JUDGMENT OF: His Honour Deputy President Judge JP McCusker

Workers Compensation Tribunal (SA)|2000-12-06

Barber v South Australia Police Department [2000] SAWCT 185 (6 December 2000)

Barber v South Australia Police Department [2000] SAWCT 185

HEARING DATES: 13, 14, 15 March 2000, 4 May 2000

JUDGMENT OF: His Honour Deputy President Judge JP McCusker

Judicial Determination - Worker suffered stroke at home - Work stress - Causation - Whether the disability arose out of worker's employment - Conflicting medical opinions - Use of epidemiological studies - Connection must be probable not possible - Cases discussed - Expert evidence - Opinion evidence - Causal link found - S 30(1) and s 30(2)(b)(i) Workers Rehabilitation and Compensation Act 1986.

Favelle Mort v Murray [1976] HCA 13; (1976) 133 CLR 580

Adelaide Stevedoring Co Ltd v Forst [1940] HCA 45; (1940) 64 CLR 538

Monroe Australia Pty Ltd v Campbell (1995-96) 65 SASR 16

Sotiroulis v Kosak (1978) 80 LSJS 112

Bonnington Castings Ltd v Wardlaw [1956] UKHL 1; (1956) AC 613 at 621

Kop v The Home for Incurables (1970) SASR 139

Darling Island Stevedoring and Lighterage Co Limited v Hankinson [1967] HCA 10; (1967-68) 117 CLR 19

SA Health Commission v Spurling (1992) 4 WCATR 43

Byrnes v Repatriation Commission [1991] FCA 481; (1991) 103 ALR 422

Caswell v Powell Duffryn Associated Collieries Ltd (1940) AC 152

Executive Director of Health v Lily Creek International Pty Ltd (2000) WASCA 258

Sydney County Council v Furner (1991) 7 NSWCCR 210

Fernandez v Tubemakers of Australia Ltd (1975) 2 NSWLR 190

Tubemakers of Australia Ltd v Fernandez (1976) 10 ALR 303

Australian Iron and Steel Ltd v Connell [1959] HCA 54; (1959) 102 CLR 522

Department of Defence v Speed, unreported, Federal Court of Australia, 30 March 1993

EMI (Australia) Ltd v Bes (1970) 2 NSWR 238

Seltsam Pty Limited v McGuiness; James Hardie & Coy Pty Limited v McGuiness (2000) NSWCA 29

McGhee v National Coal Board [1972] UKHL 7; (1973) 1 WLR 1

Birkholz v RJ Gilbertson Pty Ltd (1984-85) 38 SASR 121

Hillier & Carney v Lucas (2000) SASC 331

Farrell v The Queen (1998) 194 CLR 286

R v Perry (No 3) (1981) 28 SASR 112

Geste v Pereira (1991) 161 LSJS 260

Pipikos v. W Brown & Sons Pty Ltd (1970) SASR 508

1 In the morning of the 28 December 1997, the worker suffered a stroke. In technical terms this was a thromboembolic occlusion of the left middle cerebral artery. It was due to an embolus arising from thrombus detaching from atheroscleratic plaque lying at the origin of the left internal carotid artery (AB 75). She was at home at the time, resting in bed when she suffered this stroke. Counsel agree the only issue in this case is causation (6, 289). The key provision reads:-

"30 (1) Subject to this Act, a disability is compensable if it arises from employment.

(2) Subject to this section, a disability arises from employment if -

(a) in the case of a disability that is not a secondary disability or a disease - it arises out of or in the course of employment; or

(b) in the case of a disability that is a secondary disability or a disease-

(ii) the disability arises in the course of employment and the employment contributed to the disability."

2 In this case the worker must satisfy the test in s 30(2)(b)(i). That is if anything the higher of the two causal tests; see Favelle Mort v Murray [1976] HCA 13; (1976) 133 CLR 580 per Mason J at 598.

3 At the outset of the case, Ms Kelly, of counsel for the worker explained the worker, aged 48 years at the time of the stroke, was employed by the Police Department from 1995 as the computer Help Desk Operator and Coordinator. This made her a trouble shooter for computer problems in the Department (3). The parties tendered a statement of agreed facts (Exhibit A 2). It records the following:-

"1. From 1995 and throughout 1996 and 1997, June Barber, in her work as a Help Desk Officer and Help Desk Coordinator for the Respondent, was engaged in work at an objectively stressful workplace.

2. Ms June Barber felt stressed during this period."

4 In the final address Ms Kelly emphasised the lay evidence describing the nature and scale of this stress, (Exhibit A 1, at 1 - 15).

5 Ms Josephine Weepers, one of the worker's colleagues, commenced at the Help Desk in March 1995. Her recollection of stressful factors are as follows (AB 1):-

"Late 1996 discussions commenced between Help Desk Staff and management in relation to the Help Desk Officer positions being reclassified from ASO2 to ASO3. In June 1997 the Help Desk Coordinator (Sharon Jamison) applied for and was successful in gaining a temporary position with another Government Agency. Given that the Help Desk Coordinator vacancy was temporary and the reclassification of the Help Desk Officer positions hadn't been finalised it was mutually agreed that une (sic) and I would share the acting position of the Help Desk Coordinator a month at a time and that the vacancy of a Help Desk Officer would be temporarily filled. The frequent staff turnover and the subsequent training load proved to be very stressful. Additionally the suspense waiting for the reclassification issue to be resolved resulted in June becoming more and more frustrated, to the extent that she registered her interest in an ASO1 Station Clerk position in August 1997."

6 Ms Weepers detailed the restructuring and increased workloads in particular. She stated, (AB 2):-

"Since the inception of the Help Desk as a formal service to SAPOL computer users the following changes have occurred:

* increase in local area networks from approximately 2 to 30;

* increase in personal computers from approximately 500 to 3,000;

* outsourcing computing services to EDS resulting in more complex notification procedures, increased negotiation and consultation;

* constant changes in technology eg compact disks, scanners, software upgrades including network software and desktop software;

* outsourcing SAPOL Radio Section staff resulting in fax support becoming a Help Desk responsibility;

* threat of Help Desk operational hours changing from 0800 to 1700 Monday to Friday to 24 hour service."

7 Ms Weepers formed a close bond with the worker and they shared a confidential relationship. She says she knew of no stressors in the worker's life save her employment. But the employment was highly stressful. Moreover she had observed the deterioration of the worker's emotional state in the period leading up to her stroke. Another worker, Ms Pauline Kellaway said the same thing. The worker's husband, Kelvin Barber, confirmed the same. His description is of her work conditions becoming unreasonable and oppressive. She would manifest the effects of all this stress when she got home (AB 11, 12).

8 The evidence demonstrates to the balance of probabilities that work conditions took a great toll on the worker's reserves of psychological strength. The evidence paints a highly unsatisfactory industrial situation and one that persisted for an extensive period. While all doctors have acknowledged the difficulty of measuring this stress, I find she was severely stressed particularly from late 1996 to the date of her stroke.

