Hunt and Repatriation Commission (Veterans' entitlements)
[2016] AATA 554
•29 July 2016
Hunt and Repatriation Commission (Veterans' entitlements) [2016] AATA 554 (29 July 2016)
Division
VETERANS' APPEALS DIVISION
File Number(s)
2014/6051
Re
Mr Gordon HUNT
APPLICANT
And
Repatriation Commission
RESPONDENT
DECISION
Tribunal Mr Conrad Ermert, Member
Date 29 July 2016 Place Melbourne The Tribunal affirms the reviewable decision
...........[s[.............[sgd]..............................
Mr Conrad Ermert, Member
VETERANS AFFAIRS - Operational service - Hereditary Neuropathy with predisposition to Pressure Palsy (HNPP) - Carpal Tunnel Syndrome - whether caused by war-service - whether aggravated by war-service - satisfied beyond reasonable doubt - decision affirmed
Legislation
Veterans' Entitlements Act 1986
Cases
Bull v Repatriation Commission [2001] FCA 1832
Commonwealth Banking Corporation v Raymond William Percival 20 FCR 176
REASONS FOR DECISION
Mr Conrad Ermert, Member
29 July 2016
INTRODUCTION
Mr Gordon Hunt, the Applicant, served in the Australian Army from 21 February 1966 to 20 February 1972. He rendered operational service in Vietnam from 6 November 1969 to 6 May 1970. Mr Hunt’s duties in Vietnam were those of a cash office clerk.
On 21 December 2011 Mr Hunt submitted claims to the Repatriation Commission, the Respondent, for medical conditions to be accepted as war-caused disabilities. The conditions included tomaculous neuropathy, mild gastritis and carpal tunnel syndrome left wrist. On 14 May 2012 the Respondent rejected the claims. Mr Hunt applied to the Veterans’ Review Board (VRB) for a review of the Respondent’s decision. On 9 September 2014 the VRB affirmed the decision.
On 21 November 2014 Mr Hunt lodged an application for a review of that part of the VRB decision that relates to the condition of tomaculous neuropathy.
HEARING
Due to difficulties in arranging for the attendance of the two principal medical witnesses, the hearing was listed on two separate dates, 9 June and 21 June 2016. Ms Rachel Walsh of Counsel represented Mr Hunt. Mr Ken Rudge of the Department of Veterans’ Affairs represented the Respondent. I heard evidence from Mr Hunt, Dr Thomas Kraemer, Consultant Neurologist, and Associate Professor Brian Chambers, Consultant Neurologist.
I had before me the documents provided by the Respondent in accordance with section 37 of the Administrative Appeals Tribunal Act 1975 (the T-documents).
For Mr Hunt I took into evidence the following:
·Exhibit A1 – Statement of Gordon Edward Hunt dated 11 September 2015;
·Exhibit A2 – Report of Dr Thomas Kraemer dated 1 November 2011;
·Exhibit A3 – Report of Dr Thomas Kraemer dated 16 February 2012;
·Exhibit A4 – Report MRI Left Wrist of Ballarat MRI dated 17 April 2012;
·Exhibit A5 – Report Dr Thomas Kraemer dated 26 April 2012;
·Exhibit A6 – Report of Dr Timothy J Day dated 12 July 2012;
·Exhibit A7 – Report of Dr Thomas Kraemer dated 31 July 2012;
·Exhibit A8 – Report of Professor Garth A Nicholson dated 13 November 2014;
·Exhibit A9 – DNA Analysis report by Professor Garth Nicholson dated 13 November 2014;
·Exhibit A10 – Report of Dr Thomas Kraemer dated 29 May 2013;
·Exhibit A11 – Report of Dr Thomas Kraemer dated 9 March 2016; and
·Exhibit A12 – Paper titled Hereditary neuropathy with predisposition to pressure palsy by Dr Francisco Gondim and Dr Florian Thomas.
For the Respondent I took into evidence the following:
·Exhibit R1 – Transcript of the VRB hearing dated 9 September 2014;
·Exhibit R2 – Brendan G. O'Keefe and F.B.Smith, Medicine at War: Medical aspects of Australia's involvement in Southeast Asia 1950-1972 (Allen & Unwin in association with the Australian War Memorial, Sydney, 1994), title page and pages 180-187;
·Exhibit R3 – Wilson EJ, Horsley KW, van der Hoek R. Dapsone exposure and Australian Vietnam Service: Mortality and Cancer Incidence (Canberra: Department of Veterans’ Affairs, 2007), title page and pages i–3, 119-123 and 144-145;
·Exhibit R4 – Report of Associate Professor Brian Chambers dated 25 February 2015;
·Exhibit R5 – Report of Associate Professor Brian Chambers dated 18 November 2015; and
·Exhibit R6 – DNA analysis report by Professor Garth Nicholson dated 16 August 2012.
LEGISLATION
The relevant legislation is contained in the Veterans’ Entitlements Act 1986 (the Act).
ISSUES
Both parties agree that Mr Hunt suffers from the condition diagnosed as hereditary neuropathy with liability to pressure palsies (HNPP).
Mr Hunt contends that he suffers also from the separate condition of Carpal Tunnel Syndrome.
I must determine whether Mr Hunt’s HNPP and Carpal Tunnel Syndrome are war-caused within the meaning of the Act.
