Pollock and Comcare - [2002] AATA 753

DECISION AND REASONS FOR DECISION [2002] AATA 753

ADMINISTRATIVE APPEALS TRIBUNAL )

) No A2000/352

GENERAL ADMINISTRATIVE DIVISION       )              A2001/444
           Re      Gail Lorraine Pollock
  Applicant
           And    Comcare
  Respondent

DECISION

Tribunal Mr G A Mowbray

Date2 September 2002
PlaceCanberra

Decision The Tribunal sets aside the decisions under review, being decisions made by the Respondent dated 18 August 2000 and 24 September 2001, and remits the matters to the Respondent for reconsideration with a direction to give effect to the findings of the Tribunal as set out in the reasons for decision that:

(a)on the morning of 22 September 1997 Mrs Pollock slipped and fell on her left side in the foyer of a building in the Defence Department complex in Canberra
(b)as a consequence she suffered a soft tissue injury to her left shoulder/arm and muscle strain to the left knee
(c)these injuries are attributable to her employment
(d)Mrs Pollock continues to suffer from these injuries
(e)Mrs Pollock suffered and continues to suffer from a thoracic spinal pain syndrome, including an intervertebral disc lesion at T9/10
(f)this condition was caused, or at least substantially aggravated, by the accident on 22 September 1997
(g)Mrs Pollock continues to suffer an aggravation of her pre-existing lumbar and neck condition consequent upon the 22 September 1997 accident
(h)this condition includes a diffuse cervical spinal pain syndrome and a lumbar spinal pain syndrome both resulting from the accident
(i)Mrs Pollock suffered and continues to suffer from cervicogenic headaches caused by the accident of 22 September 1997
(j)in terms of section 4(9)(a) of the Act Mrs Pollock suffers "an incapacity to engage in any work" as a result of work caused injuries.
The Tribunal orders the Respondent to pay the Applicant's costs as agreed or taxed.

..............................................
Member
CATCHWORDS
COMPENSATION – whether thoracic spine condition attributable to work related accident – whether aggravations of cervical and lumbar spine conditions continue as a result of accident – whether cervicogenic headaches attributable to accident – whether incapacitated as a result of compensable conditions

Safety, Rehabilitation and Compensation Act 1998 ss 4(1), 4(9), 14, 19

Re Carson and Telstra Corporation (2001) 33 AAR 351
Lees v Comcare (1999) 29 AAR 350; 56 ALD 84
Comcare v Nichols [1999] FCA 209
Re Quinn and Australian Postal Corporation (1992) 15 AAR 519
Commonwealth v Borg (1991) 20 AAR 299n
Re Lewis and Comcare [2002] AATA 197
Guides to the Evaluation of Permanent Impairment, American Medical Association, 5th Edition, 2000

REASONS FOR DECISION

2 September 2002 Mr G A Mowbray

This matter involves two applications by Mrs Gail Lorraine Pollock for review of decisions by Comcare. The first application (A2000/352) is for review of a decision dated 18 August 2000 denying liability for Mrs Pollock's headaches and thoracic spine condition. The second application (A2001/444) is for review of a decision dated 24 September 2001 ceasing liability for Mrs Pollock's lumbar and cervical spine conditions. The 2001 decision also found that although liability continued for Mrs Pollock's left shoulder and left knee symptoms she was no longer entitled to incapacity payments for these conditions.
The hearing of A2000/352 commenced on 12 November 2001 but was adjourned during Mrs Pollock's evidence with directions that both applications be heard together at a date to be fixed once preparations for A2001/444 were completed. Thanks to the prompt cooperation of both parties the hearing was resumed on 26 November 2001 and concluded the following day. Mrs Pollock was represented by Dr Max Spry of Counsel, and Comcare by Ms Lorraine Gabriel of Counsel.
Background
Mrs Pollock was born on 22 August 1953. She is married with two daughters. Her previous medical history includes a back injury sustained at the age of 21 while working as a nurse, which resulted in ongoing problems. In about 1985 she developed pain in her neck and right arm that eventually led to two fusion operations in her cervical spine, performed in about 1990 and 1995 respectively.
In November 1996 Mrs Pollock began working for the Department of Defence as a trainee ASO1 performing a range of clerical work. Her duties included distribution of mail, which reportedly involved a lot of walking in and between buildings at the Department's complex of offices in the Canberra suburb of Russell.
On the morning of 22 September 1997 (that is, approximately ten months after her employment began) Mrs Pollock slipped and fell on her left side in the marble foyer of one these buildings. The severity of the fall and the extent of the injuries sustained has been a matter of contention between the parties, but it is not in dispute that Mrs Pollock was taken by ambulance to Canberra Hospital and treated in the emergency department.
Comcare subsequently accepted liability for a "soft tissue injury to L[eft] shoulder/arm and muscle strain to L[eft] knee" and approved treatments such as physiotherapy and pain management along with home help services. On 26 March 1998 liability was extended to include aggravation of Mrs Pollock's pre-existing lumbar (ie lower back) and neck conditions. This led to approval of treatment including surgery on her lumbar spine (which occurred on 30 July 1998 but was not formally approved until October) and several admissions to St Vincent's Private Hospital in Sydney.
On 19 May 2000 Comcare determined it had no liability for Mrs Pollock's headaches or for the condition of her thoracic region (ie upper back) as it was not satisfied that either of these was a compensable sequel of the fall and injury of 22 September 1997. Mrs Pollock requested a reconsideration of this determination but it was affirmed on 18 August 2000, leading to her application to this Tribunal (A2000/352).
On 1 June 2001 Comcare informed Mrs Pollock of its intention to cease liability for any costs arising out of the aggravation of her pre-existing lumbar and neck conditions and to cease any ongoing entitlement to incapacity benefits. That intention was carried out in a determination made on 26 June 2001. Mrs Pollock requested a reconsideration of this determination but it was affirmed on 24 September 2001, resulting in her second application to this Tribunal (A2001/444).
Legislation
This case is to be decided under the Safety, Rehabilitation and Compensation Act 1988 ("the Act"). The relevant provisions are as follows
"4 Interpretation
(1) In this Act, unless the contrary intention appears:
…
"injury" means:
(a) a disease suffered by an employee; or
(b) an injury (other than a disease) suffered by an employee, being a physical or mental injury arising out of, or in the course of, the employee's employment; or
(c) an aggravation of a physical or mental injury (other than a disease) suffered by an employee (whether or not that injury arose out of, or in the course of, the employee's employment), being an aggravation that arose out of, or in the course of, that employment;
but does not include any such disease, injury or aggravation suffered by an employee as a result of reasonable disciplinary action taken against the employee or failure by the employee to obtain a promotion, transfer or benefit in connection with his or her employment.
…
(9) A reference in this Act to an incapacity for work is a reference to an incapacity suffered by an employee as a result of an injury, being:
(a) an incapacity to engage in any work; or
(b) an incapacity to engage in work at the same level at which he or she was engaged by the Commonwealth or a licensed corporation in that work or any other work immediately before the injury happened.
…"
"14 Compensation for injuries
(1) Subject to this Part, Comcare is liable to pay compensation in accordance with this Act in respect of an injury suffered by an employee if the injury results in death, incapacity for work, or impairment.
…"
"19 Compensation for injuries resulting in incapacity
(1) This section applies to an employee who is incapacitated for work as a result of an injury, other than an employee to whom section 20, 21, 21A or 22 applies.
(2) Subject to this Part, Comcare is liable to pay compensation to the employee in respect of the injury, for each of the first 45 weeks (whether consecutive or otherwise) during which the employee is incapacitated, of an amount calculated using the formula:
NWE – AE
where:
NWE is the amount of the employee's normal weekly earnings; and
AE is the amount per week (if any) that the employee is able to earn in suitable employment.
(3) Subject to this Part, Comcare is liable to pay to the employee, in respect of the injury, for each week during which the employee is incapacitated, other than a week referred to in subsection (2), compensation:
(a) where the employee is not employed during that week—of an amount equal to 75% of his or her normal weekly earnings less the amount (if any) that he or she was able to earn during that week in suitable employment;
(b) where the employee is employed for 25% or less of his or her normal weekly hours during that week—of an amount that, when added to the amount that he or she was able to earn during that week in suitable employment, results in an amount equal to 80% of his or her normal weekly earnings;
(c) where the employee is employed for more than 25% but not more than 50% of his or her normal weekly hours during that week—of an amount that, when added to the amount that he or she was able to earn during that week in suitable employment, results in an amount equal to 85% of his or her normal weekly earnings;
(d) where the employee is employed for more than 50% but not more than 75% of his or her normal weekly hours during that week—of an amount that, when added to the amount that he or she was able to earn during that week in suitable employment, results in an amount equal to 90% of his or her normal weekly earnings;
(e) where the employee is employed for more than 75% but less than 100% of his or her normal weekly hours during that week—of an amount that, when added to the amount that he or she was able to earn during that week in suitable employment, results in an amount equal to 80% of his or her normal weekly earnings; and
(f) where the employee is employed for 100% of his or her normal weekly hours during that week—of an amount that, when added to the amount that he or she was able to earn during that week in suitable employment, results in an amount equal to 100% of his or her normal weekly earnings.
…"

Documentary Evidence

The Tribunal had before it the following documents which were taken into evidence. The parties agreed that all evidence was to be admitted in relation to both applications

