Wall and Repatriation Commission (Veterans' entitlements) - [2018] AATA 2573

Wall and Repatriation Commission (Veterans' entitlements) [2018] AATA 2573 (7 June 2018)
Division:VETERANS' APPEALS DIVISION
File Number(s): 2017/1215
Re:Norman Wall
APPLICANT

AndRepatriation Commission
RESPONDENT

DECISION
Tribunal:Senior Member A.A. Nikolic AM CSC
Date:7 June 2018
Place:Melbourne

The Tribunal affirms the decision under review.
[sgd]........................................................................
Senior Member A.A. Nikolic AM CSC
CATCHWORDS
VETERANS’ AFFAIRS – pension – left optic atrophy – major depressive disorder – operational service – whole of the material does not raise a reasonable hypothesis connected to circumstances of operational service – decision affirmed
LEGISLATION
Veterans’ Entitlements Act 1986 (Cth)
CASES
Blain v Repatriation Commission [2017] FCA 114
Bushell v Repatriation Commission (1992) 175 CLR 408
Cameron v Repatriation Commission (2003) FCA 1323
Repatriation Commission v Cooke [1998] FCA 1717
Deledio v Repatriation Commission (1997) 47 ALD 261
East v Repatriation Commission (1987) 16 FCR 517
Repatriation Commission v Deledio (1998) 83 FCR 82
SECONDARY MATERIALS
Statement of Principles No. 83 of 2015: Depressive Disorder
REASONS FOR DECISION
Senior Member A.A. Nikolic AM CSC
7 June 2018

Mr Norman Wall has asked the Tribunal to review a decision by the Veterans’ Review Board (VRB) made on 25 November 2016,[1] affirming the Repatriation Commission’s decision,[2] that Mr Wall’s primary optic atrophy (left) and major depressive disorder were not war-caused.
[1] Exhibit R1 (T-documents numbering 155 pages), pp.2a-2k.
[2] Ibid, pp.98-108.
The hearing was conducted during 15-16 May 2018. Mr Wall was represented by Ms Fiona Spencer of counsel, instructed by Williams Winter Solicitors. The Commission was represented by Mr Ken Rudge, a departmental advocate.
For the reasons that follow, the decision under review is affirmed.
BACKGROUND
Mr Wall is a 70 year-old veteran who served with the Royal Australian Navy (RAN) for approximately eight years from 1964 until 1972.[3] During an 11-day period of operational service between 25 January and 5 February 1968, Mr Wall was serving on HMAS Stuart, while she escorted HMAS Sydney to and from Vung Tau, South Vietnam. HMAS Stuart was anchored in Vung Tau Harbour for approximately eight hours on 3 February 1968 while helicopters unloaded stores from HMAS Sydney.[4] Crew members did not go ashore. Mr Wall contends that during this 11-day period of operational service, the primary optic atrophy in his left eye was caused by local environmental factors or infection. In the alternative, Mr Wall contends he did not receive appropriate medical treatment for this condition.
[3] Ibid, p.2e.
[4] Exhibit R3 (HMAS Stuart Report of Proceedings for February 1968, pp.1-2). HMAS Stuart anchored of Ganh Rai Point at approximately 0650 hours and cleared the Vung Tau Harbour entrance at approximately 1200 hours. HMAS Stuart and two helicopters subsequently escorted HMAS Sydney to sea at approximately 1430 hours for passage to Singapore. HMAS Stuart berthed in Singapore on 5 February 1968 before sailing to Hong Kong on 13 February 1968, arriving in Hong Kong on 17 February 1968.
RELEVANT LEGISLATION AND AUTHORITIES
Operational Service. The expression ‘operational service’ is defined at sections 6 to 6F of the Veterans’ Entitlement Act 1986 (the Act). Under section 6C, a person renders operational service if they, inter alia, are allotted for duty in an operational area. It is not contested that Mr Wall had operational service on HMAS Stuart between 25 January and 5 February 1968.
War-Caused Injuries or Diseases. Section 9 of the Act relevantly provides that:
(1)Subject to this section and section 9A, for the purposes of this Act, an injury suffered by a veteran shall be taken to be a war-caused injury, or a disease contracted by a veteran shall be taken to be a war-caused disease, if:
(a)the injury suffered, or disease contracted, by the veteran resulted from an occurrence that happened while the veteran was rendering operational service;
(b)the injury suffered, or disease contracted, by the veteran arose out of, or was attributable to, any eligible war service rendered by the veteran;
(c)…
(d)…
(e)The injury suffered, or disease contracted by, the veteran:
(i) …
(ii) Was suffered or contracted before the commencement of…eligible war service rendered by the veteran, but not while the veteran was rendering eligible war service;
And, in the opinion of the Commission, the injury or disease was contributed to in a material degree by, or was aggravated by, any eligible war service rendered by the veteran, being service rendered after the veteran suffered that injury or contracted that disease;
Standard of Proof. As Mr Wall’s claim relates to operational service, the applicable standard of proof is defined in section 120(1) and section 120(3) of the Act:
(1)Where a claim under Part II for a pension in respect of the incapacity from injury or disease of a veteran, or of the death of a veteran, relates to the operational service rendered by the veteran, the Commission shall determine that the injury was a war-caused injury, that the disease was a war-caused disease or that the death of the veteran was war-caused, as the case may be, unless it is satisfied, beyond reasonable doubt, that there is no sufficient ground for making that determination.
Note: This subsection is affected by section 120A.
(2)...
(3)In applying subsection (1) or (2) in respect of the incapacity of a person from injury or disease, or in respect of the death of a person, related to service rendered by the person, the Commission shall be satisfied, beyond reasonable doubt, that there is no sufficient ground for determining:
(a)that the injury was a war-caused injury or a defence-caused injury;
(b)that the disease was a war-caused disease or a defence-caused disease; or
(c)that the death was war-caused or defence-caused;
as the case may be, if the Commission, after consideration of the whole of the material before it, is of the opinion that the material before it does not raise a reasonable hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the person.
Note: This subsection is affected by section 120A.
Under section 120(4) of the Act, the standard of proof for assessment or reassessment of the rate of pensions, is ‘reasonable satisfaction,’ which is also referred to as the ‘balance of probabilities.’[5] The standard of proof for diagnosis is also reasonable satisfaction.[6]
[5] D. Pearce, Administrative Appeals Tribunal (4th Ed.) 2015, p.152.
[6] Repatriation Commission v Cooke [1998] FCA 1717.
Section 120(6) of the Act provides in effect that neither party has any onus of proving any matter relevant to the determination of the claim.
Reasonableness of Hypothesis. As Mr Wall’s claim was lodged after 1 June 1994, section 120A of the Act is enlivened, requiring that I assess the reasonableness of the hypothesis connecting his primary optic atrophy - left with his service, against any existing Statement of Principles (SoP). Section 120A(3) of the Act provides:
(3) For the purposes of subsection 120(3), a hypothesis connecting an injury suffered by a person, a disease contracted by a person or the death of a person with the circumstances of any particular service rendered by the person is reasonable only if there is in force:
(a)a Statement of Principles determined under subsection 196B(2) or (11); or
...
that upholds the hypothesis.
If I find that a hypothesis is raised connecting Mr Wall’s left eye condition and depressive disorder to his service, its reasonability and validity must then be determined. The methodology established by the Federal Court in Repatriation Commission v Deledio (Deledio)[7] is routinely applied in this regard. As held in Deledio (at 97-98):
‘At the risk of being repetitious we would restate the course which the Tribunal is to take in a case, such as the present, (i.e. one involving a claim to be decided after the 1994 Amendments) in respect of the incapacity of a person from injury or disease, or in respect of the death of a person related to service rendered by that person as follows:
1.        The Tribunal must consider all the material which is before it and determine whether that material points to a hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the person. No question of fact finding arises at this stage. If no such hypothesis arises, the application must fail.
2.        If the material does raise such a hypothesis, the Tribunal must then ascertain whether there is in force an SoP determined by the Authority under s 196B(2) or (11). If no such SoP is in force, the hypothesis will be taken not to be reasonable and, in consequence, the application must fail.
3.        If an SoP is in force, the Tribunal must then form the opinion whether the hypothesis raised is a reasonable one. It will do so if the hypothesis fits, that is to say, is consistent with the "template" to be found in the SoP. The hypothesis raised before it must thus contain one or more of the factors which the Authority has determined to be the minimum which must exist, and be related to the person's service (as required by ss 196B(2)(d) and (e)). If the hypothesis does contain these factors, it could neither be said to be contrary to proved or known scientific facts, nor otherwise fanciful. If the hypothesis fails to fit within the template, it will be deemed not to be "reasonable" and the claim will fail.
