the Safety, Rehabilitation and Compensation Act 1988 (Cth) (Act), a decision affirmed on review on 1 March 2010.
  4. On 1 April 2010, Ms Ashley sought a review of that decision by the Tribunal.

History

  1. Ms Ashley was born in 1960. She commenced employment with ACT Health in approximately 1976. She worked as a senior sonographer at The Canberra Hospital from 1990 until her voluntary redundancy in 2007. Her duties involved her bending from the waist and applying downward pressure on a patient’s body in order to perform ultrasounds.
  2. Ms Ashley said she first noticed problems with her lower back in 1996. Initially the problems settled with rest and physiotherapy. However, the pain returned after a busy period at work.
  3. In her workers’ compensation claim dated 1 November 1996, she claimed she suffered an L5 facet joint strain, which developed from May 1996 to October 1996. She noticed pain in the right hip, some tingling down the right leg to her right foot, and in her lower back when bending and stretching in the ultrasound rooms, the nursing bay and when moving ultrasound equipment. She had X-rays at the time but no further treatment. Prior to 2001, Ms Ashley said she consulted an osteopath, Ms Belinda Livis, and the pain would again settle with massage, rest, and anti-inflammatory and analgesic tablets.
  4. However, in an accident report dated 21 March 2001, Ms Ashley said she had experienced increasingly severe lower back, hip and neck pain in the previous few weeks. She claimed that the factors contributing to her condition were continual scanning in awkward positions without adequate breaks, prolonged staff shortages, and little assistance for load-bearing tasks, like patient transfers, moving ultrasound machines to wards and positioning heavy beds. She first sought medical attention from Dr Stephen Jamieson, her treating general practitioner, on 21 May 2001.
  5. On 22 May 2001 she lodged a worker’s compensation claim stating she could ‘no longer stand or sit for any longer than 15 minutes’, she could not ‘move freely’, and she had a ‘constant ache’ in her lower back which increased to pain during the day depending on her activities. She claimed that this was an exacerbation of her pre-existing lumbar disorder. Her May 2001 claim was accepted on 13 June 2001, her injury being described as ‘an aggravation of intervertebral disc disorder – lumbar region’ with a date of injury of 21 May 2001.
  6. Subsequently she continued to suffer episodic back pain due, she said, to the nature and conditions of her employment. She claimed that she experienced pain in her lower back, right hip, right buttock, down the right outer calf, with tingling sensations in the calf and foot, and pins and needles in her right leg coinciding with the pain. She experienced the same symptoms on the left side but not as often. The pain was constant in her lower back but elsewhere the pain varied with activity. In an inactive week, pain could occur two to three times a week; in an active week, every day.
  7. Ms Ashley’s current treatment for her conditions is osteopathy and medication (Celebrex and Digesic), heat packs, and use of her electric blanket. Ms Ashley retired from work on medical grounds in 2007 and has not worked since.
  8. At the hearing, Ms Ashley said she did not remember whether the reports of varying measurements of her thighs by Mr Coyle and Dr Richard Evans involved the right or the left thigh. However, she maintained that her right leg was strongest, so the right thigh measurement should be greater than the left. In response to questioning, Ms Ashley noted that she had experienced knee problems in the 1990s, and had undergone operations on both knees in 1999 and again in 2002. She had not noticed any reduction in the size of either thigh at that time.
  9. She submitted a claim for permanent impairment dated 3 March 2009 in respect of ‘injury to back and both legs – lower back disc disorder – lumbar region’.