Exhibit T1-T227 – the documents lodged (initially for A2000/352) under section 37 of the Administrative Appeals Tribunal Act 1975
Exhibit S1-S30 – a supplementary set of documents lodged under section 37, primarily to cover the determinations relevant to A2001/444
Exhibit A1 – Applicant's Statement of Facts and Contentions for A2000/352 dated 22 February 2001
Exhibit A2 – medical report of Dr G. David Champion dated 22 November 1999
Exhibit A3 – medical report of Dr Timothy Steel dated 11 October 2000
Exhibit A4 – medical report of Dr Alan Searle dated 4 August 2001
Exhibit A5 – letter from Dr G. David Champion to Baker Deane & Nutt dated 24 September 2001
Exhibit A6 – clinical notes from The Canberra Hospital dated 22 September 1997
Exhibit A7 – Applicant's (amended) Statement of Facts and Contentions dated 21 November 2001
Exhibit A8 – statement of Kerry Andreas Wilson dated 22 November 2001
Exhibit A9 – letter from Dr Kathleen Calder to Lieutenant Hartigan dated 25 July 1997
Exhibit A10 – a bundle of documents, the first page of which is headed 'Department of Defence' and relates to the Comcare Claim of Mrs Gail Pollack (sic) and is dated October 1997
Exhibit R1 – Respondent's Statement of Facts and Contentions for A2000/352 dated 7 March 2001
Exhibit R2 – medical report of Professor Paul Gatenby dated 10 December 1995
Exhibit R3 – medical report of Professor Paul Gatenby dated 6 January 1996
Exhibit R4 – medical report of Professor Paul Gatenby dated 24 February 1996
Exhibit R5 – medical report of Professor Paul Gatenby dated 9 August 1996
Exhibit R6 – medical report of Dr Neil McGill dated 29 March 2001
Exhibit R7 – medical report of Dr Neil McGill dated 29 October 2001
Exhibit R8 – a transcription of the clinical notes of Dr Rosenmann, covering the period 30 March to 8 July 1999
Exhibit R9 – medical report of Dr K. Nadana Chandran dated 26 February 1996
Exhibit R10 – Respondent's Further Statement of Facts and Contentions dated 14 November 2001
Exhibit R11 – supplementary medical report of Dr David Brownbill dated 2 November 2001
Exhibit R12 – supplementary medical report of Mr H. Schaeffer dated 31 October 2001
Exhibit R13 – a collation of the Applicant's "radiological" history (including reports from numerous types of imaging such as X-ray, CT scan, ultrasound and MRI) consisting of 54 numbered pages in chronological order (13 January 1987 to 8 August 2000)
Exhibit R14 – clinical notes from the Isabella Medical Centre, covering the period 30 July 1987 to 16 November 2000
Exhibit R15 – record of a meeting to discuss the Applicant's return to work dated 12 October 1998
Exhibit R16 – Respondent's Schedule of Documents (with references to the Respondent's Further Statement of Facts and Contentions) and attachments

Issues

The issues before the Tribunal are as follows

whether Mrs Pollock suffers from an injury to her thoracic spine as a result of the 22 September 1997 accident
whether Mrs Pollock continues to suffer from a lower back and neck condition as a result of that accident
whether Mrs Pollock suffers from headaches as a result of that accident
whether Mrs Pollock remains incapacitated as a result of conditions causally related to that accident.

Mrs Pollock's Evidence

Mrs Pollock gave oral evidence to the Tribunal. She related how she went in to work early on the morning of 22 September 1997 and going to another building to pick up some 'signals' slipped on something in the foyer, stumbled and fell onto her left side. She described the fall as being so heavy that she slid on the floor. She was winded and thought that she had broken something. She had pain in the left arm and shoulder, left hip and left knee, the shoulder pain being predominant. Mrs Pollock does not recall any lower back or cervical pain at the time, but stated she "hurt all over". She was unable to get up and called for help. An ambulance took Mrs Pollock to The Canberra Hospital, where x-rays were performed. She was told she had suffered soft tissue damage and that she would be back at work after three days. She was given a sling for her arm and some pain relief.
Mrs Pollock gave evidence that as she was getting dressed to leave the hospital pastry was found on her skirt and the heel of her shoe. It was put to her in cross-examination that the presence of pastry was a later invention designed to bolster a negligence claim. Mrs Pollock strongly denied this asserting that it was in fact the nurses helping her dress that had noticed the pastry and brought it to her attention. The reason it did not appear on the first Accident Report form – a second version does mention the pastry – was that this version was begun by an office manager, not Mrs Pollock.
The opinion that Mrs Pollock would shortly return to work proved inaccurate. Her first attempt to return, possibly in November 1997 although she was unsure as to this, lasted a few days during which she felt drugged and disoriented. On a second occasion, which documentary evidence shows was in October 1998, she only returned to work for a few hours. Mrs Pollock still believes she could work part-time, and has told her case manager she wants to return, but has found her condition keeps deteriorating.
Prior to this fall Mrs Pollock had a number of other medical problems during her probationary traineeship. She asserted that she had completed all the required courses and worked hard, but had taken time off work several times because of health issues including a heliobacter infection and chronic sinusitis.
In July 1997 she had slipped on a stair at work. She told a supervisor about this but did not fill out an accident report because she had already had a lot of sick leave and was afraid she would lose her job. A few days after the slip, however, she was sent home because she was considered to be in too much pain to work. As she left she was crying in frustration at yet another setback to her employment. She immediately went to see Dr Calder – not her regular doctor, but at the same practice – who ordered a MRI scan. The scan showed prolapsed discs and Mrs Pollock was told her recovery would take 3-6 weeks. She had about three weeks off work after which she returned with no ongoing symptoms. She had been back at work for about seven weeks before her next accident.
On the first day of the hearing Mrs Pollock's evidence of this incident in July was challenged in cross-examination, it being put to her that there was no slip at work. This line was not pursued when the hearing resumed a fortnight later at which time the statement of Mr Kerry Wilson, Mrs Pollock's direct supervisor, was tendered (Exhibit A8).
Mrs Pollock underwent two medical examinations in relation to her employment with the Department of Defence, one before she commenced and another after the July slip which was ordered because of her considerable time off work throughout her employment thus far. At the first examination she disclosed her pre-existing back problem, neck fusions and other medical conditions. She was passed fit for her duties on both occasions with limitations on the weight she should be expected to lift.
Mrs Pollock outlined her treatment since the fall on 22 September 1997. Initially she consulted her general practitioner and a physiotherapist, followed by Dr Cassar for pain management. Dr Cassar's treatment had included acupuncture and facet joint blocks, but with little success.
On 13 October 1997 she was visited at home by her general practitioner because she had limited mobility. The following day she was taken to hospital by ambulance because she was unable to get out of bed. She again went to hospital for similar reasons in May 1998, and in June or July Dr Newcombe performed lower back surgery to correct her diagnosed foot drop. This was the first time she had had back surgery. Mrs Pollock noted this resolved a lot of her pain as well as correcting the foot drop. She also stated the foot drop '"recurs a bit" if she is overly active.
She began to see Dr Champion in late 1998, and continued to do so. His treatment had included injections into her back. She continues to take morphine twice a day, having been unable to reduce her intake, which she finds makes her confused or lost.
At one stage she attended a psychiatrist (Dr Rosenmann) at Dr Champion's suggestion, but had been told she no longer needed to attend. She acknowledged having seen a psychiatrist on other occasions well before the September 1997 fall, and also recalled telling Dr Rosenmann of numerous other issues and problems that predated that fall. She also recalled being admitted to hospital after an overdose of pills in January 1996, but did not accept she had told carers at the hospital that she wanted to die. In fact she had called the ambulance herself after realising she had taken an overdose.
Mrs Pollock gave extensive evidence of her symptoms and their onset. She reports that she currently experiences symptoms 24 hours a day, although she considered herself to be overall much better now than at the time of the fall or when first examined by Dr Champion in December 1998. Areas affected include her knee, hip, lower back and both legs. She limps because her left knee is stiff, although she in fact ends up bearing weight on her left leg. In her opinion this is because this leg is shorter. Prior to the fall she had never had symptoms in her right leg and her lower back pain had not been continuous as it was now. She acknowledged she had been involved in a motor vehicle accident in November 1995 but disavowed any symptoms arising from this. She said that Dr Chandran (Exhibit R9) was mistaken. Her left leg and buttock symptoms had actually begun in 1994.