4.        The Tribunal must then proceed to consider under s 120(1) whether it is satisfied beyond reasonable doubt that the death was not war-caused, or in the case of a claim for incapacity, that the incapacity did not arise from a war-caused injury. If not so satisfied, the claim must succeed. If the Tribunal is so satisfied, the claim must fail. It is only at this stage of the process that the Tribunal will be required to find facts from the material before it. In so doing, no question of onus of proof or the application of any presumption will be involved.’
[7] Repatriation Commission v Deledio [1998] FCA 391, 83 FCR 82 (at 97-98).
Reference to the Deledio principles is not intended to infer that decision-makers should rely on this methodology alone or in preference to the applicable legislative provisions. The guidance in Deledio, however, can usefully inform a decision-makers consideration of veteran’s matters. Logan J’s recent decision in Blain v Repatriation Commission [2017] FCA 114 at [9] is instructive in this regard.
The plain meaning of ‘hypothesis’ was considered by the Full Court of the Federal Court in East v Repatriation Commission (East)[8] at [41-42]:
‘A hypothesis may be conveniently defined as: ‘proposition made as basis for reasoning, without assumption of its truth; supposition made as starting point for further investigation from known facts; groundless assumption’: The Concise Oxford Dictionary.
…
…[T]o be reasonable, a hypothesis must possess some degree of acceptability or credibility – it must not be obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous. For a reasonable hypothesis to be ‘raised’ by material before the Board, we think it must find some support in that material – that is, the material must point to, and not merely leave open, a hypothesis as a reasonable hypothesis...
…A reasonable hypothesis requires more than a possibility, not fanciful or unreal, consistent with the known facts. It is a hypothesis pointed to by the facts, even though not proved upon the balance of probabilities.’
[8] East v Repatriation Commission [1987] 16 FCR 517.
Mason CJ, Deane and McHugh JJ elaborated upon section 120(3) in Bushell v Repatriation Commission[9] (Bushell) at [6]:
“…Sub-section (3) is concerned with whether ‘the material’ raises a reasonable hypothesis that the relevant injury, disease or death was connected with the service of the veteran. It is not concerned with conflicts in the material, whether they be of opinion or fact…
The material will raise a reasonable hypothesis within the meaning of s 120(3) if the material points to some material fact or facts (‘the raised facts’) which support the hypothesis and if the hypothesis can be regarded as reasonable if the raised facts are true.”
[9] Bushell v Repatriation Commission [1992] HCA 47.
Citing East, their Honours further held at [9], that a hypothesis is not reasonable if it is:
"obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous"
The High Court held in Byrnes v Repatriation Commission[10] at [13]:
‘The position may be summarised as follows:
(1)First, subs (3) of s 120 is applied: do all or some of the facts raised by the material before the Commission give rise to a reasonable hypothesis connecting the veteran’s injury with war service? The hypothesis will not be reasonable if it is contrary to known scientific facts or is obviously fanciful or untenable. If the hypothesis is not reasonable the claim fails. Proof of facts is not in issue at this point.
(2)If a reasonable hypothesis is established subs (1) of s120 is applied. The claim will succeed unless:
(a) one or more of the facts necessary to support the hypothesis are disproved beyond reasonable doubt; or
(b) the truth of another fact in the material, which is inconsistent with the hypothesis, is proved beyond reasonable doubt, thus disproving, beyond reasonable doubt, the hypothesis.’
[10] Byrnes v Repatriation Commission [1993] HCA 51.
In Repatriation Commission v Bey[11], the Court endorsed the position established by East, Bushell and Byrnes, stating:
‘Any doubt that attends the status of East as a correct exposition of the law relating to s 120(3) should be dispelled. This Court re-states the position established by East, Bushell and Byrnes. A "reasonable hypothesis" involves more than a mere possibility. It is a hypothesis pointed to by the facts, even though not proved upon the balance of probabilities. That understanding of the expression gives force to the word "reasonable", is strongly supported by the history of the relevant provisions, and accords with the intention appearing in the Minister's second reading speech and with authority.’
[11] Repatriation Commission v Bey [1997] FCA 1347.
With that guidance in mind, it follows that I must consider all of the material before me in forming an opinion about whether it raises not just a hypothesis, but a reasonable hypothesis that connects factors in an applicable SoP with the circumstances of Mr Wall’s service. Where there is no SoP for a claimed condition, I must form an opinion with regard to the whole of the material before me. Allsop J has noted in Cameron[12] at [42] that the distinction between forming an opinion about the existence or otherwise of a reasonable hypothesis, and impermissible fact finding, is often a fine line to tread:
‘The dividing line between impermissible fact finding and permissible (indeed mandated) assessment of all the material, weighing it and concluding whether or not, as a whole, it points to the posited reasonable hypothesis, is not necessarily easy. The characterisation of Dr Burns’ views as assertions may be seen to be part of this weighing process of all the material. On the other hand, there is force in the applicant’s submissions that if the medical opinion is, in terms, in accordance with the hypothesis, to conclude that the hypothesis is unreasonable involves a finding that the medical opinion is without basis. I have not found this distinction easy to resolve.
[12] Cameron v Repatriation Commission (2003) FCA 1323.
THE ISSUES
The issues for determination are whether the claimed conditions of primary optic atrophy - left and major depressive disorder, arose out of or are attributable to any eligible war service, and if so, whether Mr Wall is entitled to an increase in his disability pension.
EVIDENCE
Evidence of Mr Wall
I have had regard for Mr Wall’s statement taken on 23 February 2017.[13] Mr Wall also gave oral evidence at the hearing and was cross-examined. Mr Wall contends that he had no previous problems with his vision prior to 25 January 1968, and connects optic atrophy in his left eye with war service on the following basis:
(a)He first noticed a rapid deterioration of his vision[14] during an 11-day period of operational service on HMAS Stuart between 25 January and 5 February 1968. He became aware of this deterioration when unable to facially recognise colleagues on adjoining ships during refuelling or replenishment, something he previously had no difficulty with;
(b)Optic atrophy in his left eye was caused by exposure to an unspecified ‘environmental influence or infection,’[15] during that 11-day operational tour;
(c)He reported the rapid deterioration in his vision approximately two weeks later in Hong Kong, electing not to do so during an intervening nine day stop in Singapore, as he did not wish to appear alarmist and thought his vision problems may have been temporary;
(d)After HMAS Stuart’s arrival in Hong Kong on 17 February 1968, he reported problems with his vision and was referred by a member of the ship’s medical staff to an eye specialist in Hong Kong;
(e)Tests undertaken by the Hong Kong specialist confirmed the problem was solely in Mr Wall’s left eye and he was provided with spectacles that day; and
(f)In the alternative, Mr Wall contends he did not receive appropriate medical treatment for his left eye condition.
[13] Exhibit A1, Mr Wall’s Statement dated 23 February 2017.
[14] Ibid, p.1, paragraph 2.
[15] Ibid, p.2.
In relation to his depressive disorder, Mr Wall submits in his statement that he first developed depression between his ‘1968 tour to Vietnam and the surgery performed by Prof Bradley.’ He identifies a service medical record dated 20 November 1969, which records him suffering anxiety and depression. He submits that he has ‘continued to suffer ongoing chronic depression,’ requiring referral to a psychiatrist. Mr Wall contends that his mental health problems relate to ‘the emotional distress caused by the optic nerve damage’ and the devastating impact his eye condition and the loss of smell resulting from surgery in July 1970 had on his naval career.
At the commencement of his oral evidence, Mr Wall stated that the reference in his statement about a rapid deterioration in vision ‘affecting both eyes,’ required elaboration. He said this was true only until he saw the specialist in Hong Kong, who performed tests and confirmed that only Mr Wall’s left eye was affected.
Mr Wall said he had aspired during his early Navy career to be a pilot or an officer. The former required good eyesight, which he said was assessed as normal on enlistment in 1964 and remained so until after HMAS Stuart departed Vung Tau Harbour on 3 February 1968. Mr Wall said he never got the opportunity to attend an officer selection board because of events that followed the deterioration of his eyesight in January-February 1968.
Mr Wall stated that leading up to his Vietnam service he had undertaken numerous replenishments at sea and had no problems seeing colleagues on adjoining ships when they came together for refuelling or replenishment. He submits this changed after leaving Vung Tau Harbour, when he noticed that he could no longer facially recognise colleagues on adjoining ships. Notwithstanding the rapid deterioration in his vision, he did not report this to HMAS Stuart medical staff during the transit to Singapore and a nine-day stopover there, because he did not wish to appear alarmist and thought his vision problems were temporary and may resolve without medical intervention.

