Jeffs and Repatriation Commission
[2001] AATA 615
•30 June 2001
DECISION AND REASONS FOR DECISION [2001] AATA 615
ADMINISTRATIVE APPEALS TRIBUNAL )
) No. N1999/220
VETERANS' APPEALS DIVISION )
Re Jean Patricia Jeffs
Applicant
And Repatriation Commission
Respondent
DECISION
Tribunal Mrs M T Lewis, Senior Member
Date30 June 2001
PlaceSydney
Decision The Tribunal sets aside the decision of a delegate of the Repatriation Commission dated 8 November 1997, and in substitution therefor determines that the death of Stanley Charles Jeffs was war-caused pursuant to s8 of the Veterans' Entitlements Act 1986 and that Jean Patricia Jeffs is entitled to payment of war widow's pension on and from 25 August 1997.
..............................................
M T Lewis
Senior Member
CATCHWORDS
VETERANS' AFFAIRS – War widows pension – reasonable hypothesis – Statement of Principles applied - Veteran suffered from war-caused smoking habit and ischaemic heart disease – Veteran suffered from non war-caused Parkinson's Disease and Alzheimer's Disease - whether Veteran suffered from "cerebral ischaemia" – diagnosis of condition –- whether cerebral ischaemia contributed to dementia - whether each medical condition in the causal chain of the hypothesis must be proved on the balance of probabilities – whether hypotheses disproved beyond reasonable doubt
Veterans' Entitlements Act 1986: ss120(1), 120(3)
Statement of Principles, Instrument No. 142 of 1996 (Cerebrovascular Accident) as amended by Instrument No. 85 of 1997
Byrnes v Repatriation Commission (1993) 177 CLR 564
East v Repatriation Commission (1987) 16 FCR 517
McKenna v Repatriation Commission (1999) 86 FCR 144
Munt v Repatriation Commission, Full Federal Court, 28 July 1996,
Repatriation Commission v Bey (1997) 79 FCR 364
Repatriation Commission v Cooke (1998) 90 FCR 307
Repatriation Commission v Gosewinckel (1999) 59 ALD 690
Repatriation Commission v Owens, High Court Special Leave Application, 5 August 1996, 147/1995
REASONS FOR DECISION
Mrs M T Lewis, Senior Member
This is a review of a decision of the Repatriation Commission ("the Respondent") dated 8 November 1997 that determined that the death of Stanley Charles Jeffs ("the Veteran") was not war-caused and that his widow, Jean Patricia Jeffs (the Applicant) was not entitled to a war widow's pension. The Respondent's decision was affirmed by the Veterans' Review Board ("the VRB") on 30 November 1998. The Applicant lodged a claim for review with this Tribunal on 17 February 1999. The Veteran died on 24 August 1997 and the Applicant lodged her claim on 3 November 1997. All applications for review were in time, and therefore the earliest date from which payment of war widow's pension is payable is 25 August 1997, being the day after the Veteran's death.
At the hearing the Tribunal had before it the documents provided by the Respondent pursuant to s37 of the Administrative Appeals TribunalAct 1975. The Applicant gave oral evidence at the hearing. Dr Mullany and Dr Miller also gave oral evidence, called by the Applicant. The Respondent called Dr McLeod to give oral evidence. The following documents were tendered on behalf of the Applicant:
Statement of Applicant dated 24 January 2000 with Certificate of Marriage (exhibit A)
Statement of Mervyn Woods dated 10 July 2000 (exhibit B)
Statement of Walter Clarence Woods undated (exhibit C)
Reports of Dr G Miller, consultant physician, dated 22 November 1999 and 3 July 2000 (exhibit D) and 24 March 2001 and attachment, being extract on "Vascular Dementia" from Harrison's "Principles of Internal Medicine" (14th edition) (exhibit H),
Report of Dr M Mullany, general medical practitioner, dated 17 July 2000 (exhibit E)
Report of Dr T Weerasinghe, physician and Senior Staff Specialist, John Hunter Hospital, dated 4 August, 2000 with letter of instruction from the Applicant's solicitors (exhibit F)
Pharmaceutical Data Sheet in respect of Sinemet dated 2 March, 1999 (exhibit G)
Repatriation General Hospital Concord discharge summary dated 17 July, 2001 (exhibit J)
The following documents were tendered as evidence on behalf of the Respondent –
Reports of Professor J G McLeod, neurologist, dated 7 June, 2000, 1 August, 2000 and 8 August 2000 (exhibit 1), and 25 August, 2000, 30 August, 2000 and 1 September, 2000, together with letters of instruction from Respondent (exhibit 2), Letter of Instruction from Respondent to Professor McLeod dated 2 April, 2001, report of Professor McLeod dated 3 April, 2001 and copy of article entitled "Binswanger Disease – Revisisted" (exhibit 4), and reports dated 4 December, 2000 and 12 December, 2000 (exhibit 9)
Clinical Notes of Mercy Care Centre, Young (exhibit 3)
Letter of instruction from Respondent to Dr J Korber, radiologist, dated 2 April, 2001 and supplementary report of Dr Korber dated 3 April, 2001 (exhibit 5), 7 November, 2000 and letter dated 22 November, 2000 (exhibit 7)
Letter of instruction from Respondent to Associate Professor J Roche, radiologist, dated 2 April, 2001 and reports of Professor Roche dated 4 April, 2001 (exhibit 6), 14 November, 2000 and Curriculum Vitae dated October 1999 (exhibit 8)
Article entitled "Windows to the Brain" (exhibit 10)
Extracts from Young District Hospital clinical notes (exhibit 11).
The Veteran served in the Royal Australian Air Force from 5 August 1940 to 7 January 1946. As he served in New Guinea the whole of his service constituted operational service. Therefore, this matter is to be determined pursuant to s120(1) and (3) of the Veterans' EntitlementsAct 1986 ("the Act"). This section requires the Tribunal to determine that the Veteran's death was war-caused unless it satisfied beyond reasonable doubt that there is no sufficient ground for making that determination. The Tribunal shall be satisfied beyond reasonable doubt that there is no sufficient ground for determining that the Veteran's death was war-caused if, after consideration of the whole of the material, it forms the opinion that the material before it does not raise a reasonable hypothesis connecting the Veteran's death with the circumstances of his service.
The hypothesis being advanced on behalf of the Applicant is that the mechanism connecting the Veteran's death with his war service is –
he developed a smoking habit on service;
the smoking habit led to his suffering a "cerebrovascular accident";
the cerebrovascular accident contributed to his dementia;
dementia contributed to his immobility; and
immobility contributed to pneumonia which caused his death.
The Applicant has chosen to rely on her accrued right to have the matter determined according to the Statement of Principles that applied at the date of the primary decision, that is, 8 November, 1997: Keeley v The Repatriation Commission (2000) FCR 108. Thus the relevant Statements of Principles is Instrument No.142 of 1996 for Cerebrovascular Accident amended by Instrument No.85 of 1997. "Cerebrovascular accident", for the purpose of this Instrument, means –
cerebral ischaemia or intracerebral haemorrhage, attracting ICD code …, 437.1 …".
"Cerebral ischaemia" is defined in the Instrument as –
a reduction or interruption of blood supply to an area of the brain causing a transient ischaemic attack (TIA), verterbrovasilar ischaemia, cerebral infarction, or focal brain necrosis, attracting ICD code … 437.1 …"
Factor 5(j) provides –
For cerebral ischaemia only, smoking at least five cigarettes per day or the equivalent thereof, in other tobacco products, for at least five years before the clinical onset of cerebrovascular accident and where smoking has ceased, the clinical onset has occurred within 15 years of cessation;
It was conceded for the Respondent that the Veteran had a war-caused smoking habit, and that he met the smoking aspects of factor 5(j). The Tribunal finds that this concession was properly made.
The Veteran had ischaemic heart disease accepted as a war-caused disability. His non-accepted disabilities prior to his death were lumbar spondylosis, Parkinson's disease, Alzheimer's disease and benign prostatic hypertrophy.
The Veteran was admitted unconscious to Young District Hospital on 6 March 1993. He was initially diagnosed as having suffered from a stroke. He recovered consciousness about 24 hours later and his condition was much improved. A CT scan of his brain was performed on 19 March 1993. Shortly prior to the CT scan, the Veteran had told one of the medical staff that he had overdosed on Sinequan, medication he was taking at the time for his Parkinson's Disease.
the evidence
The ApplicantIn her oral evidence the Applicant said she did not recall her husband being unwell before his heart surgery in 1988. He tended the garden, played snooker and also the violin. He did not have any mobility problems, and he walked around the town. After his heart surgery he "slowed down a lot". His mood changed, and he no longer tended the garden. Although he continued his walks because he was advised by his doctor to do so, they became shorter. Eventually, he felt that he could no longer walk because his legs became very tired. The Applicant said this was around the time the Veteran was diagnosed with Parkinson's disease.