9 The applicant's case was that this stress was a cause of her stroke. The suggested mechanisms were presented as culminative or alternative. Firstly, that chronic stress accelerated vascular disease in the carotid artery in persons with hyper sensitive vascular responses. This mechanism operated alongside the mechanisms due to genetics and smoking (AB 77). That the latter were factors was not disputed by any witness.

10 The second mechanism was the endocrine response explained in terms of this worker's insulin resistance condition. The latter, when taken together with the stress, accelerated the vascular disease that led to the stroke (9, 10). The nature of the particular stroke was not in dispute (11). The worker herself was not able to give evidence by reason of her disability (12).

11 I now turn to deal with the medical evidence. Before doing so I record that this evidence was of the highest standard and each witness a highly respected member of his profession.

12 Dr J.F. Hallpike, the Emeritus Neurologist of the Royal Adelaide Hospital, provided three reports, (AB 74 - 80), in addition to his oral evidence. I set out the clinical information recorded by Dr Hallpike as it contains a number of the premises which underlie the various experts' opinions:-.

"Taken by husband to MPH Emergency Department on 28/12/97 (received at 1015) complaining of right-sided weakness that morning and frontal headache. Aged 48 at that time. Noted to be afebrile, with regular pulse, BP 110/60, alert and orientated with CGS (sic) (Glasgow Coma Scale) score 15/15 [normal] and triaged priority 3. Seen by doctor at 1040. Mrs Barber told him that she had `flashes and dots' in her vision and inability to speak lasting 10-15 minutes at about 0900 that morning. Also that her right arm became weak and that she had been unable to dress herself. That loss of right arm strength had persisted. The doctor recorded that while he was taking her history, she became aphasic [unable to speak]. That at that time there was no facial weakness, that her right arm would only flex to pain [severe degree of neurogenic weakness] and that she was moving her right leg to command. Notes of BP 140/80, afebrile and with no neck stiffness. A right carotid bruit but no left carotid bruit. A normal ECG. Sent for an urgent CT head scan - result phoned through by radiologist - `normal'. A lumber puncture was undertaken [clear fluid, under normal pressure, no cells, normal chemistry]. At 1515 `vomited and urinary incontinence'. Given 100ml 20% mannitol intravenously [a treatment for brain swelling] between 1520-1530. At 1610 `opening eyes to pain, not obeying commands, a right hemiplegia [`flicker' of movement right leg, no movement of right upper limb]. Conclusion `ischaemic CVA'. A repeat CT head scan on 29/12/97 showed `an extensive area of decesaed (sic) density involving the territory of the left middle cerebral area ... associated mass effect with incomplete effacement of the left lateral ventricle plus almost complete effacement of the cerebral sulci of both cerebral hemispheres ... also subfalcine herniation to the right ... consistent with an area of recent cerebral infarction [tissue changes due to loss of blood supply] with associated significant mass effect [brain swelling]'. Treated with intravenous mannitol, intravenous methylprednisolone, dexamethasone [to reduce the brain swelling associated with the infarct]. An ECHOcardiogram on 30/12/97 was normal. An ultra sound scan of the carotid arteries on 2/1/98 was reported to show on the left side `a large soft atherosclerotic plaque near the origin of the internal carotid artery producing a diameter reduction of approximately 90%' and on the right side `a little atherosclerotic plaque formation at the origin of the internal carotid artery'. Not diabetic. Normotensive. Was not taking the oral contraceptive pill and was not on any form of hormone replacement therapy. No cardiolipin antibody activity was detected. Antinuclear antibody activity [test for lupus] was not detected. She was a smoker (20-24/day), according to the hospital notes. Mildly raised serum cholesterol of 6.6 mmol/L [blood taken 29/12/97] (normal <5.6). Mrs Barber's mother is recorded as having died of a heart attack aged 51, her father to have died of a heart attack aged 60, and an aunt to have died of a heart attack aged 56."

13 Dr Hallpike then went on to describe the stroke in the following terms:-

"In summary, development on 28/12/97 of a stroke-in-evolution [`stuttering stroke'] progressing to a completed stroke [stable vascular deficit] within 4-6 hours of the initial symptoms. The CT scan on 29/12/97 showed extensive ischaemic cerebral infarction, with brain swelling, in the left internal carotid-middle cerebral artery distribution. The carotid artery ultrasound indicates that the cause of the stroke was almost certainly a thromboembolic occlusion of the left middle cerebral artery from an embolus [circulating plug] or emboli, arising from thrombus detaching from atherosclerotic plaque lying at the origin of the left internal carotid artery. Such thrombo-embolism from atherosclerosis of the large arteries supplying the brain is the commonest cause of ischaemic cerebral hemisphere infarction both in younger and older age groups. There is the adverse family history of atheroslerotic (sic) vascular disease. Being a smoker, and a raised serum cholesterol, are also risk factors for atherosclerosis."

14 Dr Hallpike describes the stress factor in much the same terms as I have set them out above. By that I mean he has made an assumption that accords with the finding I have made.

15 He observes that because stress is hard to measure it is a difficult subject to study scientifically. More so because of the range and complexity of personality types. He acknowledges a "clinical impression that emotional stress and anxiety are risk factors for the development or expression of atherosclerotic vascular disease". And psychological stress has been accepted as a possible risk factor in ischaemic stroke in the leading text, CP Warlow, citing a study by Harmsen of risk factors for stroke in middle-aged men in Gottenberg Sweden (Stoke 1990). Dr Hallpike reinforced this point in his testimony (22). Warlow's work is an arbiter of accepted views in neurology.

16 In contemplating the evidence, a distinction should be kept in mind. That is between studies and research that conclude there is a link between carotid artery atherosclerosis and stress and such papers that postulate a mechanism for that link. As Dr Hallpike explained medicine can make a link between a factor and a disease without being able always to explain the mechanism (33 - 35, 59). The issue for the worker is to prove that link in her individual case to the balance of probabilities. While it would be preferable to know the mechanism of that link, the mechanism is not one of the requirements to validate the expert's opinion.

17 It should also be recorded that Dr Hallpike approached the issue in this case with a contrary view (23) but his researches on the discrete topic resulted in an opinion that there was a link in this case (AB 77, 38). He was engaged to express an opinion in the first instance by the employer.

18 His first report (AB 76) referred to a number of published studies. In considering this material a distinction must be kept in mind between those suffering a fixed raised blood pressure condition (hypertension) for whom stress is a recognised factor in the acceleration of vascular disease (182, 200, 215) and those with a variable presentation. The worker's history does not involve the presence of essential hypertension operating as a medium between the stress and the vascular disease.

19 Dr Hallpike's first reference was to Harmsen et al (Sweden 1990). That investigated cardio-vascular risk factors in 1000 men aged 47 - 55 over a four-year period. The psychological stress defined as a feeling of tension, anxiety and irritability, was scored on an analogue scale. The result of the study was that severe psychological stress was associated with a significant increase in the risk of all types of stroke (AB 76). Dr Hallpike also referred to House et al (Journal of Neurology Neurosurgery and Psychiatry 1990) which demonstrated a link between high long-term threat ratings and stroke though little effect in short-term equivalents. Lastly he relied on Everson et al (BMJ 1979) which again demonstrated a positive correlation between stress-induced change in blood pressure and progression of carotid artery atherosclerosis. This was a mechanism different from essential hypertension.