It was not until approximately two weeks later, when HMAS Stuart was alongside in Hong Kong, that Mr Wall reported his vision problems. He says one of the medical staff on HMAS Stuart arranged for him to see an eye specialist in Hong Kong, who performed tests and confirmed there was an issue only with Mr Wall’s left eye. The specialist provided spectacles, which allowed Mr Wall to ‘see the lights of Hong Kong much better.’ In the statement he adopted at the hearing, Mr Wall contends that he believes an attendance in his records at the British Naval Base (HMS Tamar) on 21 February 1968,[16] relates to the initial complaint about his vision. This entry is contained within a table in Mr Wall’s Service Medical Records (SMR) as follows:
[16] Exhibit R2, p.5. HMS Tamar is where HMAS Stuart berthed in Hong Kong on 17 February 1968.

TABLE 6A – MICROPHOTOGRAPHIC X-RAY

Date

Film No.

Spool No.

Examined at

Result

Inits of MO

21-2-68

633

55

TAMAR HK

N

[initials]

Mr Wall stated in his oral evidence, however, that he doesn’t recall ever attending HMS Tamar.
Approximately a year later in January 1969 and after returning to Australia, Mr Wall said he believed his vision had further deteriorated. He returned to HMAS Stuart’s sick bay where an appointment was organised with a consultant ophthalmologist in Sydney. Tests were performed and myopia diagnosed, resulting in a prescription for glasses. Problems with Mr Wall’s eyesight persisted, however, leading to further specialist appointments and an assessment that his left optic nerve may have been compressed by a cancerous tumour or lesion. Surgery was recommended to investigate this possibility and Mr Wall recalls understanding the seriousness of these investigations when his parents made the ‘expensive and difficult’ trip from Perth to be by his side. After surgery he recalls being advised about primary optic atrophy in his left eye. He submits that the vision in his left eye became worse after the surgery, with ‘most of the left side gone – a blind spot.’ He also lost his sense of smell as a result of the surgery, which is commonly referred to as anosmia. Over the years he says the sight in his left eye has gotten progressively worse.
Mr Wall states that the surgical findings effectively ended his aspirations to become a Navy pilot. Moreover, his anosmia rendered him unable to continue in his trade as a weapons/radio technician, because he could not smell if something was burning and could only work in company with others and not independently as was often required. He says the combined effects of his left eye condition and anosmia caused him to become progressively ‘despondent, angry, depressed, and anxious. He over-consumed alcohol and submits these problems persist to the present day and require ongoing medication.
Mr Wall states that as a result of the medical limitations on his career aspirations he took discharge from the Navy some four years before his term of enlistment expired. He was subsequently unemployed for 5-6 months and then succeeded in finding work in a ‘clerical environment.’ He then decided to do his VCE certificate at night school and to undertake tertiary study as a way of transitioning to other employment.
Mr Wall said he had no previous psychological issues prior to the deterioration of his left eye and the surgery that followed. That changed after commencing university, where he was ‘initially OK’ and studied economics. But he subsequently had trouble coping and recalls seeking assistance from the university medical centre. He also withdrew from a number of subjects and received exemptions from a number of tests. But he persisted and subsequently graduated from university with a degree in economics and later qualified for a master’s degree in strategic planning. He worked as an economist for a number of years and then as a marketing manager at Monash University for approximately 14 years. Mr Wall agreed that he had worked for approximately 40 years after leaving the Navy, enjoyed a successful career, and had chosen to retire at the age of 65.
In relation to his depressive disorder, Mr Wall submits in his statement that he first developed depression between his ‘1968 tour to Vietnam and the surgery...’ He identifies a service medical record dated 20 November 1969, which records him suffering anxiety and depression, submitting that he has ‘continued to suffer ongoing chronic depression.’ Mr Wall contends that his mental health problems relate to ‘the emotional distress caused by the optic nerve damage’ and the impact this had on his naval career. At the hearing Mr Wall said the career implications of his deteriorating eyesight had caused him to seek assistance from the Medical Officer at HMAS Albatross on 20 November 1969. A clinical record on this date refers to him being ‘upset, has a tendency to tears, agitated, tremor, nail biting…insomnia.’[17] The treating Lieutenant Surgeon diagnosed: ‘apparently situational anxiety / depression,’ but did not refer to a cause for Mr Wall’s presentation in that clinical record. Mr Wall was asked about a document immediately adjacent to the clinical record relating to his situational anxiety. It relates to a Ministerial Representation dealing with correspondence dated 7 November 1969, from a woman who had written to the Minister a week earlier requesting to know Mr Wall’s blood group. The request was based on the woman’s belief that Mr Wall may be the father of her child.[18] Mr Wall was asked about the relevance of this correspondence and its connection to the depressive episode he was suffering at the time. Mr Wall stated this issue was unrelated to his situational anxiety/depression at this time, insisting his symptoms resulted entirely from fears about his eye condition and future in the Navy.
[17] Ibid, p.37.
[18] Ibid, p.36.
Mr Wall was asked to elaborate on the above response, given that at the time of this depressive episode, the career implications arising from his eyesight appeared to be unknown and unrealised. On the date of this depressive episode, his SMR reveals only a single presentation about eye problems on 14 January 1969 and a subsequent diagnosis of myopia requiring glasses in March 1969. The identification of a field defect in his left eye and the surgery to investigate a potential tumour only occurred approximately 6-7 months after this depressive episode. Mr Wall insisted that the Ministerial Representation regarding his possible paternity was unrelated to his situational depression, which resulted entirely from concerns about his eyesight and career implications.
Mr Wall said he had also seen psychiatry registrar Dr Sam Margis in March 2006, some 35 years after leaving the Navy and consultant psychiatrist Dr Paul Collier in July 2015. He said Dr Collier’s reference about the commencement of his left eye problem in 1969 instead of 1968 was erroneous, as was the reference to seeing an eye doctor in Singapore, which should have stated Hong Kong. Mr Wall also recalls seeing consultant psychiatrist Dr Gregor Schutz in August 2017, at a time he claims to have been drinking approximately a bottle of wine per day. He continues to take the anti-depressant Aropax prescribed by Dr Margis in 2006 to the present day, to stabilise his ‘mood, ups-an-downs, and paranoia about being a victim…’ He continues to ruminate about being a ‘high achiever’ in the Navy, with prospects of becoming an officer, when his military career was cut short and ‘everything fell apart.’ He says ‘it boils over’ even today.
Mr Wall said in addition to his left eye condition he also suffers from short-sightedness in his right eye, but has ‘no idea’ if it was in any way related to his left eye deficiency. He had worn contact lenses for many years and in recent years had transitioned to bifocal lenses. He said he could ‘cope most of the time’ if he ‘had lots of light.’ He said he was able to drive without restriction. He has been careful over the years not to reveal to anyone at work that he had a problem, but often ran into things due to the blind spot in his left eye.
During cross-examination, Mr Wall was also taken through aspects of HMAS Stuart’s Report of Proceedings in January and February 1968[19] regarding instances of refuelling when he may have first experienced problems with facially recognising colleagues on adjoining ships. These records showed an instance of refuelling on 28 January 1968 and jackstay transfers on 29-30 January 1968, which is when other ships were likely to have been alongside during Mr Wall’s operational service.[20] Due to the passage of time, however, he could not recall which of these events may have been the first time he noticed deterioration in his vision. Mr Wall was asked whether he had experienced eye problems in 1967, prior to his 1968 operational service, given the notation in his Navy Personnel File dated 31 October 1967 that:
‘He has been before a Suplementary (sic) List Selection Board and failed – he states it was eyesight. If this is so, it appears he can only become an Upper Yardman and follow on a technical specialisation…’[21]
[19] Exhibit R3.
[20] Ibid, p.22.
[21] Exhibit R4, p.25.
In relation to whether he could recall any eyesight problems consistent with this 1967 record or earlier, Mr Wall stated: ‘No it doesn’t reflect my recollection.’
Mr Wall was taken through entries in his SMR that showed his eyesight was assessed as normal until a presentation in Australia in early 1969. Mr Wall was asked if it was unusual there was no record in his files about the referral to an eye specialist in Hong Kong a year earlier, or the glasses the specialist had prescribed for him, or the lack of any follow-up. He claimed it was not unusual and follow-up would only have been initiated if he had returned to the sick bay, which he had not. He said questioning medical staff about follow-up in these circumstances was ‘unheard of.’ When asked who had referred him to the specialist in Hong Kong, he replied: ‘it would have been the leading sick berth attendant or ship’s surgeon.’ He was asked if he was given a referral or any other notes to take to the eye specialist but said he had not been given anything. He was asked if the eye specialist in Hong Kong had given him any documents, to which he replied ‘no.’