Medical evidence

  1. In a radiological report relating to the right hip dated 27 October 1992 Dr N Smith, radiologist, reported no abnormality of her hips or sacro-iliac joints. Dr Smith reported a slight retrolisthesis at the L5/S1 level.
  2. In a radiological report dated 13 July 1993 Dr S Bell, radiologist, reported that Ms Ashley’s cervical vertebra and disc spaces appeared normal, the nerve root exit space was unimpaired and there was no cervical rib shown.
  3. In a radiological report of the lumbo-sacral spine dated 15 June 2001, Dr A Robertson, radiologist, noted a history of back pain. He identified a decrease in the intervertebral disc heights, particularly at the L5/S1 and L3/L4 levels. He considered that degenerative spondyloarthropathy was seen, particularly at the L5/S1 level and to a lesser degree at the L3/L4 and T12/L1 levels. He considered that the intervertebral foraminae were patent.
  4. A medical report by Dr John Lange, occupational physician, dated 15 December 2001, diagnosed L5/S1 disc degeneration, of which 70 to 80 per cent could be attributable to the natural ageing process. Dr Lange considered [Ms Ashley] was fit to resume work and that it would be reasonable for her to work eight hour days, of which two hours should be devoted to administrative duties.
  5. An MRI of Ms Ashley’s spine reported on by Dr John Ly on 18 November 2002 concluded that there was a ‘moderate sized posterior central disc protrusion at the L5/S1 level on a background of disc degeneration and annular bulge’. However, he said ‘right-sided nerve roots do not appear to be impinged upon’, and that he was therefore ‘unclear as to the cause of the patient’s symptoms’.
  6. A medical report of Dr Colin Andrews, neurologist, dated 15 January 2003, considered that the symptoms suggested a right S1 nerve root irritation. Dr Andrews considered that the MRI showed a moderate central disc protrusion at the L5/S1 level, which he considered was in close proximity to both S1 nerve roots. Dr Andrews considered that there was little doubt that the disc lesion at L5/S1 was the cause of [Ms Ashley’s] symptoms. He observed that her symptoms were resolving.
  7. The 2002 MRI was reviewed by Dr Malcolm Thomson on 28 February 2010. He concluded that there were ‘degenerative changes involving the L4/5 and L5/S1 intervertebral discs. Potential for compromise of particularly the left L4 nerve root at L4/L5 and for the S1 nerve roots at L5/S1. The right L4 nerve root is less convincingly compromised’. In the body of his report, he said that at the L4/5 level, ‘there was a moderate left posterolateral disc protrusion potentially compromising the left exiting L4 nerve root.’ He also recorded ‘Bilateral facet joint osteoarthosis at L4/5 and L5/S1’. In his opinion, the ‘associated inflammatory change may well irritate both S1 nerve roots’.
  8. In a medical report dated 16 October 2003, Dr David Burke, rehabilitation medicine physician, diagnosed degenerative changes in lumbosacral discs with bulging of the L5/S1 intervertebral disc. Dr Burke found that the injury sustained on 21 May 2001 was an aggravation of a pre-existing condition. He considered that Ms Ashley’s condition was unlikely to resolve or stabilise in the near future. In support of his opinion, Dr Burke referred to the MRI scan which showed a mild to moderate central disc bulge at the L5/S1 level.
  9. In a report of 11 March 2005, Dr Virginia Pascall, occupational physician, said Ms Ashley had suffered an aggravation of her underlying degenerative condition in 2000-2001 as a result of maintaining abnormal postures for long periods of time as well as general manual handling tasks, including pulling patients on trolleys and the ultrasound machines, and assisting patients from their wheelchairs onto the ultrasound table and vice versa. She considered that Ms Ashley’s lower back problems commenced in 1992 when she was in her mid-thirties. She noted that Ms Ashley had a significant disc protrusion at the L5/S1 level which extended close to, if not touched, the S1 nerve root which might have caused some radicular symptoms.
  10. Dr Pascall considered that the peripheral symptoms in Ms Ashley’s right leg and foot were not radiologically supported by nerve root impingement. She found that Ms Ashley had also suffered degenerative changes in the lumbosacral spine, and it was likely that she also suffered degenerative change in her cervical spine. She considered sustained abnormal posture was the activity most likely to have caused Ms Ashley’s increasing back pain during 2000-2001. She also considered the degenerative changes in Ms Ashley’s lumbar and cervical spine would increase over time and her ability to undertake sonography would diminish, unless there were significant changes in the technology providing sonographers with better ergonomic practices.

Dr Jamieson

  1. Dr Stephen Jamieson, Ms Ashley’s treating general practitioner, reported on 29 May 2002 that Ms Ashley had a work-related lumbar disorder. He identified the cause of this disorder as being due to staff shortages, and Ms Ashley being ‘forced to carry out more clinical work,’ exacerbating her lumbar pain. He certified that she should be limited to five hours of clinical work per day. A second report dated 18 November 2002 referred to her ‘intervertebral lumbar disc disorder’. He denied a report by Dr Lange that her condition had resolved and said her condition continued to be exacerbated by excessive bending or twisting at her workplace. He rejected Dr Lange’s assessment that 70-80 per cent of her lumbar condition was due to ageing on the basis that there could be no scientific explanation for the figures. He also asserted that it was Ms Ashley’s occupation was renowned for chronic spinal problems. In a report to Comcare dated 24 August 2003, Dr Jamieson rejected Dr Low’s medico-legal report that Ms Ashley’s symptoms were due to ‘disturbance of psycho-social functioning’. In Dr Jamieson’s view, her symptoms were ‘mechanical in nature’ due to ‘changes at the L5-S1 disc’, and he said that this was confirmed in an opinion he had sought from Dr Garth Eaton.
  2. His clinical notes refer to the following:
  3. The notes also record measurements of the thigh circumferences in 1997 and 1999. On both occasions, the left thigh circumference was 1.5 cm less than the right thigh.

Dr Low

  1. Dr Ian Low, occupational physician, reported on 5 March 2003, that Ms Ashley had been doing ultrasounds for ACT Health for 24 years. He reported her saying she developed an ‘intermittent sore back with tingling down her right leg’ about ten years previously. The condition, which was not triggered by any particular action, worsened over the working week and improved over the weekend. She had tried reducing her work hours and had been on restricted duties since 2001. By 2003, her back condition was no longer improving with rest.
  2. Dr Low found ‘no evidence of nerve root compression’ and said ‘the MRI scan of 18 November 2002 is reported to show, at L5-S1, a moderate sized posterior central disc protrusion abutting the left S1 nerve root with no evidence of impingement of the right S1 nerve root’. In his view, Ms Ashley’s movement of the ultrasound machines would not cause degenerative change in the spine, in particular disc damage.
  3. Dr Low’s opinion was that ‘disability due to low back pain depends more on complex individual and work-related psychosocial factors than on clinical features or physical demands of work’. Given this viewpoint and the absence of neurological damage, in Dr Low’s assessment, Ms Ashley’s ‘low back pain is due to a disturbance in her psychosocial functioning with associated tightness in her spinal musculature’. As he said:

The persistence of her pain will be related to reinforcement of her belief that she is suffering from a physical disorder, a lack of insight into the impact of her personality functioning on her emotional functioning and musculature, her frustration at not being able to perform more clinical work and probably, her beliefs about management’s failure to provide adequate staffing levels as a result of which she perceives she has been physically injured.

  1. In his view there was no indication for any physical therapy and there was no physical pathology which would preclude her from working full time in her usual duties.