EVIDENCE
Mr Hunt
Mr Hunt confirmed the following facts contained in his statement dated 11 September 2015:
·he served in Vietnam from 6 March 1969 to 6 May 1970;
·he was in Nui Dat from November 1969 to March 1970;
·he was in Saigon from March to May 1970; and
·he was employed as a clerk in the cash office.
Mr Hunt stated that, as part of his duties in Vietnam, he used an adding machine. He said the machine had mechanical keys which he had to push hard. He then had to pull a handle with his left hand to enter the transaction. He estimated that he would pull the handle more than 50 times every hour. He said that while he was stationed in Nui Dat he used the adding machine between four and six hours per day. When he was in Saigon he used the adding machine up to eight hours per day. He said he worked seven days per week in both locations. Mr Hunt said he has not used an adding machine since leaving Vietnam.
Mr Hunt described the webbing he wore each day on his way to and from his place of work. He said it comprised a waist belt with braces over each shoulder, joined at the back below the neck. Attached to the belt were two water bottles and pouches containing 200 to 300 rounds of ammunition. Mr Hunt said the webbing weighed approximately 10 kilograms. At Nui Dat he would wear it while walking about 200 metres each way. In Saigon he would wear it while travelling in the back of a truck for about half an hour each way. He said he would be wearing the webbing when he jumped off the back of the truck, a height about a metre and a half. He said the webbing was not comfortable. Mr Hunt said he had not worn webbing since leaving Vietnam.
When asked whether he experienced symptoms of HNPP while in Vietnam Mr Hunt said he would wake up with the feeling of pins and needles in his hands, mainly his left hand. He said the feeling would last for hours. He first noticed the symptoms in Nui Dat. They occurred infrequently and would gradually go away. He said they later became a permanent symptom.
Mr Hunt described two specific incidents of paralysis in his left arm and right leg. The first incident was in May 1970. On waking up his left arm was paralysed. He sought treatment on his first day back from leave. The symptoms gradually improved but then he suffered the second incident in August 1970. This time his right leg was affected as well as his left arm. He had difficulty walking and could not drive the car. He sought treatment from a medical centre.
Mr Hunt said he could not relate either incident to any activity. He specifically denied the suggestion in the report of Professor Chambers that he had been binge drinking. He said that on the first occasion he had been staying with his future in-laws and on the second occasion he was travelling at the time.
Under cross-examination Mr Hunt corrected his statement regarding the pins and needles sensation saying that the feeling was not “infrequent” but did not occur in a regular pattern. He agreed that he had them before going to Vietnam but they lasted for only minutes. He agreed that he had suffered paralysis in his leg for three days at age seven when he had the measles. He said he had had no similar problems from that time to 1966.
Asked about his activities at Nui Dat, Mr Hunt stated that he participated in two or possibly three clearing patrols. He said he generally worked seven days per week with occasional days off. He worked eight to 10 hours per day at Nui Dat with breaks for morning and afternoon tea and lunch.
Turning to the use of Dapsone, Mr Rudge referred Mr Hunt to the document Medicine at War (page 187) which recorded that an order was issued on 10 February 1970 that all Australian Forces in Vietnam were to stop taking Dapsone. Mr Hunt stated that he was working in a very small unit and they were unaware of the order. He and others just continued to take their Dapsone daily on a self-help basis. The Dapsone was stored in a steel cupboard and was readily available.
Asked whether he took Dapsone while in hospital from 10 April 1970 to 4 May 1970 Mr Hunt said he could not say, as he was taking a lot of medications at the time.
In regard to his employment after his discharge from the Army, Mr Hunt said he worked in various jobs, including selling cars and at Woolworths. He came to Victoria in 1975 and worked in a domestic timber yard until the mid-1980’s; after which he became an assessor in the timber industry. He agreed he had good strength and balance but said he started to deteriorate in the 1990’s. He ceased his work as a trainer in 2003. Mr Hunt agreed that he had served in the Country Fire Authority but ceased operational duties in the early 1990’s. He continued to instruct in the use of chain saws until March 2011.
In re-examination, Mr Hunt stated that while in Vietnam he frequently woke up with pins and needles. He said that he never fully recovered the strength in his left arm after his second incidence of paralysis.
Dr Kraemer
Dr Kraemer described HNPP as being a genetically induced neuropathy affecting the PMP 22 gene which maintains the myelin around the nerves. The history he obtained from Mr Hunt was that in 1970 Mr Hunt had the pins and needles sensation in his left arm; he had a paralysis in his left arm and later a paralysis in his left arm and right leg. He said the pins and needles indicated a motor weakness and might be a symptom of HNPP.
Dr Kraemer agreed it was probable that wearing webbing twice a day weighing approximately 10 kilograms and involving jumping from a truck could bring on symptoms of HNPP. He agreed also that using an old-style adding machine eight hours a day and seven days a week could bring on such symptoms. He said that each activity would aggravate the condition. It was a high probability that the activities described would add to the condition.
Asked to comment on the time delay between Mr Hunt ceasing to take Dapsone and the first incidence of paralysis, Dr Kraemer said that after stopping the drug the condition does not get worse but the residual damage remains. His advice to patients with HNPP is to avoid abnormal activities and be careful with medications.
Asked whether any of Mr Hunt’s activities would be associated with Carpal Tunnel Syndrome, Dr Kraemer nominated the use of the adding machine; particularly as the old machines required more force to operate the keys and the lever. Asked about an association between Mr Hunt’s HNPP and his Carpal Tunnel Syndrome, Dr Kraemer said that Mr Hunt’s nerves were more vulnerable and highly susceptible.