Mr Wall was asked if anyone had told him his eyes had deteriorated between the time of the initial consultation recorded in his SMR (January 1969) and March 1969,[22] to which he replied: ‘not that I can recall.’ He was asked if the glasses prescribed for him had worked and whether he had worn them, to which he replied: ‘I tried to…I recall having glasses but found them very uncomfortable.’ He said he had not complained about his eyesight from the time of the initial consultation with the eye specialist in Hong Kong, until about a year later in January 1969, because he was able to function reasonably well with the spectacles given to him in Hong Kong, which he used if he ‘had a problem.’ He said he was able to continue looking after radar, missile and communications systems on HMAS Stuart during this time, because even though many of the components were small, they were not miniaturised. He agreed that he was able to function as an electronics technician 14 months after first claiming to have reported deteriorating eyesight in early 1968, and ‘didn’t ever get to the stage’ of not being able to perform that work.
[22] Exhibit R1, p.31.
In relation to a clinical note by consultant ophthalmologist Dr P. Hardy-Smith stating Mr Wall had been prescribed glasses in 1969,[23] Mr Wall submitted this should have stated 1968, because he believed he had told treating doctors about the consultation with the eye specialist in Hong Kong a year earlier.
[23] Ibid, p.39
Mr Wall was taken through a number of specific records from his SMR,[24] which refer to:
(a)an initial presentation on 14 January 1969 relating to ‘Difficulty with distant vision…Pain after reading for a time;’
(b)his subsequent referral to consultant ophthalmologist Mr E. Freshney on 13 March 1969, who noted Mr Wall had complained about ‘trouble with distant vision and near vision’ during the previous 12 months, resulting in a provisional diagnosis of myopia;
(c)his referral to Dr P. Hardy-Smith, who examined Mr Wall on 6 May 1970 and 1 June 1970 in the context of a presentation for: ‘Difficulty with distance vision for last 18/12;’[25] and
(d)his referral to specialist Dr E. Graeme Robertson on 5 June 1970, who diagnosed problems with the visual field in his left eye.
[24] Exhibit R2.
[25] Ibid.
Mr Wall was again asked to confirm whether he had advised these physicians about the ‘rapid deterioration in eyesight’ during early 1968, or the referral to a specialist while HMAS Stuart was in Hong Kong. Mr Wall said he believed he had told these doctors about that history, and could not explain why there was no record of the 1968 consultation, or the previous provision of glasses by the Hong Kong specialist.
Mr Wall was asked about his functional vision after surgery, which he said had worsened. He described not being able to play squash, because the ball would disappear as it entered the blind spot in his left visual field. He said his vision did stabilise around January 1972, but was worse at various times. Even though his vision was corrected to near normal with glasses, the visual field problem has persisted since that time, causing him to bump into things when walking or moving around. He said it often became worse when wearing glasses, which made him feel uncomfortable and nauseous.
Mr Wall was taken through documents at the time of his discharge from the Navy, in which he opined that his left eye condition was ‘possibly due to working conditions.’ In a letter dated 27 October 1970 relating to a claim he had previously made under the Commonwealth Employment Compensation Act 1930, he had relied at that time on possible exposure to ultraviolet light. This was refused on the basis that ultraviolet light may cause burns, but not optic atrophy.[26] In his oral evidence, Mr Wall said he had tried until 1977 to progress a compensation claim on this basis but had been unsuccessful. He said that ‘deep down’ he still believes the cumulative effect of the electromagnetic environment he was exposed to as a result of his trade was the causal factor of this left eye condition. He acknowledged in response to questions, however, that even if that were the case, the electromagnetic exposure was present during his entire three-year posting on HMAS Stuart, not just during a specific 11-day operational tour in early 1968.
[26] Ibid, p.100.
In relation to Mr Wall’s alternative hypothesis that he did not receive appropriate medical treatment for his left eye condition, he did not advance this hypothesis in any substantive way during his oral evidence. I note the Applicant’s Statement of Facts, and Contentions (ASFIC), however, contains a number of submissions in this regard, including:
(a)‘…the Applicant suffered a “primary atrophy of the left optic nerve” following the craniotomy;’[27] and
(b)‘…the optic nerve was damaged in the surgery.’
MEDICAL EVIDENCE
[27] Applicant’s Statement of Facts, Issues and Contentions (ASFIC) dated 5 December 2017, p.3.
Primary Optic Atrophy - Left
Mr Wall’s SMR details an initial presentation to HMAS Stuart medical staff on 14 January 1969 for ‘Difficulty with distant vision…Pain after reading for a time.’[28] He was subsequently referred to consultant ophthalmologist Mr E. Freshney, who saw Mr Wall on 13 March 1969 and noted in a clinical record that Mr Wall had complained about ‘trouble with distant vision and near vision for 12/12.’[29] Mr Freshney’s provisional diagnosis was myopia, which is commonly referred to as near-sightedness.[30]
[28] Exhibit R2, p.31.
[29] Ibid.
[30] See, for example, Dorland’s Illustrated Medical Dictionary, 27th Edition, p.1215.
Mr Wall’s vision problems persisted and he was referred to consultant ophthalmologist Dr P. Hardy-Smith on 6 May 1970, with the referral stating: ‘This sailor complains of blurring of distant vision, progressively worsening. Could you please assess.’[31] Dr Hardy-Smith examined Mr Wall on 6 May 1970 and noted: ‘Difficulty with distance vision for last 18/12.’[32] Dr Hardy-Smith’s record of that consultation states in part:
‘…had glasses prescribed in 1969 but wasn’t happy with them…
…
He says he had a head injury with a cricket ball at 11 or so – unconscious. No other known head injury or other relevant injury or disease. He was not aware of the field defect Left. (The left pupil reaction is definitely less well sustained than right.)
This sailor needs further investigation. Please arrange for X-ray of skull, particularly pituitary fossa and optic foramina. I also wish him to have a fluorescein angiogram of optic discs at Melbourne University Department of Opthalmology…
Could I then see him again, in the meantime I will order above glasses.’
[31] Exhibit R2, p.39.
[32] Ibid.
Mr Wall was referred to specialist Dr E. Graeme Robertson, who examined him on 5 June 1970.[33] Dr Robertson’s clinical note appears to quote Mr Wall directly in relation to this presentation as follows:
‘About two years ago my eyes started playing up. I could not focus distant things properly, e.g. when driving on a country road I could not see cars sharply and could not see whether the car was coming or going…Scenery appeared hazy. It has become worse and worse, so that now I can’t recognise faces across the road. I can read quite well, but my eyes get tired.
I do not suffer from headache.
When I was nine I was knocked unconscious by a cricket ball which hit the back of my head. I was O.K. after a couple of minutes and I think I went on playing.
I cannot concentrate as well as before. I realized this when doing a refresher course in the last six months. I found it harder than the original course in 1996.
I don’t get irritable. Sleep is normal. Sense of smell is normal.’
[33] Ibid, pp.44-46.
After examining Mr Wall and considering the available diagnostic information, Dr Robertson concluded:
‘The visual fields suggest impairment of conduction in the lower half of the left optic nerve. This might be due to compression from below by a neoplasm or a destructive lesion in the nerve itself, such as a glioma of the optic nerve. An atrophic lesion is unlikely to cause such a picture. Arachnoiditis is remotely possible.
The field pattern is not usual for neoplasm, but this seems the most likely diagnosis, and, at all events, full investigation to recognise or exclude such a cause is necessary. A carefully performed and pneumoencephalogram would be the most informative investigation.
Mr Wall was admitted to the Royal Australian Navy Hospital at Cerberus and the Epworth Hospital for further tests and surgery between 17 June 1970 and 19 August 1970. This encompassed a three-week period of sick leave. On 23 July 1970, Surgeon Lieutenant W.J Berry recorded a summary of Mr Wall’s hospitalisation, including an observation from the surgical notes about ‘a primary atrophy of the left optic nerve.’[34] A craniotomy performed by consultant neurosurgeon Professor K. Bradley on 11 July 1970 to examine the optic nerve had revealed that:
‘The left optic nerve appeared to taper as it was traced anteriorly from the chiasma and was at least 1mm. narrower from this point compared with its width at the chiasma.
The right optic nerve also showed some evidence of this change.[35]
[34] Ibid, p.53.
[35] Ibid.
Mr Wall was subsequently reviewed by Professor Bradley on 25 August 1970, who confirmed a ‘loss in the field of vision for the left eye.’[36] Interference with Mr Wall’s olfactory pathways during surgery had also resulted in anosmia. As a result of these medical investigations and results, Professor Bradley recommended on 25 August 1970 that Mr Wall be placed in a non-seagoing category and be subject to further medical review as to his future in the Navy.
[36] Ibid, p.54.