Mrs Pollock agreed there had been occasions prior to the September 1997 fall when she had not been able to get out of bed because of neck or back pain. Mrs Pollock also agreed she had had spontaneous recurrences of lower back pain in the past, but these episodes would last a few days rather than the four years of her current condition.
Mrs Pollock also acknowledged her pre-existing neck pain, but stated it had resolved well before the fall in September 1997. It had resolved with her first cervical fusion in 1990 but had recurred in 1995 due to a traumatic incident. Shortly afterwards she underwent the second fusion operation and by about May 1996 she had no neck problems and ceased taking any medication for that condition.
She also reports a constant burning sensation in her thoracic area. In cross-examination she asserted that this was present from shortly after the fall. She did not report it because she thought it was simply a consequence of having her arm in a raised position in a sling. She mentioned it to her physiotherapist but did not realise its true significance until she was told of the herniation of a disc in her thoracic spine. Also for some time it was a relatively minor problem in comparison to her shoulder and lower back pain. As these other pains reduced the thoracic pain did not and thus it became relatively more prominent.
She considers her shoulder to be crooked, which pulls on muscles and leads to headaches, although these occur less frequently then they used to thanks to physiotherapy and her own ability to recognise their onset and take preventative action. Muscle relaxants for her shoulder and neck will fix the headache. The headaches did not start immediately but a mild form commenced 3-4 days after the fall. She still has at least two headaches per week. She was adamant these are quite different to her previous migraine headaches which ceased in 1995 and her sinus headaches which ceased after her sinus operations earlier in 1997. She admitted having had antibiotics to treat sinus problems "a couple of times" since then.
Mrs Pollock described herself as having been "very fit" before the fall in September 1997. She cycled, played tennis and squash, swam 20 laps and walked with her dogs up to 12 kilometres. She held dinner parties and contributed food to other events. In contrast, her activities were now very limited. She can no longer entertain at home – she only cooks "simple" meals – or walk to the top of the road. She is able to do some light household tasks such as sweeping but cannot clean bathrooms or garden. She had attempted activities such as walking, cycling, horseriding and tennis with little success. The horseriding for example was limited to walking pace and her knee locked.
Mrs Pollock presented her evidence in an open forthright manner. I believe she was honest. She did not appear to exaggerate or overstate her case. Her evidence was cogent and consistent, despite being strongly tested in cross-examination.
The Medical Evidence
Dr Alan Searle
Dr Searle, a consultant orthopaedic surgeon, gave oral evidence further to his written report (Exhibit A4). In his opinion Mrs Pollock's thoracic disc prolapse at T9/10 in the lower half of the thoracic spine, revealed in a MRI scan dated 1 June 1998, was the result of a traumatic injury. He gave a number of reasons why he considered it "very unlikely" to be a degenerative condition – the size of the prolapse, the fact that it was causing some pressure on the spinal cord, the lack of evidence of damage to the facet joint, the lack of similar degenerative changes at adjacent levels, and the absence of other side effects such as osteophyte formation that would have been associated with degenerative change before the prolapse. Arthritic changes reported in a CT scan dated 16 February 1999 could probably be observed within a year of the prolapse of a disc.
He was aware of the problems in Mrs Pollock's cervical and lumbar spine and agreed it was probable she would have eventually experienced problems in those regions in any event. However these were much more likely to undergo degenerative changes than the thoracic spine. He also acknowledged that degenerative processes would usually spread and affect other levels of the spine, but emphasised these would be adjacent levels.
Dr Searle knew of the operation performed by Dr Newcombe to treat Mrs Pollock's foot drop – a laminectomy, removing part of the lumbar disc pressing on the nerve root. It was very common to have a recurrence after an operation of this type. It was also quite common to have continuing minor symptoms after a cervical spinal fusion. The levels above and below the fusion would be slightly more likely to undergo degenerative changes than in a normal spine.
Dr Searle had been told by Mrs Pollock about the accident in July 1997. He considered this to be a much less serious injury than the one in September 1997.
Dr Searle agreed that someone with a spine as degenerated as Mrs Pollock's could experience back pain intermittently. It was unlikely this would occur without some precipitating incident, even if it were relatively minor such as a sneeze. Pain would probably be experienced almost immediately in this situation. However in re-examination Dr Searle stated it was quite common for a disc to prolapse but not produce symptoms for a few days or even a week. The pain was often caused by processes other than the actual prolapse.
Ms Gabriel asked Dr Searle to comment on whether a hypothetical job description involving light clerical work would be suitable for Mrs Pollock. He replied that Mrs Pollock may be able to do it part-time but could not imagine her being able to do it full-time even though it was light work. The distance she could walk would decrease through the day, probably to the point of hardly being able to walk at all. He considered all of her injuries to now be permanent, including her hip and knee injuries, that she was severely incapacitated and that she was unfit for work. She was unlikely to see any improvement over time. In his written report he concluded
"Comparing her condition now with her activity level prior to the injury on 22/9/97 it is obvious that the fall caused severe aggravations of her pre-existing lumbar and cervical problems, as well as traumatic capsulitis of the left shoulder with possibly a small rotator cuff tear, a contusion of the left ilium, and a sprain of the left knee with traumatic chondromalacia of the left patello-femoral joint. The ongoing symptoms from these injuries and aggravations are permanent and cause a severe degree of disability.
She is unfit for work and this work incapacity is permanent.
With regard to prognosis there will be gradually increasing symptoms and disability in the cervical and lumbar regions as the degenerative changes progress. This progress will occur more rapidly than might otherwise have been expected because the fall has also accelerated these degenerative changes. There will probably be no change in the conditions in the other regions ie. left shoulder, left ilium, and left knee." (Exhibit A4, p.7)
Dr G. David Champion
Dr Champion, a consultant physician in rheumatology, musculoskeletal medicine and pain medicine, gave oral evidence in addition to the considerable body of his reports and correspondence before the Tribunal. He had been involved in treating Mrs Pollock since late 1998. His last formal consultation with her was in August 2000 but they had had telephone conversations since then regarding her treatment.
Dr Champion was aware that Mrs Pollock had slipped on stairs at work in July 1997 causing a relatively brief exacerbation or experience of back pain. This would, however, have added to the predisposition to injury in her next accident. He also outlined the early history of Mrs Pollock's condition after the fall on 22 September 1997 as given to him. She had gradually and increasingly acquired symptoms until about three weeks after the fall, when she was taken to hospital with pain in her lower back and legs and paralysis.
Dr Champion said that this was when Mrs Pollock presented with foot drop. When it was suggested to him that the foot drop did not present itself until May 1998, he acknowledged this would change his understanding of the time course of Mrs Pollock's condition, but nevertheless a description of stiffness and low back pain in October 1997 was consistent with his understanding. He initially indicated that Mrs Pollock's foot drop was not consistent with the evolution of a degenerative process. He subsequently agreed, as a general proposition, that the final rupture of a degenerative disc leading to nerve root compression did not require any greater trauma than a sneeze or bend. Dr Champion explained why it could take up to three weeks for a disc injury to be fully expressed, outlining the processes involved in creating a sensation of pain from the injury.
Dr Champion rejected the proposition that all disc herniations are degenerative in origin. He acknowledged that a degenerate disc was more likely to protrude, rupture or herniate, but it was entirely possible and indeed common for these injuries to be provoked by single or repetitive stresses or forces. In cross-examination he agreed that a disc protrusion at L5/S1 predated the fall, and that therefore one of his reports should be amended to cite the fall as probably aggravating this without any suggestion it was the original cause. However the leg weakness and foot drop experienced by Mrs Pollock was related to the L4/5 level.
At Dr Champion's initial assessment in late 1998 tenderness in Mrs Pollock's thoracic spine was not as significant a feature as it was subsequently. It became a higher priority once her back and left leg pain had been dealt with as well as possible. He also agreed that the thoracic spine was probably not a significant part of Mrs Pollock's presentation when Dr Billett assessed her in late 1997. In Dr Champion's view neither Dr Billett's nor Mr Schaeffer's reports indicated they had performed sufficiently detailed examinations of the thoracic area to pick up abnormalities. Dr Champion himself had missed much of the pathology in the thoracic area in his first assessment.
The disc lesion at T9/10 was clearly the result of trauma or repetitive biomechanical stress, and from the history Dr Champion had there was no alternative candidate to the September 1997 fall as its cause. In addition the onset of Mrs Pollock's thoracic pain postdated the fall. However the disc lesion was not in itself a sufficient explanation for her low thoracic back pain, as the lesion was predominantly right sided and the pain predominantly left sided.
Dr Champion was cross-examined at length on the finding in his report of 2 December 1998 (T108) of "tenderness in the left leg consistent with secondary allodynia", and in particular on the meaning of secondary allodynia. The essence of his explanation was that this involved abnormal sensory processing in the central nervous system, because of sensitisation of touch pressure nerves (or "mechano-receptor afferents"). Whereas these nerves normally would relay a sensation of pressure, in secondary allodynia the signal from these nerves is interpreted by the central nervous system as pain. This has certain characteristics enabling it to be distinguished from the sensation transmitted by pain nerves. The condition is described as secondary because the pathology is not in the tissue where pain is experienced. In Mrs Pollock's case, the pain experienced in her leg related to pathology in her lumbar spine. The distribution of this kind of response was commonly within the same region as referred pain for a particular site of origin as in Mrs Pollock's case, but occasionally could have a much wider distribution.
Dr Champion agreed that the fact Mrs Pollock was limping and bearing more weight through her left leg rather than her right was unusual, but one did see this on occasions. He did not remember recording any muscle wasting but did not regard wasting as something to be expected in her. He recorded tenderness in Mrs Pollock's hip and would have considered it most surprising if the fall as described to him had not caused a disorder in that area. At the time of his initial assessment Mrs Pollock was suffering a major depression of mood which would influence her ability to cope with her pain. There was no doubt that her pain was real. There was a very high level of internal consistency in her responses related to the underlying pathology and it was "virtually unimaginable" that this could be feigned or imagined.
In his report of 22 November 1999 (Exhibit A2) Dr Champion summarised his diagnosis of the conditions caused or aggravated by the 22 September 1997 accident as follows
"? A diffuse spinal pain syndrome and prominent cervicogenic headaches.
?        Thoracic spinal pain syndrome including intervertebral disc lesion at T9-10.
?        Lumbar spinal pain syndrome at L4-5 and L5-S1 with left L5 radiculopathy, perhaps also S1 radiculopathy.
?        Left supraspinatus tendonitis.
?        A patellofemoral pain syndrome at the left knee.
?        Pelvic injury with some possible symphysis pubis pain.
?        In addition, pain related distress and other psychosocial consequences, with major interference with capacity to work and to function generally for activities of daily living."