Dr Kraemer said that the nerve conduction studies and the DNA analysis confirmed the diagnosis of HNPP.
Dr Kraemer affirmed his opinions reported in Exhibits A10 and A11, that HNPP can be worsened by exposure to neurotoxins. Referred to the paper Hereditary neuropathy with predisposition to pressure palsy by Dr Francisco Gondim and Dr Florian Thomas, Dr Kraemer agreed with the following statements:
·“the condition may occasionally be revealed in later life when individuals develop an acquired unrelated neuropathy due to metabolic derangements, autoimmunity, or neurotoxic drugs”;
·“In typical HNPP, motor symptoms predominate over sensory symptoms. Patients often report that after resting on a limb in an awkward position, the resulting weakness and dysesthesias last weeks to months, rather than seconds to minutes”;
·“Most attacks are of sudden onset, painless, and initially followed by recovery”;
·“Precipitating trauma, such as carrying heavy loads, writing, or playing musical instruments”;
·“Del Colle and colleagues (Del Colle et al 2003) reported carpal tunnel syndrome without episodes of nerve palsy as the presentation in a PMP22 deletion family”;
·“HNPP rarely presents in childhood”;
·“Secondary preventive measures focus on education and awareness and avoidance of … neurotoxic drugs”;
·“It is important to prevent, look for, and treat acquired neuropathies as well as avoid compression neuropathies”; and
·“Patients, family members, and physicians need to be aware of drugs and vitamin supplements that can affect the peripheral nervous system. Drugs and vitamins with various degrees of neurotoxicity include the following: … Dapsone …”.
Dr Kraemer agreed that the report had been written by experts and he had no reason to disagree with it.
Asked about Mr Hunt’s paralysis when aged seven, Dr Kraemer said it was likely to have been a spinal condition related to the measles.
Referred to the Executive Summary of the report Dapsone Exposure, Vietnam Service and Cancer Incidence Dr Kraemer agreed with the statement “Adverse reactions to its use include … peripheral neuropathy”.
Ms Walsh referred Dr Kraemer to the report of Professor Chambers dated 25 February 2015 which recorded:
·The question arises whether Army Service was responsible for development of pressure palsies in a genetically predisposed individual. It is interesting that when he first presented with pressure palsies in June 1970 and August 1970, he woke up with paralysed limbs on those two occasions. It is more than likely, that around that time when he was binge drinking, he fell asleep in a drunken state, sleeping so heavily that he developed the pressure palsies.
Dr Kraemer said the Mr Hunt’s nerve roots were susceptible to pressure whether drunk or not.
Referring to the report of Professor Chambers dated 18 November 2015, Dr Kraemer disagreed with the report saying:
·There is evidence that HNPP can be aggravated by Dapsone;
·Mr Hunt’s peripheral neuropathy became clinically significant in the 1990’s; and
·A relationship with Dapsone is likely.
Under cross-examination, Dr Kraemer said that when he first saw Mr Hunt he did not think he had Carpal Tunnel Syndrome. Dr Kraemer said he referred Mr Hunt to Dr Day with suspected HNPP. Mr Rudge asked if Carpal Tunnel Syndrome is a separate condition. Dr Kraemer said the HNPP contributes to Carpal Tunnel Syndrome which is part of HNPP. He added that HNPP sufferers have a greater incidence of Carpal Tunnel Syndrome.
Mr Rudge asked Dr Kraemer a number of questions arising from the paper on HNPP by Dr Francisco Gondim and Dr Florian Thomas. Dr Kraemer responded as follows:
·The onset of HNPP can be at any age;
·The onset is insidious;
·The effect often occurs after sleeping with a limb in an awkward position;
·The effect can last for weeks and months; and
·Minor everyday activities can bring on the effects.
Mr Rudge suggested that it was unlikely that wearing 10 kilograms of webbing to and from work would constitute the heavy loads referred to in the paper. Dr Kraemer said that carrying heavy loads during his previous training may have been involved as Mr Hunt had a predisposition to HNPP. Dr Kraemer agreed that general activities can bring on pressure palsies but heavier loads bring them on more often.
Mr Rudge asked if it was normal that peripheral neuropathy does not occur until later in life. Dr Kraemer said that the condition may not be clinically confirmed even though the nerves are already struggling. Mr Rudge put to Dr Kraemer that Mr Hunt had had a long working life after his Vietnam service, including working in timber yards, becoming a trainer, serving in the CFA and instructing in the use of chain saws. Mr Rudge asked if Mr Hunt’s condition differed in any way from the normal progression of the disease. Dr Kraemer said the Mr Hunt had pressure palsies during his time in the Army and he took Dapsone. Dr Kraemer said the clinical symptoms were just the tip of the iceberg. He opined that Mr Hunt’s nerves were already struggling but his Army activities put extra pressure on the nerves and, in addition, he took Dapsone.
Professor Chambers
Referring to his report dated 25 February 2015, Professor Chambers confirmed the diagnosis of HNPP. He said it was a hereditary condition which carried an underlying ability to develop pressure palsies such as Carpal Tunnel Syndrome, and other neurologies. He said that pressure palsies can occur with anybody, such as from sleeping awkwardly. Those with HNPP were more vulnerable. As there was some bruising from repeated actions, it could take weeks or months to resolve. However, the palsies usually did resolve.