Mr Wall was again referred to Dr Robertson on 9 November 1970 for post-operative review. Dr Robertson concluded:[37]
‘Thus the cause of the optic atrophy remains obscure. I hope that the right optic nerve is not becoming affected. Leber’s optic atrophy comes to me as a possible cause - is there any family history of visual failure?
The well-defined area of non-filling in the chiasmatic cistern might have been an arachnoid cyst, but Professor Bradley found no evidence of arachnoiditis.
It is hoped that his sense of smell will improve.
[37] Ibid, p.64.
Mr Wall was again referred to Dr Hardy-Smith on 18 November 1970, who concluded:[38]
‘The (R) optic disc appears normal: (L) still pale. I would think on all the evidence that the (L) eye trouble may be long-standing, in fact there is a possibility that it may be related to his head injury at…11 with subsequent optic atrophy…’
[38] Ibid, pp.65-66.
Consultant neurosurgeon Professor Bradley noted on 18 November 1970 that he had seen the reports of Dr Hardy-Smith and Dr Robertson, concluding that:[39]
‘The optic atrophy affecting the left optic nerve has not been explained and no treatment can be suggested. Whether or not, it is of long standing or whether it would be progressive cannot be stated.
I consider the prognosis indefinite. There is no evidence that the (R) optic nerve is being affected.’
[39] Ibid, p.68.
As a result of an increasingly restricted field of vision in his left eye and anosmia, Mr Wall was periodically reviewed by Medical Boards of Survey. Professor Bradley provided a report to assist the Board’s deliberations, stating on 9 July 1971 that:[40]
‘Atrophy in the left optic nerve has progressed and the field of vision is quite constricted. Also anosmia[41] persists. He is of course permanently unfit for sea duty but his visual acuity is good in the right eye and 6/12 with correction in left eye.
However anosmia precludes him from continuing as an electrician…
Vision will progressively deteriorate in the left eye.’
[40] Ibid, pp.73-74.
[41] The loss of sense of smell.
Professor Bradley provided a further report to the Medical Board dated 1 December 1971, stating in part:[42]
‘…All one can say is that this is probably a progressive condition and also that anosmia is likely to be permanent. He is unfit for sea duty but can, I believe do an efficient job in radio etc., providing he is working in company. He has a marked disability both physically and in relation to civilian employment.’
[42] Exhibit R2, p.83.
Mr Wall was again referred to consultant ophthalmologist Dr Hardy-Smith, who noted on 12 January 1972 that the problem with Mr Wall’s eyesight was stable at that time.
A referral by Surgeon Lieutenant D. Laing to consultant ENT surgeon Mr P. Freeman on 17 January 1972 states a diagnosis of ‘(L) Optic Atrophy, Anosmia’ noting:
‘This sailor has a complicated history beginning approx. 1969 at which time he noted problems with his (L) eyesight…’[43]
[43] Ibid, p.85.
Mr Freeman regarded Mr Wall’s anosmia permanent and that it rendered him ‘unfit for service at sea.’[44]
[44] Ibid, p.86.
Almost half a century later, a report by consultant ophthalmologist Dr Robert Nave dated 16 October 2015,[45] confirmed a diagnosis of ‘left optic atrophy, consistent with primary optic atrophy,’ and notes that the clinical onset of the condition was January 1969. Dr Nave’s report states in part:
‘A diagnosis of primary optic atrophy would suggest that the cause of the condition is unknown. There are very many predisposing causes to the development of optic atrophy, such as multiple sclerosis, neuromyelitis optica, trauma, trauma including optic nerve compression, ischaemia, glaucoma, etc. However in this case, there would not appear to be any known predisposing factor.’
[45] Exhibit R1, pp.76-86,
A further report by Dr Nave dated 16 August 2017 was accepted into evidence.[46] Dr Nave considers that Mr Wall’s service and medical history do not indicate a cause for left optic atrophy. He considers the four options contained in Associate Professor White’s report, the cricket injury and venereal disease as possible causes, but either dismisses those as being causes or considers them ‘highly unlikely.’
[46] Exhibit R9.
Dr Nave gave oral evidence at the hearing and was cross-examined. He said the words ‘primary’ or ‘idiopathic’ were interchangeable in describing Mr Wall’s optic atrophy, meaning that no cause was known. He said Mr Wall had mentioned becoming aware of his deteriorating vision in Vietnam during their consultation, but after considering the available records, he could not find any cause or predisposing factor. When asked to express an opinion about the two possible options referred to by Associate Professor White, Dr Nave said this ‘would have affected the other eye and optic nerve as well.’ When asked whether he had noted any evidence to support either of the possible causes proposed by Associate Professor White, Dr Nave stated: ‘I don’t think so. Extensive tests were done. The metabolic thing is guesswork.’ He agreed that the visual field defect in Mr Wall’s left eye may not have been initially picked up in January 1969 and wouldn’t have necessarily shown up if all that was being conducted was an acuity test. He said detection of optic atrophy depended on its stage of development and there were degrees of optic atrophy that could be very mild. When asked if Mr Wall had a visual field defect caused by optic atrophy during his operational service in early 1968, would it have been picked up, Dr Nave said he ‘certainly would have expected optic atrophy to have been picked up.’ When asked if it should have been picked up approximately 13 months later at the time of Mr Freshney’s examination in March 1969, Dr Nave responded it should have been picked up, but noted Mr Wall’s vision was assessed as ‘pretty good’ at that time. He couldn’t say that optic atrophy was not present in March 1969, but noted that ‘if vision was 6/6, then it may not have been investigated unless he was complaining about it.’ He said it was possible Mr Wall’s optic atrophy may have existed since February 1968.
During cross-examination, Dr Nave was asked about Associate Professor White’s views regarding an immune response or toxic cause. He replied that it may be a hypothesis that cannot be proven. He agreed that the surgery Mr Wall had undergone caused anosmia, which was a regrettably common complication. He also speculated that Mr Wall’s visual field defect could have been greater after surgery as a result of the blood supply in the eye being affected.
An MRI performed at Cabrini Health on 22 June 2016[47] and interpreted by Dr Ian Cox concludes:
‘There is focal encephalomalacia in the gyrus adjacent to the left optic nerve. This could be the sequelae of previous head injury, it could be the result of surgery if this gyrus were retracted in order to gain access to the adjacent optic nerve, or could be the sequelae of previous compression on the gyrus by tumour, e.g. meningioma. The left optic nerve is atrophic, with associated abnormal signal. The portion of the nerve immediately anterior to the optic canal is most severely abnormal, and definite integrity of the nerve cannot be confirmed. There is no dural thickening to suggest residual tumour, and no treated aneurysm is seen.
[47] Exhibit R1, p.131
Neurologist, Associate Professor Owen White, has penned four pieces of correspondence in relation to this matter as follows:
(a)In a letter dated 28 June 2016,[48] Associate Professor White states in part:
[48] Ibid, p.132.
‘…
The question arises as to the cause of his original visual loss rather than his final visual loss. It is speculation at this stage but may well have been environmental and toxic or otherwise immune and triggered by something in the environment. It cannot be determined with any certainty.
The only thing one can say with certainty, is that this occurred during his service in Vietnam. I’m happy to provide further opinions if required and if there are specific questions…’
(b)In a letter dated 7 July 2016 to Mr Wall’s RSL Advocate, Associate Professor Owen White states in part:
‘…
With regards to his original visual loss and its cause, rather than his final visual loss, it is speculative. It remains possible that he had several different causes including:
(1)Autoimmune optic neuropathy, possibly triggered by local environmental factors infection.
(2)Compressive neuropathy with the tumour not being identified at surgery.
(3)Local effective pathology that was cleared at the time and not recognised. This seems unlikely.
(4)Toxic optic neuropathy. This seems significantly less likely as such neuropathy is generally bilateral rather than unilateral.
I do note that he has been potentially, and possibly probably, two numerous toxic agents as listed in your letter. It remains possible that these have contributed to the development of an optic neuropathy but, as a direct cause they are unlikely to be responsible in the absence of bilateral disease.
Nonetheless, it is more than likely that a local organism or environmental agent has been involved in the triggering of an immune response. There is no doubt that such a patient would not be operated on in this day and age and a trial of steroid, in the absence of infection, would have been considered. It is not immediately clear that would have been the case at the time for surgery.
...
(c)At the request of the Applicant’s solicitor, Associate Professor White wrote on 18 September 2017 stating in part:[49]
‘…
In this situation, it is more appropriate to say that Mr Wall has idiopathic optic atrophy in no identifying cause was proven. It is important to be aware of the time and circumstances under which this occurs. The more such pathologies are investigated, the more there are causes for the optic atrophy and, primary optic atrophy is not a diagnosis by itself.
…
Most cases of “primary optic atrophy,” so-called, have been bilateral except in situations where there has been direct compression.
There is no doubt that there was an underlying cause for progressive visual loss as described in my original correspondence. There is equally no doubt that at the time, and under the circumstances, the available investigations would probably not have been adequate to try and identify the pathological entity.
That said, there was a substantial deterioration in vision after exploratory surgery.
It remains my opinion that primary optic atrophy is not a diagnosis and would be difficult to maintain. The name itself implies there is no cause for that degeneration in the nerve and this is improbable to the extreme. Identifying the cause of this distance of time is not possible but, given his circumstances, it is more than probable that his original condition was inflammatory or compressive and that the subsequent surgery resulted in devitilization and death of the optic nerve. It seems most probable that this was associated with events associated with his war service.
[49] Exhibit A3
Associate Professor White gave evidence at the hearing and was cross-examined. He said that primary optic atrophy is a descriptive term that was used in the 1970’s ‘in the absence of an identifiable diagnosis.’ He submitted Mr Wall’s condition could be characterised as ‘ideopathic optic atrophy,’ which was a ‘lovely way of masking total ignorance and means I don’t know.’ He said the word ‘ideopathic’ related to the fact that the precise cause of Mr Wall’s optic atrophy was unknown and that the term ‘atrophy’ conveys that ‘the optic nerve is sick,’ which could arise from a number of causes. Associate Professor White said the terms optic atrophy and optic neuropathy were used interchangeably, and a number of factors could cause it, including direct compression within the orbit of the eye, infective involvement of the optic nerve caused by parasites or bacteria, autoimmune optic neuropathy where antibodies caused inflammation of the optic nerve, metabolic abnormalities that could occur in one or both eyes, or small vessel disease.
Associate Professor White was taken through a number of potential causes for Mr Wall’s left optic atrophy. This included small vessel disease, which he said was very unlikely given Mr Wall’s age at the time, and the absence of diabetes or other co-morbid conditions. He said that in any event, this was usually painless and accompanied by sudden visual loss. He also considered that a fungal compression was an unlikely cause of Mr Wall’s optic atrophy, because patients often became progressively and profoundly ill from such a cause – often leading to death. Associate Professor White said he considered direct infective involvement of a parasite as being a ‘conceivable’ but unlikely cause, because he would have expected Mr Wall to be ‘sicker’ than the records suggest and the surgeon would have found evidence of infective involvement during surgery. Associate Professor White was asked about Dr Hardy-Smith’s reference to Mr Wall being knocked unconscious by a cricket ball at the age of 11 and whether this could have caused or contributed to the development of left optic atrophy. Associate Professor White said he ‘thought it was unlikely,’ but ‘couldn’t deny that possibility.’ During cross-examination, when asked again about this issue, he stated: ‘It’s a possibility not a probability. The other two are more probable.’
Associate Professor White stated that the tests conducted for eye problems in the 1960s and 70s were ‘much more rudimentary’ offering a ‘limited capacity to investigate.’ He said the surgery performed on Mr Wall in 1970 was in order to determine if a tumour may have been directly compressing his optic nerve. He believes the surgery ruled out such a cause and discovered nothing further relating to other potential causes. He noted that the surgery had nevertheless identified a ‘narrowing of the optic nerve fibres,’ confirming the integrity of the optic nerve ‘had been diminished.’ He considered there may have been some disturbance of blood supply to the optic nerve during surgery, which was a potential consequence of operating so closely to the optic nerve or its sheath. He believes the deterioration in Mr Wall’s eyesight in the months after surgery may have been a vascular event caused by some manipulation of the nerve or disruption of the blood supply, or perhaps the blood supply had already been compromised as a result of lower blood pressure under anaesthetic. In relation to Mr Wall’s anosmia, Associate Professor White said this was one of the more common nerves damaged with surgery in this area, which was a known risk and common complication, with ‘no surgeon’ able to say ‘they’ve never had that complication.’ In essence, the olfactory pathway was located above the nose, with nerves adhering to the frontal lobe, which, if manipulated during surgery, risked stretching or breaking the olfactory nerve roots.
Associate Professor White said that in light of the exclusionary process he had considered, the two possible causes he ‘can’t rule out’ were a ‘para infectious immune response or toxic episode of some sort.’ He said there were other possibilities, but considered these two ‘more probable.’ He said there was nothing in the material he had seen that changes his view in relation to these two possible causes. He said it was unlikely Mr Wall had significant myopia in January 1968 and explanations for why he says he could not facially-recognise shipmates on adjoining ships could have been that his ‘eyes were not lined up correctly’ or a ‘field defect.’ When asked to speculate on the most probable cause, Associate Professor White stated:
‘At this distance of time it is not possible to be absolutely conclusive, but it is something I would be concerned about.’
When asked again to provide his best assessment, Associate Professor White said he ‘couldn’t differentiate between a para infectious immune-related optic neuropathy or a toxic optic neuropathy,’ and that one of these is ‘more likely than the other causes he had considered.’ He believe onset had occurred during the 11-day period of Mr Wall’s operational service from 25 January – 5 February 1968. When I asked Associate Professor White how he was able to localise the possible causes he advances with onset to a precise 11-day period some 50 years ago, he stated it was entirely based on Mr Wall’s claim regarding first noticing a rapid deterioration in his vision during this period of operational service. Associate Professor White explained that ‘we doctors have a different level of evidence to the courts’ and he had inferred from Mr Wall’s claim about a visual disturbance during this 11-day period that this was ‘when the pathological process commenced.’
Associate Professor White was taken through the investigations undertaken in response to Mr Wall’s initial presentation in Australia in January 1969 and the subsequent diagnosis of a field defect in his left eye. He stated that ‘people can go through life with a field defect.’ He expressed concerns about the consistency of some medical records in Mr Wall’s SMR, including in places there was no record of Mr Wall’s uncorrected visual acuity. When asked about the timeliness of the diagnosis relating to Mr Wall’s field defect, he said it would have taken ‘time for a field defect to come on.’ He said the likely cause of Mr Wall’s progressively worsening eyesight at this time was a visual field defect and not his myopia. Associate Professor White opined that atrophy doesn’t develop quickly and ‘you won’t see it for two months from an acute lesion.’
During cross-examination, Associate Professor White was asked about some of the physicians who had treated Mr Wall during 1969-1972, describing Dr Robertson as a ‘one of the doyens of Australian neurology.’ He was also asked whether he agreed the cause of Mr Wall’s optic atrophy remained obscure, to which he replied: ‘Yes – there has to be doubt.’ When it was put to him that ‘we’re in the dark about the cause of Mr Wall’s condition,’ he replied: ‘Yes – we can make inferences, but without certainty.’ He was taken through Mr Wall’s evidence about consulting with an eye specialist in Hong Kong and being prescribed glasses, but stated that he ‘didn’t have enough information’ or the facts relating to Mr Wall’s visual acuity in February 1968.
Associate Professor White said there were circumstances where visual acuity could be corrected to perfect or near perfect vision, because what was being corrected was the central 2.5% of visual field. But someone with perfect vision in that narrow corrected field could still have a profound visual defect. Associate Professor White said if Mr Wall had long-standing optic atrophy at the time of his examination in March 1969, it would have been a ‘very poor physician not to notice it.’ He agreed that if left optic atrophy was present at this time, which was some 13-14 months after Mr Wall’s operational service, it should have been seen. He concluded therefore it was not present at that time. Associate Professor White was then taken a further 14 months forward in the available records to May 1970, which was some 28 months after Mr Wall’s operational service, where optic atrophy was first identified. He was asked if Mr Wall’s left optic atrophy had developed at some stage between 1969-1970 rather than in early 1968 at the time of his operational service. Associate Professor White responded:
‘Yeah – I would expect to see the optic atrophy certainly by 6 months.’
When asked if he could say when the onset of Mr Wall’s optic atrophy was, he replied:
‘I can’t say – the only marker I have is his visual complaints.’
During re-examination, Associate Professor White was asked if there was anything in the material he had been taken through that was inconsistent with onset of left optic atrophy while Mr Wall was on HMAS Stuart. He said it was not possible to be conclusive.
In response to questions about his two possible causes he had referred to for Mr Wall’s optic atrophy, Associate Professor White stated they were reasonable ‘on balance – clinically – not on certainty,’ and that ‘one of the two environmental causes’ he had referred to were ‘more likely’ than the other possible causes he had discussed.
Depressive Disorder