In his opinion Mrs Pollock was permanently incapacitated for work.
Dr Neil McGill

The oral evidence of Dr McGill, a consultant rheumatologist, supplemented his two written reports (Exhibits R6 and R7). He had examined Mrs Pollock on one occasion, for an hour or possibly a bit longer. He did not think she was being evasive or dishonest in the history she gave.
Dr McGill did not think he could realistically locate the source of Mrs Pollock's headache or distinguish it from the ones she experienced prior to September 1997. He had been told her previous history included migraines, and other headaches which she attributed to sinus problems. Headaches could also be derived from the cervical spine or from muscle tension.
Dr McGill strongly disagreed with the contention that a disc prolapse necessarily indicated there had been trauma. The vast majority of disc protrusions occurred as a result of degenerative change in the absence of trauma. Inheritance was the most important factor in disc prolapse, although it was not possible to determine the importance of inheritance in an individual person's case.
To have a significant effect on a disc, a trauma would need to be substantial. Symptoms may not be immediate, but would develop within two to three days rather than occurring weeks or months later. Dr McGill accepted that the fall of 22 September 1997 had the capacity to cause a temporary aggravation of Mrs Pollock's lower back pain. He accepted that if she had reported an increase in pain 2-3 days later then the fall had caused this but the first report of an increase that he had was on 13 October 1997, three weeks after the fall. There would not be any ongoing effect.
Dr McGill was asked for his understanding of the concept of "central sensitisation of nociception". His answer described it as a hypothesis to explain people reporting pain in the absence of a physical explanation for that pain. Such people may experience sensations as painful that the rest of the population experienced as non-painful.
It was a very reasonable hypothesis that central processing, particularly depression or anxiety, could influence the way that pain was felt. However there was no need to apply the concept to Mrs Pollock's case. She had a clear origin for her pain in the degenerative changes in her spine. The concept was of no assistance in diagnosing the physical origin of pain, as the whole point of the hypothesis was that there was no known origin.
Dr McGill had not found any evidence of muscle wasting in Mrs Pollock's limbs. Whether or not he would expect to find any would depend on the nature of the disability. Dr McGill made specific reference to several shoulder conditions that would produce wasting.
In his report of 29 October 2001 (Exhibit R7) Dr McGill concluded
"There is no doubt that she had pre-existing degenerative change in the cervical and lumbar spine regions and also had a long history of headache. I think her thoracic spine abnormalities reflect the same degenerative processes that have affected her cervical and lumbar spine.
… I think, on the balance of probabilities, that the September 1997 fall was not responsible for any significant change in her cervical, thoracic or lumbar spine problems nor responsible for any change in her state in regard to headache. I think the problems in her spine, including the cervical, thoracic and lumbar regions, and her headaches are constitutional and related to problems that had developed prior to September 1997 and will continue in the future."
Mrs Pollock's shoulder and knee conditions, while restricting some activities, would not have a substantial effect on her work capacity. Her knee would not impact on her ability to walk distances, but would affect climbing stairs. In his report of 29 March 2001 (Exhibit R6) he concluded
"With the exception of at or above shoulder height work with her left arm and squatting/repetitive stair climbing, I think her current work capacity would have been the same had the September 1997 fall not occurred.
Although I think her spine related symptoms would have prevented her from working in the past, on the basis of her current symptoms and her physical examination, I think she is currently fit to resume the type of duties she was performing previously with the Department of Defence."
Mr H. Schaeffer
Mr Schaeffer, a consultant neurologist, gave oral evidence to supplement his three written reports regarding Mrs Pollock (Exhibits T185, T200 and R12). He had examined Mrs Pollock on one occasion for about one hour. He rejected the suggestion that this was insufficient time in which to obtain a complete medical history from Mrs Pollock given its extent, a suggestion put to him because of his finding that she was an unreliable and selective historian. The basis of that finding was the failure of Mrs Pollock to tell him about the incident in July 1997 and his later discovery in the material provided by Mrs Pollock of the MRI scan taken in that month. Mr Schaeffer would not have read reports provided to him by Comcare prior to the examination but would have read them before preparing his own report.
Mr Schaeffer considered that a thoracic disc problem would present itself completely differently from problems with the L4/5 and L5/S1 discs. It was extremely uncommon for pains to arise from problems with thoracic discs. There would be spinal cord involvement and lower limb weakness, which Mrs Pollock had never had. A right-sided disc herniation would not be expected to produce left-sided pain.
Mr Schaeffer stated it is a prerequisite of disc prolapse that there is existing degeneration of the disc. In 40 per cent of cases disc herniation occurs spontaneously, in the other 60 per cent an injury acts as an aggravating factor precipitating the final rupture. The trauma could be very indefinite such as turning in bed or a cough or rather more significant such as a bending and/or lifting strain.
Symptoms would be experienced within 24 hours. On the information that Mrs Pollock only complained of back trouble three weeks after the fall on 22 September 1997, this was too long an interval to postulate an association between the incident and the subsequent back symptoms. When it was put to Mr Schaeffer that Mrs Pollock had been aware of pain earlier than this, Mr Schaeffer was reluctant to go into the matter further without an objective report. He emphasised he had found no evidence there was any actual structural injury to the lumbar spine in the September fall. Any soft tissue injury would resolve within a few weeks.

Mr Schaeffer reiterated in his oral evidence his report findings that he found inconsistencies in Mrs Pollock's presentation. One of the two specific inconsistencies mentioned was in the straight leg raising test, which is used to artificially produce pressure on the sciatic nerve in patients with disc herniation. It was a standard diagnostic test for nerve root compression. A definite inconsistency meant that one had to think of non-physical reasons for those responses.
The fact that Mrs Pollock had alternated between sitting and standing during Mr Schaeffer's examination could, he conceded, indicate she was experiencing some discomfort, but this was very non-specific. It was most unusual for someone to bear weight on a painful limb, and Mr Schaeffer could not recall having seen an example.
Mrs Pollock's symptoms of headache were not specific to any type of headache. There was no physical correlation between pre-existing lumbar and neck complaints and symptoms of headache. Ordinary tension headache could occur in association with any disease or injury and the relationship was non-specific.
In summary, Mr Schaeffer's view was that

Ms Pollock's claimed conditions of cervical, thoracic and lumbar spinal problems and headache were not the result of and were not contributed to by her fall at her place of employment on 22 September 1997
any physical symptomatology that Ms Pollock may experience occasionally resulted from an underlying disease process, this being degenerative spondylosis of her spinal column
additionally, there were non-physical factors contributing to her situation
the physical aspect of her current incapacity was a consequence of her pre-existing underlying condition.