Professor Chambers said that peripheral neuropathy was a more generalised condition. In regard to Mr Hunt’s condition, he said that Mr Hunt had episodes of pressure palsies but his symptoms of peripheral neuropathy started in the 1990’s. He said there was nothing remarkable about Mr Hunt’s condition. It fitted within the common history of peripheral neuropathy. Asked about the investigations into Mr Hunt’s condition, he noted the report of Dr Day dated 12 July 2012 and said that the findings relating to the median and ulnar nerves at the wrists supported the diagnosis of HNPP. Professor Chambers said that the DNA analysis made the diagnosis of HNPP 100 per cent certain.
Asked about Charcot-Marie-Tooth Disease (CMT Disease), Professor Chambers said it was different from and distinguished from HNPP. He said CMT Disease presents between 20 and 30 years of age, with a wasting of the lower legs, spreading upwards causing a swelling commonly referred to as champagne bottle legs. The disease then causes a weakness of the arms and forearms.
Professor Chambers recorded the pressure palsies which occurred a month after Mr Hunt returned from Vietnam as the earliest signs of HNPP. Mr Rudge asked if the wearing of webbing with 10 kilogram loads to and from work, the jumping off the truck and the use of the adding machine would be causal factors for HNPP. Professor Chambers said:
·they were probably co-incidental;
·the palsies appeared after Mr Hunt had left Vietnam; and
·back packs can cause pressure palsies but they present differently, affecting the shoulder girdle not the peripheries, as in this case.
In regard to Carpal Tunnel Syndrome, Professor Chambers said that Mr Hunt’s pins and needles in Vietnam could have been the earliest manifestation of Carpal Tunnel Syndrome. He said that people with HNPP are more susceptible to Carpal Tunnel Syndrome. He agreed that the use of the adding machine could be a contributory factor for people with HNPP. Asked whether pressure palsies would be contemporaneous with the use of the adding machine, Professor Chambers said it was possible but they were not always apparent for people with HNPP.
Asked about the possible effects of Dapsone, Professor Chambers said the proposition was extremely tenuous, just speculation. He said Dapsone can cause generalised symmetrical peripheral neuropathy affecting motor functioning but not sensory functions. He added that people usually recover when they stop taking Dapsone. They do not develop peripheral neuropathy decades later. He is not aware of any evidence linking Dapsone with pressure palsies.
Professor Chambers agreed with Dr Kraemer that pressure palsies could be linked with Army service but they would not connect with peripheral neuropathy 20 years later. Professor Chambers said Mr Hunt’s HNPP had not been made worse by his Army service as Mr Hunt had recovered from each episode of pressure palsy. Professor Chambers said he disagreed with Dr Kraemer’s statement in the report of 9 March 2016, that Mr Hunt’s exposure to Dapsone can contribute to the worsening neuropathy, similar as in CMT.
Professor Chambers said he was not familiar with the report on HNPP by Dr Gondim and Dr Thomas. He did not agree that all the drugs listed in the report were causative of the condition. He said that, for people with the underlying condition, the drugs may make the condition worse. He agreed with the statements in the report that the onset of the neuropathies typically occurs during a person’s third or fourth decade. He agreed that common, everyday activities can bring on pressure palsies.
Asked to comment on Dr Kraemer’s opinion that the condition is made worse by each incident, Professor Chambers said that was a difficult question. In the long term it may be true and nerve conduction studies may find residual changes. Given that Mr Hunt had had a full working life with good strength and balance during it, Professor Chambers said Mr Hunt may have had some subtle residual effectZs, but any worsening of the condition from that of 1969 and 1970 was fairly trivial.
Under cross-examination, Professor Chambers agreed that he met Mr Hunt on only the one occasion. In preparing his report he relied on the Service records, the clinical records and the clinical history given by Mr Hunt. Professor Chambers said that his observations from the physical examination all showed signs of peripheral neuropathy with sensory deficit.
Professor Chambers agreed that at the time of preparing his report he was not aware of the details of Mr Hunt’s post-service employment including his work as a car salesman, a supermarket manager, that his work in the timber industry involved working in a domestic timber yard, and as a trainer and assessor.
He said he was aware that Mr Hunt worked in a cash office while in Vietnam but he agreed that he was not aware of the details of his activities. His knowledge of Mr Hunt’s activities in Vietnam is confined to what is included in the report. He was not aware of Mr Hunt’s wearing webbing with 10 kilogram loads and jumping one and a half metres off a truck twice a day.
Professor Chambers was questioned about the basis for his statement It is more than likely, that around that time when was binge drinking, he fell asleep in a drunken state, sleeping so heavily that he developed the pressure palsies. He agreed that it was his own conclusion from what he thought was most likely.
Professor Chambers was asked about the statement in his report that Military service is relevant. He said that Mr Hunt may have done something that aggravated the condition. Professor Chambers was told that Mr Hunt’s evidence was that he operated an old adding machine left-handed on a repetitive basis four to ten hours per day. He agreed that such an activity could well cause neuropathy considering Mr Hunt’s pre-disposition to the condition.
At the time of preparing his report Professor Chambers was not aware of the studies on the effects of Dapsone, nor of the report by Dr Gondim and Dr Thomas.
In re-examination, Professor Chambers agreed that Mr Hunt’s repetitive use of his left hand to operate the adding machine could be related to the reported median compression and could be related to Carpal Tunnel Syndrome. Professor Chambers was asked about the reported incidents of weak left hand in June 1970 and paralysed left forearm and right foot in August 1970. He said they were atypical of Carpal Tunnel Syndrome but could be pressure palsies.