Dr Eaton

  1. Dr Garth Eaton, occupational physician, reported on 23 May 2003. He confirmed that it was common for ultrasonographers to be affected by ergonomic and postural factors in the course of their employment. He conceded that psychological and emotional difficulties can also play a part, but disagreed with Dr Low that in Ms Ashley’s case all of her problems were of that nature. As he said:

I would certainly not feel confident saying there is no physical component to [Ms Ashley’s] aches and pains, particularly when she was scanning’. As he said ‘There is likely to be a neurogenic component to her pain, which may well be aggravated by various workplace environmental factors.

Dr Evans

  1. Dr Richard Evans, physician, prepared two reports: both are dated 18 March 2010. The second report clarified a reference to a table in the Comcare Guide to the Assessment of the Degree of Permanent Impairment (2nd ed, 2005) (Comcare Guide). He concluded Ms Ashley’s level of permanent whole person impairment was 13 per cent under Table 9.17 of the Comcare Guide. He did not resile from this assessment at the hearing.
  2. Dr Evans’s measurements of Ms Ashley’s thighs showed a right thigh circumference of 37cm and a left thigh of 35cm. The right calf was 31.1cm and the left, was 30.2cm, a small difference that could be expected between a dominant and non-dominant leg. In his initial statement to the Tribunal Dr Evans said he thought the difference in diameter – the wastage - of Ms Ashley’s left thigh and calf was consistent with radiculopathy. At the hearing he acknowledged that the difference in measurements in 2010 ‘could be radiculopathy and it would fit with S1 nerve irritation, but I can’t be dogmatic about it’.
  3. He also noted that ‘The numbness and tingling experienced by Ms Ashley in the backs of the thighs and calves ... are suggestive of irritation of the first sacral nerve root’, resulting from ‘irritation of the S1 nerve roots at the L5/S1 segment of her back’. As he said, ‘the most likely cause of the current back pain and stiffness is the L5/S1 disc protrusion, though it is not possible to exclude a contribution from the L4/5 protrusion’. He conceded that minor symptoms of pressure on a nerve root would be ‘irritation of the nerve’, but ‘significant’ alteration of a nerve would occur as compression on the nerve becomes worse.
  4. He also conceded calf wasting rather than thigh wasting would, more typically, flow from damage to or irritation of the S1 nerve roots. However, he said such damage can cause thigh wasting since the S1 nerve root was one of the three nerves supplying the quadriceps muscle, the main muscle at the front of the thigh. The Tribunal, however, noted that according to Gray’s Anatomy,[1] the L2 to L4 nerve roots connected with the quadriceps muscle, while the S1 nerve was related to the biceps femoris muscle. Dr Evans said he was relying on the neurology text by Russell Brain.[2]
  5. In response to the report of Mr Coyle for Comcare that there was ‘non-verifiable radicular complaints’, Dr Evans said ‘I do not think that this is fair. She has pain and abnormal sensations in a dermatomal distribution (S1) and a radiologically verified disc herniation consistent with the radiculopathy’. In his opinion Ms Ashley’s work was a more likely cause of ‘disc damage and associated degeneration than any constitutional factor’.
  6. Dr Evans noted there was looseness in usage of the term ‘sciatica’, commonly employed to mean any pain radiating down the leg. The technically correct meaning of sciatica is pain due to the sciatic nerve. According to Dr Evans, it was rare for so-called sciatic pain to be correctly attributed. He said the term ‘radiculopathy’, meant irritation of or damage to a nerve root. This can present as pain, numbness and tingling, or weakness, or any combination of the three. He did not agree with Mr Coyle’s description of the distinction.
  7. In Dr Evans’ view, sciatica is almost always due to radiculopathy. He also observed straight leg raising for Ms Ashley of 60 degrees right and 70 degrees left, and noted that this was consistent with radiculopathy. He said that clinical evidence of radiculopathy was indicated predominantly by pain and/or numbness and tingling radiating down a leg. In his view, it ‘was significant’ that ‘sensory impairment’ was also present. He noted that Ms Ashley had ‘unilateral atrophy above or below the knee’ and that these symptoms were ‘caused by the left S1 nerve root being irritated by the disc‘. The ‘history of a herniated ... disc on the level ... consistent with objective clinical findings’ was also evidence of radiculopathy.
  8. In response to a suggestion that the pain in Ms Ashley’s legs was not dermatomal in distribution, he said as the pain was present intermittently, he had reached no firm conclusion on the cause. He said Ms Ashley’s description of the site of the leg pain was dermatomal in distribution in that it was consistent with S1 nerve root damage. He said he thought the symptom of ‘numbness was much more important’ than pain and he had relied more on her sensation of numbness, than of pain, for his assessment.
  9. He disagreed with Mr Coyle’s report of 22 September 2011 in relation to the relevance of ‘right thigh muscle wasting’, since he found wasting of the left, not the right thigh. Nor, for the same reason, did he agree with his reference to ‘lateral right foot sensory symptoms’. Finally, he disagreed with the source of the numbness in the right foot since he had found no abnormality in the reflexes, nor evidence of L3 or L4 nerve irritation. He conceded, however, that Gray’s Anatomy could well indicate that the L4 dermatome includes the front of the toes and the sole of the foot on the medial aspect.
  10. In cross-examination he acknowledged that ‘pins and needles’ would amount to ‘altered’, not ‘loss of’ sensation. He also conceded that an observed alteration of calf measurements was more significant than of thighs for an S1 nerve root damage. Other effects such as reflex loss, sensory loss, weakness and atrophy can all occur, but do not have to be present. He affirmed that the reported numbness in Ms Ashley’s right foot was consistent with radiculopathy, since the disc lesion was capable of affecting both S1 nerve roots.
  11. Dr Evans’s comment on the findings by Dr Thomson on the MRI was that they appeared to be ‘consistent with ... the clinical picture’.