Comcare's Submissions

Ms Gabriel for Comcare submitted there was ample evidence that Mrs Pollock's spine was, to use a vernacular term, "stuffed". There were many levels of degeneration and the process of degeneration had been proceeding for quite some time (referring to a MRI scan of the lumbar spine performed on 3 August 1995, Exhibit R13 at p.18). Mrs Pollock had a known prior history of lumbar back pain, sciatica and pain in her left leg. Her cervical spine was also severely affected. She had undergone fusion at two levels. There was evidence that this in itself could affect the surrounding levels of the cervical spine.
Mrs Pollock had clearly been plagued throughout life with extensive illness. She had not presented as someone who was perfectly well before 22 September 1997. In the time she was working for the Department of Defence she had significant physical problems. There was also evidence of prior psychological stresses in her life and a tendency to somatisation.
Ms Gabriel submitted that Ms Pollock while not a dishonest witness downplayed events in her earlier history that she did not consider relevant. Ms Gabriel made reference to specific instances of this tendency in relation to the motor vehicle accident in 1995, the alleged attempted suicide in 1996 and the slip at work in July 1997.
Comcare did not dispute that Mrs Pollock was in fact injured on 22 September 1997. Indeed she continued to suffer effects to her left shoulder and left knee. These effects were not, however, major or incapacitating. It was also not disputed that she had a physiological basis for ongoing pain.
Mrs Pollock's first complaint of lumbar back pain was over three weeks after the fall. Her general practitioner's description of this as a recurrence of lumbar back pain was not a reference to something that had occurred on 22 September, because nothing was recorded at that time. She had a known predisposition to lumbar spine problems. Her own evidence was that she had experienced spontaneous events in the past, and doctors had given evidence she had a condition that could be provoked by something as simple as a sneeze or a twist in bed.
Dr Searle's evidence was that it could take up to a week for a disc injury to be expressed and Dr McGill and Mr Schaeffer had given shorter periods. Yet it was more than three weeks before there was any objective evidence. Even taking the medical evidence at its highest, any aggravation to Mrs Pollock's significantly degenerative spine would have now long ceased.
Mrs Pollock was unable to remember when her other problems commenced, other than to say that it was after the fall. This was in contrast to her extremely clear and specific evidence on some other matters. The symptoms had developed over time. Headaches started to become a feature towards the end of 1997 and the thoracic spine was not really a problem until Mrs Pollock was made aware of MRI results in mid-1998. Even then the pain was on the opposite side to what was expected. In the absence of recollection from Mrs Pollock to the contrary, the Tribunal should rely on the contemporaneous medical reports.
Dr Champion's views on the explanation of pain were not widely accepted, and so far as he sought to rely on those views to support a link between Mrs Pollock's back conditions and the fall of 22 September 1997 his evidence ought to be disregarded. In his reports he was clearly advocating on behalf of Mrs Pollock.
Ms Gabriel also submitted that Dr Searle's evidence was affected because he had not been presented with as full a chronological history as many other doctors. She submitted that he took a different view when asked to assume facts as recorded in the general practitioner's and hospital notes. However, following a close reading of the transcript I cannot accept Ms Gabriel's characterisation of Dr Searle's evidence.
Mrs Pollock's Submissions
Dr Spry for Mrs Pollock submitted that she had given her evidence, both in chief and under cross-examination, in a straightforward, clear and non-evasive fashion. A number of matters had been put to her to question the credibility or at least reliability of her evidence, and her evidence has subsequently been supported by documentary evidence. In that regard Dr Spry referred specifically to the occurrence of a slip at work in July 1997 and the presence of pastry in the September 1997 fall.
Mrs Pollock had never denied or sought to obscure her past medical history. She had given a full history when examined before starting her employment with the Department of Defence. It was submitted that much of that history was irrelevant to the present proceedings, for example the number of miscarriages Mrs Pollock had had.
Not only had Mrs Pollock in fact reported the July 1997 incident, the leave she took was unpaid leave and she made no claim for compensation. She also returned to work more quickly than was anticipated, as was recorded in the second medical examination by the Department of Defence.
A number of hypotheticals put by Ms Gabriel to Dr Searle were based on propositions for which there was no evidence. For example there was no evidence that Mrs Pollock had gone home crying as a direct consequence of her accident in July 1997, nor was there evidence of her complaining of incontinence.
Mrs Pollock had given evidence of the conditions she continues to suffer and of the activities undertaken prior to the fall that she can no longer perform. There was evidence that she became more aware of pain in her knee, neck and back as the pain in her left shoulder decreased in early October 1997.
Dr Champion had given his evidence in a dispassionate manner and in no way could be said to be an advocate for Mrs Pollock. He has seen Mrs Pollock on many occasions and is her treating pain management specialist. This was in contrast to Dr McGill and Mr Schaeffer who had each seen Mrs Pollock on a single occasion for no more than an hour. Far from being on his own, Dr Champion's views on Mrs Pollock's condition were supported by Dr Searle. The Tribunal was referred to Exhibit A2 as a good summary of Dr Champion's views which he had maintained in later reports.
Dr Ashman writing his report in February 1998 (T43), was of the opinion that the fall in September 1997 had an aggravating effect on both Mrs Pollock's neck and low back conditions. Dr McGill had thought it unlikely there was any aggravation, but this was in conflict with the opinions of Drs Billett, Brownbill, Searle and Champion.
Mr Schaeffer's opinion of Mrs Pollock as a poor historian had coloured his views on her symptoms and condition. The basis for this opinion was that Mrs Pollock had not mentioned the MRI taken in July 1997, but she had actually provided this MRI to Mr Schaeffer.
Consideration of Issues and Findings
"Cease liability/effects" decisions
As I have said before, in many "cease liability" or "cease effects" decisions made under the Act there appears to be a misunderstanding of the nature and effect of the determination that is made and of the statutory provisions relied upon.
In Re Carson and Telstra Corporation (2001) 33 AAR 351 Deputy President Estcourt stated
"49. It would only be a rare case where a reconsideration of the substantive determination under s.14 that Comcare was liable to pay compensation in accordance with the Act would be warranted. Such a case might arise, for example, if it was subsequently discovered that the injury had never in fact occurred or that the person claiming was never in fact an employee.
50. In such a case a reconsideration of the s.14 determination under s.62 resulting in a revocation would surely carry with it the result that no future claims in respect of that incident could properly be made, but in other cases, the revocation of a determination under relevant sections would not have the effect of preventing altogether further or other claims for compensation.
…
55. Telstra by its determination of 21 February 1995 was not, properly understood, denying those findings implicit in the original determination, it was merely determining that, on the available medical evidence, it was no longer liable for payment of medical expenses or incapacity payments.
56. That is to say the effect of the determination that "liability in respect of this injury ceased on and from 5 February 1995" was not a decision to "cease liability" altogether or to "cease liability" under s.14, but rather a purported determination to cease the payment of compensation under s.16 and s.19 of the Act.
…
58. The conclusion I have reached, namely, that at its highest, Telstra's determination only ceased payment of compensation under s.16 and s.19 of the Act and did not effectively revoke the early determination to accept liability under s.14, thereby preventing further claims of compensation being made at a later time, is also consistent with the reasoning of the Full Court in Plumb v Comcare (1992) 39 FCR 236."
Implicit support for this approach is found in Lees v Comcare (1999) 29 AAR 350; 56 ALD 84, especially at [34], upon which Deputy President Estcourt relies. I agree with and adopt the views of Deputy President Estcourt, which have been followed elsewhere in the Tribunal.
The burden of persuasion
It is neither particularly apt nor appropriate to refer to a common law concept of a burden or onus of proof placed on a particular party in administrative proceedings in the Tribunal. However there has been a line of authority in both the courts and the Tribunal on what has been described as "the burden of persuasion" in these matters.
First, in relation to claims to establish liability for an injury, or to establish sequelae or incapacity flowing from an injury, the Tribunal must be satisfied on the balance of probabilities of the existence of the injury, the sequelae or the incapacity and that they were work-related. A succinct statement of this is found in Comcare v Nichols [1999] FCA 209 where Justice Heerey said at paragraph 23
"However Mrs Nichols also contended that (i) she had a cervical spondylosis (ii) which was work-related and (iii) which contributed to her present incapacity. If all three elements were established she would have an entitlement to compensation. The Tribunal had to be satisfied of the existence of each element."
Secondly, where the reviewable decision is one ceasing liability Justice O'Connor and Mr Barbour in Re Quinn and Australian Postal Corporation (1992) 15 AAR 519 at 525 spoke of an obligation to produce material supporting a change in circumstances
"In our view, as it is clear from the statutory intention that the respondent can only reconsider a determination when there has been a change in circumstances, it seems justifiable to expect the respondent to be able to produce material in these proceedings supporting its assertion that the applicant is no longer entitled to compensation. There is no strict burden of proof as such but there must be additional evidence to indicate that there has been such a change in circumstances."

Justice Jenkinson in Commonwealth v Borg (1991) 20 AAR 299n at 307 put it in these terms

"I think that the Act required on its proper construction that the delegate should not make the determination he did make unless he was persuaded that one of the entitling circumstances had on or before 28 July 1988 ceased to exist."

In Comcare v Nichols Justice Heerey said at paragraph 22
"In the present case, Mrs Nichols was receiving compensation in respect of an injury (RSI) which had been found in 1985 to result in incapacity for work. Comcare contended in 1996 that she no longer suffered from RSI. Comcare therefore had to establish this fact. Perhaps more accurately, it was the Tribunal, as an administrative decision-maker, which had to satisfy itself that this was the case. It was so satisfied."

Nichols is consistent with the earlier authorities and is the approach I will adopt in considering the "cease liability" matter in these proceedings.

Uncontentious matters

There are a number of matters before the Tribunal on which there is no disagreement between the parties

on the morning of 22 September 1997 Mrs Pollock slipped and fell on her left side in the foyer of a building in the Defence Department complex in Canberra
as a consequence she suffered a soft tissue injury to her left shoulder/arm and muscle strain to the left knee
these injuries are attributable to her employment
Mrs Pollock continues to suffer from these injuries.

The evidence clearly supports findings along these lines and I accept them. Both parties also agree that nothing turns in these proceedings on the disease/injury simpliciter distinction.
Does Mrs Pollock suffer from an injury to her thoracic spine as a result of the 22 September 1997 accident?
Mrs Pollock gave evidence that she experiences a constant burning sensation in her thoracic area. She first noticed it shortly after the fall but thought it was a consequence of having her arm in a sling. She therefore did not report it, apart from mentioning it to her physiotherapist. It had been a minor problem at that time in comparison with her shoulder and lower back pain. But as these other pains reduced it became more prominent.
On 16 July 1997 a MRI of Mrs Pollock's lumbosacral spine recorded multiple level degenerative changes, but the report made no mention of the thoracic spine (Exhibit R15). This is not surprising as there is no indication that the thoracic spine was scanned.
However, a MRI of 1 June 1998 found T9/10 right lateral disc herniation deforming the spinal cord (Exhibit T63). This led Dr Newcombe, a neurosurgeon, to conclude on 27 August 1998
"Some continued thoraco-lumbar pain is to be anticipated from the T9-10 thoracic disc protrusion. This is also a new finding since the fall and on the basis of this history given, there is likely to be a connection with the fall of September, 1997. This is more likely to be an aggravation of pre-existing thoracic disc degeneration than a new phenomenon though if present earlier, was then asymptomatic." (Exhibit T81)
On 26 August 1998 Mrs Pollock reported "aching in her back just under the shoulder blades" to Mr Brownbill, a consultant neurosurgeon (Exhibit T83). This was burning in nature and present all the time. However, the report focuses on the lumbar and cervical spine conditions.
Dr Steel, a consultant neurosurgeon and spinal surgeon, noted "a different pain that was developing high in the low thoracic region on the left side… [radiating] around to the armpit and… separate from the low back pain" on 11 February 1999 (Exhibits T121 and A3). He diagnosed "T9/10 thoracic disc".
In his report of 14 September 1999 Dr Champion, Mrs Pollock's treating physician, specifically addressed "the thoracic disorder with chronic pain and disc lesion" (Exhibit T173). His assessment was
"There is no doubt about the pathological significance of the T9-10 disc lesion however, while it is predominantly right posterolateral, the symptoms and signs have been predominantly left posterolateral and have extended beyond the T9-10 segment (typically T8 to T12). This disorder is a post injury condition. It has gradually worsened from a few months after the accident to the present and has become a really high priority.
Unfortunately, the early history and early examination of the thoracic spine after the accident, on the information available to me, has not been adequately described and recorded. My assessment is that this was because of the prominence of the left shoulder region and low back pain disorders. Sometimes a spinal injury with or without significant pathology, is not very symptomatic at first, but becomes so in the course of a few weeks, or a few months. That latency relates to the very complex changes that occur in nociceptive functioning over time. I conclude that the lower thoracic spinal pain syndrome which includes the T9-10 disc lesion was caused, or at least substantially aggravated by, the fall at work on 22.9.97."

He later stated that the consequences of the 22 September 1997 fall accounted for "100% of the thoracic pain syndrome" (Exhibit A2).

In his oral evidence Dr Champion

rejected the view that all disc herniations were degenerative in origin
asserted that it was common for ruptures to be provoked by a single or repetitive stress
acknowledged that a degenerative disc was more likely to rupture
noted a T9/10 disc rupture was not common
expressed the opinion that the T9/10 lesion was the result of biomechanical stress and that there was no alternative cause to the 22 September 1997 incident
agreed that the right-sided T9/10 lesion was not itself "a sufficient explanation for the predominantly left-sided low thoracic back pain". "Post-injury factors were germane".