Professor Chambers was asked about the significance of his examination findings of bilateral effects. He said that they were indicative of symmetrical peripheral neuropathy. He said the finding of subtle wasting of the left hand was not related to Carpal Tunnel as it involved the ulnar nerve. He said it was the result of pressure, commonly from leaning on the left elbow.
Professor Chambers agreed he had heard no history of the webbing worn by Mr Hunt in Vietnam but he did not think it was relevant to Mr Hunt’s conditions. Had there been an effect, he would have expected to see a different type of pressure palsy.
TRIBUNAL CONSIDERATION
Section 9(1) of the Act states relevantly that an injury suffered by a veteran or a disease contracted by a veteran shall be taken to be war-caused 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;
…
(e)The injury suffered, or disease contracted, by the veteran:
(i) Was suffered or contracted while the veteran was rendering eligible war service, but did not arise out of that 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;
The standard of proof to be applied in the case of operational service is prescribed in section 120(1) of the Act which states relevantly:
Where a claim under Part II for a pension in respect of the incapacity from injury or disease of the veteran … relates to the operational service rendered by the veteran, the Commission shall determine that … the disease was a war-caused disease … unless it is satisfied, beyond reasonable doubt, that there is no sufficient ground for making that determination.
Section 120(3) states relevantly:
In applying subsection (1) … 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 … ;
(b)That the disease was a war-caused disease …; or
(c)…
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.
In this matter two conditions are in contention: HNPP and Carpal Tunnel Syndrome. I will consider each condition in turn.
HNPP
Ms Walsh contends that Mr Hunt’s HNPP arose out of or was attributable to his operational service satisfying section 9(1)(b) of the Act. In the alternative, Ms Walsh contends that his HNPP was contributed to in a material degree or was aggravated by his operational service satisfying section 9(1)(e) of the Act.
Ms Walsh submits that the evidence points strongly to a reasonable hypothesis connecting the condition with Mr Hunt’s operational service. She refers to the evidence of Dr Kraemer that the use of the adding machine in the way described, wearing the webbing including when jumping off the truck, and taking Dapsone brought on the symptoms of the HNPP disease, thus aggravating the underlying condition.
Mr Rudge contends that the HNPP was neither caused nor aggravated by operational service.
In considering whether the hypothesis is reasonable, I turn first to section 120A which provides for the determination of the reasonableness of hypotheses by reference to Statements of Principles (SoP). Section 120A(3) provides that an hypothesis is reasonable only if there is in operation an SoP that upholds the hypothesis. However, subsection (4) states that subsection (3) does not apply in relation to a claim in respect of the incapacity if the Authority has not determined an SoP in respect of the relevant injury or disease.
Ms Walsh acknowledges that there is no specific SoP for HNPP but urges the Tribunal to consider HNPP as analogous to CMT Disease, for which there is an SoP. SoP No.21 of 2015 relates to CMT. It defines CMT as one of a group of genetic disorders of myelin structure or function, characterised by distinct peripheral neuropathies which are manifested clinically by muscle atrophy, weakness and sensory abnormalities.
In his report dated 9 March 2016, Dr Kraemer states that HNPP is a demyelinating congenital illness with effects on the myelin similar to Charco-Marie-Tooth. Although they are different in regards to the genetic defect, the genetic defects in both condition affects the PMP22 gene... In his oral evidence, Professor Chambers said CMT was different from and distinguished from HNPP. He confirmed the statement in his report dated 18 November 2015, that HNPP is the deletion of the PMP22 gene whereas CMT disease is due to the duplication of the PMP22 gene. He gave evidence of clinical symptoms clearly distinguishable from those of Mr Hunt.
From the medical evidence, I am satisfied that HNPP is different from CMT Disease and is not included within the provisions of SoP No.21 of 2015. I find that there exists no SoP in respect of HNPP. As a result, I must apply section 120A(4) of the Act and apply the standard of proof provided for in sections 120(1) and 120(3) of the Act.
Section 9(1)(b)
In considering whether the HNPP disease arose out of or was attributable to Mr Hunt’s operational service (section 9(1)(b) of the Act), I note the following medical evidence:
·Report of Dr Kraemer dated 29 May 2013 which records:
Genetic testing positive for hereditary neuropathy with propensity to pressure palsy.
·Report of Professor Nicholson dated 16 August 2012 which records:
The deletion of the peripheral myelin protein 22 gene (PMP22) is most probably the cause of Hereditary Neuripathy with Liability to Pressure Palsies in this patient. This mutation is inherited as an autosomal dominant trait.
·Report of Professor Nicholson dated 13 November 2014 which records:
In conclusion, Mr Hunt has a genetic predisposition pressure palsy but he does not have a familial condition. … In this case, environmental factors such as pressure precipitate the disorder.
·Report of Professor Nicholson dated 13 November 2014, DNA Analysis for HNPP and CMT, which records:
The result confirms a diagnosis of Hereditary Neuropathy with Liability to Pressure Palsies in this patient … The HNPP deletion is inherited as an autosomal dominant trait.
·Report of Professor Chambers dated 25 February 2015 which records:
Mr Hunt is suffering from hereditary neuropathy with liability to pressure palsies …Hereditary neuropathy with liability to pressure palsies is genetically determined. Despite there being no family history of the condition, Mr Hunt has the genetic mutation, which was present at birth.
·Report of Dr Kraemer dated 9 March 2016 which records:
In my opinion, his hereditary neuropathy with pressure palsy, although congenital, has been brought on and worsened by his time serving with the Army.