Mr Coyle

  1. Mr William Coyle, orthopaedic surgeon, provided five reports dated 14 October 2009, 26 July 2010, 24 August 2010, 21 April 2011, and 22 September 2011.
  2. In his October 2009 report, he diagnosed ‘chronic symptomatic lumbosacral disc disease, degeneration and prolapse, substantially contributed to by [Ms Ashley’s] strenuous physical work as a sonographer over many years’. He said the condition ‘probably became permanent in 1996’. He assessed whole person impairment due to work at 6 per cent, having deducted 2 per cent for age related degeneration. In his opinion she has ‘non-verifiable radicular complaints’ and ‘radiologically demonstrated disc herniation consistent with radiculopathy’.
  3. His supplementary report of 26 July 2010 substantially agreed with his initial report. However, at the hearing, he said he resiled from those views ‘to a certain extent’. As he said, the MRI report and both radiologists who had reported on it said the prolapse of the disc was on the left-hand side, but Ms Ashley’s view was that her symptoms were on her right side. He concluded ‘You’ve just got to accept that happens’.
  4. In his supplementary report of 24 August 2010, Mr Coyle noted that he could ‘find no objective clinical signs of neurological deficit in the lower limbs’, despite Ms Ashley saying she ‘had intermittent paresthesia on the lateral aspect of her right ankle and heel’. In support he said ‘there was no limitation of straight leg raising of either lower limb to indicate significant sciatic nerve root irritation’.
  5. He also explained:

I do not agree that ‘sciatica’ is a colloquialism for ‘radiculopathy’, as I do not agree that they mean the same thing. ‘Sciatica’ to me means pain or non-verifiable sensory change in the distribution of the sciatic nerve or of a sciatic nerve root and is the result of irritation of the sciatic nerve or nerve root only. ‘Radiculopathy’ to me means that the nerve has been so irritated or compromised that its function is impaired’.

In other words, a nerve affected by radiculopathy will cause verifiable changes in the distribution of the sciatic nerve such as absent or diminished deep tendon reflexes, muscle weakness or muscle wasting.

  1. However, in his 21 April 2011, report he noted ‘The straight leg raising test for sciatic nerve root irritation was on this occasion somewhat limited, to 70 [degrees] on the left side and 60 [degrees] on the right side, both causing ipsilateral buttock pain’. He concluded that ‘Ms Ashley has chronic symptomatic lower lumbar disc degenerative disease, affecting the L4/5 and, especially L5/S1 intervertebral discs, substantially contributed to by her strenuous physical work as a sonographer over many years’. He also noted ‘more abnormal clinical signs on this occasion’ and that ‘her lumbar spinal movements are quite grossly restricted and obviously painful ....and that there is some definite irritation of her sciatic nerves, especially the right’. He said his re-examination had not caused him to change his opinion about her level of impairment, which in his view under AMA 5 would be 7 per cent whole person impairment due to her work-related lumbar spinal condition.
  2. He reported on 22 September 2011 that the results of Ms Ashley’s straight leg raising tests had not altered since his April 2011 report. He detected no neurological deficit in the lower limbs; she had intermittent paraesthesia in the lateral aspect of her right ankle and heel; her mid- right thigh was 1.5cm less than the mid left thigh, indicating some left thigh muscle wasting; but there was no calf muscle wasting. He confirmed that the imaging evidence from 2002 supported a diagnosis of a herniated disc or discs. He said that the radiation of pain to her right lower limb was ‘sciatica’ which was not the same as thing as ’radiculopathy’.
  3. In his view ‘Ms Ashley’s right lower limb pain is widespread and cannot be described as dermatomal in distribution’. By contrast, her ‘intermittent paraesthesia ... in the lateral aspect of her right ankle and heel ... is in the S1 dermatomal distribution’. He found no ‘apparent loss of muscle strength of either lower limb assessed clinically’. He also concluded that the difference he had detected in muscle bulk [as previously] between the two thighs was ‘probably not related to any nerve root impairment’ and was ‘probably more likely related to Ms Ashley favouring her right lower limb because of the right lower limb pain’.
  4. He said ‘The only clinical sign I have found which could possibly be the result of radiculopathy is relative muscle wasting of the right thigh which could mean compromise of function of right L3 or L4 nerve roots’. He said this was consistent with disuse of the right lower limb, ‘because that’s the painful one’. He found that ‘‘She relied more on her left lower limb than her right lower limb,’ and this was ‘the most likely explanation’ for the ‘relative muscle wasting in her right thigh’. In his view, Ms Ashley did not have any clinical signs to indicate S1 radiculopathy but she does have ‘a convincing history of symptoms suggesting irritation of the right S1 nerve root’. He did not alter his assessment of her level of impairment of 7 per cent under the AMA 5 Guidelines. .
  5. He agreed that paresthesia in the form of ‘pins and needles’ was evidence of ‘sensory change, not necessarily loss’. He found that ‘It may or may not be associated with numbness. But it’s not verifiable; it’s a subjective complaint’. In cross-examination, however, he conceded that numbness ‘would constitute a complaint of sensory loss’. He also noted that for a ‘verifiable’ diagnosis, there would need to be something ‘you can see or measure’ such as ‘absence of tendon reflexes, muscle weakness of specific muscle groups, or muscle wasting of specific muscles’. He also denied that a difference of 10 degrees in straight leg raising would be an indicator of radiculopathy. In his view, an asymmetric loss of range of motion was an indicator under AMA 5 Table 15.3 DRE II, not III.
  6. Mr Coyle’s notes indicated that the thigh measurement ‘right side [was] one and a half centimetres less than left side’. He also indicated that irritation of the nerve roots was not the same as radiculopathy. He said that in September 2011 he had tested Ms Ashley’s lower limb muscle strength and both legs were weak. He also agreed that weakness was one of the significant signs of radiculopathy.
  7. However, in cross-examination, when taken to his September 2011 report, Mr Coyle indicated that he held clinically to the view that ‘There is no apparent loss of muscle strength of either lower limb assessed clinically’.. He denied the statements he made earlier during the hearing, concerning loss of muscle strength in both lower limbs. He confirmed that the limitation on straight leg raising was due to pain but said that ‘unilateral muscle wasting was due to disuse’.
  8. At the hearing, Mr Coyle admitted, in response to a question by the Tribunal, that he had not tested biceps femoris and disagreed to an extent with the Tribunal’s information from Gray’s Anatomy as to which nerves related to the biceps, knee flexion, and gluteus maximus and minimus muscles. Mr Coyle said he had relied for many years on Last’s Anatomy.[3]