In 1991 the Veteran was admitted to the Young Retirement Village because of Parkinson's disease and slight dementia, where he resided for about four years. The Applicant said he was not very happy about this move. His unit was cleaned for him, his bed was made for him and he was assisted with showering - he did little for himself. She could not recall how the Veteran's heart condition and other "circuitry problems" were at this time, but she recalled that his legs were still affecting him and the problem got worse over time. The Applicant said during this time they did not communicate well. However, he would sometimes play the violin for concerts held at the Retirement Village.
The Applicant noted that over a period of months prior to the Veteran's admission to the Young District Hospital for suspected stroke, he appeared very depressed. He no longer read books or watched television and he had more or less "thrown the towel in".
The Applicant said the Veteran appeared "different" after regaining consciousness. She found it difficult to relate to him and he just "wasn't with it". After that "his mind" progressively became worse. She was aware there was some suggestion that he had taken too many tablets before his admission to hospital. However, no empty containers were found in his room. She said the Veteran had said to her that he had taken "too many tablets" but he did not say how many or when he had taken them. She assumed he had taken them the previous night. She said he had been taking Sinequan as a sleeping tablet, and was also taking blood pressure tablets and tablets for Parkinson's disease.
The Applicant said she was told or became aware that her husband had Parkinson's disease around 1990 or 1991, and he had been receiving treatment for this condition prior to his admission to hospital in March 1993. She said for some time prior to his admission the Veteran walked like a "dummy or robot" and she believed this to be one of the effects of Parkinson's disease. She considered he did not understand what was happening to him.
The Applicant said she had doubt in her mind that the Veteran had taken an overdose because of the lack of proof to establish this. She also admitted she was upset and confused at the time. She recalled being told by the duty doctor at the time, Dr Hamilton-Gibbs, that her husband had suffered a stroke in the main brain stem and that "in 48 hours it would all be over". She understood this to mean that he would be dead. She was not told of any other possible causes for his hospitalisation.
In cross-examination the Applicant said that she could not recall having spoken to a social worker at the time of her husband's discharge from hospital. However notes from the Young District Hospital around that time noted that the Applicant appeared "tired, emotionally drained and extremely concerned about her husband's safety in view of his depression and attempted suicide" (exhibit 11, p358).
The Applicant said that she recalled speaking with Dr Mullany about whether her husband should go into the retirement village. Dr Mullany had recommended that the Veteran go into the home because he needed full-time care as a result of his stroke. However, on a claim for Disability Pension, on 8 May 1995, the Applicant indicated that one of the disabilities suffered by the Veteran was depression. Next to this disability, Dr Mullany opined that the Veteran had "established depression" and was "suicidal". The Applicant said that Dr Mullany had never mentioned any overdose to her.
The Applicant said the Veteran became completely immobile around 1996, 12 months before his death, and was bound to a wheelchair. He also had Alzheimer's disease for about three years before his death. The Applicant conceded that her husband's condition deteriorated gradually from the time he was diagnosed with Parkinson's disease until his death.
Dr MullanyDr Mullany was the Veteran's general medical practitioner from 1989 to late 1995 or 1996. Although not a specialist in geriatric medicine, he took an active interest in this area, including attending conferences and clinics to keep up-to-date. He said he treated the Veteran when he was admitted to the Mercy Care Centre and whilst he was in the Retirement Village. The Tribunal notes that Dr Mullany did not treat the Veteran at the time of his death. Dr Maher signed the death certificate.
Dr Mullany provided a report dated 12 July 2000 (exhibit E) and gave oral evidence, by conference telephone, at the hearing. He said the Veteran had peripheral vascular problems, particularly in his lower left limb, dating back to 1989 when he had by-pass surgery. The Tribunal notes a report from Dr O'Neill dated 7 March 1989, indicating that the Veteran had refused surgery for his peripheral vascular disease.
In his report (exhibit E) Dr Mullany noted that 18 months before the Veteran's death he deteriorated very rapidly. In oral evidence, Dr Mullany said he was "amazed" how quickly the Veteran deteriorated in his last few years of his life, from around 1995. He considered this suggested vascular disease as a background to his Parkinson's disease.
In relation to the incident in March 1993 Dr Mullany said that on admission the Veteran was unconscious (exhibit E). However he opined that the Veteran's unconsciousness was due to a stroke, ie. cerebrovascular accident, and not because of an overdose of Sinequan. Dr Mullany recorded other differential diagnoses in order of clinical significance, namely, "brain tumor, Parkinsons (Off-on freeze phenomenen) (sic) and iatrogenic". He noted that his opinion was confirmed by Dr Weerashigna.
In cross-examination he considered, on the clinical evidence, that the possibility of the Veteran having had a stroke was 90 percent, there was a 1 percent chance of there having been brainstem involvement and a 2 percent chance of iatrogenic involvement.
In an undated report received by the VRB on 3 July 1998 (T21), Dr Mullany noted the Veteran suffered from "depression, Parkinson's disease, Coronary Artery Disease, Anginal Heart Disease, Cardiac Hypertension, Ischaemic Heart Disease, Congenital Spinal Disease and Alzheimer's Disease". He acknowledged there was no reference to cerebrovascular accident, but explained that as an omission because his "memory had failed" him. He also noted that he failed to record peripheral vascular disease. He admitted that there were no written records of his opinion that the Veteran had suffered a cerebrovascular accident in March 1993. He conceded that on the admission form for the Mercy Care Centre dated 10 March 1993 (exhibit 11, p335) he noted that the Veteran was "depressed" and that other conditions also present were "Parkinson's" and "overdosage Sinemet" but there was no reference to cerebrovascular accident.
The Young District Hospital notes regarding the Veteran's admission in March 1993 (exhibit 11) include a consultant's report dated 19 March 1993 (p338) that states –
Going to have CAT scan – took overdose of medication when "churned up". Says there was no reason. Presents with worried look and depressed. Was on Sinequan at night before. Had been depressed "2-3 months". Slept well. Sinequan 1. Eating OK. Lives in Village. Has had bi-pass surgery on heart 4 years ago. Memory ?, concentration ?. ….
CT scan of the brain on 19 March 1993 (exhibit 11, p.339) was reported thus:
No facal intra or extra axial lesion is demonstrated.
The subarachnoid spaces are prominent but consistent with patient's age. No gross abnormality seen within the paranasal sinuses or orbits.A multi-disciplinary discharge summary was made before the Veteran's discharge (exhibit 11, pp344-349). In the "summary of hospitalisation" it was noted that the Veteran's admission was treated as "suspected brain stem infarct" and he was "much improved within 48 hours". It was also noted that "it was not known until day of discharge that Mr Jeffs had taken overdose of Sinequan". That entry does not sit well with the consultant's report dated 19 March or the admission form dated 10 March. The Veteran was discharged on 31 March 1993.
In his report dated 1 August 2000, Professor McLeod, neurologist, stated in respect of the Veteran's CT scan –
Mr Mullany has evidently misread the report of the CT brain scan. The statement made by the radiologist is "no gross abnormalities seen within the paranasal sinuses or orbits". This has no relevance at all to the remainder of the examination of the brain where the radiologists states "no focal intra – or extra-axial lesion is demonstrated". He does not state that there was no gross abnormality in the whole of the brain, merely in the sinuses and orbits which is irrelevant to the illness of Mr Jeffs.
In commenting on Professor McLeod's observations, Dr Mullany said he did not completely trust CT scans because sometimes they do not demonstrate problems. He said, however, he did not send the Veteran for further investigations given the travelling distances from Young. He said there was doubt on the CT scan given it was taken about 19 March 1993, some days after his admission. He felt that if the scans were followed up it might have helped to clear up the diagnosis. He said a subsequent scan would "hopefully" have revealed an increase in brain space, specifically the sub-arachnoid spaces. He clarified that a follow up scan would have shown a subsequent infarction, rather than an old infarction that occurred at the time the Veteran lost consciousness for 24 hours. He said the CT scan, taken 13 days later, could have shown up an infarct but not a haemorrhage.
In his report Dr Mullany also considered the issue of the Veteran's alleged overdose. He noted that there had been domestic problems at home between the Veteran, his wife and his 39 year old retarded son. His wife believed that the Veteran was not acting in the son's best interests and so he had to remain at the Young Retirement Village. Dr Mullany said the Veteran had spent several years trying to get home and as a last resort the Veteran used suicide to influence his wife to take him home. However, Dr Mullany concluded that all the clinical evidence "pointed to CVA preceded by hypertension and arteriosclerosis".
In relation to the Veteran's alleged drug overdose, Dr Mullany said that about a day before the Veteran was due to return home, he overheard a sister at the Mercy Care Centre say that the Veteran had taken on overdose. Dr Mullany acknowledged that at the time the Veteran was "desperate" to get home and thus he kept on "open-mind" about whether or not he had overdosed, although he did say it took him by surprise. (The Tribunal notes Dr Mullany's admission notes dated 10 March 1993, on which he acknowledged that the Veteran had taken an overdose. This does not sit comfortably with Dr Mullany's oral evidence about his "surprise"). He described the Webster system for distributing drugs to patients, whereby the pharmacist would supply the drugs on a weekly basis. He understood that the pharmacist had not observed anything unusual in his Web packing, and the sister in charge of the retirement village had not seen anything that suggested the Veteran took an overdose. He said however that the sister had told him that the Veteran had had upsetting meetings with his wife and a few days of "things not being really smooth".