20 Dr Hallpike also sought out available studies that reached contrary conclusions (36). In Macko et al (Stroke 1996) the study found no significant link between stroke and the incidence of stressful life events in the month preceding the stroke; ie in the case of recent psychological stress and acute brain infarction.

21 Dr Hallpike then listed the accepted risk factors namely genetic, age, hypertension, diabetes mellitus and tobacco. While hyperlipidaemia was a risk factor for coronary artery disease, it seemed less significant for strokes. In the case of younger adults, cardiogenic emboli and premature atherosclerosis were the commonest causes of ischaemic cerebral infarction.

22 Dr Hallpike stated his conclusion in the following terms (AB 77):-

"... According to the literature surveyed above, there is acceptable scientific evidence that sustained stress is a risk factor for stroke. The stress experienced by Mrs Barber at work hasn't been scientifically evaluated by an appropriately experienced psychologist and I am unable to form a judgement about to what extent the conditions described in Ms Weepers' statement represented `above average' psychological stress in contemporary terms. Nevertheless, this statement gives information about a number of stressful aspects of the employment during 1997 and indicates that Mrs Barber was exhibiting noticeable signs of stress in the period before the stroke occurred. So the answer to this question is in the affirmative.

... My assessment of the relevant information about the illness itself is that the stroke [ischaemic cerebral infarction] resulted from thromboembolism from left internal carotid artery atherosclerosis. I think that the family history of atherosclerotic disease and the cigarette smoking were the most significant and uncontentious independent risk factors for development of the premature atherosclerosis underlying the stroke in this case. In terms of relative contibutions (sic) to her stroke of the identified risk factors - the family history(1), the smoking(2), and the work-related stress(3) - an, admittedly arbitrary, assignment of 60%(1), 30%(2) and 10%(3) for the proportions of risk under these 3 headings is suggested."

23 In his second and third reports (7 August 1999 and 12 September 1999), Dr Hallpike added details of the study of Matthews et al (Stroke 1998). This study, while concluding a link between stress and atherosclerosis of the carotid artery, was also concerned to reveal a mechanism. Measured thickening of the carotid artery in middle-aged women was compared to the magnitude of change in pulse pressure during mental stress tasks independent of age, hormone replacement therapy, base line measures of pulse pressure, smoking and tri-glyceride levels. It concluded a mechanism of deterioration where a large pulse pressure response was produced in response to mental pressures (AB 78). This demonstrated in Dr Hallpike's opinion that hypertension, an acknowledged factor, was not a pre-condition for the link. It demonstrated a link between vascular disease and stress in those with normal blood pressure readings. Dr Hallpike stated (AB 78):-

"... It follows that sustained hypertension is not after all a pre-requisite for stress-related acceleration of carotid atherosclerosis."

24 As will emerge in the course of these reasons, the lack of discrete proof that the worker here had the characteristic vascular response to a short term mental stress test as did the subjects of the Matthews studies, became central to the argument of Mr Lines, of counsel for the respondent (290). That in turn will depend on my understanding of what the worker had to establish by way of evidence for there to be an evidential foundation upon which the causal linkage could be established, ie, did the worker have to prove there was a causal linkage or did she have to show the actual mechanics of the linkage. I indicate it is the former, but I will return to this later in these reasons.

25 Dr Hallpike referred to Barnett et al (Hypertension 1997). That study concluded that (AB 80):-

"... `reactivity to psychologic stress is not only a correlate at baseline, but also a significant predictor of the progression of extent of atheroscerosis'. (sic)"

26 Dr Hallpike also cited studies by Agewall et al (American Journal of Hypertension 1996), Matsumoto et al (Stroke 1993), O'Leary et al (New England Journal of Medicine 1999) and Jennings et al (Australian NZ Journal of Medicine 1999). These studies pointed to a causal link between psychological stress and the development of carotid atherosclerosis though the explanations of the mechanism were uncertain. Vascular reactivity does appear to be one mechanism emerging from the research.

27 I will discuss Dr Hallpike's evidence further in these reasons, but I comment at this point in that Dr Hallpike gave his evidence in a measured, impressive and careful way. He chose his words with deliberation. I cite part of his evidence with this in mind (23):-

"Q. You summarise those papers by saying, `These authors hypothesise that acceleration of the atherosclerotic process might result from neuro-endocrine responses to stress or interaction with hypertension'.

A. I think the important thing about the papers is that they were serious epidemiological studies that had as their conclusion that there was evidence in different ways that backgrounds of stress were, unexpectedly I think in both papers - because that point is clearly made - epidemiological risk factors for stroke."

28 In Dr Hallpike's opinion the causal link is established though there is variation and in some aspects inadequacy in terms of explaining the mechanism. However the presence of chronic long-term stress was necessary (27). Hyper-lipidaemia (cholesterol), unlike its role in the case of coronary disease, had not been established as a risk in stroke (28). The worker did not have significant cholesterol readings.

29 In cross-examination Dr Hallpike was challenged on the level of acceptance of the causal linkage of chronic stress and carotid atherosclerosis. He stated (42):-

"A. I don't think it has much, if any - I mean, `acceptance' is quite a sweeping word and the jump between research and what then becomes something to be put into practice is obviously a very big jump.

A. And what I do say, and what all the papers would say, is that the relevance of these findings in relation to, for instance, chronic work-related stress and so on - workplace stress - is something that needs to be considered, but I - because that's not exactly what the papers are necessarily about, that they work on a mechanism."

"Q. So it is a fair thing to say that this issue of the relationship between chronic stress and vascular disease and stroke is still in the area of debate.

Q. Yes. And although the results of some studies are suggesting that chronic stress be considered as a possible risk factor, it's not been concluded that it is a definite risk factor.

A. Yes. I think - could - would you allow me to say - - -

A. One might ask, you know, why is such a rather important matter - I mean, we are spending a lot of time and effort on this for - you know, I mean, for very important reasons - why hasn't this been - why is this still for debate and so on. And the fact is that, you know, what measurements to make and how to produce appropriate studies is extremely difficult. ... We haven't actually been primarily that interested in this rather artificial model, but it seemed to be the only way in which we could get any measurements at all. I think that's how its sort of proceeding."

30 Mr Lines tested the hypothesis of vascular reactivity as explaining the mechanism of the linkage. Dr Hallpike accepted those studies that sought to illuminate a mechanism had tested their subjects as to low or high vascular activity (51) and such a test had not been conducted on the worker (51, 52). Moreover the vascular reactivity tests had not specifically been trialed for the purpose of making conclusions about workplace stress (57, 58). Thus the mechanism of vascular reactivity had arguable significance as an explanation for the link in Mrs Barber's case, (61).