Other evidence

  1. A statement by Ms Ashley’s supervisor, Mr John Ryan, dated 1 November 1996 noted that ‘the practice of diagnostic ultrasound is physically demanding, with “unergonomic” postures required. Adjustable height trolleys have been introduced to assist and staff advised to relieve physical strain by movement’. Mr Ryan had also noted that staff had been reduced as a result of an Operational Efficiency Review.
  2. Ms Ashley’s supervising officer, Dr Bill Mouratidis, on 23 May 2001, described her injury as ‘chronic low back pain’. He said the condition as reported by Ms Ashley was due to ‘chronic repetitive musculoskeletal stress causing exacerbations of chronic low back pain, hips, knees, neck, shoulders, elbows’. He observed ‘stiffness, limited movement, acute severe, painful episodes’.

Legislation

  1. Section 24 of the Safety, Rehabilitation and Compensation Act 1988 (Cth) (Act) provides for payment of compensation for permanent impairment. Section 27 sets out the pre-requisites for compensation for non-economic loss. Section 24(3) provides that the amount of compensation is an amount ‘not exceeding the maximum amount at the date of the assessment’. Section 24(4) provides that the amount ‘is the same percentage of the maximum amount as the percentage determined by Comcare under subsection (5)’.
  2. Section 24(5) provides that ‘Comcare shall determine the degree of permanent impairment of the employee resulting from an injury under the provisions of the approved Guide’. No compensation is payable if ‘the degree of permanent impairment is less than 10 per cent’.[4] A Guide has been approved and its second edition has been in force since 2005.
  3. Relevant definitions in the Act are:

4(1) Interpretation

‘approved Guide’ means:

(a) the document, prepared by Comcare in accordance with section 28 under the title ‘Guide to the Assessment of the Degree of Permanent Impairment’, that has been approved by the Minister and is for the time being in force; and

(b) if an instrument varying the document has been approved by the Minister--that document as so varied.

‘impairment’ means the loss, the loss of the use, or the damage or malfunction, of any part of the body or of any bodily system or function or part of such system or function.

‘permanent’ means likely to continue indefinitely.

  1. The relevant table in the approved Guide is Table 9.17 – Lumbar Spine – Diagnosis-Related Estimates. However, as there is a dispute about Ms Ashley’s level of impairment which was assessed by Mr Coyle as either 7 or 8 per cent, and by Dr Evans, as 13 per cent, there is the potential for the Tribunal to be required, under principles established in Comcare v Broadhurst,[5] to rely on an alternative guide to the Comcare Guide. In these circumstances, Table 15.3 of the American Medical Association’s Guides to the Evaluation of Permanent Impairment (5th edn) (AMA Guides) was relied on as an alternative. However, since Table 15.3, in its description of the criteria for level of impairment, is in identical terms to Table 9.17, little turns on the distinction. Two differences are first in relation to the percentage of impairment listed alongside the criteria, and second that DRE Category III states also that ‘impairment may be verified by electrodiagnostic findings’. It was common ground that no electrodiagnostic findings had been undertaken since 2002.
  2. The text of the relevant columns in Table 15.3 is set out below.
DRE Lumbar Category I
0% Impairment of the Whole Person
DRE Lumbar Category II
5-8% Impairment of the Whole Person
DRE Lumbar Category III
10-13% Impairment of the Whole Person
No significant clinical findings, no observed muscle guarding or spasm, no documentable neurologic impairment no documented alteration in structural integrity, and no other indication of impairment related to injury or illness; no fractures.
Clinical history and examination findings are compatible with a specific injury; findings may include significant muscle guarding or spasm observed at the time of the examination, asymmetric loss of range of motion, or nonverifiable radicular complaints, defined as complaints of radicular pain without objective findings; no alteration of the structural integrity and no significant radiculopathy.
Significant signs of radiculopathy, such as dermatomal pain and/or in a dermatomal distribution, sensory loss, loss of relevant reflex(es), loss of muscle strength of measured unilateral atrophy above or below the knee compared to measurements on the contralateral side at the same location; impairment may be verified by electrodiagnostic findings.