It was submitted by counsel for the Applicant and accepted by the Respondent, that the condition of major depressive disorder in this matter was consequential on the acceptance of Mr Wall’s left optic atrophy as being war-caused. I have considered the available evidence in relation to depressive disorder as follows:
(a)I note a medical record in Mr Wall’s SMR dated 20 November 1969, in which Surgeon Lieutenant P. Ainsworth diagnoses ‘Anxiety State’:
Upset, has a tendency to tears, agitated tremor, nail biting. Anorexic, insomnia, Apparently a situational anxiety / depression.
(b)10mgs of an unspecified drug was prescribed to Mr Wall in relation to this presentation, but no further reference is made in his SMR to any subsequent episodes.
(c)Immediately adjacent to this medical record is correspondence in Mr Wall’s SMR dated 7 November 1969, relating to Ministerial correspondence from a woman seeking to know Mr Wall’s blood group, on the basis that she suspected he was the father of her child. Mr Wall contends this issue was not the cause of his situational anxiety/depression at that time, insisting it resulted entirely from fears about his eye condition and future in the Navy.
(d)I note the report of psychiatry registrar Dr Margis at the Alfred in March 2006, approximately 35 years after Mr Wall’s discharge from the Navy, which refers to a two year deterioration in Mr Wall’s mental state. The issues encompassed in that report include family issues, work-related concerns, reference to a previous episode of counselling while a first year university student, and reference to a possible genetic vulnerability to depression and anxiety disorders.
(e)I note a report by consultant psychiatrist Dr Paul Collier dated 17 July 2015,[50] who met with Mr Wall on 10 June and 16 July 2015. Dr Collier’s report states in part:
[50] Exhibit R1, pp.87-93.
‘He states that his vision was perfect before 1969, but he began to experience problems in this regard in the first half of that year. He saw an eye doctor in Singapore and was prescribed spectacles. They did not help very much. He was eventually taken off HMAS Stuart and transferred to HMAS Albatross. He was worried about his sight and uncertain about what was going on. He was concerned about the potential impact on his career. Numerous medical tests were performed, but he reports that he was given minimal explanation about his situation.
A brain tumour was suspected. In this context he underwent a craniotomy at Epworth Hospital on 11 July 1970. He does not recall meeting the neurosurgeon, Professor Keith Bradley, until the day of the operation. No tumour was found. The operation left him with reduced peripheral vision, loss of the senses of smell and taste, and headaches. He has been diagnosed with optic atrophy, but cannot now state whether this problem, as such, develop before or after his cranial surgery….
…
The range, duration and severity of the above symptoms indicate that Mr Wall’s condition meets the diagnostic criteria for major depressive disorder, according to DSM IV…
…
The above history indicates that Mr Wall’s condition met the diagnostic criteria for alcohol use disorder, according to DSM 5, during his time at HMAS Albatross. His alcohol use disorder is still active today.
…
Mr Wall recalls seeing a clinician at HMAS Albatross as noted in the Daily Medical Record of 20 November 1969. He does not recall a great deal about this interaction. He does recall that he was worried and uncertain about his eyesight, and his career.
…
In 2006 he was assessed by Dr Marcus at the Alfred Hospital. He has taken Aropax, an antidepressants medication, ever since.
…
I have presented information above indicating that Mr Wall’s condition meets the diagnostic criteria for major depressive disorder according to DSM IV, and alcohol use disorder, according to DSM 5.
Mr Wall was assessed for psychological reasons at HMAS albatross in 1969 he was suffering from depressive and anxiety symptoms sufficient to attract the label of “anxiety/depression” at the time. I consider it appropriate to date the clinical onset of Mr Wall’s depressive disorder to that time of his life.
(f)I note a report by consultant psychiatrist Dr Gregor Schutz dated 27 August 2017.[51] Dr Schutz’s report states in part:
[51] Exhibit R5.
‘…
He stated that the issues in the military were with his eyesight. It deteriorated rapidly… He stated he thought his eye problem was related to the electromagnetic environment. He had surgery. He had left optic nerve atrophy and is blind on the left eye. He was medically discharged primarily because of anosmia (a lack of sense of smell) and lack of taste which he stated was the result of surgery. When he was discharged he felt that he was ‘kicked out before I died’ so that no one would become responsible. He stated that this drove him into a mess for 12 months…
…
… He denies any traumatic exposures in the Military…
In terms of his symptoms he stated that at the time he was discharged he had a bit of a meltdown. He had ups and downs. He was in the sickbay with anxiety. He felt everyone was against him. He felt upset because his performance was at a high level. He was drinking a lot. He felt let down… After a year he was able to get on with his life and “get back to basics”…
In terms of stressors over the years he denies any “exceptional issues”…He has been made redundant on three occasions… He was always able to find other jobs…
He reports that during his adult life he had no clinical depression until stressors in 2006 while working at Monash University. He stated that there were issues with his [family member]… He saw a psychiatrist at The Alfred. He was prescribed a medication Aropax (paroxetine), an antidepressant which he has continued on subsequently. He reports feeling easily offended and the people were against him. He reports around this time he had no confidence at work. He felt intimidated by managers and academics and is drinking increased. He stated that he had conciliation in relation to the workplace issues. He had a meltdown. He had some reduction in sleep, some ruminating, some low confidence and some difficulties with writing.
…
SUMMARY AND ASSESSMENT:
Mr Wall… was in the Military between 1964 and 1972. He was discharged reportedly on medical grounds in relation to anosmia and left optic atrophy. He reported subsequently becoming obsessed with this for a period of the year and then not reflecting on this until a few years ago. He continues to be resentful in relation to the manner in which he was discharged from the Military.
Mr Wall has had psychological difficulties over the years best characterised as intermittent depression or dysthymic disorder complicated by alcohol abuse. He is currently drinking at unhealthy levels and may meet the criteria for an alcohol use disorder. There is insufficient evidence that he is currently clinically depressed. There is no evidence of Post-Traumatic Stress Disorder, a personality disorder or psychotic disorder.
The causes of his depression have been multifactorial. He has resentment as to his perceived treatment by the Military around the time of his discharge. He attributes this to the development of optic atrophy and anosmia. It is beyond my scope to determine if the optic atrophy and anosmia were related to military exposures. He has also had periodic difficulties in his marital relationship as outlined in the report from 2006…. His alcohol consumption has been a major contributor to his mental health issues. His alcohol use disorder can be at most partially related to his Military exposure in terms of the reported drinking culture.
… His initial depression and alcohol use disorder commenced towards the end of his Military career.
There has been no incapacity for work. He has functioned at a high level for many years in the workplace including in a management role and then chose retirement several years ago.
Other Evidence
I note from Mr Wall’s SMR:
(a)The disabilities he listed on discharge were:[52]
[52] Exhibit R2, p.93.
‘(1) No smell.
(2) Left optic Atrophy. (Blind spot (L) eye)
(3) Long sighted.’
(b)In response to a question on his Discharge Medical Statement, Mr Wall lists the approximate date his ‘Left Optic Atrophy’ occurred as ‘Jan ’69.’[53] The question immediately following asks whether Mr Wall considered the condition was due to or had been aggravated by service, to which he responded: ‘possibly due to working conditions;
[53] Ibid.
(c)A service letter dated 27 October 1970 relating to a claim Mr Wall had made under the Commonwealth Employment Compensation Act 1930, states:[54]
[54] Ibid, p.100.
‘The cause of this sailor’s Left Optic Atrophy is most unlikely to have been due to the causes stated. D of T states that he would have only been exposed to ultraviolet light, and this would not cause optic atrophy but burns. There is no record of any retinal burning or its sequelae…
…
The cause of the (L) optic nerve atrophy has not yet been proven.’
(d)A service letter dated 24 February 1971, relating to Mr Wall’s anosmia, was provided in response to Mr Wall’s claim under the Commonwealth Employees Compensation Act 1930.[55] Consultant neurosurgeon Professor K. Bradley states:
‘The incidence of loss of smell depends entirely on the area investigated by craniotomy. In the case in question where the optic nerves were being explored, the incidence of post-operative anosmia would be high as the olfactory nerves are adjacent to the optic tracts and may suffer damage during exploration. Conversely where areas of the brain remote from the olfactory nerves are being explored the incidence of anosmia would be low.
In the type of operation performed in this case there is always an inherent risk of post-operative anosmia.’
(e)A service letter dated March 1972, referring to Mr Wall’s Left Optic Atrophy as ‘constitutional and not the result of naval service under the provisions of the Repatriation or C(CE) Acts.’[56]
(f)A Report of the Medical Board of Survey dated 2 March 1972 states:
‘Recorded Facts: This LEMP first presented with difficulty with vision in his (L) eye in Jan 69…’[57]
(g)Correspondence dated 1 June 1972 regarding Mr Wall’s discharge, states:
‘In June, 1970, after complaining that his distant vision had worried him for about two years…’
[55] Ibid, p.102.
[56] Ibid, p.109.
[57] Ibid, p.92.
TRIBUNAL’S DELIBERATIONS
Ms Spencer, counsel for Mr Wall, submits that the material before me points to a reasonable hypothesis connecting the onset of Mr Wall’s left optic atrophy with his 11-day period of operational service in early 1968. Counsel further submits that the visual defect in Mr Wall’s left eye ‘could have been missed’ until diagnosed over two years later in mid-1970. Ms Spencer said the Applicant relied on the two possible causes referred to by Associate Professor White, contending it was not necessary to identify a definite cause, just a hypothesis pointed to by the material before me that was reasonable.