.
Both parties agree that the diagnosis of the condition is HNPP caused by the deletion of the PMP22 gene. Professor Nicholson’s reports, with which Dr Kraemer and Professor Chambers agree, state that Mr Hunt’s HNPP is a genetic predisposition and inherited. Professor Chambers states that Mr Hunt’s genetic mutation was present at birth. Dr Kraemer states that the condition is congenital.
I am satisfied from the medical evidence that Mr Hunt’s HNPP was congenital, inherited and present at birth. There is no material that points to the condition arising out of or being attributable to Mr Hunt’s operational service.
As a result, I am satisfied beyond reasonable doubt that there is no reasonable hypothesis that Mr Hunt’s HNPP arose out of or was attributable to his operational service. I find that section 9(1)(b) is not satisfied in regard to HNPP.
Section 9(1)(e)
Section 9(1)(e) requires consideration of whether the disease, in this case HNPP, was contributed to in a material degree by, or aggravated by, any eligible war service rendered by the veteran.
The hypothesis contended for Mr Hunt is that the use of the adding machine, the wearing of the webbing, including when jumping off the trucks, and the taking of Dapsone brought on the symptoms of the HNPP disease, thus aggravating the underlying condition. Ms Walsh contends that the symptoms of a disease are a part of the condition. She contends that in this case the war-service aggravated, or contributed to in a material degree, the symptoms of HNPP, thus aggravating or contributing to the HNPP in a material degree. In support of this contention, Ms Walsh refers to the judgement of the Federal Court in Re Commonwealth Banking Corporation v Raymond William Percival [1988] 20 FCR 176, in which their Honours said at paragraph 11:
No doubt, for many medical purposes, it is useful and often necessary to distinguish between the underlying pathology of a disease and mere symptoms of the disease. For some legal purposes, eg. s.104(2) of the Act, the distinction is also pertinent. … But that is not to say that the symptoms of a disease are not a part of the disease. It is indeed fundamental to compensation law that a symptom of an injury or disease is a part of the condition in respect of which compensation for incapacity is granted.
In contrast, Mr Rudge contends that symptoms are not evidence of the worsening of an underlying disease. He referred to the judgement of the Federal Court in Re Repatriation Commission v Darryn Paul Yates [1995] FCA 1234 (1995) 21 Aar 331, (1995) 38 ALD 80. Mr Rudge referred me to the following passages from Justice Lindgren’s reasons for the decision:
41. Symptoms worsened by service activity may or may not, depending on the medical evidence, be evidence of a defence-caused aggravation of the underlying injury or disease. …
42. … Those passages recognise that an occurrence or worsening from time to time of symptoms caused by work or service may not compel an inference that there has been an aggravation, caused by work or service, of a pre-existing disease.
…
45. … I think it was seeking to emphasise the Act’s insistence that an aggravation be of an injury or disease and that this is not necessarily indicated by a temporary worsening of the symptoms with consequential temporary incapacity. Like the AAT in Heaps’ case, I would expect, in the absence of medical evidence to the contrary, that an aggravation of an underlying disease would have a duration at least longer than the period of worsening of symptoms caused by service, although it may not necessarily be as long as the duration of the disease itself. …
…
47. In my view the AAT was distracted from addressing the question whether there had been aggravation of Yates’ spondyloarthritis as distinct from a temporary worsening of symptoms.
I conclude from these citations that I must determine whether or not Mr Hunt’s HNPP has been contributed to in a material degree by or aggravated by his operational service; and that, depending on the medical evidence, symptoms worsened by Mr Hunt’s service activities may be evidence of a war-caused aggravation of the condition.
Dr Kraemer’s oral evidence is that wearing webbing with 10 kilogram loads twice a day, including while jumping off the back of a truck, and using an old-style adding machine can bring on the symptoms of HNPP. He said that each activity aggravates the disease and adds to the condition and that heavier loads bring on the condition even more.
In regard to Mr Hunt’s taking of Dapsone, Dr Kraemer said the drug can affect the functioning of the nerves. He added that after ceasing taking the drug the condition does not get worse but the residual damage remains.
Asked by Mr Rudge whether the progression of Mr Hunt’s HNPP was any different from the normal progression of the condition, Dr Kraemer said that Mr Hunt experienced the pressure palsies during his Army service and that he had been exposed to Dapsone. Dr Kraemer said that the clinical symptoms are the tip of the iceberg. He said the Mr Hunt’s nerves were already struggling from the HNPP and his Army service put extra pressure on his nerves.
In contrast, Professor Chambers said that there was nothing remarkable about the history of the development of Mr Hunt’s HNPP. When asked to comment on Dr Kraemer’s proposition, that each occasion of pressure made the condition worse, Professor Chambers said It is a difficult one. In the long term it may be true. One may find residual changes from nerve conduction studies. Asked if there was any evidence of the worsening of Mr Hunt’s condition, Professor Chambers said “he may have had some subtle residual effects … fairly trivial”.
Asked about the possibility of Dapsone affecting HNPP, Professor Chamber said that any connection was extremely tenuous, speculation. He said that people usually recover when they stop taking Dapsone and do not develop peripheral neuropathy decades later. Professor Chambers agreed that when preparing his reports he was not aware of the paper on HNPP by Dr Gondim and Dr Thomas. When asked to comment on the inclusion of Dapsone in the list of drugs that can affect the condition Professor Chambers said they are not causative of the condition but they may make the condition worse for people with an underlying condition.