  1. Relevant definitions for the purposes of the AMA5 Guides are:

Radiculopathy

Significant alteration in the function of a nerve root or nerve roots and is usually caused by pressure on one or several nerve roots. The diagnosis requires a dermatomal distribution of pain, numbness, and/or paresthesias in a dermatomal distribution. A root tension sign is usually positive. The diagnosis of herniated disk must be substantiated by an appropriate finding on an imaging study. The presence of findings on an imaging study in and of itself does not make the diagnosis of radiculopathy. There must also be clinical evidence as described above.

Weakness and loss of sensation

To be valid, the sensory findings must be in a strict anatomic distribution, ie, follow dermatomal patterns. ... Motor findings should also be consistent with the affected nerve structure(s). Significant, long-standing weakness is usually accompanied by atrophy.

Atrophy

Atrophy is measured with a tape measure at identical levels on both limbs. For reasons of reproducibility, the difference in circumference should be 2cm or greater in the thigh and 1cm or greater in the arm, forearm, or leg. The evaluator can address asymmetry due to extremity dominance in the report.

Issues

  1. The agreed statement of issues is:

Consideration

Whether Ms Ashley continues to suffer from the effects of the May 2001 injury?

  1. Ms Ashley’s claim, which was accepted, was for a condition she described as episodic back pain. She says the pain is constant in her lower back but varies in intensity. She also gets pain in the right hip, right buttock, down the right outer calf, and tingling sensations in the calf and foot. She gets the same symptoms on the left side but not as often. The intensity of the pain varies with activity. On an inactive week, it can occur two to three times a week; in an active week, it can occur every day. The sites and precipitating activities giving rise to her pain are similar to those she experienced in 1996. She maintains that the pain is due to the nature and conditions of her employment, and has continued since 2001.
  2. The clinical notes of Dr Jamieson confirm that the predominant reason for her consultations since 2001 to mid-2010, the period of the notes, has been her complaint of lumbar pain. No doctor has denied that she experiences pain.
  3. Ms Ashley, Mr Ryan, Mr Coyle, Doctors Mouratidis, Evans, Eaton, Jamieson, Pascall, and Burke all accepted that her back conditions were substantially caused by her sonography work. Only Dr Lange and Dr Low considered that the contribution of her work was at most minimal in a causal sense. Given the preponderance of medical evidence, the Tribunal finds that Ms Ashley continues to suffer pain in the lower back, lower legs, buttocks and feet consistent with an aggravation of an intervertebral disc disorder which was work-related.

Degree of whole person impairment that resulted from the May 2001 injury

  1. The principal focus for this application has been the degree of whole person impairment suffered by Ms Ashley due to her employment. It was accepted that the assessment was to be undertaken using AMA5 Table 15.3.[6]
  2. Despite some deficiencies in the medical evidence, and disagreements about the nature and source of the symptoms suffered by Ms Ashley, the Tribunal considers that it has sufficient information to reach a conclusion in this matter.
  3. Ms Ashley submits that her evidence, coupled with the evidence of Dr Jamieson, Dr Evans, and Mr Coyle was that she has:

... dermatomal pain as well as a dermatomal distribution with respect to the bilateral incidence of paraesthesia, sensory loss based upon her evidence and the confirmation of Mr Coyle that numbness equates to sensory loss and loss of muscle strength and a measured unilateral atrophy which is noted by both Mr Coyle and Dr Evans... On the basis of those assessments, [Ms Ashley] asserts that she has established ...the ‘significant signs of radiculopathy criteria’.