Dr Mullany said his "gut feeling", from a clinical perspective, was that the Veteran had suffered a stroke, despite the fact that a CT scan showed no areas of infarction in his brain which would have indicated a stroke. However he said the CT scan was taken a little bit late - 13 days after the stroke occurred - to detect whether there was a bleed or a small leak from a vessel.
In his report dated 1 September 2000, in reply to questions by the Respondent in a letter dated 31 August 2000, Professor McLeod noted –
The CT scan would positively exclude a cerebral haemorrhage as even a very small amount of blood shows up sharply on a CT scan. I can see no grounds for diagnosing a cerebral haemorrhage in Mr Jeffs. If he had been rendered unconscious by a cerebral haemorrhage, he would not have recovered in 24 hours. A lumbar puncture will usually demonstrate blood in the cerebrospinal fluid after cerebral haemorrhage, but a scan is a more accurate and safe test…for the reason given above and also loss of consciousness for 24 hours would be very rare as a manifestation of vertebrobasiliar insufficiency and if unconsciousness were due to cerebrovascular disease it would be caused by cerebral infarction or haemorrhage.
Mr Jeff's recovery was too rapid for a cerebral infarction and a CT scan would have been expected to show an infarct 13 days after the event if the infarct were of sufficient size to cause loss of consciousness for 24 hours.In cross-examination Dr Mullany said he did not agree with Professor McLeod's opinion, except that he agreed if unconsciousness were due to cerebrovascular disease it would have been caused by cerebral infarction or haemorrhage. He said that cerebral haemorrhage could be anything from a tiny microscopic drop of blood to a haemorrhage. He said that if the veteran had bled it could have been absorbed by the time of the CT scan and agreed with Dr Broe in that regard. He did not agree that a small amount of blood would show up on a CT scan. He also did not agree that a CT scan would have showed an infarct 13 days after the event even if it caused loss of consciousness. He said that he had seen both large and small, multiple and singular infarctions on CT scans that all disappear after 13 days.
Dr Mullany did not consider that the Veteran suffered from an "intra-cerebral haemorrhage" as mentioned in factor 2(b) in the Statement of Principles. However he considered "cerebral ischaemia" was relevant. He did not know if there was any "focal brain necrosis" since there was no post mortem to establish that. He agreed there was no evidence of cerebral infarction without having conducted further scans.
Dr Mullany was referred to the following extract from Professor McLeod's report of 1 September 2000 -
Common symptoms of vertebrobasilar TIAs are transient double vision, slurred speech, difficulty in swallowing, weakness of both legs causing the patient to drop to the ground, blurred or loss of vision in both eyes, vertigo and ataxia. There may be brief loss of consciousness associated with one or more of these symptoms, but loss of consciousness alone is very rare in the condition, and is usually cardiac in origin.
Dr Mullany said these were not the only symptoms of vertebrobasilar ischaemia, nor did he agree that it was very rare. He did agree that it was rare for vertebrobasilar ischaemia to cause a loss of consciousness. Dr Mullany considered that some of the Veteran's symptoms, such as giddiness, might have been suggestive of vertebrobasilar episodes, but he conceded he did not make such a diagnosis.
Professor McLeod defined a "transient ischaemic attack" as "a neurological deficit or deficits of duration no more than 24 hours caused by insufficient blood supply to the brain. The usual duration is a few minutes but in some cases full recovery may take up to 24 hours". He also said the "usual symptoms of carotid TIAs are transient speech impairment, hemipraesis, hemianaesthesis, loss of vision in one eye or a visual half-field". Dr Mullany agreed with this definition.
Dr Mullany did not agree that there was no evidence that pointed to the Veteran suffering from a TIA. He said there was evidence of "unsteadiness" at the Retirement Village although he acknowledged there was no written evidence. The evidence was based on his recollection and memory back to 1995.
Dr Mullany did not agree that the Veteran's admission to Young District Hospital in March 1993 is explained by an overdose of Sinequan medication. He agreed, however, that an overdose might explain the episode of unconsciousness for 24 hours. He agreed there were several explanations for each of the symptoms he attributed to cerebrovascular accident.
Dr Mullany said that on the assumption the Veteran had taken a week's supply of medication at the one time, he doubted the Veteran took an overdose. He expected that the side effects of an ingestion of an excessive amount of the medication would have been nausea, imbalance, or toxicity. Dr Mullany conceded that the Veteran had recurrent bouts of depression, but he also noted that the Veteran played his violin at the Retirement Village and would challenge him to a game of billiards. He attributed the Veteran's depression to the fact that he had to live at the Retirement Village, and in particular, the friction that had developed between the Veteran and his son.
Dr Mullany noted that around the time the Veteran went to the Retirement Village he had to rest every 50 yards when walking in the street. He did not think this was because of pain from his lumbar spondylosis, and the Veteran had not complained of backache at that stage. He also noted that the Veteran had venous problems in his legs. However he did not arrange arteriogram or ultrasound examinations to explore these symptoms, which he said he regretted. He now considered that he should have investigated the veteran's peripheral circulation problems.
Dr Mullany noted carotid bruits that he considered significant. He considered this was an indicator of vascular problems. He said "they are not easy to pick up,…but I heard them in this case and that was it. Maybe other people didn't…but at least I heard it and that's why I put it down and it's definitely hearing a bruit". This finding was also noted by Dr Miller in his report dated 22 November 1999.
When the Veteran lodged a claim on 5 May 1995 in respect of a number of conditions, including depression, Dr Mullany provided medical information to the effect that the Veteran had an "established depression" and was "suicidal" (T5, p26). Dr Miller relied on that opinion of Dr Mullany in his report dated 22 November 1999.
In relation to the same claim, Dr Mullany noted in a medical report dated 12 July 1995, that the Veteran had recurrent attacks of depression every six weeks, and that arising from an attempted suicide the Veteran "has been unconscious for 3 days" (T7, p36). In cross-examination, Dr Mullany agreed that this referred to the Veteran's admission to the Young District Hospital in March 1993. However he said that he was recording the story as it was told to him, acknowledging that he failed to qualify that he had received this information from a third party. He said he wrote it down because it was an important part of the Veteran's history.
In his report dated 4 August 2000 (exhibit F), Dr Weerasinghe noted –
The term "dementia of mixed aetiology" refers to Mr Jeffs' confusion at the time I saw him. The clinical features of progressive onset, with no clear evidence of step-wise progression favours Alzheimer's Disease with Parkinson's Disease, causing the dementia. It is however possible that the vascular pathology could have a minor role in the clinical picture
In cross-examination, Dr Mullany said he did not agree with Dr Weerasinghe's opinion of a progressive onset of dementia, rather than any dramatic deterioration, but he was unable to comment on Dr Weerasinghe's opinion of "the vascular pathology" having a "minor role in the clinical picture":
Dr Mullany was also referred to the opinion of Professor McLeod in his report dated 30 August 2000 (exhibit 2) where he opined there was a "gradual progression of dementia due to Parkinson's and Alzheimer's Disease". Dr Mullany agreed this did not indicate a rapid deterioration. However he said that his opinion that there was a rapid deterioration found support in Dr Baggott's observations that there was such deterioration. The observations made in a letter from Dr Baggott to Dr Mullany dated 7 September 1995 (exhibit 3, p16) were that Dr Baggott noted the Veteran had deteriorated since he last saw him and that his problems were mainly "those of confusion due to his Alzheimer's disease". Dr Mullany agreed that the Veteran's problems arose from Alzheimer's disease and at that stage he had had Parkinson's disease for many years. Dr Mullany agreed that in July 1995 he described the Veteran's deterioration as "progressive" (T7, p35).
In his report dated 17 July 2000 (exhibit E) Dr Mullany stated –
When admitted to hospital on 6/3/93, it was diagnosed as a stroke…Dr Weeransingha confirmed stroke C.V.A…on 15/3/93 Stan put a spanner in the works and said he took an overdose of Sinimet or Sinequan…as a last resort I feel Stan used suicide to influence his wife to take him home. My considered opinion is that all the clinical evidence pointed to CVA proceeded by hypertension and Arteriosclerosis.
In cross-examination Dr Mullany continued to maintain that the Veteran did not overdose on Sinequan.
In his report dated 25 August 2000, Professor McLeod stated –
Sinequan doxepin is a tricyclic antidepressant used in the treatment of major depression. The fact that he was taking Sinequan prior to admission, indicates that he had been diagnosed as having a major clinical depression…It is difficult to be specific about the doses of these drugs required to cause coma. Given Mr Jeff's age of 79 at the time of his admission in March 1993, 150 milligrams (15, 10 milligram tablets, or 6, 25 milligram tablets) could cause coma.
Dr Mullany agreed that the dosage suggested by Professor McLeod could cause coma, although he thought the Veteran might have needed a slightly higher dose. However he still maintained his opinion that the Veteran did not overdose, based on clinical observation. He said he held this position in March 1993 and in 1995.