Section 120(1) of the Act requires me to find that the condition has been aggravated by Mr Hunt’s war-service unless I am satisfied, beyond reasonable doubt, that there is no sufficient ground for making that determination. Section 120(3) of the Act requires me to be satisfied, beyond reasonable doubt if, after considering the whole of the material before me, I am of the opinion that the material does not raise a reasonable hypothesis connecting the disease with the circumstances of Mr Hunt’s service.
In considering the reasonableness of the hypothesis, I am conscious of the finding of the High Court in Re Bushell v Repatriation Commission [1992] HCA 47; (1992) 175 CLR 408 (7 October 1992) in which their Honours said “… the case must be rare where it can be said that a hypothesis, based on the raised facts, is unreasonable when it is put forward by a medical practitioner who is eminent in the relevant field of knowledge. Conflict with other medical opinions is not sufficient to reject a hypothesis as unreasonable”.
However, I note also the finding in the judgement in Re Bull v Repatriation Commission [2001] FCA 1832, where Justice Moore wrote at paragraph 5:
… The law presently is that it is not sufficient that the material raise a hypothesis. In addition the hypothesis, to constitute a “reasonable hypothesis” for the purposes of s120, must be one to which the material points: see East v Repatriation Commission [1987] FCA 242 (1987) 16 FCR 517 at 533.
In regard to the hypothesis that the wearing of the webbing and the use of the adding machine aggravated the HNPP Ms Walsh submitted the following material:
·the evidence of Mr Hunt’s symptomatic episodes in May and August 1970;
·Mr Hunt’s evidence that the weakness in his left arm did not fully resolve after his May paralysis; and
·the paper by Dr Gondim and Dr Thomas which, on page 3, includes carrying heavy loads and playing musical instruments as precipitating trauma.
I note however that Drs Gondim and Thomas also record:
Patients often report that after resting on a limb in an awkward position, the resulting weakness and dysesthesias last weeks to months, rather than seconds to minutes. Slight compression of peripheral nerves and repeated local exercise leads to episodes of weakness with decreased perception to touch and pain. Most attacks are of sudden onset, painless, and initially followed by recovery. Attacks most often present with a single nerve involvement, with onset on awakening. They are usually triggered by mild compression that resolves in days to months.
This report points to the immediate onset of the symptoms of HNPP brought on by a compression of the nerves. The report includes no material that points to delayed onset of symptoms, as occurred in Mr Hunt’s case. He was on leave at the time of his episodes. Indeed, he had been in hospital for some time before the May 1970 episode. There is no material to indicate that Mr Hunt was carrying heavy loads or performing an activity equivalent to playing a musical instrument, such as the use of an old adding machine, before the May and August 1970 episodes.
I note the evidence that, apart from the continuing weakness of his left hand, Mr Hunt recorded no symptoms of HNPP until the 1990s.
The paper by Drs Gondim and Thomas records:
The onset of neuropathies associated with PMP22 deletions or mutations typically occurs during the third or fourth decade but ranges from the first to the eighth …
HNPP rarely presents in childhood …
In general, patients with hereditary liability to pressure palsies have excellent quality of life. About 10% of patients make an incomplete recovery from episodes of nerve palsy.
I have no material before me that indicates that Mr Hunt’s HNPP followed any course other than that described as typical by Drs Gondim and Thomas. I am satisfied that there is no material before me that points to an aggravation of Mr Hunt’s HNPP resulting from his wearing of webbing and using an old adding machine.
The remaining part of the hypothesis relates to the affect of Mr Hunt’s use of Dapsone while on operational service. Ms Walsh contends that the following material points to this hypothesis:
·the paper by Drs Gondim and Thomas which records:
The condition may occasionally be revealed in later life when individuals develop an acquired unrelated neuropathy due to … neurotoxic drugs;
…
Secondary preventive measures focus on education and awareness and avoidance of … interventions that can lead to systemic or focal neuropathies (eg, … neurotoxic drugs, …)
…
It is important to prevent, look for and treat acquired neuropathies … Patients … need to be aware of drugs … that can affect the peripheral nervous system … Dapsone … ;
·the Dapsone Exposure Survey that referred to Dapsone as a cause of peripheral neuropathy among servicemen in Vietnam (Exhibit R3); and
·The evidence of Dr Kraemer that HNPP is part of the family of conditions referred to as peripheral neuropathy.
I note however that Drs Gondim and Thomas relate the effect of neurotoxic drugs and the preventative measures to acquired unrelated neuropathies, not to HNPP itself.
The Dapsone Exposure Survey refers to Dapsone as a cause of peripheral neuropathy. I note Dr Kraemer’s opinion that HNPP is part of the family of conditions referred to as peripheral neuropathy. However, the evidence is that HNPP is genetically and clinically distinguished from CMT, another condition characterised by peripheral neuropathy. There is no material in the Dapsone Exposure Survey that connects the use of Dapsone with the condition of HNPP. Accordingly, I have no material that points to the hypothesis that Mr Hunt’s HNPP was aggravated by his use of Dapsone.
I have no material before me that points to an aggravation of Mr Hunt’s HNPP resulting from his use of Dapsone.
I have no material that points to the hypothesis that Mr Hunt’s HNPP was contributed to, or aggravated by, his operational service. I am satisfied that the material does not raise a reasonable hypothesis connecting Mr Hunt’s HNPP with his operational service. In accordance with section 120(3) of the Act, I am satisfied beyond reasonable doubt that there is no sufficient ground for determining that Mr Hunt’s HNPP was war-caused.