  1. Ms Ashley also accepts ‘that she must establish that she has at least two significant signs and submits that she has established no less than five significant signs of radiculopathy’. She also submits she is not required to establish that she has radiculopathy simpliciter but merely that she has to establish, in accordance with the DRE III Table, ‘significant signs of radiculopathy’.
  2. As a preliminary matter the Tribunal notes there appears to be some misunderstanding of the meaning of ‘signs’ as used in the relevant Table, as compared with ‘symptoms’. The Tribunal notes that a ‘symptom’ is purely subjective, that is, it is how the person describes the nature of their complaint. In the case of Ms Ashley, her symptoms are low back pain radiating to both lower limbs and her intermittent paraesthesia and numbness in the lower limbs.
  3. By contrast, ‘signs’ are objective and usually elicited on physical examination by a medical practitioner. Evidence of a ‘sign’ on investigation, generally by a medical practitioner, would follow measurement of limbs, or testing of reflexes or strength, and be based, for example, on MRI findings, an X-ray, or loss of body mass in the limbs. These distinctions are relevant to the issue of whether Ms Ashley meets the criteria in Table 15.3 for either DRE II or DRE III. The Tribunal reads the criteria in DRE III as referring to objectively identified and significant indications of radiculopathy.
  4. However, the Tribunal notes that there also appears to be confusion between the use of ‘signs’ and ‘symptoms’ in Table 15.3. That table states for DRE III, ‘Significant signs of radiculopathy, such as dermatomal pain’. This criterion uses ‘symptom’ and ‘sign’ interchangeably in relation to radiculopathy, pain being a symptom, not a sign. Despite this confusion, it is possible to discern an intention from the criteria read as a whole, that a prerequisite for a finding of radiculopathy is pain in a dermatomal distribution. Therefore the signs, as listed, must also be in a dermatomal distribution, and the Tribunal so finds.
  5. A further ambiguity in Table 15.3 DRE III is the use of ‘and/or’ in the descriptions of the criteria, following the reference to ‘dermatomal pain’. At first sight, a reading of the criteria in light of the use of ‘or’, suggests that only ‘significant signs of radiculopathy’ or any one of the criteria following the reference to ‘radiculopathy’ such as ‘sensory loss’ would be sufficient for an assessment of 10-13 per cent level of impairment.
  6. Equally, the reference to ‘signs’ in the introductory criterion ‘Significant signs of radiculopathy’, could be interpreted to mean simply that there is more than one indicator of radiculopathy, any one of those listed being sufficient to indicate radiculopathy. The Tribunal raised this interpretive issue with counsel who helpfully made submissions after the hearing had concluded.
  7. Both counsel maintained that use of ‘signs’ in the expression ‘Significant signs of radiculopathy’ was intentional and indicated more than one ‘sign’ was required. The submission for Comcare also indicated that the need for more than one ‘sign’ was accepted in Thurling v Comcare.[7] The Tribunal notes the absence of argument about the alternative interpretations in Thurling v Comcare. Nonetheless, the Tribunal accepts the submission of counsel and of Comcare. The Tribunal also notes that a finding that only one ‘sign’ of radiculopathy is required to meet an assessment under DRE III would be to ignore the ‘and’ in the expression Hence ‘signs’ should be taken to mean that at least two objective indicators of radiculopathy are required to meet the criteria in DRE III. In these circumstances, although the Tribunal considers there is ambiguity in the wording and this warrants reconsideration of the drafting, the Tribunal finds that more than one objective sign of radiculopathy is required for an assessment of level of impairment to fall within DRE III.
  8. The Tribunal has focused on whether an assessment of the effects of Ms Ashley’s conditions can bring her within Table 15.3 DRE III, so as to enable her to meet the minimal 10 per cent impairment level required by section 24(7)(b) of the SRC Act. If her level of impairment does not fall within DRE III, Ms Ashley’s application for review will be unsuccessful.
  9. The Tribunal also accepts that given the need for objective indications of radiculopathy, the evidence should be capable of showing that the nerve root affected by radiculopathy has caused verifiable changes such as absence of, or diminished, deep tendon reflexes, muscle weakness or muscle wasting.
  10. Turning to the ‘signs’ exhibited by Ms Ashley, the medical evidence indicates she has not experienced ‘loss of relevant reflexes’. Nor, despite Mr Coyle’s September 2011 report to the contrary, from which he later resiled at the hearing, does she appear to have experienced ‘loss of muscle strength’.
  11. The evidence about ‘measured unilateral atrophy above or below the knee’ was equivocal. Ms Ashley’s evidence was that her right leg was the stronger of the two and its measurement should be greater than for the left. That is consistent with the measurements taken by Dr Evans which showed her right thigh as 2cm larger than the left, and her right calf as less than one cm larger than the left. At the same time, that evidence is inconsistent with Ms Ashley’s submission that she experiences symptoms more on the right than the left side. That evidence is consistent with Mr Coyle’s findings that her right thigh was 1.5cm less than the left thigh with no calf muscle wasting. The evidence is also inconsistent with the majority medical and radiological opinion that potential nerve root compromise was more likely on the left than the right side.
  12. As it happens, nothing turns on these findings. As Dr Evans conceded, to be consistent with S1 nerve damage, it would be expected that the calf measurement was the more significant. The difference in girth of Ms Ashley’s calf that he detected is less than the minimum of one cm required in the notes to the Table 15.3. The difference, as he accepted, would be no more than could be expected between a dominant and a non-dominant limb. Dr Evans also said that although his findings about the differences in measurements were indicative of S1 nerve irritation, ‘I can’t be dogmatic about it’. In these circumstances, the Tribunal finds that Ms Ashley’s measured atrophy in her calf is not sufficiently significant to be an indicator of radiculopathy.
  13. Whether Ms Ashley suffered ‘sensory loss’ was another matter of dispute in the discussions and the evidence. Dr Jamieson’s clinical notes over a ten year history were of reports of ‘tingling’ and ‘numbness’ in Ms Ashley’s right foot and lower leg. The complaints of these sensations at consultations were, until 2004, made roughly once a year. There is then a break of some 4 years, to 2008, before the next report, and a further two years, till 25 February 2010, for the most recent report.