Dr Mullany was referred to documents from the Young District Hospital (exhibit 11, p338) where in a referral to Dr Bircher, psychiatrist, he noted "recent overdosage, Domestic situation not good". Again, Dr Mullany acknowledged that he did not qualify this statement with any doubt he had about whether the Veteran had overdosed. An entry recorded on 31 March 1993 (exhibit 11, p377) noted - "Seen by Dr Mullany this am…who informed staff the pt [patient] had overdosed on Sinequin due to depression which resulted in unconsciousness". In cross-examination Dr Mullany said he referred the Veteran to a psychiatrist because he was depressed. He said he had received a history that the Veteran had overdosed. He acknowledged that the histories recorded contradict his opinion that the Veteran did not overdose. However he said "I still had an open mind about his overdosage, and when I have an open mind about something, I refer the patient to a psychiatrist to get a full story".
Dr Mullany said he did not speak to the Applicant about the incident and did not know who informed her. He confirmed there was trouble at home; there was no doubt that the late Veteran was depressed; and that he was prescribed Sinequan, an antidepressant that could cause coma.
White Matter DiseaseDr Miller provided reports and gave oral evidence at the hearing. He qualified as a consultant physician in 1970. His main specialty is general medicine with a particular interest in cardiology and geriatrics. As a general physician he has had many years' experience as a geriatrician, including the investigation and diagnosis of dementia.
Professor McLeod referred to an article by Caplan (exhibit 4). Dr Miller noted from that report that dementia, associated with cerebro-vascular disease, can be divided into two general categories: multi-infarct dementia and diffuse white matter dementia. White matter dementia is also known as subcortical arteriosclerotic encephalopathy or Binswanger's Disease. However, the term Binswanger's Disease should be used with caution as the condition is not often identified as a single, discrete entity and may have multiple causes.
Dr Miller clarified that subcortical arteriosclerotic encephalopathy (also known as micro angiopathy, and also known as white matter disease) was an aspect of Binswanger's Disease and should not be used synonymously with it. Dr Miller noted that Caplan's article (exhibit 4) stated that "micro angiopathic vascular dementia of the Binswanger type is a common cause of vascular dementia and invalidism". Caplan also referred to it as "white matter ischaemic disease". White matter dementia may be of subtle onset and slow progression. It is likely to result from chronic ischaemia due to occlusive disease of small penetrating cerebral arteries and arterioles. Dr Miller considered the Veteran might have suffered the second category of dementia, namely white matter disease (or small vessel disease), that contributed to his dementia. The Tribunal notes that throughout this decision, the terms "White matter disease" and "Binswanger's Disease" are used interchangeably. Both terms refer to a common cause of vascular dementia.
Dr Miller was referred to Caplan's article where he wrote "Time and experience have taught that white matter abnormalities and CT MRI are very common and they are not at all specific". Dr Miller said he would not adduce a reasonable hypothesis that the condition existed without radiological support, but he also deferred to Caplan's article. He regarded Dr Caplan as a leading radiology expert.
Despite the opinion he provided in his report of 22 November 1999 (exhibit D), in his oral evidence Dr Miller agreed with Professor McLeod that the Veteran's loss of consciousness, prior to his admission to the Mercy Care Centre on 10 March 1993, was more likely due to an overdose and was not due to cerebrovascular disease. In particular, Dr Miller had noted in that report that the Veteran suffered from cerebrovascular disease and that small vessel atherosclerotic cerebrovascular disease could not be excluded by the negative CT brain scan of 19 March, 1993.
On the basis of Dr Miller's change of opinion, the Tribunal interprets that in effect he was discounting the opinion evidence provided by Dr Mullany, and had withdrawn his support for the hypothesis that the Veteran suffered a CVA in 1993 that caused or contributed to his dementia. Multi-infarct dementia is characterised by a step-wise progression. He could find no evidence of multi-infarct dementia in the Veteran.
However, Dr Miller concluded there was a possibility that the Veteran had Binswanger's disease (ICD code 437.0), a form of cerebro-arteriosclerosis. By contrast, Binswanger's disease (also known as diffuse white matter disease) is characterised by slow onset and subtle abnormalities in the symptoms. It was a form of vascular dementia rather than multi-infarct dementia. He considered there was support to his hypothesis in that there is a radiological abnormality and the clinical features of the dementia could not be explained by multi-infarct dementia. He added that it was more than a possibility that the Veteran suffered from a degree of small vessel arteriosclerosis, but nonetheless he did not consider it proven on the balance of probabilities. Dr Miller admitted that he has diagnosed only one case of Binswanger's Disease, that being about 15 years ago.
In his view, therefore, the Applicant was suffering from arteriopathy, that is, generalised arteriosclerotic involvement of the arteries. He said that a diagnosis of arteriopathy was satisfied where there is at least three separate diagnoses of arteriosclerotic disease in three different places and he considered it was highly likely that the Applicant suffered from arterial problems in the coronary artery, carotid artery and peripheral vascular system, that is, the likelihood was 50 percent or more.
Dr Miller considered that each doctor providing an opinion in this matter had identified symptoms that in fact were evidence of arteriosclerosis.
Dr Weerasinghe, in his report of 4 August 2000, considered it "possible that vascular pathology could have had a minor role in the clinical picture" (exhibit F) and that there was a reasonable hypothesis that the Veteran suffered from cerebrovascular disease. Dr Miller considered Dr Weerasinghe's opinion provided further evidence of vascular disease that was relevant for the diagnosis of Binswanger's disease.
Professor McLeod, in his report dated 1 September 2000, concluded on the basis of the clinical evidence that there was no cerebral ischaemia. Dr Miller disagreed with this on the basis that he considered Dr Mullany and Dr Weerasinghe, provided documented evidence of cerebral ischaemia.
Based on the radiological findings of Professor Roche and Dr Korber, Dr Miller formed the view that there was a reasonable hypothesis that the Veteran suffered from white matter disease (Binswanger's Disease). Dr Miller understood the term reasonable hypothesis to mean more than a possibility that was not fanciful and tenuous, but not necessarily proven on the balance of probabilities.
Dr Miller considered that the history of the Veteran's condition was consistent with the description of white matter disease in Harrison's Principles of Internal Medicine, 14th Edition, p2352 (exhibit H). He had a gait disorder that appears in half the patients who suffer from white matter disease. Dr Miller noted that the Veteran's Parkinson's Disease would completely mask any changes in the Veteran's gait that might have been caused by white matter disease. He also noted that the Veteran had a history of hypertension, that would not be implicated in Alzheimer's or Parkinson's disease.
In his report dated 4 April, 2001 (exhibit 6) Professor Roche, Associate Clinical Professor in Radiology, noted the single CAT scan film of 19 March 1993 that was provided showed changes in the Veteran's deep white matter. Professor Roche noted these findings were common in a patient of the Veteran's age of 79 years. The changes have no direct correlation with the diagnosis of dementia, but "such changes are found more frequently in demented patients, but in an individual case one cannot infer anything from these changes". Dr Miller considered this comment supported his view. Professor Roche noted -
The CT scan of 19 March 1993 is consistent with Dr Miller's diagnosis of vascular dementia, but it is also consistent with normality.
Dr Miller also considered this supported his hypothesis, and noted that he would not have made such a diagnosis without radiological support. Dr Miller took issue with Professor Roche's reference to age-related changes. Dr Miller considered that the changes noted represented a pathological narrowing of the vessels. It was not merely a physiological process that is part of ageing.
Professor McLeod provided a supplementary report dated 3 April 2001 (exhibit 4) in which he discussed the findings of low density changes in the white matter. He considered that "most white matter imaging abnormalities are not related to Binswanger Disease". Dr Miller noted, however, that he was not referring to Binswanger Disease but to subcortical arteriosclerotic encephalopathy, or small vessel disease. Professor McLeod concluded there was no convincing evidence the late Veteran suffered from subcortical arteriosclerotic encephalopathy. It is not clear from his report, however, what level of proof he was seeking in forming his view.
Professor McLeod opined in his report dated 3 April 2001 that "there is no clinical evidence of Mr Jeffs having had cerebral ischaemia at any time". Similarly, in his report dated 25 August 2000 (exhibit 2) Professor Roche opined there was "more than a reasonable doubt that Mr Jeffs suffered from cerebral ischaemia" (exhibit 2).
In his report dated 4 April 2001 (exhibit 6) Professor Roche wrote –
I stand by my report of 14 November 2000 on the single CAT scan film provided of 19 March 1993. There are changes in the deep white matter. These are common findings in a patient of the age of 79, as was [the veteran] in 1993. They have no direct correlation with the diagnosis of dementia as they are found in both non-demented and demented patients. Certainly such changes are found more frequently in demented patients, but in an individual case one cannot infer anything from these changes.
These changes are age-related changes and it is the presumption that these are due to focal changes in the cell structure, presumably on the basis of decreased oxygen supply, secondary narrowing of the small vessels of the brain (Tribunal's emphasis)
Dr Miller conceded that Professor Roche was an eminent radiologist. However, Dr Miller did not agree that there was no evidence in the radiological material to support the hypothesis, as there is definite evidence of periventricular hypo-density.