Carpal Tunnel Syndrome
Ms Walsh contends that Mr Hunt was asymptomatic to Carpal Tunnel Syndrome before commencing operational service. She contends that Mr Hunt first become symptomatic during his operational service and subsequently suffered further symptoms soon after his operational service. Ms Walsh contends that his Carpal Tunnel Syndrome arose out of or was attributable to his operational service satisfying section 9(1)(b) of the Act. In the alternative, Ms Walsh contends that Mr Hunt’s HNPP was contributed to in a material degree or was aggravated by his operational service satisfying section 9(1)(e) of the Act.
Mr Rudge contends that Mr Hunt’s Carpal Tunnel Syndrome does not satisfy the requirements of the Statement of Principles (SoP) for the condition. Accordingly, he contends, the hypothesis cannot be reasonable and the condition cannot be attributed to his operational service.
In considering whether the hypothesis is reasonable, I turn to section 120A which provides for the determination of the reasonableness of hypotheses by reference to Statements of Principles (SoP). Section 120A(3) provides that an hypothesis is reasonable only if there is in force a SoP that upholds the hypothesis.
Statements of Principal No.7 of 2013 relates to Carpal Tunnel Syndrome. Paragraph 6 of the SoP lists the factors that must as a minimum exist before it can be said that a reasonable hypothesis has been raised connecting Carpal Tunnel Syndrome with the circumstances of a person’s relevant service. Paragraph 6(a) states relevantly :
Performing any combination of repetitive activities or forceful activities with the affected hand for at least 130 hours within a period of 120 consecutive days before the clinical onset of carpal tunnels syndrome, and where the repetitive or forceful activities have not ceased more than 30 days before the clinical onset of carpal tunnel syndrome;
Mr Rudge concedes that the requirement for at least 130 hours of repetitive activities within a period of 120 consecutive days is satisfied by the evidence. Mr Rudge contends however that the relevant activities of Mr Hunt’s using his left hand to operate an old adding machine ceased more than 30 days before the clinical onset of the condition. Mr Rudge refers to the uncontested evidence that Mr Hunt was in hospital or in transit back to Australia from 10 April 1970 to 27 May 1970, during which time Mr Hunt did not use an adding machine. Mr Rudge contends that the onset of the condition was when Mr Hunt woke with a weak left hand while on leave after his discharge from hospital; or when it was diagnosed following nerve conduction studies on 17 April 2012.
In support of his contention regarding the clinical onset of the condition, Mr Rudge referred to the decision of this Tribunal in the matter of Kathleen Robertson and Repatriation Commission [1998] AATA 127 (2 March 1998). The Tribunal said at paragraph 23:
On that evidence we consider that there is a clinical onset of a disease, either when a person becomes aware of some feature or symptom which enables a doctor to say the disease was present at that time, or when a finding is made on investigation which is indicative to a doctor of the disease being present at that time.
In his statement, Mr Hunt recorded that during a period of leave in late May 1970 he woke up suffering paralysis in his left arm. The evidence of Dr Kraemer is that he suspected the existence of Carpal Tunnel Syndrome only in November 2011, at which time he referred Mr Hunt for nerve conduction studies. Professor Chambers stated in evidence that the symptoms reported by Mr Hunt in June and August 1970 were atypical of Carpal Tunnel Syndrome.
I am satisfied that in late May 1970 Mr Hunt did not become aware of a feature or symptom which enabled a doctor to say that Carpal Tunnel Syndrome was present at that time. From the medical evidence, I am satisfied that the first occasion that enabled a doctor to say that Carpal Tunnel Syndrome was present was on 17 April 2012, following the analysis of the nerve conduction studies. Accordingly, I find that the clinical onset of Capral Tunnel Syndrome was in November 2011, a date which is clearly beyond the 30 consecutive days required by factor 6 of the SoP.
There is no other factor in the SoP relevant to Mr Hunt’s circumstances. I find that Mr Hunt’s circumstances do not satisfy the requirements of SoP No.7 of 2013.
Section 120A(3) provides that an hypothesis is reasonable only if there is in force an SoP that upholds the hypothesis. I have found that the relevant SoP does not uphold the hypothesis. I am therefore of the opinion that the material does not raise a reasonable hypothesis connecting Mr Hunt’s Carpal Tunnel Syndrome with his operational service.
As a result, I am satisfied beyond reasonable doubt that there is no sufficient ground for determining that Mr Hunt’s Carpal Tunnel Syndrome is a war-caused disease. In accordance with section 120(1) of the Act I find to that effect.
CONCLUSION
I have found that Mr Hunt’s HNPP was not aggravated by his operational service and is therefore not war-caused. I have also found also that his Carpal Tunnel Syndrome is not connected with his operational service and is therefore not war-caused.
Accordingly, the reviewable decision of the VRB is correct.
DECISION
The Tribunal affirms the reviewable decision of the VRB.
I certify that the preceding 108 (one hundred and eight) paragraphs are a true copy of the reasons for the decision herein of Mr Conrad Ermert, Member ..........................................................
Associate
Dated 29 July 2016
Dates of hearing 9 June 2016 and 21 June 2016 Counsel for the Applicant Ms Rachel Walsh Solicitors for the Applicant Williams Winter Advocate for the Respondent Mr Kevin Rudge
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