31 The last questions of the cross-examination demonstrate that having taken all these considerations into account, Dr Hallpike's opinion was that there was a causal linkage between the work stress and the stroke in this particular case. I quote it as the shortest summary of his evidence over a number of the proceeding pages of the transcript. He stated (65):-

"Q. But whether stress played an influencing role in Mrs Barber's stroke is something that you're not really in a position to given (sic) an opinion about.

A. I think I have indicated uncertainty about that.

McCUSKER DP: That's the point though, I think - if I could articulate my understanding of Dr Hallpike's position - he is not asserting it as a scientific fact to which dissent should not be available. He is expressing it in this particular case as an opinion on the totality of the material and on the basis that yes, as a fact the thing is a possibility and then in the opinion, in this case - in his judgment in this case - it has a contributory factor. It has been a contribution, albeit a lesser one than other factors.

A. Yes. I wanted to qualify what I said and that was the way I did it. Thank you.

Q. On that same page you have answered another question about whether it's possible to estimate the contributory extent of the stress. Correct me if I am wrong but from what you have said it seems to me that you can't actually conclude whether stress influenced Mrs Barber's condition and the onset of the stroke but you are prepared to say that it may well have done.

32 I find that on a proper understanding of his evidence, Dr Hallpike testified that in his opinion there was a causal link in this worker's case. In his final address Mr Lines did not suggest that the effect of his evidence was otherwise.

33 Dr Peter Hetzel cardiologist (179) was called by the Crown. His reports dated 19 July 1999 and 25 August 1999 were before me (AB 81-87). As Dr Hallpike has stated, (37), the conflict of views between him and Dr Hetzel amount to whether hypertension is a precondition for stress to effect or contribute to stroke. There seems little doubt there was no evidence of hypertension either before or at the time of Mrs Barber's stroke. Dr Hetzel's view as to Dr Hallpike's opinion is stated as follows (AB 83):-

"Dr Hallpike comments that according to the literature surveyed above, `There is acceptable scientific evidence that sustains stress as a risk factor for stroke.' I would disagree with that conclusion formed from the evidence he has quoted. The Everson and House reports do not suggest this. Everson's evidence indicates that in men who were not high reactors (not hypertensive responders) there was no increased rate in the development of carotid artery atherosclerosis. We know that women have a lower rate of development of atherosclerosis in the pre-menopausal phase of their lives. This applies to non-smokers in particular. The paper by Harmisen refers to the significance of hypertension.

In my opinion the evidence indicating stress as a risk factor in women without the development of hypertension, is lacking."

34 In Dr Hetzel's second report he deals with the study of Matthews which he classifies as unsatisfactory because of the techniques and methods used to reproduce stress circumstances and measure the effect. In particular the interval between the stress tests and carotid artery measurements, over two years on average was a major defect in being able to establish a relationship. There was an absence of a base line. The techniques used to measure the blood pressure effects and variations were in Dr Hetzel's opinion unsound. He rejected the study as demonstrating any link between work stress and for the progression or development of the coronary artery disease in Mrs Barber (AB 87).

35 In his oral evidence, Dr Hetzel dealt with the Everson studies that had influenced Dr Hallpike's conclusions. He was dubious as to the validity of the comparative measurements of the carotid artery (184). Also that it was a study of men only (185). Because of these reasons he thought the report did not establish anything (187). His evidence seemed to provide some shift in position in comparison to his report, though not to the extent of agreement with Dr Hallpike or support for a link in this case.

36 As to Matthews, Dr Hetzel expanded on his criticisms in the second report (188). In his view an underlying difficulty in this area was that as yet there is not a test good enough to determine who are and who are not in the reactor group (190). Thus the Matthews study in his view failed to establish a link between stress and the progression of vascular disease in the carotid artery in middle aged women. His evidence-in-chief then went on to deal with the opinions of Dr Gale and I will return to those at the appropriate stage of these reasons.

37 Under cross-examination, when Dr Hallpike's evidence (57) differentiating hypertension and vascular reactivity was described, Dr Hetzel's response was in terms of labile hypertension in the case of the person who responded to stress by fluctuations in blood pressure. This accords with Dr Hallpike's characterisation of their respective stances and differences on the issue (37). Dr Hetzel was of the view that to develop arterial disease you needed to have fixed hypertension (200, 216). Anything beyond that in Dr Hetzel's opinion was not sustained by evidence he regarded as satisfactory (217).

38 Dr Hetzel acknowledged that he did not have expertise in epidemiological methods (209). Dr Hallpike clearly had expertise in that area inter alia in his noted contribution to the study of multiple sclerosis (17, Exhibit A3). Dr Hetzel felt the results of the epidemiological research was not enough to persuade him of the linkage (221) and he felt more needed to be done to convince him it was a proven risk factor (222). This was particularly so in his mind for the following reason (220):-

"If you postulated an epidemiological relationship, you have to have some sort of idea of a mechanism because otherwise you can be comparing - I mean, somebody may develop the epidemiological figures, and then somebody goes back and tries to point out why - I don't object to that, but you have to find out why, if you're going to have a satisfactory analysis of it. I don't think we have got good epidemiological evidence in this lady so far.

... and I think the problem about these studies is that they're not scientifically tight enough in the techniques they have used to be able to say yes or no. It isn't strong enough to say, `Yes, there is a relationship'."

39 Dr Hetzel accepted Matthews and Everson had not been subjected to criticism in medical journals (219). He felt publication in a medical journal did not per se provide credence (225). Yet Dr Hallpike was able to refer to numerous studies indicating the link; (see also Tennant and McLean at 32). Not only were the publishers ones of reputation but it is interesting to note Dr Gale had his studies rejected (76) indicating the need for the studies to satisfy certain acceptance by the editors before publication. I note that Dr Hallpike as a neurologist is directly concerned in his learning and experience with the condition under examination here. I felt in the course of Dr Hetzel's evidence a significant element of scepticism for the essential hypothesis of a link outside of hypertension which may have coloured his approach.

40 Professor Craig Anderson was the other witness whose testimony was relevant to Dr Hallpike's contentions. He is the Professor of Geriatric Medicine at the University of Auckland in New Zealand. His specialties are clinical neurology, geriatric medicine and clinical epidemiology, (see Exhibit R7). He had been awarded a Ph.D. in epidemiology upon the thesis of stroke related disability frequency patterns and determinants of care in 1995. That thesis had included some examination of causality (228). His continued involvement with epidemiological studies included the areas of cerebral-vascular disease and stroke (229).