Dr Miller said that "technically" his hypothesis of a diagnosis of small vessel disease was not supported by any reference in the material from Dr Mullany, Dr Weerasinghe and the specialist psychiatrist, Dr Bircher, but he considered that the following opinion of Dr Weerasinghe (exhibit F) supported his opinion, where he said:
The term "dementia of mixed aetiology" refers to Mr Jeffs' confusion at the time I saw him. The clinical features of progressive onset, with no clear evidence of step-wise progression favours Alzheimer's Disease with Parkinson's Disease, causing the dementia. It is however possible that the vascular pathology could have had a minor role in the clinical picture.
….Mr Jeffs suffered from cerebrovascular disease
Dr Miller conceded, however, that there was no specific reference to small vessel disease in this report. He also said he relied on the reports of Dr Mullany or Dr Weerasinghe, to the extent their opinions referred to the Veteran's dementia; no reliance was made on the Veteran's episode of unconsciousness.
Dr Miller said that the Veteran had dementia that was probably associated with Parkinson's disease and Alzheimer's disease. He conceded these diseases could possibly explain all the Veteran's symptoms, and that the contribution of small vessel disease to the Veteran's dementia was not likely to be great.
In conclusion, Dr Miller said his opinion was based on the fact that the Veteran had dementia and evidence of arteriopathy. He also had hypertension. In his opinion there was a reasonable hypothesis that the dementia could be due to small vessel disease such as subcortical arteriosclerotic encephalopathy. He conceded that this hypothesis arose only in the course of his giving oral evidence.
Dr Miller was referred to the Statement of Principles for Cerebrovascular Accident, in particular, to the definition of "cerebral ischaemia". He said it would only be possible to clarify that the Veteran had focal brain necrosis in a post mortem. He insisted that his opinion was more than speculation; indeed it was based on his reading of the documents. He clarified that the condition of white matter disease would satisfy the definition of "cerebral ischaemia, ICD code 437.1".
Emeritus Professor McLeod, neurologistProfessor McLeod provided a number of reports in relation to this matter, and gave oral evidence at the hearing. He had been provided with all the documentary evidence before the Tribunal, and had heard a significant amount of the oral evidence of Dr Miller. He considered that there was no evidence that the Veteran had suffered from Binswanger's Disease or white matter disease. He noted that it was very difficult to diagnose clinically and that radiological findings are taken into account. However, he considered the radiological changes necessary to make the diagnosis "are usually much more extensive than we see" in the Veteran's CT scan. The only conclusive way of resolving the question of diagnosis in this case would be to have performed neuropathology tests following death. He also noted that in most cases where Binswanger's Disease has been diagnosed there has been a history of hypertension and "little strokes". He said "I'm not talking about multi-infarct dementia but stepwise progression".
In relation to the radiological changes, Professor McLeod said there was no evidence in the Veteran's CT scan of little infarcts in the brain and more extensive changes. On his CT scan there was no evidence of any infarction but there was evidence of atrophy that one sees in Alzheimer's Disease or Parkinson's Disease. Professor McLeod noted that the Veteran did have some evidence of large vessel disease in that he had peripheral vascular disease, and he may have had a carotid bruit. However, these are large vessels, not small vessels.
The Tribunal notes the specific langauge used by Professor McLeod in giving his evidence, eg.
Where a person suffers from dementia of a cerebrovascular type, would you expect to see those changes here --- Yes, but they'd probably be more definite than they are here…
Would they become more dense as the condition progresses? --- Well, the density is rather patchy, and you can usually see areas where there have been infarcts or necrosis, if you like, of the brain, focal necrosis, and I think Caplan makes that point in his article also, and if we use the term, Binswanger Disease as one of them, you nearly always see in it much more dense and patchy changes
Progressive sub cortical arteriosclerotic encephalopathy is a rare cause of dementia? --- Yes. What I'm saying is that they're a rare cause of dementia, but the white matter changes that we see on the scan here are very, very common in older people. So, I don't think that that provides any convincing evidence that he was suffering from any of those white matter conditions.
It is consistent though, isn't it? --- You can't deny the possibility, I think I make that point, yes.
And he [Caplan] says that that type of vascular dementia is a common cause of vascular dementia … Now, that suggests something far greater than what might be defined from when you were saying on that first page "It's a rare cause of dementia"? --- Well, I think it still is a very rare cause of dementia, and probably he would agree with that, but he's saying that if you can diagnose it, then it's worthwhile doing, and he says micro angiopathic vascular dementia of the Binswanger type is a common cause of that is an – he doesn't say this, but this is the fact, I think, that … vascular dementia is a fairly uncommon disorder, but Binswanger type is a common cause of this uncommon condition.
(Tribunal's emphases).
Professor McLeod said that it was not possible from a clinical perspective to distinguish the dementia arising from the Veteran's Parkinson's Disease from that arising from some other condition. He could not exclude the possibility that the Veteran's dementia arose, in part, from something other than Parkinson's Disease.
Professor McLeod was asked whether he could exclude beyond reasonable doubt that the Veteran did not suffer from Binswanger's Disease. He said "I think beyond reasonable doubt, one can't exclude it entirely". He added "No, I don't think you can disprove it, but there's no positive evidence to support it, where there is positive evidence to support the other diagnoses.
Professor McLeod was aware that the Veteran suffered from coronary atherosclerosis and peripheral vascular disease, and agreed that cerebrovascular disease is more common in people who have vascular disease elsewhere. However, the clinical picture was not that of the Veteran having vascular dementia. There was no evidence of him having strokes or any other evidence of cerebrovascular disease, which one would expect. In people with cerebrovascular disease there are episodes of stroke – this is a point also made by Caplan. He noted that with vascular dementia there are usually episodes of little strokes that are clinically evident. Most vascular dementias deteriorate in steps.
Professor McLeod had no difficulty with Dr Weerasinghe's opinion (exhibit F). His comment was "I can't disagree with that". Again, he said he could not exclude vascular pathology playing a very minor role in the clinical picture. Dr Weerasinghe's report stated –
…My comments on the specific questions are as follows:
1.Evidence of cerebrovascular disease on my examination on 11.3.1993.
I examined Stanley Jeffs on 11.3.1999, at the request of Dr M Mullany, following his admission to Young District Hospital in an unconscious state on 6.3.1999. He had regained consciousness on 7.3.1999 and had been noted to have "a speech deficit" and "weakness of the left side".
When I examined him, he was conscious, alert, but had difficulty in word finding. On physical examination he had weakness of his left leg with absent ankle jerk and an equivocal plantar response on the left, in addition to his Parkinsonian features.
Based on these physical signs and the history of vascular disease, I consider it a reasonable hypothesis that Mr Jeffs suffered from cerebrovascular disease.2.Whether a "dementia of mixed aetiology" - refers to a possible vascular component of Mr Jeffs dementia?
The term "dementia of mixed aetiology" refers to Mr Jeffs' confusion at the time I saw him. The clinical features of progressive onset, with no clear evidence of step-wise progression favours Alzheimer's Disease with Parkinson's Disease, causing the dementia. It is however possible that the vascular pathology could have had a minor role in the clinical picture.
In relation to the definition of "cerebral ischaemia", Professor McLeod considered there was no evidence that the Veteran's dizzy spells, etc. were transient ischaemic attacks (TIAs); rather they were due to light headedness due to lowering of blood pressure when he stood up. However, he said that a good clinician would consider cerebrovascular disease was something that at least needed to be excluded. He also noted an inconsistency that if the Veteran had suffered a stroke in March 1993 there was no evidence of it on the CT scan that was taken shortly afterwards. He noted that if one has a stroke after a haemorrhage there might not be definite radiological evidence of it for the first five days. However by 13 days it should be visible on the scan, "unless it's a tiny, tiny, thing".
Professor McLeod also said that if the Veteran did suffer from Binswanger's Disease the contribution it made to the Veteran's dementia was very small, because the main cause of his dementia was Alzheimer's Disease and Parkinson's Disease. If it existed at all its contribution would be 10 percent or less. However, he said he did not consider there was any contribution. He considered that Alzheimer's Disease and Parkinson's Disease explained the chain of events leading to the Veteran's death. The general thrust of Professor McLeod's position was that there was an easily identifiable cause for the Veteran's dementia in Parkinson's disease and Alzheimer's disease, and therefore it was not necessary to import another condition that was extremely difficult to diagnose – white matter disease. However, one cannot say it is impossible that the Veteran did not have white matter disease.
submissions
RespondentIt was submitted for the Respondent that there was an abundance of evidence demonstrating that the Veteran had been admitted to Young District Hospital because of a drug overdose. He had been depressed, and he had been taking Sinequan. It was submitted that Sinequan could induce coma when taken in sufficient quantity, and the Veteran had informed the Applicant that he had "taken too many tablets". His recovery from the coma within 24 hours was consistent with his having taken an overdose.
It was submitted that Dr Mullany had completed a claim form for depression, being evidenced by a suicide attempt, and the Applicant had counter-signed that form. It was submitted that if Dr Mullany did not consider that the Applicant was suffering from depression, as he indicated during oral evidence, then his support of the claim for depression was compromised. Dr Miller agreed that the Veteran's admission to hospital unconscious was referable to an overdose.