Ms Spencer stated that atrophy takes time to develop and could have been ‘slowly progressive,’ which may explain why it may have been missed. It was put that other compelling evidence before me related to the glasses Mr Wall claims to have been given during the specialist consultation he says occurred in Hong Kong in February 1968, which ‘didn’t help.’ Moreover, there was a progressive worsening after he was given glasses in March 1969 to address his myopia. Ms Spencer said the likely explanation in the absence of any other, is that Mr Wall’s visual defect had first developed during the 1968 operational service when he claims to have first noticed a rapid deterioration in his vision. Although there were no service records available to support Mr Wall’s claimed eyesight deterioration in early 1968, or about the Hong Kong eye specialist consultation, Ms Spencer said this was because his service records were incomplete, which is evidenced by the absence of x-rays or results of the selection board he is alleged to have failed in 1967 because of his eyesight.
Ms Spencer said the consequences of Mr Wall’s surgery, subsequent anosmia and the implications for his career, caused him to suffer depression, That was because ‘he knew things were not right and were getting worse.’ She referred to SoP No. 83 of 2015 relating to Depressive Disorder, submitting that if Mr Wall’s left optic atrophy were found to be war-caused, his depressive disorder should consequently be accepted. Mr Rudge for the Commission agreed that if Mr Wall’s left optic atrophy was accepted by the Tribunal as war-caused, the Commission would not dispute that he suffered a consequential depressive disorder consistent with the requirements of the SoP.
In closing, Mr Rudge submitted there was a major problem with the hypothesis supported by Associate Professor White of two possible causes for Mr Wall’s left optic atrophy. He said there was no evidence in Mr Wall’s service records of an infection of the eye or exposure to a toxin– including during the 11-day period of operational service. Mr Rudge contended this was only ‘half a hypothesis,’ which did not causally-relate any infection or toxin exposure to that 11-day period of operational service. He said the conclusions of all the doctors were speculative at best and terms like ‘idiopathic’ or having no known cause, was an appropriate descriptor for the whole of the evidence in this matter. He said the material had to point to more than a possibility or assertion to take it beyond the realm of possibility, which it did not.
In considering the material before me, there is no reference in Mr Wall’s SMR or other service documents about:
(a)the initial report he claims to have made about his eyesight in early 1968 while HMAS Stuart was alongside in Hong Kong; or
(b)attendance at an eye specialist in Hong Kong who performed tests that determined the problem was with Mr Wall’s vision left eye alone and prescribed spectacles; or
(c)any outcome or follow-up in relation to that Hong Kong specialist appointment; or
(d)any reference to the above events in any of Mr Wall’s consultations with doctors in Australia from 1969 until his discharge, or in his medical claims on discharge, or in the initial compensation claims he lodged following discharge.
None of the doctors Mr Wall saw after his initial presentation with eye problems in Australia in January 1969, make any reference to the claimed presentation a year earlier. This is despite Mr Wall’s contention at the hearing that he believes he would have told these treating physicians about the 1968 presentation in Hong Kong. Ms Spencer submits that the SMR is incomplete, as evidenced, for example, by the absence of x-rays referred to in his service documents. But it is clear on the material before me that the clinical notes of Surgeon Lieutenant Norgate, Mr Freshney, Dr Hardy-Smith, Dr Robertson, and Professor Bradley relate to Mr Wall’s presentation with predominantly distance vision problems. The earliest recorded presentation in his SMR was a year after the acute onset Mr Wall claims he noticed during an 11-day period of operational service in 1968. Similarly, none of the available service records following surgery in mid-1970 refer to the claimed February 1968 presentation to an eye specialist in Hong Kong, but solely to a report of deteriorating vision in January 1969. This includes Mr Wall’s own claims about the date of onset (1969) in his Medical Statement on Discharge, and attribution of cause in that statement as ‘possibly due to working conditions.’
The earliest reference in the documentary material before me to a specific problem with Mr Wall’s left eye is Dr Hardy-Smith’s observation on 6 May 1970, that Mr Wall’s ‘left pupil reaction is definitely less well sustained than right.’ Approximately a month later, on 5 June 1970, Dr Robertson confirmed impairment of conduction in the lower half of Mr Wall’s left optic nerve, which was suspected to have been caused by a tumour or other lesion. This was over two years after Mr Wall claims a specialist in Hong Kong had first identified a specific problem with his left eye, for which there is no corroborating, subjective evidence in the material before me. Associate Professor White’s evidence is instructive in this regard. He agreed that if left optic atrophy was present in March 1969, which was some 13 months after Mr Wall’s operational service, it should have been seen. He agreed therefore it was likely not to have been present at that time. After being taken a further 14 months forward in the available records to May 1970, which was some 28 months after Mr Wall’s operational service, Associate Professor White was asked if Mr Wall’s left optic atrophy had developed at some stage between 1969-1970 rather than in early 1968 at the time of his operational service. He responded:
‘Yeah – I would expect to see the optic atrophy certainly by 6 months.’
When asked if he could say when the onset of Mr Wall’s optic atrophy was, he replied:
‘I can’t say – the only marker I have is his visual complaints.’
Primary Optic Atrophy - Left
Step 1: Hypothesis connecting Mr Wall’s left eye condition with war service?
In considering the specific circumstances of his case, I am mindful of the guidance in Meehan v Repatriation Commission,[58] where Wilcox J held that when considering the first stage as set out in Deledio, the Tribunal must consider ‘whether it is reasonably satisfied, pursuant to s 120(4), that there is a disease…as claimed.’ In Mr Wall’s case, I am reasonably satisfied on the medical evidence before me that he suffers from left optic atrophy.
[58] Meehan v Repatriation Commission [2001] FCA 597
I find there is no SoP in force for this condition or for the descriptive variations preferred by the specialists who gave evidence at the hearing, which they agree can be used interchangeably. I must therefore consider all of the material before me to determine whether it points to the hypothesis relied upon by Mr Wall, connecting his left optic atrophy with war service.
I acknowledge that no question of fact finding arises at this stage, but if no such hypothesis arises, the application must fail.
There is plentiful speculation in the material before me, as evidenced by the following extracts from the evidence (emphasis added):
(a)Professor Bradley, observed the optic nerve during craniotomy, stating after surgery that the cause of its atrophy ‘had not been explained.’ He could not say whether or not it was of long standing or progressive in nature. On 1 December 1971, Professor Bradley wrote that it was ‘probably a progressive condition;’
(b)Dr Robertson said ‘the cause of the optic atrophy remains obscure.’ He felt that compression from a neoplasm or destructive lesion in the optic nerve could have been the cause, or that it ‘might have been’ an arachnoid cyst. After surgery, Dr Robertson speculated on whether there was ‘a possible’ inherited or hereditary cause – Leber’s hereditary optic neuropathy was proposed;
(c)Dr Hardy-Smith opined on 18 November 1970 that the atrophy ‘may be’ long-standing and there was ‘a possibility…it may be related’ to the cricket injury Mr Wall had aged 11;
(d)More recently, consultant ophthalmologist Dr Robert Nave noted that the cause of the condition was unknown and while there were very many predisposing causes, in this case ‘there would not appear to be any known predisposing factor;’
(e)An MRI performed at Cabrini Health on 22 June 2016[59] and interpreted by Dr Ian Cox noted the presence of ‘focal encephalomalacia in the gyrus adjacent to the left optic nerve – again speculating that this ‘could be the result of surgery, or the sequelae of previous compression on the gyrus by a tumour, for example meningioma.
(f)Associate Professor White’s correspondence in relation to this matter, referring to the question of cause as ‘speculation at this stage’ - possibly environmental and toxic or otherwise immune and triggered by something in the environment. It cannot be determined with any certainty.’ In a similar vein, in a letter to Mr Wall’s RSL advocate dated 7 July 2016, Associate Professor White states that it ‘remains possible that there were several different causes.’ On 18 September 2017 he states that ‘no identifying cause was proven.’ His conclusion is qualified by the words: ‘Identifying the cause of this distance of time is not possible…’
(g)At the hearing, Associate Professor White submitted that his description of Mr Wall’s condition as ‘ideopathic optic atrophy,’ could also be interpreted as a ‘lovely way of masking total ignorance and means I don’t know.’ Associate Professor White considered a number of causes as conceivable but unlikely. Using an exclusionary methodology, he considered there were two possible causes which ‘couldn’t be ruled out,’ and that he considered ‘more probable’ than those excluded or considered unlikely. Associate Professor White said he ‘couldn’t differentiate between a para infectious immune-related optic neuropathy or a toxic optic neuropathy,’ and that one of these is ‘more likely’ than the other causes considered. He said that likelihood and reasonableness were founded ‘on balance clinically’ and not on legal certainty. Moreover, Associate Professor White’s conclusion that one of the possible causes he proposes had an onset coinciding with Mr Wall’s 11-day period of operational service some 50 years ago in 1968, was based entirely on Mr Wall’s contention that this was when he first noticed a deterioration in his vision. He had concluded on that basis alone, that this was ‘when the pathological process commenced.’
(h)Associate Professor White agreed that the cause of Mr Wall’s optic atrophy ‘remained obscure,’ and that we were ‘in the dark about the cause. Given that the diagnosis of a visual field defect in Mr Wall’s left eye was made approximately two-and-a-half years after Mr Wall’s operational service in 1968, Associate Professor White agreed during the hearing that left optic atrophy could have developed at some stage between 1969-1970 rather than in early 1968 at the time of his operational service.
(i)At the time of his discharge, Mr Wall himself opined that his left eye condition was ‘possibly due to working conditions.’ In a letter dated 27 October 1970 relating to a claim he had made under the Commonwealth Employment Compensation Act 1930, he relied at that time on possible exposure to ultraviolet light. At the hearing Mr Wall continued to believe ‘deep down’ that the cumulative effect of the electromagnetic environment he was exposed to during naval service was a causal factor.
[59] Exhibit R1, p.131