41 Two reports were tendered (AB 112, Exhibit R4). At the outset Professor Anderson "defined his terms" which assists in appreciating the effect of his evidence. I quote (AB 113):-

"... Whatever the exact mechanisms, it is quite clear that there are certain individual and population characteristics (risk factors) which make the clinical consequences of atheroma, in this case that of ischaemic stroke, more likely. In some, but no means all, instances, there is a clearly plausible biological explanation for the connection between a risk factor, through atherothrombotic arterial disease, to the subsequent clinical syndrome. It is, however, important to be clear that a risk factor indicates an association between that factor and the disease of interest, and a causal relationship between a risk factor and disease is only supported by the fulfilment of several criteria: a strong association between the risk factor and the disease of interest (often expressed as a high relative risk or odds ratio compared to normal controls or those free of disease); consistency of the association across several studies; a dose response relationship, (i.e, the greater the exposure to the risk factor, the greater the risk of disease); independence of the risk factor from other associated (confounding) variables; a clear temporal sequence of exposure to the risk factor before disease onset; biological and epidemiological plausibility; and, most convincingly of all but not always feasible, demonstration that the incidence of disease falls following modification or removal of the risk factor of interest, preferably by means of a randomised controlled trial. However, even if a risk factor is associated with stroke, an (sic) even if the relationship is potentially causal, the factor may have very little impact on the overall burden of the disease in the community if the particular risk factor is rarely present in the population and the baseline risk of disease in that population is low."

42 This quote is important because the opinion of Professor Anderson which is against a link, is in part influenced by the failure of the evidence to satisfy these criteria. But the test in civil law of the balance of probabilities may not always equate with the level of demonstration required in science. After all, the law distinguishes between various burdens of proof dependent upon the nature of the proceedings (ie criminal and civil) and matters of scientific proof are not necessarily the equivalent of one or the other. But I will return to this later in these reasons.

43 Professor Anderson emphasised what he saw as the key factors in Mrs Barber's case namely, cigarettes, genetics, above average cholesterol and impaired glucose tolerance (AB 114).

44 He dealt with the evidence of work related stress as a causal factor in the development of her carotid atheroma at large. In his conclusion the epidemiological evidence is minor compared with the well known factors "in part related to the complexities of measurement, not least the difficulties with the operational definition of stress". As to the studies of House and Harmsen, Professor Anderson admitted they suggest a link between psychological stress and stroke but he was not satisfied with them as convincing studies. As to Everson which describes a mechanism explaining the link, Professor Anderson's position was that there is no indication of blood pressure variation (vascular reactivity) in Mrs Barber's medical records. However Professor Anderson did not address Everson in terms of being an unsatisfactory study for demonstrating a causal link between stress and stroke in people with a history of apparent normal blood pressure. That of course is also the conclusion of House and Harmsen. On the other hand, he accepted that as a mechanism for vascular disease, blood pressure is plausible. He reiterates this in evidence in the case of essential hypertension (237).

45 He referred to studies of the role of stress in coronary artery disease by Hlatky (Circulation 1995) and Willich (New England Journal of Medicine 1993) as evidence to provide an important counter argument for the importance of stress and vascular disease if one assumes coronary artery disease as a useful surrogate. One of Dr Hallpike's points was that such a comparison was not always valid (19, 28, 49, cf 32).

46 The final part of Professor Anderson's first report emphasised the far greater significance of the established risk factors set out above and criticises Dr Hallpike's view as "an exaggeration of the importance of a possible (or somewhat uncertain) risk factor for ischaemic stroke (eg job strain or work-related stress)" and that there is "little scientific support" for the link because further research is required to confirm (or refute) the association. Moreover he was of the view that if an association exists, it is modest.

47 Because of the circumstances in which the case was conducted this was as much of Professor Anderson's evidence as Dr Hallpike had opportunity to answer. He was of the opinion that Professor Anderson had not given the evidence of the mechanism of vascular reactivity its due weight (37). Moreover as to Professor Anderson's criticisms of the reports that favoured the link, Dr Hallpike accepted that there was space for dissent and that the studies did incorporate an element of judgment by the medical scientists conducting them (35). But accepting that the existence of the link still allowed legitimate debate (49) his conclusion remained (38, 65).

48 This element of weighing the evidence and then making a judgment and the role of probabilities particularly in epidemiology was acknowledged by Professor Anderson (233). This was to be contrasted with other forms of medical research securing conclusion definitely yes or no. Professor Anderson pointed out that epidemiology used expressions like "most unlikely", "uncertain", "probable", "possible", "strong effect", "black and white", and presented things as statistics and numbers as well as probabilities, though the latter in protocol terms.

49 Professor Anderson put his opinion on the link as follows, (233-234):-

"A. ... All the time we're making judgments and weighing up probabilities and likelihoods. It's never definitely no and it's never definitely yes. But for all intensive (sic) purposes and practicalities and sensibilities I'd have to say it's a no.

Q. And no to job strain contributing to adverse health or development of premature vascular disease. Is that what you mean.

A. To the development of premature vascular disease.

Q. When you refer to the probabilities, do I understand you to be using that term in a statistical sense.

A. Purely statistical, because that's what epidemiology is. Epidemiology is the science of probabilities and statistics and numbers."

50 On the association between blood pressure and vascular disease he pointed to the fact that traditionally medicine categorised pathological processes. You either did or did not have high blood pressure. You either did or did not have high cholesterol. Professor Anderson said the correct approach was as follows (235):-

"A. ... we should actually be counting every level of blood pressure, and so it's not that some of us are at risk and others aren't, it's that we're all at risk, but some of us are a bit more at risk than others. None of us are at zero risk. ... we all develop atheroma. It happens very early in our life and it continues on for the duration of our life. ... the relationship is linear. ...

... all of us here in the courtroom would do ourselves a justice to try and reduce our blood pressure at the lowest possible level, and in fact this is a very powerful message that we can't seem to get across from a public health perspective, ... if we can reduce our blood pressure then we prevent a lot of strokes. So the individual risk goes up for every little rise in your blood pressure. So this is a continuous relationship, that we're all at risk. Its just that some of us are a bit more at risk.

... Whatever this process is of hardening of our arteries happens very early in life and it continues on, and for those of us who have various predispositions this process can occur at a premature and accelerated rate - and what are those mechanisms we know somewhat about, but we don't know the whole answer, but we know a lot about and we know what does that. So one of the key things that is important is blood pressure. Now we're not exactly sure why blood pressure causes us to harden our arteries, but it's got something to do with a - just if you could imagine pipes, the volume or the pressure down pipes - excessive strain on the blood vessel wall or whatever the mechanism, there is some process by having our pressure raised that accelerates this degree of atherosclerosis, and what is most important, because this is a chronic disease, is chronic exposures."

51 Professor Anderson then dealt with the stroke event and the rupture of the plaque (238):-

"A. ... What causes that final sort of trigger to erupt no-one really knows, but one of the plausible mechanisms is acute changes in physiology. It might be acute changes in our clotting mechanisms; it may be acute changes in blood pressure. So what I've tried to say here in my report ... is firstly this issue of continuous relationships with risk factors - we are all at risk and some of us are more at risk than others. It' s not a yes or a no issue. ... The second point I'm trying to make, ... is that there is some complication that might trigger it and one of the potential mechanisms is transient elevations in blood pressure that happen very quickly; talking about within hours, minutes to hours, that something might happen to blood pressure or clotting or some other physiological variable."