It was submitted that Dr Mullany was "an enthusiastic proponent" of the hypothesis that the Veteran's admission to Hospital in 1993 represented a frank incident of stroke. It was submitted that his evidence was partisan and misleading, and he had lost his professional objectivity by becoming an advocate for the Applicant. Notwithstanding his opinion that the Veteran suffered a stroke he did not conduct any investigations along those lines but he did refer the Veteran to a psychiatrist, Dr Bircher, noting a history of depression and attempted suicide. Dr Mullany had also informed the staff at the hospital of the overdose.
In documentary evidence Dr Mullany referred to the Veteran suffering from conditions including Parkinson's disease, coronary artery disease, anginal heart disease, cardiac hypertension, ischaemic heart disease, congenital spinal disease and Alzheimer's disease. In his oral evidence he said he had forgotten to include CVA in his report of July 1998. It was noted for the Respondent, however, that Dr Mullany had also included "depression". Moreover, there were numerous other documents written by Dr Mullany that did not contain any suggestion that the Veteran suffered from CVA at any stage.
It was submitted that Dr Miller's evidence cannot be accepted because of his lack of expertise in radiology, and there was no challenge to Professor Roche's eminence or competency in radiology.
Dr Miller admitted that he had not seen the CT scans but was aware that Dr Korber and Associate Professor Roche considered the changes were non-specific and age related. On the one hand Dr Miller considered his diagnosis was supported by the opinion of Professor Roche but on the other hand he considered the condition could not be diagnosed radiologically. While at times Dr Miller embraced the opinion of Professor Roche, at other times he challenged Professor Roche's opinion.
It was submitted that there was no suggestion by Dr Miller, prior to the cross-examination of Dr Mullany, of the diagnosis by Dr Miller of Vascular Dementia/Binswanger's Disease/ white matter disease, and that the new hypothesis had been proposed when he was on notice about the strong suggestion that the Veteran had overdosed.
It was submitted that Dr Miller has mischievously misinterpreted Dr Caplan's article entitled "Binswanger's Disease – Revisted" by suggesting that Vascular Dementia of the type he had diagnosed was common. The quotation in full is –
Dementias, including vascular dementias, are an important public health problem that is becoming more common and important as the population ages. Micro angiopathic vascular dementia of the Binswanger type is a common cause of vascular dementia and invalidism.
It was submitted that Dr Miller's evidence that the condition can be very obvious is inconsistent with the essence of Dr Caplan's article about the difficulty diagnosing the condition. Dr Miller's evidence that white matter disease was common represents a contradiction given his evidence on 7 September 2000 that white matter disease was "not all that common and is difficult to detect".
In respect of Dr Miller's qualifications, it was submitted for the Respondent that he had a primary specialty in cardiology and to a much lesser extent in geriatrics. It was submitted that Dr Miller could not raise a reasonable hypothesis as he is not "eminent in the relevant field": Repatriation Commission v Bey (1997) 79 FCR 364.On the other hand Professor McLeod has relevant specialist qualifications. It was submitted that the evidence of Professor McLeod about the rarity of the condition, in the context of dementia, was not impugned by the Applicant's case.
It was submitted that Dr Weerasinghe's evidence goes no further than Professor McLeod's belief that it was "possible" there was a vascular dementia, however labelled. However Professor McLeod considered it was unlikely given there was no evidence of step-wise deterioration; rather there was a gradual progression consistent with Alzheimer's and Parkinson's Disease. The significance of the lack of a step-wise progression was supported by Dr Miller. Dr Miller appears to rely on Dr Weerasinghe's report, but there is no clinical material that would support any such hypothesis.
It was submitted that Professor McLeod's evidence was cogent, consistent and transparent. It was submitted that he has disputed the alternative hypothesis of stroke /frank incident in 1993, and white matter disease/Binswanger's disease.
It was submitted for the Respondent that the hypothesis raised on behalf of the Applicant was not impossible, fanciful or incredible, but it was too tenuous, having regard to the whole of the evidence. The hypothesis was not pointed to by the evidence, but was raised only as a possibility. Indeed, it was raised by Dr Miller who is not eminent in the relevant field. Thus, it was submitted for the Respondent that, relying on the decisions of the Federal Court in Repatriation Commission v Bey (1997) 79 FCR 364, and East v Repatriation Commission (1987) 16 FCR 517, the hypothesis is not pointed to by the material before the Tribunal. In this regard, it was submitted that Dr Miller referred to "focal brain necrosis" that could only be confirmed by way of autopsy, that was not performed.
It was also noted that in commenting on the likelihood of the hypothesis, Dr Miller said there was more than a possibility that the brain was so affected to a greater or lesser degree. This was probably about 50 percent he thought. It was submitted that this underscores the theoretical nature of the hypothesis. Dr Miller relied on radiological material to support his hypothesis, but that radiological evidence was interpreted by Professor Roche and Dr Korber as representing changes that are age-related and non-specific, and from which nothing can be inferred. Dr Miller was unable to point to any clinical findings that supported his hypothesis. There was no evidence of any frank CVA, and Dr Miller said himself that the condition was "very hard to demonstrate". It was also noted by Professor McLeod that Dr Miller was addressing the presence of disease in large vessels, and not small vessels which are relevant in the hypothesis.
It was submitted that the hypotheses were not pointed to on the clinical material, nor on the radiological material, nor on the history. The evidence is of a gradual progressive dementia and not of a step-wise deterioration, and it is clearly explained by non-war-caused conditions. It was also submitted that the fact that the symptoms of white matter disease would completely mask the symptoms of Parkinson's Disease suffered by the Veteran does not help the Applicant. It merely confirms the tenuous nature of the hypothesis.
Even if the Tribunal finds that a reasonable hypothesis has been raised on the whole of the material, it is still open to find on the facts that there is more than a reasonable doubt that there is no sufficient grounds to determine that the Veteran's death was war-caused. On the evidence of Professor McLeod, the chain of events concerning the Veteran's dementia, leading to his immobility is entirely and adequately explained by his Parkinson's disease and Alzheimer's disease.
The Respondent noted that this matter was adjourned so that the Applicant could adduce further evidence in the form of a report from a neurologist. No further evidence from a neurologist was forthcoming. The Respondent relied on the decision of the Full Federal Court in Munt v Repatriation Commission, 28 July 1986, SA G42/1985 where the Court held that the principle in Jones v Dunkel was applicable in such cases, that it is a case of "plain common sense". It was submitted that in these circumstances an adverse inference should be drawn against the Applicant. The Applicant's failure to adduce such evidence should be interpreted as the Applicant's failure to raise a reasonable hypothesis and that the hypothesis advanced by Dr Miller is not a reasonable hypothesis. On the issue of the Jones v Dunkel principle, it was submitted for the Applicant in reply that there is no basis for the Respondent's speculation on this issue. Moreover, material that is inconsistent with an hypothesis will not prevent a reasonable hypothesis from being raised: Byrnesv Repatriation Commission (1993) 177 CLR 564.
It was submitted for the Respondent that, relying on the decisions of the Federal Court in Repatriation Commission v Gosewinckel (1999) 59 ALD 690 and Repatriation Commission v Cooke (1998) 90 FCR 307, that are binding on the Tribunal, the diagnosis of the condition that caused the Veteran's death must be made on the balance of probabilities. The Respondent noted the concession made by Dr Miller that white matter disease would not be diagnosed on the balance of probabilities.
It was submitted that the causal factor has already been conceded for the Respondent that is, the smoking factor in Instrument No. 142 of 1996. Whilst the definition of "cerebral ischaemia" appears to be more liberal in the later Statement of Principles, nevertheless, it is stated that cerebral ischaemia "… usually presents as a Transient Ischaemic attack (TIA) or stroke". The Respondent relies on the clinical material before the Tribunal and the reports of Dr Weerasinghe, Professor McLeod, Dr Korber and Professor Roche. There is no evidence of a frank "stroke". Moreover, in relation to TIAs, the Respondent noted that there is no evidence that is pointed to on the whole of the material before the Tribunal that established that the Veteran ever suffered from TIAs.
ApplicantThe hypothesis being pursued on behalf of the Applicant has been outlined at paragraph 5 of these reasons for decision.
In relation to the Respondent's submission that the Applicant's hypothesis was too tenuous, having regard to the whole of the evidence, it was submitted for the Applicant that, relying on Byrnes (supra), the High Court (at 570) confirms that a hypothesis may properly rely on only part of the material before the Tribunal:
The remarks of the majority in Bushell were directed specifically to a situation where the raised facts giving rise to the hypothesis covered "the whole of the material" bearing on the hypothesis. They were not directed to a case where the veteran relies on only part of the material before the decision maker. Proof beyond reasonable doubt of a fact inconsistent with the reasonable hypothesis would, by implication, demonstrate that "the factual foundation upon which the hypothesis can operate does not exist".
It was submitted for the Applicant that the following material points to the hypothesis –
The Respondent conceded that the Veteran had a war-caused smoking habit sufficient to meet the Statement of Principles for Cerebrovascular Accident, Instrument No.142 of 1996.