The material points to a possible onset of optic atrophy in Mr Wall’s left eye in January 1969, approximately a year after the brief period of operational service he relies upon. By 5 June 1970, impairment of conduction in the lower half of Mr Wall’s left optic nerve had been diagnosed and surgery performed soon after to explore what was suspected to be a cancerous cause. The surgery revealed existing atrophy of Mr Wall’s left optic nerve, but not a cause for it. In relation to cause, the material before me points in many possible directions. What it doesn’t do, however, is raise facts that point to a connexion between Mr Wall’s left optic atrophy and that 11-day period of operational service on HMAS Stuart some 50 years ago.
The material also does not point to other than appropriate clinical responses and management following Mr Wall’s presentation with eye problems in January 1969. The submissions advanced in the ASFIC that Mr Wall suffered atrophy of his left optic nerve ‘following the craniotomy,’ and that his ‘optic nerve was damaged in the surgery,’ is inconsistent with the surgical findings in 1970. Professor Bradley found the left optic nerve was already diminished when he observed it during surgery. Moreover, these submissions are inconsistent with counsel for the Applicant’s contention at the hearing that onset of left optic atrophy had occurred during operational service, some two-and-a-half years before Mr Wall’s surgery. The evidence before me points to an initial indication of problems with Mr Wall’s left eye during Dr Hardy-Smith’s examination in early May 1970, when he noted that the ‘left pupil reaction was less sustained than the right.’ Within a month, specialist Dr Robertson had diagnosed a problem affecting the left optic nerve and surgical investigation followed soon after.[60]
[60] Exhibit R2, pp.44-46.
Similarly, Associate Professor White’s evidence that a deterioration in Mr Wall’s eyesight after surgery in 1970 may have been a vascular event caused by manipulation of the optic nerve, or disruption of the blood supply, or perhaps due to the blood supply being compromised as a result of lower blood pressure under anaesthetic, rises no higher than speculation almost 50 years after the event. There is no doubt that the eyesight in Mr Wall’s left eye deteriorated after surgery, but the extent to which that may have resulted from or been contributed to by the surgery, or results from the unknown process that caused atrophy of his left optic nerve in the first place, is not able to be determined on the material before me. No submissions were made during the hearing regarding sub-optimal medical responses or treatment. Ms Spencer noted in her closing submissions that ‘no-one is suggesting anyone did anything wrong in the operation.’ Moreover, Associate Professor White’s evidence is that the anosmia suffered by Mr Wall during his surgery was commonplace, describing it as ‘a known risk’ that ‘no surgeon can say they’ve never had that complication.’ I am therefore satisfied beyond reasonable doubt that there is no sufficient ground for determining that Mr Wall’s left optic atrophy arose as a consequence of receiving medical treatment that could be regarded as deficient.
I find that no reasonable hypothesis has been raised connecting Mr Wall’s left optic atrophy with his operational service. I also find that the whole of the material before me does not support Mr Wall’s alternative hypothesis that he did not receive appropriate medical treatment. It is therefore not necessary to consider the subsequent Deledio steps, or to consider whether the depressive order claimed by Mr Wall was war-caused.
CONCLUSION
I acknowledge how worrying and difficult the consequences of Mr Wall’s left eye condition and anosmia must have been for him as a high performing young sailor. Based on periodic performance reports compiled at the time, he undoubtedly possessed qualities that would have been highly regarded in a Navy officer. He would also have experienced considerable stress from May-June 1970, when the potential seriousness of his left eye condition was diagnosed. His parents must also have been very concerned at the time, travelling from Western Australia to be with him when surgery was undertaken to investigate a possible cancerous cause. A common complication of such surgery is loss of smell, which had further devastating consequences for Mr Wall’s ability to continue his military career. Following discharge, it is to his great credit that he found work and undertook additional study and professional development. This enabled him to enjoy a 40 year working life after leaving the Navy, working as an economist and in managerial roles in the tertiary education sector.
Counsel for the Applicant submitted that Associate Professor White’s evidence supported the proposed hypothesis. But as held in Bey, my task is not to determine the existence of a hypothesis, but a reasonable hypothesis. Force must be given to the word ‘reasonable,’ which requires ‘more than a mere possibility.’ The evidence before me points to many possible causes for the atrophy in Mr Wall’s left optic nerve. Associate Professor White has used an exclusionary methodology to identify two possible causes he considers more probable than those rejected. He also connects onset of optic atrophy to a specific 11-day period of operational service some 50 years ago, purely on the basis of Mr Wall’s claim that this is when he first noticed a rapid deterioration in his vision. At the hearing, however, Associate Professor White agreed that if onset of left optic atrophy occurred at the time of Mr Wall’s operational service, he would have expected to ‘see the optic atrophy certainly by 6 months.’ The evidence before me shows that Mr Wall’s left optic atrophy was diagnosed in mid-1970, approximately 28 months after his operational service.
The proposed hypothesis is too tenuous and is therefore not reasonable. I am satisfied beyond reasonable doubt that there is no sufficient ground for determining that Mr Wall’s left optic atrophy, or the depressive disorder he says arose from it, was war caused.
DECISION
It therefore follows that the decision under review is affirmed.

98. I certify that the preceding 97 (ninety-seven) paragraphs are a true copy of the reasons for the decision herein of Senior Member A. Nikolic

[sgd]........................................................................
Associate
Dated: 7 June 2018

Date of hearing: 15-16 May 2018

Counsel for the Applicant:

Solicitors for the Applicant:

Ms Fiona Spencer

Ms Elle Kulesza, Williams Winter

Advocate for the Respondent: Mr Ken Rudge

TABLE 6A – MICROPHOTOGRAPHIC X-RAY
Date	Film No.	Spool No.	Examined at	Result	Inits of MO
21-2-68	633	55	TAMAR HK	N	[initials]