"Q. What sort of event or circumstance are you referring to there as ---

A. Lifting, a sudden strain or lifting, and there's some good data to suggest that sudden unaccustomed exertion, heavy exertion, can precipitate myocardial infarction heart attack. ... So sudden triggers can precipitate this event, and it probably happens just for stroke - that it does for heart attack, but our evidence relationship to stroke is less than it is to heart attack. The final point that you're trying to make is this issue of fluctuations in blood pressure or consistency of blood pressure, and I must say this is a new area, a very new area, and this is why a lot of the cardiovascular doctors and cardiologists are doing research with 24 hour blood pressure control, ... These are people who have changes in their blood pressure at certain time of the day. And people are thinking up various mechanisms and reasons why this might happen and whether it's an important clinical syndrome or not, and at the moment it's of uncertain significance and most people agree that it is of minor significance in comparison of the chronicity of your absolute level of blood pressure.

Q. Is another term for this fluctuation in blood pressure `vascular reactivity'.

53 Professor Anderson then dealt specifically with Dr Hallpike's opinion (241):-

"Q. And I believe you've looked at Dr Hallpike's reports ... which raise the concept of vascular reactivity as a possible mechanism for the development or contribution to the development of athersclerosis.

A. It's a hypothesis, isn't it? It's a hypothesis that is not substantiated by any evidence. I mean, I can give you another 10 hypotheses. They're hypotheses.

54 Professor Anderson dealt with Dr Hallpike's reliance on Everson. He quoted the paper's conclusion that "our findings are limited to employed middle-aged white men. Additional research is needed to determine if these relations are also evident in non-white or female populations or among other age groups."

"Furthermore, work is only (sic) aspect of life. Therefore it is important to consider a variety of social and interpersonal contacts that may be potential sources of stress in an individual's life."

"A. ... So, you know, my own summation of the study is that it's very interesting and it leads us in an area of hypothesis generation and for further research. It would certainly not be classed as strong evidence. It would not be classed as the definitive conclusion. It provides us with some thoughts that maybe stress might be related to changes in thickening of the blood vessel, but there's a lot of uncertainty, which the authors have been quite open and concluded themselves."

56 Professor Anderson then dealt with his own view (242-243):-

"A. ... The quick answer is, completely uncertain and likely to be - if it's there at all it's likely to be extremely small. And if it is there - and again these are my hypotheses; there's no evidence to substantiate this - but, you know, if there is any role it's what we call - the epidemiological lingo is `modest, modest effect', which is basically small, marginal. It's probably likely to occur in those who are predisposed for whatever reason. In the otherwise well individual it is extremely hard to think of a clearly biological or mechanisimal (sic) way, in the absence of any other predisposition, that work stress can cause you to harden your blood vessels. It's ridiculous to expect that. You're talking about a chronic disease that occurs over your life span and here we have a small window when we work six, seven or eight hours of the day that's going to cause us to harden our blood vessels? In light of all the other evidence that we've accumulated related to the causation of artheroma it's implausible. That's the short answer."

57 Professor Anderson returned to the topic (254) in cross-examination in the following context:-

"Q. ... Do I understand you to be saying that you agree that there is epidemiological evidence that work stress is a casual (sic) factor in the development of atheroma, but there's less evidence, or it is less important, than the link with smoking, family history and hypertension.

A. Well, what I'm saying here is that the role of stress in general - not just work stress, but stress in general, whatever that is - may in some way - is possibly associated with premature cardiovascular disease, stroke or heart attack ... So what I'm trying to convey is that there's this overwhelming strength of established risk factors that are clearly defined, unrefutable, but probably still underestimated, and we have this possibility of stress playing some role, and some imprecision - even imprecision there."

58 This comparison of the significance of the known risk factors ie hypertension, genetics, smoking and cholesterol with the contribution that stress might play was emphasised in the evidence given by Professor Anderson. And understandably, as he explains (256) from a public health perspective the admitted factors are in the main reversible, (ie smoking, overweight). Directing attention to factors not of significance, caused him trouble (257), (viz the British Researches perspective, contra the Americans). He agreed the evidence of causal linkage has appeared relatively recently, in particular in the past five years (260).

59 He differed from Dr Hallpike as to the need to differentiate between studies in coronary disease and those studies specific to stroke. As to vascular reactivity he opined that not only was there no proof the worker here had vascular reactivity, but one would have expected raised blood pressure during the stroke process if she did (263-264). He then added:-

"Q. Would you agree that vascular reactivity is possible even though there has been no diagnosis of hypertension.

A. Well, I'm an epidemiologist so I don't say no very often. So I see if I can get away with saying extremely unlikely, which is close to saying no."

60 Having suggested (264) that the Everson and Matthews studies do not provide an adequate foundation for the link of stress and stroke Professor Anderson gives the following answer in the context of the particulars of Mrs Barber's case (267):-

"A. ... The evidence is very strong in terms of chronic exposures and causation of disease."

"Q. Can I paraphrase what you say by saying this - and tell me whether you agree or not - that work stress is a risk factor for ischaemic stroke. Well, possibly; that's somewhat uncertain, but it still exists as a risk factor, even though it's much less than other far more important risk factors. Is that a fair paraphrase. There's little scientific support for that hypothesis.

Q. That's why you give a low odds ratio, but you give an odds ratio; you're not saying that there's nothing. I think Dr Hallpike said that if you were to say there's no risk, it would be less than the 1.5 you've given. Is that right.

A. Yes, well, I think this comes back to my introduction here in the very few minutes I was here, is that this is why doctors have difficulty in courts of law, and particularly epidemiologists, is that we don't talk in the absolutes, and I do have difficulty saying no ... and I suppose what I'm trying to say there is that it is my belief, however, that any association, should it exist, is modest, weak, small, and for all intensive (sic) purposes at the moment, I think we just have to say that it is very uncertain. I think if we're going to make very important - far-reaching and important decisions based on strong definite evidence, you can't assign the same weight of risk of stress and stroke with the same degree of credibility that you can assign to cigarette smoking, premature vascular disease, high insulin, raised cholesterol."

61 It is a fair representation of Professor Anderson's position that while he accepts the possibility of the link, though it is poorly evidenced even to the word "improbable", he is of the opinion that for this individual worker the link is most unlikely (274). Thus there is a clear conflict between Dr Hallpike on the one hand and Dr Hetzel and Professor Anderson on the other. Part of my task will be to resolve that conflict.

62 The second contest over the causal link between stress and stroke, including a mechanism for that relationship involved the evidence of Drs Allen Gale, Philip Harding and Professor Anderson. I deal with their evidence in turn.

63 Dr Gale is a physician specialising in allergy (73). However he has made a particular study of the role of insulin resistance in disease (74). He supplied two reports, dated 23 March 1999 and 17 August 1999. The first of those sets out the worker's history in the same terms as described herein. In the process of clinical investigation, he obtained a two hour glucose and insulin tolerance test that revealed levels consistent with impaired glucose tolerance and significant hyper-insulinaemia (89, 91). He concluded these placed the worker in the second phase of patho-physiology of Type II diabetes. He stated that stress is a known factor for unmasking Type II diabetes. The mechanism is the elevation of serum cortosol which can be up to five fold in chronic stress. In saying that he acknowledged the well known factors contributing to atherosclerotic disease and consequent stroke, (genetic, tobacco, weight and exercise). However assuming the stress consistent with that in the worker's case, in his opinion her employment was causally linked to her stroke (89).