There is clinical evidence that the Veteran suffered a stroke or that he was suffering from cerebral ischaemia in 1993. He was seen by Dr Weerasinghe, specialist geriatrician, on 11 March 1993, who recorded that the Veteran was a "severely Parkinsonian" man with a recent history of fall and unconsciousness. He diagnosed –
1. Probably CVA w/mild L weakness and dysphasia
2. Parkinsonism & confusion (? Dementia of mixed aetiology) …
It later became apparent that the Veteran's admission to hospital might have been the result of an overdose, perhaps of Sinequan. However, in a further report of Dr Weerasinghe dated 4 August 2000 (exhibit F) he adhered to his initial clinical impression. At examination on 11 March 1993 Dr Weerasinghe noted speech problems, left leg weakness and absent ankle jerk, and "equivocal plantar response on the left". Dr Weerasinghe was asked to provide a report on whether he considered cerebrovascular disease was suffered "on the balance of probabilities" or as a "reasonable hypothesis", namely as "more than a mere possibility. He concluded:
Based on these physical signs and the history of vascular disease, I consider it to be a reasonable hypothesis that Mr Jeffs suffered from cerebrovascular disease.
Dr Mullany, the Veteran's general practitioner, considered that all the clinical evidence pointed to CVA, "proceeded by hypertension and arteriosclerosis". He said that the Veteran (exhibit E) –
… had plenty of TIA's, light-headedness, hypertension attacks, off balance, unsteady on his feet, hazy feeling, disorientated, confused, we would be putting our head in the sand to say there was no cerebro-vascular disease.
In his oral evidence Dr Mullany noted his amazement at how quickly the Veteran's condition had deteriorated in his last few years, and more quickly than it had in the previous years. Dr Mullany confirmed that the Veteran suffered a stroke in 1993.
Professor Roche (exhibit 8) commented in respect of CT scans that they have significant limitations in diagnosing brainstem infarct or haemorrhage, and while a small brainstem infarct or haemorrhage could have been present there was no evidence of either on the scan.
Professor McLeod (exhibit 1) did not see any "definite evidence" of a stroke, but he noted that if the Veteran had had a minor stroke he could have been much improved in 48 hours. If he had had a minor stroke then it would most likely have been a transient ischaemic attack of a lacunar infarct in the brainstem. He also opined that it was more probable than not that the Veteran would not have recovered as quickly if he had had a significant cerebral infarct or haemorrhage. He also said that if the Veteran had had a stroke in 1993 it would have confirmed the existence of cerebrovascular disease.
Putting aside the 1993 incident, it was submitted that there is a great deal of opinion evidence of the various experts qualified in this matter, including Dr Mullany and Dr Weerasinghe, that cerebral ischaemia was present. Without specific reference to the 1993 incident, however, there was greater focus on the nature of possible cerebral ischaemia.
Dr Miller proposed in his oral evidence that the Veteran suffered from white matter disease as a form of cerebral ischaemia, in which dementia is characteristically exhibited. The matter was then adjourned to enable the parties to obtain further evidence. Dr Miller noted the observations of Dr Korber and Professor Roche, of evidence on the CT scan of periventricular low density, that he concluded was evidence to support his hypothesis that the Veteran had white matter disease. He also noted (exhibit D) that the negative brain scan of 19 March 1993 does not exclude small vessel atherosclerotic cerebrovascular disease.
It was submitted that the experts qualified by the Respondent admit the possibility of small vessel cerebral ischaemia on the basis of the clinical evidence. Dr Korber (exhibit 7) noted that periventricular low density was evident, and it was a common degenerative finding in the CT scans of older people. Moreover, atherosclerosis, under the hearing of Degenerative Diseases of the Brain (that is, Binswanger's disease) is described in the literature as showing periventricular hyperintensities on MRI, that on a CT is described as periventricular low density. It was submitted, therefore, that Dr Korber was by his evidence confirming that the CT scan appearance was consistent with the presence of small vessel ischaemia.
Professor Roche noted, in relation to the CT scan of 19 March 1993, that there were poorly defined low density changes in the deep white matter that were non-specific in nature, and most probably age-related "on the basis of small vessel ischaemia". He noted that such changes were found in demented and non-demented people, but more frequently in demented people. He noted that the changes are age-related, and the presumption is that they are due to focal changes in the brain cell structure, on the basis of decreased oxygen supply, secondary to narrowing of the small vessels of the brain. Professor Roche confirmed that the CT scan of 19 March 1993 was consistent with Dr Miller's diagnosis of vascular dementia, but it is also consistent with normality. It was submitted that on this basis no issue about Dr Miller's expertise and the correctness of his reasoning should remain.
It was submitted that Professor McLeod's final position was that the Veteran might well have had vascular disease. He noted there was no question but that the Veteran had periventricular low density changes in the white matter, as shown on the CT scan. He noted that progressive subcortical arteriosclerotic encephalopathy was a rare cause of dementia whereas white matter changes seen on CT and MRI are common. On this basis he opined there is "no convincing evidence" that the Veteran suffered from white matter disease, and it was more likely than not that he suffered from subcortical arteriosclerotic dementia at the time preceding his death. It was submitted that therefore Professor McLeod conceded that there were changes in the Veteran's brain and that it was possible that he suffered from vascular-related dementia. He also conceded that the changes on the CT scan were consistent with white matter disease. He did not agree with the opinion of Professor Roche (exhibit 6).
It was submitted that the Veteran suffered from vascular disease at other sites, and he had ischaemic heart disease accepted as war-caused. There is evidence of peripheral vascular disease that, on the opinion of Dr Weerasinghe and Dr Miller, increased the likelihood of the presence of white matter disease.
It was submitted that the evidence clearly established that the Veteran suffered from dementia, and that dementia being a result of Alzheimer's disease was recorded on the death certificate as the condition present at the time of death. The material pointing to the contribution of cerebral ischaemia to the Veteran's dementia is supported by Dr Weerasinghe, Dr Miller and Professor McLeod.
The death certificate listed immobility as a cause of death. The Respondent conceded (Statement of Facts and Contentions dated 5 April 2001) that broncho-pneumonia was caused by immobility, albeit also contending that the immobility was caused, apparently solely, by Parkinson's disease.
The Applicant disagreed with the Respondent's interpretation of the Federal Court decisions of Cooke (supra) and Gosewinkel (supra) that the diagnosis of the Veteran's "cerebrovascular accident" must be determined on the balance of probabilities. The presence of cerebrovascular accident is part of the hypothesis. Accordingly, it need only be established at the level of the reasonable hypothesis. It is not the proximate cause of death, viz. broncho-pneumonia and immobility and Parkinson's disease. It was submitted that Cooke (supra) is authority that all aspects of the hypothesis that seek to link the Veteran's service with his death are to be considered at the level of the reasonable hypothesis. In Cooke it was submitted that such an approach would result in different treatment of a disease. In that matter there was on the one hand a claim for depressive disorder and on the other a death claim where the Veteran had committed suicide as a result of the depressive disorder. The Court (at 405) said:
In our view there are two answers to these questions. First, the language of s120(1) and (3) is so clear as to not raise any doubt on the point. Secondly, any suggested illogicality disappears when one concentrates on the task in hand. In the example given above, the task at hand when deciding the incapacity claim is, initially, whether there is or was a disease. The evidence is far more readily available on that issue (in the main medical evidence one would suppose) than matters of war-causation which involve assessment of events which may have taken place as long ago as half a century.
It was also submitted that Gosewinckel (supra) simply follows Cooke.
It was noted for the Applicant that Professor Roche and Professor McLeod have provided their respective opinions on the basis of the 1996 Statements of Principles for Cerebrovascular Accident. It was submitted that Professor McLeod (exhibit 4) agreed with Dr Miller's opinion that arteriosclerotic encephalopathy due to small vessel ischaemia satisfies the definition for cerebral ischaemia in the Statement of Principles, and that Professor Roche "somewhat cryptically" seemed to be agreeing that the terms of the Instrument were met. It was submitted that given those experts agree that the matter falls within Instrument 142 of 1996, the Tribunal should be satisfied that it is applicable.
It was submitted for the Applicant in relation to s120(1) of the Act, all three qualified experts provided by the Respondent admitted the possibility of cerebral ischaemia being present in the Veteran. Accordingly their opinions offer no disproof of that part of the hypothesis. It was noted that although Professor McLeod had been opposed to the hypothesis his position had changed by the time of his last report and his oral evidence. Despite each of those experts having been taken by the Respondent to the evidence it relied on to disprove the hypothesis, none was of the opinion that the hypothesis had been disproved to their satisfaction. Professor McLeod could not exclude the presence of white matter disease beyond reasonable doubt, nor could he disprove that the Veteran suffered from white matter disease. In reply, it was submitted for the Respondent that Professor McLeod could exclude white matter disease beyond reasonable doubt, but not "entirely".