  14. The number and intervals between these reports, suggest that the sensations are intermittent, and infrequent. Additionally, there were noticeably fewer reports over the last 7 years, and the intervals between them became longer, suggesting an improvement of Ms Ashley’s symptoms. In particular, the Tribunal notes that Dr Jamieson’s clinical notes only refer to ‘numbness’ on three occasions over the ten year period.
  15. Dr Evans said he considered the ‘sensory impairment was significant’ and the sensation of ‘numbness’ was the more important indicator of radiculopathy. At the same time he conceded that ‘pins and needles’ was ‘altered’ not ‘loss of’ sensation, a view agreed with by Mr Coyle.
  16. Mr Coyle’s overall view, expressed in 2009 and affirmed in 2010, was that Ms Ashley suffered from ‘non-verifiable radicular complaints’, and that there were ‘no objective clinical signs of neurological deficit in the lower limbs’, despite her reported ‘intermittent paresthesia’. His views justified his assessment of her level of impairment as falling within DRE II, not DRE III. He maintained that these views were supported by the absence of any limitation in straight leg raising.
  17. Although by April 2011 Mr Coyle conceded that there was some limitation in Ms Ashley’s straight leg raising, and that he had also observed more ‘abnormal clinical signs’, that did not change his opinion about her level of impairment. He maintained his view that Ms Ashley’s slight muscle wasting was the only objective sign to indicate radiculopathy, and that overall his assessment of her level of impairment had not changed. His views were that she did not qualify for the minimum 10 per cent level of impairment under Table 15.3, DRE III. The Tribunal is satisfied that the predominant evidence is that Ms Ashley’s reports of sensory loss (numbness) or tingling (paraesthesia) were insufficiently frequent to be regarded as a significant sign of radiculopathy.
  18. Another disputed matter was whether Ms Ashley experienced signs or symptoms, including pain, in a dermatomal distribution. That raises the issue of the reports of nerve root compromise and damage to the discs in Ms Ashley’s spine.
  19. In his 2001 MRI report, Dr Robertson identified problems at the L5/S1 and L3/L4 levels of her spine, due to ‘degenerative spondyloarthopathy’. Dr Lange, late in 2001, confirmed the L5/S1 degeneration. A second MRI in November 2002, found ‘moderate sized posterior central disc protrusion at the L5/S1 level’ with disc degeneration. In his report on the MRI results, Dr Ly, noted that ‘right-sided nerve roots do not appear to be impinged upon’.
  20. Dr Andrews, in January 2003, agreed with the finding of disc protrusion at the L5/S1 level in ‘close proximity to both S1 nerve roots’. Dr Low also accepted that there was central disc protrusion abutting the left S1 nerve root, but he too found no impingement of the right S1 nerve root.
  21. A review of the 2002 MRI in 2010 by Dr Thomson confirmed the degenerative changes in the L4/L5 and L5/S1 discs and noted ‘potential for compromise of the left L4 nerve root at L4/L5 and for the S1 nerve root at L5/S1’. Dr Pascall, in 2005, said the S1 nerve root might have caused some radicular symptoms, but denied that Ms Ashley’s peripheral symptoms in her right leg and foot were indicative of nerve root impingement. Dr Evans conceded that Ms Ashley’s complaints of intermittent tingling and numbness were suggestive of nerve root irritation, but that this would not meet the ‘significant’ level of alteration of the nerve root needed to meet the criteria in DRE III.
  22. The upshot of the medical evidence is that there is accepted degeneration of Ms Ashley’s spine particularly at the L5/S1 level and also at the L4/L5 levels. The issue is whether there is sufficient evidence of pain in a dermatomal distribution to indicate a significant level of damage associated with radiculopathy.
  23. Ms Ashley’s evidence was that she experiences pain in her lower back, right hip, right buttock, down the right outer calf, with tingling sensations in the right calf and foot. She also experiences symptoms on the left side but with less intensity or frequency. Although the symptoms in the right outer calf occur in a dermatomal distribution relating to the L5/S1 nerve root, and Mr Coyle agreed that she had a ‘convincing history of symptoms suggesting irritation of the right S1 nerve root’, there is disagreement from medical specialists and practitioners as to whether the nerve root compromise is more marked in relation to the left or the right side.
  24. Doctors Ly, Thomson, Low, Pascall, and Evans suggest that the objective evidence is that any irritation of the nerve roots due to the disc degeneration is most likely to be on the left region; Ms Ashley, Mr Coyle, Dr Jamieson, and Dr Andrews indicated that her signs and symptoms were more prominent on the right. The Tribunal finds that the predominant medical view that the disc degeneration and nerve root irritation is more marked on the left is consistent with the radiological findings, but not with Ms Ashley’s symptoms.
  25. As it transpires, there is no need to resolve this difference of opinion. At most, it appears on the medical evidence that there is potential for, or irritation of, the nerve roots. However, this does not amount to the experience of more significant damage that is capable of leading to ‘significant signs’ of radiculopathy. In other words, the level of nerve root irritation is insufficient to lead to absence of or diminution of tendon reflexes, muscle weakness or muscle wasting, whether these are on Ms Ashley’s left or right lower limb.
  26. The Tribunal also finds that although there is evidence of S1 nerve root compromise in a dermatomal distribution, Ms Ashley’s diffuse experience of pain in the lower back, right hip, and right buttock do not appear to be dermatomal in distribution and hence do not point to radiculopathy.
  27. Accordingly, on balance the Tribunal is not satisfied that Ms Ashley’s signs and symptoms are of sufficient moment to indicate that she has experienced at least two ‘significant signs’ of radiculopathy, so as to qualify for at least 10 per cent impairment in accordance with Table 15.3 of the AMA5 Guides.

  1. The decision under review is affirmed.

I certify that the 98 preceding paragraphs are a true copy of the reasons for the decision herein of Professor RM Creyke, Senior Member.

Signed: .................................[sgd].........................................

Prishika Raj, Associate



Date of Hearing 28 October 2011
Date of Decision 5 January 2012
Solicitor for the Applicant Angus Bucknell
Maurice Blackburn Lawyers
Counsel for the Applicant Angus Bucknell
Solicitor for the Respondent Amanda Danti
Dibbs Barker
Counsel for the Respondent Declan Roche











[1] Warren H Lewis (ed), Gray’s Anatomy of the Human Body (20th edn, Lea & Febiger, 2000).
[2] Michael Donaghy (ed), Brain's Diseases of the Nervous System (12th ed, 2009).
[3] Chummy S Sinnatamby (ed), Last’s Anatomy (12th edn, 2011).
[4] Act s 24(7)(b).
[5] [2011] FCAFC 39 at [7], [15], [73], and [79] (Downes, Tracey and Flick JJ).
[6] Comcare v Broadhurst [2011] FCAFC 39.
[7] [2008] AATA 270 at [39] – [40]

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