64 In dealing with the mechanism of insulin resistance or metabolic syndrome, (sometimes referred to as syndrome X), Dr Gale referred to an editorial from the Medical Journal of Australia (1996) (95). Inter alia it states:-

"Insulin insensitivity was first described some 50 years ago and an association between the severity of insulin resistance (as measured by the insulin tolerance test) and atheromatous vascular disease in non-insulin dependent diabetes was noted in 1969 by Stocks and Martin in Australia. In 1988, Reaven coined the term "Syndrome X" to describe a cluster of diseases - obesity, hypertension, dyslipidaemia and glucose tolerance in the presence of insulin resistance and hyper-insulinaemia. It is now recognised that insulin resistance is the pre-imminent feature of syndrome X, also known as the insulin resistance metabolic syndrome (IRMS)."

65 In his second report, Dr Gale acknowledged literature identifying elevated blood sugar levels to impart the biggest risk factor in the long term management of diabetes but adds that elevated insulin levels can play a significant role in causing a diversity of clinical features (AB 96). He regarded that as conforming with information from Dr W Kidson, a specialist endocrinologist with particular expertise in the phenomenon (AB 96). I turn to that at this point as it is important material in the ensuing analysis by the main contenders.

66 Dr Kidson's report (AB 108) confirmed that the worker's glucose tolerance test was abnormal in three aspects. At 8.5 mmol/l, it is above the level permissible namely less than 7.8. Secondly the fasting serum insulin at 13 mU/l exceeds the upper level of normal at 8-9mU/l. Thirdly the one and two hour insulin levels are grossly elevated at 121 and 203mU/l the upper limit being 80mU/l with the peak occurring at one hour rather than at two hours. Thus Dr Kidson says that the worker is unquestionably suffering hyperinsulinaemia as a result of "insulin resistant syndrome". "HOMA Index" of insulin resistance was 3.1., the upper limit being 2.0 and values above 3.0 indicating moderate to severe insulin resistance. The significance was as follows:-

"i. The high levels of insulin inhibit the formation of HDL cholesterol, the so called `good cholesterol' that protects people from the development of vascular disease. The high levels of insulin, at the same time, stimulate the formation of LDL cholesterol, the so called `bad cholesterol' that increases the development of vascular disease,

ii. The high levels of insulin facilitate weight gain and make weight loss difficult. If obesity occurs in this condition, the blood fats become more abnormal, further increasing the likelihood of vascular disease.

iii. In some people, the high levels of insulin cause the blood pressure to rise, further increasing the risk of vascular disease."

67 The insulin resistance is a genetic result. However for the purposes of this case (AB 109) Kidson states:-

"It is widely assumed that stress aggravates insulin resistance. There is, however, no research data to quantify how much additional risk for vascular disease does a period of stress add to the effects of virtually life long insulin resistance."

68 The parties allowed into evidence the record of a telephone conversation between the worker's solicitors and Dr Kidson of 16 November 1999 (AB 110). This stated inter alia:-

"He then indicated there was no quantitative (sic) dated research concerning the stress aggravating insulin resistance, however it was accepted that stress does aggravate insulin resistance, this has been known for 15 years. The question is being no data about the quantitative (sic) effects of it. He said it is hard to apportion the amount of this in each case.

It is reasonable to presume that the longer the insulin resistance the greater the chance of having a stroke. The point being stress for a longer period of time means the greater the chance of stroke. Long term stress is more likely than an isolated instance of stress to cause a stroke through this mechanism. Attributing how much stress contributed to it is difficult to assess."

69 I return to Dr Gale's evidence. In his oral evidence, he reiterated his basis for concluding the worker had the metabolic syndrome or syndrome X at the relevant time (79). These included features of her pregnancy and her family history of premature death from cardiac disease as well as the definitive results of the glucose tolerance test. Though the latter was taken some 14 months after the worker's stroke, Dr Gale did not regard that fact as compromising the pre-stroke insulin resistance factor especially given these other features (80). Insulin resistance was the term Dr Gale used rather than syndrome X or metabolic syndrome, the other terms by which the pathology is labelled.

70 Dr Gale described the mechanism in its healthy setting as follows (82):-

"What all that means is that in times when the individual can't go hunting and gathering and eating food then the mechanism of insulin resistance is evoked by the body to elevate the blood sugars to nourish the tissues, so insulin resistance is a mechanism which is switched on in situations of stress to elevate the blood sugar to help the person to fight infection or to run away.

... so that adrenalin, interestingly enough, opposes the action of insulin so adrenalin elevates blood sugar, so does cortisone, so the stress hormones, both acute and chronic, elevate, oppose the action of insulin, elevate blood sugar so the person has the glucose and the oxygen to be able to feed the muscles to be able to run away or fight, so that's the mechanism and we should be talking in this patient about increase insulin resistance. ...

... but if that insulin resistance is evoked by a situation where the individual sits in a chair and doesn't require to burn up glucose then you induce a problem."

71 Dr Gale described the role of receptors in the cells enabling the acceptance of insulin (87). A situation of excess insulin overwhelms the receptors and the system breaks down (ie insulin resistance). That definition or explanation in Dr Gale's view was consistent with the generality of Dr Harding's definition of insulin resistance (89).

72 The three phases of non-insulin dependent diabetes mellitus were referred to. In the second phase the presentation is of elevated blood glucose (impaired glucose tolerance) and elevated blood insulin (hyperinsulinaemia). In Dr Gale's opinion the worker was in the second phase (93). As the underlying mechanism of this condition is insulin resistance, it is, according to Dr Gale, accepted medical science that stress is a known factor in aggravating that resistance. That in turn promotes vascular disease leading to stroke (97, 98). Moreover assuming the worker's history, in Dr Gale's opinion stress was a causal factor in her stroke (102).

73 Dr Gale turned to the reports of Dr Harding, an endocrinologist. As indicated, he accepted Dr Harding's definition of metabolic syndrome (103). However Dr Harding took the view it was insulin resistance in addition to obesity, hypertension, dyslipidaemia and glucose intolerance that led to vascular disease. Further the importance of insulin resistance was that in such circumstances it operated to increase the risk of vascular disease in much the same way as those with manifest diabetes and the other factors. Thus the presence of normal blood sugar level should be cautiously considered.

74 Dr Gale disagreed. His point of focus was the insulin resistance and not the glucose levels (103). He postulated Dr Harding's understanding had to be adjusted and refined (104). He regarded Dr Kidson as confirming his understanding of the mechanism (106).

75 Dr Gale referred to the comments of Professor Anderson in his report of 25 January 2000 addressed to the role of insulin resistance (Exhibit R4). He agreed that the level of understanding of insulin resistance as indicated by Professor Anderson was in it early stages and medical science needed to do more research in the area (107).