It was submitted for the Applicant that Professor McLean conceded the presence of Parkinson's disease and Alzheimer's disease could have masked the presence of white matter disease, even though he preferred a diagnosis of dementia arising out of Parkinson's disease. Dr Miller's evidence was that Parkinson's disease was consistent with gait problems that could "completely mask" any changes from diffused white matter disease. Hence, the possibility of masking means that there is little disproof of the possibility of vascular dementia on the basis that the Veteran was thought to suffer from Alzheimer's and Parkinson's dementia. Therefore, it was submitted the Tribunal should be satisfied that there is no material before it that disproves the hypothesis beyond reasonable doubt.
In reply, it was submitted for the Respondent, that despite the Applicant's failure to refer to the Federal Court decisions in East (supra) and Bey (supra) they are authority for the proposition that in considering whether a reasonable hypothesis has been raised consideration must be given to all of the evidence. It was also noted that the High Court, in considering the Special Leave Application in Repatriation Commission v Owens ,5 August 1996,147/1995 said –
It is not whether an hypothesis of connection would be reasonable if some facts are ignored; the question is answered by reference to the whole of the material before the Administrative Appeals Tribunal.
Applying that case law, it was submitted for the Respondent that the cause of the Veteran's dementia was due to Parkinson's disease and/or Alzheimer's disease, rather than the hypotheses advanced for the Applicant. The Tribunal is not empowered to sift through reams of evidence to find material that could benefit one party only; it must have regard to the whole of the material to determine the correct or preferable decision. It was submitted that whilst it is clear that there is a possibility of a causal connection of white matter disease and the Veteran's death, the evidence goes no further than that. It is only a mere possibility, the hypotheses not being pointed to when one has regard to the whole of the material before the Tribunal. It was submitted "it is simply too tenuous". Dr Miller has discounted that the episode in 1993 was due to a "frank stroke". Therefore, it was submitted the Applicant should not continue to press this as a reasonable hypothesis when her expert witness has abandoned it.
It was submitted for the Respondent that Professor McLeod has considered there is sufficient doubt about the diagnosis to render more than a reasonable doubt about it. He notes a lack of support in the material and the radiological evidence, and this is a relevant consideration as to whether a reasonable hypothesis has been raised.
Importantly, the Respondent conceded that on the question of contribution, if one accepts that a reasonable hypothesis has been raised in relation to white matter disease, then on the evidence of Professor McLeod it made a contribution that in the circumstances was more than de minimis to the subsequent events that led to the death of the Veteran.
consideration of evidence and findings of factAt the outset the Tribunal notes that it gives little weight to the evidence of Dr Mullany who the Tribunal found to be partisan and lacking in objectivity. Moreover, his medical opinion was given without any specialist qualifications, yet he was prepared to challenge the expert neurological evidence of Professor McLeod. The Tribunal does not find Dr Mullany to be appropriately qualified to raise a medical hypothesis of the nature raised in this matter. Moreover, on issues relevant to his role as the Veteran's treating local medical officer, he demonstrated gross inconsistency in his evidence on the issue of whether the Veteran was suffering from depression and attempted suicide and the nature of his cerebrovascular condition. Fortunately for the Applicant her case does not need to rely on Dr Mullany.
The Tribunal notes the submission for the Respondent that the hypothesis raised is not impossible, fanciful or incredible, but that it is too tenuous. The Tribunal considers that this represents a careful consideration of the raised facts, but that is not to say that the Tribunal necessarily agrees with the whole of the submission. However, it enables the Tribunal to cut through the reams of documents and evidence in this matter, and to consider the narrow issue left open, that is, whether it is too tenuous. The Tribunal is of the view that the hypothesis is not impossible, fanciful or incredible.
It is interesting that the Respondent has come to this assessment of the hypothesis but still considers that Dr Miller is not appropriately qualified to raise the hypothesis. Dr Miller is not qualified as a neurologist or a radiologist, nonetheless the Tribunal finds that he is qualified as a relevant expert to raise the hypothesis in this case. One only has to consider his ability to deal with the minutiae of the questions put to him during his oral evidence to conclude that he was relevantly qualified. Dr Weerasinghe was also appropriately qualified as the Veteran's physician and a geriatrician whom the Veteran consulted to provide evidence about that consultation and to provide an opinion as to whether the Veteran suffered from cerebrovascular disease. His opinion evidence does not take the matter very far. It is difficult to understand the minutiae of his reasoning, and this matter will certainly turn on the minutiae.
A central issue is whether the hypothesis is too tenuous. In considering that issue, it is the Respondent's submission that the Tribunal must consider whether the Veteran suffered from white matter disease on the balance of probabilities. The Tribunal does not accept that submission. The existence of white matter disease is but one link in the chain of causation of the Veteran's death. It is merely a contributory cause, and a minor contribution at that, of his dementia. At this stage it should be noted that if the Veteran suffered from white matter disease, then the Tribunal finds on the evidence that it contributed to his dementia to a minor degree but one that was more than de minimus. On the evidence of Professor McLeod, it was no more than 10 percent. That is sufficient for the contribution to be material, and the Tribunal so finds.
The Tribunal finds that, when considering whether a reasonable hypothesis of the Veteran's death has been raised, it is not necessary to determine that each medical condition included in the chain of causation exists on the balance of probabilities. The Tribunal does not accept the Respondent's interpretation of Cooke (supra) and Gosewinckel (supra) on this point. This merely is part of the totality of the evidence to be considered in determining whether there has been a reasonable hypothesis raised in respect of the Veteran's death. There is no doubt about the primary cause of his death, which was bronchopneumonia, arising from his inactivity due to dementia. Applying the decision of the Federal Court in McKenna v Repatriation Commission (1999) 86 FCR 144 is also necessary when there is a Statement of Principles relevant to any condition involved in the chain of causation, then all relevant Statements of Principles must be met. That is not to say, however, that the condition relevant to that condition must exist on the balance of probabilities.
The issue for the Tribunal to consider is whether the evidence that goes to whether or not the Veteran suffered from white matter disease is too tenuous. It has been raised and defended vigorously by a relevant specialist, Dr Miller. The Full Federal Court in East v Repatriation Commission (1987) 16 FCR 517 held (at 533) that –
A reasonable hypothesis requires more than a possibility, not fanciful or unreal, consistent with the known facts. It is an hypothesis pointed to by the facts, even though not proved upon the balance of probabilities.
There is no doubt it was possible that the Veteran could have suffered from white matter disease. The hypothesis based on that possibility was raised by Dr Miller in the context of his oral evidence at a time when a previous hypothesis was abandoned. That in itself must not go against the Applicant. He noted the Veteran's history of cardiovascular and peripheral vascular disease, and considered therefore that it was likely he also would have suffered from cerebrovascular disease. He noted the CT findings of age-related changes that he considered consistent with cerebrovascular disease. He noted the opinion of Dr Weerasinghe, who had examined the Veteran in March 1993 at the time he was admitted unconscious with a provisional diagnosis of "stroke". Dr Weerasinghe reported on his examination at that time that he had difficulty with word finding and had weakness of his left leg with absent ankle jerk and an equivocal plantar response on the left "in addition to his Parkinsonian features". This underpinned Dr Weerasinghe's consideration that there was a "reasonable hypothesis" that the Veteran suffered from cerebrovascular disease.
The Tribunal notes the definition of "cerebral ischaemia" in Instrument No.142 of 1996, the relevant Statement of Principles, and considers that the raised facts point to the Veteran having suffered from cerebral ischaemia as defined. In so doing, the Tribunal has disregarded Dr Mullany's evidence about the TIAs. The submissions for the Applicant about the existence of evidence about "cerebral ischaemia" are sufficiently persuasive.
The Tribunal considers that the raised facts meet the relevant Statement of Principles, and that a reasonable hypothesis has been raised.
Moving now to s120(1) of the Act, the Tribunal notes the vigour with which the Respondent has provided expert evidence and very cogent submissions that in part go to the test of dispelling the reasonable hypothesis beyond reasonable doubt. However, after carefully considering all the evidence, while the Tribunal has considerable doubt about the hypothesis, it cannot be satisfied to the requisite high standard, that the hypothesis has been disproved beyond reasonable doubt. The Tribunal must determine that the Veteran's death is war-caused unless it is satisfied beyond reasonable doubt that there is no sufficient ground for making that determination.
The Tribunal has been greatly assisted by both parties in the presentation of the oral evidence to the Tribunal, and in the incisive and careful written submissions that were lodged subsequently. The Respondent's medical evidence, and in particular that of Professor McLeod, provided the Tribunal with an opportunity to test the hypothesis very carefully. However, this matter, finally, turned on its own facts, thus making the process of reaching a decision a difficult one for the Tribunal.
The Tribunal therefore sets aside the decision under review, and determines that the death of the Veteran was war caused. War widow's pension is payable to the Applicant on and from 25 August 1997.
I certify that the 120 preceding paragraphs are a true copy of the reasons for the decision herein of Mrs M T Lewis, Senior Member
Signed: .....................................................................................
AssociateDate/s of Hearing 11 August, 7 September 2000 & 5 April 2001
Date of Decision 30 June 2001
Counsel for the Applicant Mr M Vincent
Solicitor for the Applicant Mr S Lurie, Dibbs Barker Gosling
Solicitor for the Respondent Mr G Wright, Dept. of Veterans' Affairs
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