Dr Champion concluded that Mrs Pollock suffered from a "thoracic spinal pain syndrome including intervertebral disc lesion at T9/10" (see Exhibit A2).

Evidence was given by Dr Searle that the T9/10 disc rupture was the result of a traumatic injury. It was very unlikely to be due to degenerative changes because of

the size of the prolapse
the pressure it was putting on the spinal cord
the lack of similar degenerative changes at adjacent levels
the absence of other indicators of degeneration such as osteophyte formation
the thoracic spine being much less likely to undergo degenerative change than the cervical or lumbar regions due to the protection of the rib cage.

Dr McGill examined Mrs Pollock for Comcare (Exhibits R6 and R7). She reported to him that she "has a burning sensation involving most of her back including the low and mid back". She told him that a few weeks after the accident she experienced tightness across the upper back. Dr McGill stated

disc ruptures commonly occur as a result of degenerative change in the absence of trauma
symptoms from a disc rupture triggered by trauma would develop within two or three days
it was unclear when the T9/10 disc rupture occurred
the T9/10 and the later T8/9 disc lesions were probably relevant to the tight feeling in Mrs Pollock's upper back
on the balance of probabilities the thoracic problem was constitutional and not due to the September 1997 accident.

Comcare also sent Mrs Pollock to Mr Schaeffer for examination. She spoke of "constant pain across the lower dorsal region which feels like a burning feeling or a stitch". He described the T9/10 radiological appearances as
"[A]n irrelevant and incidental radiological finding… not related to the subject injury of 22 September 1997.
Ms Pollock demonstrates no evidence of a spinal cord lesion which would be expected in a true case of thoracic disc herniation. There is no neurological abnormality on the examination." (Exhibit T185)

In his view

it was extremely uncommon for pain to arise from thoracic discs
spinal cord involvement and lower limb weakness would be expected, but Mrs Pollock had none
a right-sided rupture would not produce left-sided pain
all disc ruptures are degenerative in origin, although trauma precipitates the final rupture in 60 per cent of cases
symptoms from a rupture would occur within 24 hours.

Both parties accept that Mrs Pollock suffers from problems with her thoracic spine. Comcare contends that the thoracic spine condition is the result of the deterioration in her pre-existing spinal degenerative disease and not related to the 22 September 1997 incident.
The evidence before me is divided, although perhaps not as clearly as Ms Gabriel would suggest. The only medical practitioner who was decisively against a finding of liability was Mr Schaeffer. I did not find him a convincing witness. He blamed Mrs Pollock, in my view unfairly, for deficiencies in the history he took and drew certain adverse inferences from this.
Dr McGill, although also of the view that the cause of the condition was constitutional degeneration, reached this conclusion on the balance of probabilities. He was prepared to accept that there was some uncertainty.
But both Mr Schaeffer and Dr McGill only saw Mrs Pollock once. Dr Champion examined Mrs Pollock on numerous occasions as her consulting practitioner and was involved in her ongoing treatment. I do not accept Ms Gabriel's description of him as an advocate, notwithstanding that he put his views forcefully. I found them thoughtful and considered, even if somewhat controversial.
Dr Champion's diagnosis was a thoracic spinal pain syndrome, including the T9/10 disc lesion. For this he partly relies on the notion of central sensitisation of nociception or 'windup'. This concept was described by Dr Champion to the Tribunal in Re Lewis and Comcare [2002] AATA 197 as follows at paragraph 24
"The concept of sensitised nociception is relatively new. As a post injury disorder it began in approximately 1990 at least in respect of central sensitisation of nociception. After injury, the pain nerve endings (nociceptors) in the injured region become sensitised and their connecting nerve cells (neurons) in the spinal cord and higher in the central nervous system also become sensitised and will fire impulses leading to the experience of pain on minor stimuli or no stimuli at all. One of the consequences of central sensitisation of nociception is that there is a particular pattern of superficial and/or deep tenderness in tissue which is not primarily pathological and which has special characteristics referred to as secondary allodynia/hyperalgesia. Ms Lewis exhibits those features in large measure and it is this process of central sensitisation (of which secondary allodynia is a clinical counterpart) which accounts for the severity, nature and chronicity of the clinical problem. It is a disturbing experience having sensitised nociception with allodynia and it is usual that there are substantial secondary psychological consequences which in turn can augment the pain experience and further influence behaviour. Unfortunately, while this sensitised nociception concept is well-established, recorded in detail in extensive medical literature, it has not yet [sic] widely disseminated into general medical curricula and into the mind set of most medical practitioners."
Ms Gabriel submitted that in so far as Dr Champion sought to rely on this concept his views should be disregarded. Although Dr McGill described it as a "reasonable hypothesis", he did not think it applicable to Ms Pollock's situation. Nevertheless, Ms Gabriel sought to dismiss Dr Champions' explanation as "not a view which is widely accepted".
I do not accept that Dr Champion's evidence can be dismissed so easily. In particular I note the following passages from Guides to the Evaluation of Permanent Impairment, American Medical Association, 5th Edition, 2000, Chapter 18 on Pain
"18.2 Overview of Pain
18.2a Definitions
…
The concept of chronic pain as an extension of acute nociceptive pain is not valid. Chronic pain is an evolving process in which injury may produce one pathogenic mechanism, which in turn produces others, so that the cause(s) of pain change over time. Support for this concept includes evidence that primary afferent discharge actually has the ability to injure or kill spinal inhibitory neurons (excitotoxicity), leading to hyperexcitability due to disinhibition. Peripheral nerve injury can initiate evolving abnormalities in spinal cord neurons, which in turn generate abnormal responsiveness of thalamic neurons, which in turn generate cortical dysfunction. In time, these higher-level abnormalities may become independent of the abnormalities that produced them.
Even in situation that might be expected to provide clear correlations between perceived pain and identified peripheral pathology, there are perplexing observations. For example, in up to 85% of individuals who report back pain, no pain-producing pathology can be identified; conversely, some 30% of asymptomatic people have significant pathology on magnetic resonance imaging (MRI) and computed tomographic (CT) scans that might be expected to cause pain. Headache is another common disabling condition in which impairment must be assessed primarily on the basis of individuals' reports of pain rather than on tissue pathology or anatomic abnormality. The reason is straightforward: in the majority of cases there is no demonstrable tissue pathology. Thus, pain can exist without tissue damage, and tissue damage can exist without pain. In summary, there is no "pain thermometer", that is, no biological measure that correlates highly with individuals' complaints of pain.
…
18.2c Medical Advances in Understanding and Managing Pain
…
Neurophysiologic
A second major current has derived from explosive growth in our understanding of the pathophysiology of pain, which has rendered many older concepts untenable. Processes of peripheral and central sensitization have been clarified, along with such phenomena as the development of adrenergic sensitivity in injured nociceptive fibers and the accumulation of ion channels at sites of nerve injury, all of which may produce severe pain in response to trivial stimulation. Processes have been identified by which unilateral inflammation, trauma, or illness can lead to pain and sensitivity in uninvolved, often contralateral, structures. Physiologic processes underlying such symptoms, which were often dismissed as "not real", have been found at the level of the dorsal horn, thalamus, and sensory cortex. Intense stimulation and peripheral nerve damage have been found to induce persistent changes in the spinal cord that, over time, alter the receptive field mapping and the phenotype of neurons rostral to them, which in turn may induce changes at the cortical level. These findings are of major import. They demonstrate that pain need not be symptomatic of a disease or injury but, in fact, can become a disease unto itself.
A major implication of recent research on sensitization is that the failure of medical and surgical investigation to account for a given pain may result not from looking in the wrong place, but from looking at the wrong time. That is, the investigations may be directed toward the organ or body part that was historically responsible for the individual's pain, but they may be unrevealing because the pain, having been initiated by an injury or illness in the past, is now relatively independent.
Although sensitization of the peripheral and central nervous system has been demonstrated repeatedly in basic neuroscience research, there are currently no widely accepted methods for determining whether the symptoms of an individual with chronic pain can be ascribed to sensitization. Thus, while the concept of sensitization is extremely important to a conceptual understanding of chronic pain, there is currently no systematic way to incorporate it into impairment ratings.
Implications
The scientific advances described above have important implications for the assessment of pain-related impairment. The AMA Guides as a whole embodies the premise that injuries and illnesses cause deficits in the functioning of organs or body parts, and these deficits can be quantitatively assessed during an impairment evaluation. In the simplest situations, an individual experiences a definite biological insult that creates a clear-cut abnormality in his or her biological functioning. This abnormality, in turn, leads directly to deficits in activities of daily living (ADL) that can be quantified during the course of an impairment evaluation. An example is an individual who sustains a below-elbow amputation in a sawmill accident.
The behavioral concept of [Chronic Pain Syndrome] and the neurophysiologic concept of peripheral or central nervous system sensitization imply that pain and pain-related activity restrictions may be dissociated from the biological insult to which a person was exposed and from any measurable biological dysfunction in that person's organs or body parts. Both concepts thus challenge the assumed linkages among biological insult, organ or body part dysfunction, and ADL deficits that are fundamental to the AMA rating system." (references omitted)
Although Dr Champion's diagnosis is a modification of theirs, Dr Champion's conclusion that the thoracic condition was related to the 22 September 1997 accident was supported by Drs Newcombe and Searle. Dr Searle also noted that degenerative change was much less likely in the thoracic spine than in the cervical and lumbar regions.
Weighing up all the evidence, not least that of Mrs Pollock herself, I am satisfied and find that

Mrs Pollock suffered and continues to suffer from a thoracic spinal pain syndrome, including an intervertebral disc lesion at T9/10
the condition was caused, or at least substantially aggravated, by the accident on 22 September 1997.
Does Mrs Pollock continue to suffer from a lower back and neck condition as a result of the 22 September 1997 accident?