76 Finally Dr Gale produced a pulse wave analysis test. He regarded the test as demonstrating the worker had the arteries of a much older person (110). This state would result in vascular pathology if stress situations elevated her blood pressure (111, Exhibit A6).

77 In cross-examination Dr Gale repeated that the relationship between insulin resistance and the hardening of the arteries was direct. (114). Moreover the mechanism did not require the presence of hypertension (116). A patient might present with all or only some of the other factors (AB 95) (120) though each of the known factors would contribute (118). Moreover his reading of the Modbury Hospital notes indicated she had elevated cholesterol (123). Whether she was obese did not alter his view (163). While the SphygmoCor test (Exhibit A6) was a new diagnostic tool and still under research, it was valid to demonstrate the abnormal radial pulse wave (172). That demonstrated vascular disease (173). As to the need of transitory blood pressure increase, Dr Gale stated (175):-

"A. ... Prof O'Rourke who has been the leader in this area has been warning that the patient with the normal blood pressure with stiff arteries is at greater risk of vascular diseases than the person with chronic hypertension - without that. So this is the significance of the amplification. So if you do this test and an individual has normal blood pressure and you get amplification in the aortic pulse wave then you know you've got a problem and the medication can be adjusted accordingly, but, as I discussed earlier, this woman has got amplification of the radial pulse, so we know she has got stiff arteries."

78 Dr Hetzel accepted Professor O'Rourke's expertise (214), though Dr Hetzel queried whether arterial stiffness had in fact been demonstrated. He emphasised the difference between arterial stiffness (inside lining) and atheroma (wall lining). Dr Gale's opinion remained steadfast that the stress was causal to the stroke (166). I did not understand Mr Lines in his final address to contend otherwise.

79 Dr R Harding, an endocrinologist, was called by the Crown. He had provided two reports (AB 101-107). The focus of Dr Harding's attention as stated in his report (AB 102-103) was in the following terms:-

"Accordingly, any imputation of vascular risk associated with metabolic syndrome should be based on a careful appraisal of the recognised risk factors of high blood pressure, cholesterol and other blood fats and blood glucose rather than on the plasma insulin level per se."

80 However having reviewed the medical history and analysis of Dr Hallpike he stated (AB 102):-

"... In regard to vascular risk factors independent of metabolic syndrome, it is noted that she is a heavy smoker and has a very strong family history of vascular disease. The relevance of these various factors to the occurrence of her stroke is carefully analysed in Dr Hallpike's above referenced report and I would agree, with a minor modification suggested below, with his assignment of the relative contributions of the various risk factors, as referred to in the last paragraph of his report, namely 60% to the family history, 30% to the smoking and 10% to work related stress."

81 However as indicated, Dr Harding felt in the case of the suggestion of a mechanism of insulin resistance and vascular disease, more was required. His reference was to the risk factors related to metabolic syndrome. He stated, "As mentioned above, these are obesity, high blood pressure, abnormal blood lippets and glucose intolerance. There is relatively little evidence of these in Mrs Barber's case."

82 In his view, the test of 11 February 1999 by Dr Gale showed boarderline evidence of glucose intolerance and:-

"... the two hour glucose value being 8.5mmol/L; the cut off between normal and impaired glucose tolerance is 8.0mmol/L. It can be anticipated that under these circumstances her blood glucose would remain normal on an average diet."

83 In Dr Harding's view the tobacco and genetic factors were not related to metabolic syndrome or insulin resistance (AB 103) being independent risk factors. In his view Dr Gale's reliance was solely on the worker's blood insulin levels and its relationship to stress. He states:-

"The plasma insulin levels on the glucose tolerance test of 11th February 1999 are elevated, but it is difficult to interpret this without knowing the patient's weight which could well have increased during the year following her stroke. In any case, the plasma insulin level is relatively unimportant in assessing the individual's vascular risk. Hyperinsulinaemia associated with insulin resistance is certainly an underlying mechanism in generating the abnormal risk factors, but it is the risk factors themselves which are important."

84 As to the relationship of stress and diabetes, Dr Harding accepted that a causal link existed, particularly in the case of acute stress though to a lesser degree with chronic stress. But he questioned the relationship to a metabolic abnormality of which there was minimal evidence namely a minor abnormality of the glucose tolerance test. In this regard he saw the degree of risk as related to the degree of abnormality of the blood glucose. In the worker's case the abnormality demonstrated was minor. The amount of vascular risk attributable to metabolic abnormalities induced by stress would be similarly minor. Dr Harding thought the appropriate view was that these factors should be taken as included within the 10 per cent factor assigned by Dr Hallpike.

85 Dr Harding's second report sought to clarify what he saw as misunderstandings in the way his first has been interpreted. He reiterated that he accepted the worker has insulin resistance (AB 106). But it was minor. Insofar as his expertise was concerned he gave the following opinion (AB 107):-

"4. The main point I would like to make is that the question of whether or not insulin is involved here is of minor relevance, the essential point being whether Mrs Barker's (sic) stroke was precipitated by work related stress. All of this correspondence about insulin really relates to Dr Gale's view that insulin may play a role in the induction of vascular disease by stress. I do not deny that possibility, although no one would suggest it was the sole mechanism. Could you please again note that I have included consideration of these factors in my assessment of the assignment of the role of stress, as indicated ...

... any assignment of the relative contribution of stress by comparison with other factors must be arbitrary ... "

86 In his evidence, Dr Harding repeated the significance of dyslipidaemia and diabetes in vascular disease (134). The dyslipidaemia of concern was elevation of the plasma trygliceride rather than the cholesterol. In her case while the cholesterol on admission was a little elevated, the trygliceride was normal (135). Dr Harding explained the history of medical understanding in respect to the action of insulin and insulin resistance. It was found in a larger group than those with manifest diabetes and gave a partial explanation for the increased propensity for individuals with diabetes and developing diabetes to have large vessel disease particularly coronary artery disease, but including stroke (137). A characteristic of insulin resistance is obesity. On seeing the worker, admittedly far from the date of stroke, she was not overweight (138). She still evidenced insulin resistance a mechanism that generated factors like cholesterol and glucose which do cause vascular damage (140). But as an independent factor in vascular disease risk, it had to be discounted. On the other hand, Dr Harding recognised a Quebec heart study of very recent date suggesting it was an independent risk factor in coronary heart disease.

87 To put the matter in context, he reiterates his position (143) in the following terms:-

"A. ... All that had been done here was to identify that there was a high blood insulin and to focus on that situation. In other words the mechanism rather than the actual events which I would consider more important, and to answer your question, only having done that could one really make a judgment about the possible contribution of those factors to vascular disease.

Q. So the glucose tolerance test is inadequate for this discussion.

Barber v South Australia Police Department [2000] SAWCT 185

At a glance

Court

Decision date

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Catchwords

Judgment (287 paragraphs)

Barber v South Australia Police Department [2000] SAWCT 185 (6 December 2000)

Parties

Legislation Cited (1)

Cases Cited (15)