The evidence of Mr Pollock was

she had a pre-existing back problem having first injured it at the age of 21 when nursing and had had two neck fusions
on occasions prior to the accident she had been unable to get out of bed due to neck or back pain
she had recurrences of lower back pain in the past lasting a few days
she did not recall any lower back or neck pain at the time of the accident; rather she "hurt all over"
in October 1997 and again in May 1998 she had been hospitalised because of pain and being unable to get out of bed
in June or July 1998 Dr Newcombe had operated on her lower back to correct foot drop
she currently experiences symptoms 24 hours a day including to her hip, lower back and both legs.

On 9 December 1997 Mrs Pollock reported to Dr Billett that

she had a long history of lumbar and neck pain
at the time of the accident she experienced pain in her neck along with left shoulder pain
at the time of the consultation she was suffering "pain in her neck, which radiates into her left shoulder, remains constant and daily and is of varying severity" (Exhibit T22)
"[t]wo weeks ago, she experienced pain in her lower lumbar region, which now occurs intermittently during the course of the week" (Exhibit T22). Mrs Pollock says this is misleading as the pain in her back became unbearable on 14 October 1997 (Exhibit T32).

Dr Billett concluded that the 22 September 1997 accident resulted in aggravations of pre-existing asymptomatic degenerative changes in Mrs Pollock's neck and of pre-existing changes in her lumbar spine, making them both symptomatic.

Dr Ashman reported on 22 December 1997 that "she may have aggravated the pre-existing condition in her neck and low back" and that although other problems should resolve over three to six months "the symptoms in her neck and low back which have been aggravated by her fall may be more unpredictable" (Exhibit T27). Dr Ashman agreed with Dr Billett (Exhibit T29) and later noted that a MRI performed in July 1997 showed degenerative changes throughout the lumbar spine but no significant disc protrusion (Exhibit T43). He confirmed his earlier opinion that the accident had an aggravating effect on both the neck and low back conditions.
In a report of 27 August 1998 Dr Newcombe noted that MRIs had shown multiple level degenerative changes with disc protrusion at L2/3, L3/4, L4/5 and L5/S1 levels (Exhibit T81). In his view there had been a specific aggravation of the L4/5 disc herniation as a result of the 22 September 1997 accident causing both weakness and pain.
Symptoms that Mrs Pollock described to Mr Brownbill on 3 September 1998 included

aching in the lower back
neck pain posteriorly and more on the left side, present all the time and fluctuating in severity (Exhibit T83).

Mr Brownbill concluded

Mrs Pollock has longstanding degenerative changes within her cervical and lumbar spines
over the previous twelve months Mrs Pollock's back and neck pain had increased in severity
the accident aggravated the degenerative changes in the neck and back
on probability the effects of the aggravation would not cease fully in the future
ongoing back and neck pain could be anticipated to occur in a fluctuating manner indefinitely, having been contributed to by the aggravating forces of the accident.

It should be noted that Mr Brownbill subsequently expressed some reservations about his conclusion (Exhibit R11). If Mrs Pollock's history of neck and back pain were accurate, he would stand by his earlier conclusion. If reliance were to be placed solely on ambulance and doctors' records, he would have concluded that the neck and back pain was unrelated to the fall.
After examining Mrs Pollock on 2 December 1998 with a manipulative physiotherapist, Dr Champion said that two of the main features of her presentation were
"? Low back pain mainly from L5-S1, but also presumably from L3-4, somatic referred pain to the right hip region, residual (presumably L5) radicular symptoms and signs in the left.
…
? A rather diffuse cervical spinal pain syndrome and also incidentally cervicogenic headaches (she was tender bilaterally at the occiput and said that her headaches are different from her previous migraine)." (Exhibit T108)

He noted that the back was her major, disabling and distressing disorder. Diffuse tenderness to pressure in the left leg was consistently present and had the features of "deep mild secondary allodynia (referrable to her spinal and radicular lesion)".

Dr Champion concluded that the consequences of the accident included

aggravation of diffuse pre-existent lumbar osteospondylosis
cause, or at least gross aggravation, of L4/5 disc lesion complicated by left L5 radiculopathy
probable aggravation of disc protrusion at L5/S1
mechanical stress to the cervical spine leading to diffuse chronic cervical spine pain syndrome and cervicogenic headaches (superimposed on a background of cervical spinal pain disorders leading to fusion at C5/6/7).

He said that "the ongoing pain related disability is a consequence of sensitised nociception at sites of injury and central sensitisation of nociception". Dr Champion was cross-examined at length on this concept and that of "secondary allodynia" (see paragraph 42 above; also paragraph 102 and following).

Dr Champion was of the view that the accident accounted for about "80% of the left leg pain/disordered function, 75% of the low back pain, … 50% of the cervical spine pain syndrome…" (Exhibit A2).
Dr Searle on 30 July 2001 reported symptoms of constant pain on the left of the neck, aggravated by head and neck movement, which would spread into the occiput. Mrs Pollock also suffered constant low back pain aggravated by prolonged sitting, travelling, standing still, coughing or sneezing. The pain spread down the left leg and was aggravated by walking (Exhibit A2).
Dr Searle noted that it was quite common for a disc to rupture but not to produce symptoms for a few days or even a week. It was obvious, Dr Searle said, that the accident caused severe aggravations of Mrs Pollock's pre-existing lumbar and cervical problems. He said
"The ongoing symptoms from these injuries and aggravations are permanent and cause a severe degree of disability.
…
With regard to prognosis there will be gradually increasing symptoms and disability in the cervical and lumbar regions as the degenerative changes progress. This progress will occur more rapidly than might otherwise have been expected because the fall has also accelerated these degenerative changes." (Exhibit A2)
When Mrs Pollock saw Dr McGill on 29 March 2001 she reported that she continued to feel stiffness and pain in the left shoulder radiating up to the left side of her neck. This pain was increased by shoulder movement. She also continued to experience pain in her low back and legs (Exhibit R6). He concluded
"In light of the time period between her fall and the deterioration of her low back symptoms, followed by deterioration in her lower limb symptoms, particularly the development of left foot drop, I think it is unlikely that the September 1997 fall was responsible for the subsequent deterioration in her low back. I should emphasise that I cannot exclude the possibility that the fall aggravated her low back. On the balance of probabilities however, I think the most likely scenario was that the deterioration in her low back and lower limbs that occurred in the months and years following the September 1997 fall was a reflection of her pre-existing lumbar disc disease." (Exhibit R6)
"I think, on the balance of probabilities, that the September 1997 fall was not responsible for any significant change in her cervical, thoracic or lumbar spine problems nor responsible for any change in her state in regard to headache. I think the problems in her spine, including the cervical, thoracic and lumbar regions, and her headaches are constitutional and related to problems that had developed prior to September 1997 and will continue in the future. The typical history of degenerative spinal disease is for it to cause exacerbations and periods of improvement. The interval between the September 1997 fall and the subsequent exacerbation of her spinal symptoms, in light of the fact that there was no spinal symptom at the time of or immediately after the fall, makes it unlikely that the fall played any role in the subsequent exacerbations of her spinal degeneration that she experienced." (Exhibit R7)
Mrs Pollock described to Mr Schaeffer extreme pain in her back region between L3 and her sacrum and pain in her left leg (Exhibit T185). She also said that her neck and left shoulder were painful to touch. Mr Schaeffer found that Mrs Pollock suffered from degenerative disc disease of her spinal column to a moderate degree. He considered that the 22 September 1997 accident might have exacerbated her pain symptoms temporarily but no structural back injury resulted. There was too long an interval between the first back pain and the accident to postulate an association between them. When it was put to Mr Schaeffer that Mrs Pollock had given evidence that the onset of pain was somewhat earlier, he was reluctant to revise his opinion without an objective report of that onset.
He considered there to be "a substantial non physical element" in her condition. He rejected Dr Champion's diagnosis of a cervical spinal pain syndrome as "not a true diagnosis" but a "label" where a "clear diagnosis is not forthcoming" (Exhibit T200).
Comcare has submitted that Mrs Pollock did not suffer an aggravation of her lumbar or cervical spinal conditions as a result of the fall of 22 September 1997, either by way of injury or material contribution to the underlying degenerative disease. In the alternative Comcare contends that any aggravation of Mrs Pollock's lumbar or cervical spinal conditions as a result of the fall of 22 September 1997, either by way of injury or material contribution to the underlying degenerative disease, had ceased as at 29 June 2001 (Exhibit R10).

However, Comcare accepts that I have to be satisfied on the balance of probabilities that Mrs Pollock no longer suffers from the accepted condition of "aggravation of pre-existing lumbar and neck condition". I cannot be so satisfied.
There are considerable differences of view in the evidence before me. It is clear that Mrs Pollock suffered from degenerative conditions in both her cervical and lumbar spine before the 22 September 1997 accident. Mr Schaeffer accepts that the accident may have temporarily aggravated her pain symptoms but did not result in any structural change. Although he was not prepared to exclude the possibility that the fall aggravated her low back, Dr McGill thought it unlikely. All the other medical practitioners agreed that the fall did aggravate the cervical and lumbar spinal conditions. All also indicated that the effects of the aggravations would not cease fully in the future.
In addition Dr Champion found that the accident precipitated a cervical and lumbar "spinal pain syndrome", relying on the concept of central sensitisation of nociception with deep secondary allodynia. I have discussed this earlier at paragraphs 102 to 104 and for the reasons given there I am not prepared to dismiss Dr Champion's evidence as advocated by Ms Gabriel.
Furthermore, Mrs Pollock attested to her continuing ongoing pain. I accept her evidence.
Therefore, I am not satisfied on the balance of probabilities that Mrs Pollock's neck and back conditions have ceased. I find that consequent upon the 22 September 1997 accident she continues to suffer from an aggravation of her pre-existing lumbar and neck condition. I am also satisfied on the balance of probabilities that this neck and back condition includes a diffuse cervical spinal pain syndrome and a lumbar spinal pain syndrome both resulting from the accident.

Does Mrs Pollock suffer from headaches as a result of the 22 August 1997 accident?

Mrs Pollock's evidence was that she currently experiences headaches at least twice a week. This form of headache did not commence immediately after the accident but some 3-4 days later. She had in the past suffered from migraines that ceased in 1995 and she had not experienced sinus headaches after the sinus operations in 1997, although she had been treated with antibiotics for sinus problems since then.
Mrs Pollock was insistent that these headaches were quite different in nature from the sinus and migraine headaches. Furthermore, as a consequence of physiotherapy and her own ability to recognise them and take preventative action, the headaches now occur less frequently.
At an Initial Needs Assessment on 25 November 1997 Mrs Pollock reported very frequent and quite severe headaches (Exhibit T19). At a consultation with Dr Billett on 9 December 1997 he recorded
"On an intermittent daily basis she experiences occipital headaches which radiate to the vertex." (Exhibit T22)
Further early references to the headaches are found in a report of Dr Ashman of 22 December 1997 (Exhibit T27), a letter from Dr Rasaratnam, Mrs Pollock's general practitioner, on 28 January 1998 (Exhibit T36) and in an Initial Needs Assessment Update of 29 January 1998 (Exhibit T38).
On 26 August 1998 Mrs Pollock was seen by Mr Brownbill at the request of Comcare. She reported
"Headaches situated on top and in front and behind the eyes. These occur about twice per week and can last many hours at a time. They are sharp, sickening and piercing." (Exhibit T83)
At her first consultation with Dr Champion on 2 December 1998 he recorded

ever since the accident she had been troubled by chronic headaches
she stated that the current headaches were not migraine
she experienced a rather diffuse cervical spinal pain syndrome and also incidentally cervicogenic headaches.

He concluded that one consequence of the September 1997 accident was

"Mechanical stress to the cervical spine leading to diffuse chronic cervical spine pain syndrome and cervicogenic headaches (superimposed on a background of cervical spinal pain disorders leading to fusion at C5-6-7)" (Exhibit T108)

In a later report Dr Champion asserted that the accident accounted for "100% of the cervicogenic headaches" (Exhibit A2).

Dr Searle recorded Mrs Pollock reporting on 30 July 2001 that within a few weeks of the accident she had headaches emanating from the left side of the neck spreading into the occiput and then forward to the frontal region. These headaches did not cause nausea or vomiting (Exhibit A4). In his view her accident had caused severe aggravation of her pre-existing cervical problems.
Dr McGill concluded
"She has a long history of headache. The severity and frequency of her headaches has fluctuated considerably over the years. Although she distinguished between "migraine" and other headaches, I could not be confident that there was clear distinction between different types of headache. Headache has not been a major problem recently and she could not recall when her last severe headache occurred.
I think it is probable that her cervical spine disease has contributed to her tendency to develop headache. Sinus disease also appears to have contributed and there may have been some contribution from true migraine. In light of the symptoms she reported in the weeks following her September 1997 fall, I think it is unlikely that the fall made a contribution to the frequency or severity of her headaches." (Exhibit R6)

Her headaches were "constitutional and related to problems that had developed prior to September 1997 and will continue in the future" (Exhibit R7). Although it was put to Dr McGill that Mrs Pollock did not agree that her headaches were no longer a major problem, Dr McGill still was not confident that it was possible to source her headache.

On 1 December 1999 Mrs Pollock described to Mr Schaeffer "dreadful headaches" occurring about twice per week and lasting as long as three days (Exhibit T185). In his view the symptoms were not specific to any type of headache. There was a strong indication of a substantial non-physical element. It could be an ordinary tension headache.
Comcare contended that the Tribunal could not be satisfied that Mrs Pollock's current headaches result from the work-related accident of 22 September 1997. In the absence of Dr Champion's opinion, there was no reliable basis on which to attribute Mrs Pollock's headaches to that accident. Her headaches were related to her pre-existing conditions and not to that accident (Exhibit R10).
I do not intend to repeat here my views on the weight to be attached to the evidence of the various medical practitioners, especially Dr Champion. But I again note that Dr Champion was Mrs Pollock's treating specialist who examined her on numerous occasions. I also accept Mrs Pollock's evidence on the nature and onset of her headaches.
Weighing up all the evidence, and consistent with and giving due weight to my findings in relation to the cervical spine, I am satisfied and find that

Mrs Pollock suffered and continues to suffer from cervicogenic headaches
this condition was caused by the accident of 22 September 1997.
Does Mrs Pollock remain incapacitated as a result of the 22 September 1997 accident?

The reviewable decision of 24 September 2001 determined that although liability for "soft tissue injury to left shoulder/arm and muscle strain to left knee" continued, Mrs Pollock had no entitlement to compensation pursuant to section 19 of the Act as those conditions were not causing incapacity (Exhibit S28).
I have found that Mrs Pollock suffers from a range of additional conditions as a result of the 22 September 1997 accident. The question then is whether these conditions have caused incapacity or currently result in incapacity. Section 4(9) provides
"A reference in this Act to an incapacity for work is a reference to an incapacity suffered by an employee as a result of an injury, being:
(a) an incapacity to engage in any work; or
(b) an incapacity to engage in work at the same level at which he or she was engaged by the Commonwealth or a licensed corporation in that work or any other work immediately before the injury happened."
In Comcare's view Mrs Pollock is not entitled to incapacity payments because it had not accepted the other conditions as work related. However, as I have now found those conditions to be attributable to the 22 September 1997 accident, I can infer from Ms Gabriel's submissions an acceptance of total incapacity for work (see the Transcript of Proceedings on 27 November 2001, especially page 68).
Even if this inference is not open, I note the following

a number of Initial Needs Assessments spoke of Mrs Pollock's unfitness for work (see for example Exhibit T19 of 25 November 1997)
at 9 December 1997 Dr Billett did not consider Mrs Pollock "totally and permanently incapacitated" (Exhibit T22)
at 27 August 1998 Dr Newcombe said the aggravation of the L4/5 disc rupture resulted in incapacity (Exhibit T81)
on 3 September 1998 Mr Brownbill referred to Mrs Pollock's "current incapacitating factor" and the possibility of a trial return to work (Exhibit T83)
the whole of Dr Champion's evidence put Mrs Pollock as permanently unfit for work (see for example Exhibits T141 and T143). In oral evidence he confirmed that "she has a high level of incapacity"
Dr Searle reported that at 30 July 2001 Mrs Pollock was "unfit for work and this work incapacity is permanent" (Exhibit A4). He in effect confirmed this under cross-examination
on 29 March 2001 Dr McGill expressed the view that although her spine related symptoms would have prevented her from working in the past, she was then fit to resume her previous duties (Exhibit R6). He too confirmed this in oral evidence
in Mr Schaeffer's view Mrs Pollock suffered from no "continuing or permanent disability arising as a consequence of the subject injury of 22 September 1997" (Exhibit T185). Any incapacity resulted from her "pre-existing underlying condition".

Mrs Pollock also gave evidence on her capacity to undertake work. After the accident she was only able to return to work for two short periods. She still wishes to return but her condition prevents her.
Having made the findings above on the various conditions that Mrs Pollock suffers and their relationship to the accident, in my view the evidence on incapacity is clear. In terms of section 4(9)(a) of the Act Mrs Pollock suffers "an incapacity to engage in any work". This is the result of work caused injuries. I find accordingly.
Conclusions
In summary I conclude

on the morning of 22 September 1997 Mrs Pollock slipped and fell on her left side in the foyer of a building in the Defence Department complex in Canberra
as a consequence she suffered a soft tissue injury to her left shoulder/arm and muscle strain to the left knee
these injuries are attributable to her employment
Mrs Pollock continues to suffer from these injuries
Mrs Pollock suffered and continues to suffer from a thoracic spinal pain syndrome, including an intervertebral disc lesion at T9/10
this condition was caused, or at least substantially aggravated, by the accident on 22 September 1997
Mrs Pollock continues to suffer an aggravation of her pre-existing lumbar and neck condition consequent upon the 22 September 1997 accident
this condition includes a diffuse cervical spinal pain syndrome and a lumbar spinal pain syndrome both resulting from the accident
Mrs Pollock suffered and continues to suffer from cervicogenic headaches caused by the accident of 22 September 1997
in terms of section 4(9)(a) of the Act Mrs Pollock suffers "an incapacity to engage in any work" as a result of work caused injuries.

Decision

The decision of the Tribunal is to set aside the decisions under review and remit the matter to Comcare for reconsideration with a direction to give effect to the findings of the Tribunal as set out in these reasons for decision.
The Tribunal orders Comcare to pay Mrs Pollock's costs as agreed or taxed.
I certify that the 147 preceding paragraphs are a true copy of the reasons for the decision herein of Mr G A Mowbray
Signed:         .....................................................................................
  Associate
Date/s of Hearing  12, 26-27 November 2001
Date of Decision  2 September 2002
Counsel for the Applicant        Dr Max Spry
Solicitor for the Applicant         Peter Bevan, Baker Deane & Nutt
Counsel for the Respondent    Ms Lorraine Gabriel
Solicitor for the Respondent    Clare McNamara, Dibbs Barker Gosling