Braithwaite and Comcare
[2001] AATA 125
•21 February 2001
DECISION AND REASONS FOR DECISION [2001] AATA 125
ADMINISTRATIVE APPEALS TRIBUNAL )
)
GENERAL ADMINISTRATIVE DIVISION ) No Q2000/51 Q2000/725
Re MICHAEL CHARLES BRAITHWAITE
Applicant
And COMCARE
Respondent
DECISION
Tribunal Mr K L Beddoe, (Senior Member) Miss AM Brennan, AM (Member) Dr KP Kennedy, OBE, (Member)
Date21 February 2001
PlaceBrisbane
Decision The Tribunal (by majority) affirms the decisions under review.
(Sgd) K L Beddoe
Senior Member
Decision No: 125/2001
CATCHWORDS
COMPENSATION – whether the applicant qualified for compensation for an injury resulting in permanent impairment – whether the applicant suffered a sufficient increase in impairment to bring section 25(4) of the Safety, Rehabilitation and Compensation Act 1988 into operation – whether any amount was payable for non-economic loss pursuant to section 27 – whether section 124(3) of the Act operated to preclude compensation for permanent impairment.
Safety, Rehabilitation and Compensation Act 1988 ss 24, 25, 27, 124
Blackman v ATC (1990) 12 AAR 11
Brennan & Comcare (1994) 19 AAR 542
Comcare v Levett (1995) 38 ALD 518
Comcare v West (1998) 50 ALD 712
REASONS FOR DECISION
21 February 2001 Mr K L Beddoe, (Senior Member) Dr KP Kennedy, OBE, (Member)
The applicant seeks review of two decisions of the respondent.
By a claim dated 26 March 1997 the applicant claimed compensation for head injury [T98]. The respondent treated the claim as being for payment of permanent impairment for head injury resulting in left temporal lobe damage, epilepsy and personality disorders. The respondent decided that the diagnosed condition became a permanent impairment by 1986 and refused the claim [T133]. On reconsideration that decision was affirmed [T137].
The applicant also made a claim in respect of depressive illness and personality disorder said to be related to the accepted condition of epilepsy. That claim was refused, the refusal being affirmed on reconsideration and notified by the respondent by letter dated 8 August 2000.
The hearing of this matter commenced on 9 August 2000. It was accepted that there was a valid application for review before the Tribunal in relation to the reviewable decision notified on 8 August 2000. The Tribunal proceeded with the hearing of both matters on the understanding that both matters were properly before it.
The questions are does the applicant qualify within the terms of section 24, of the Safety, Rehabilitation and Compensation Act 1988 ("the Act") for compensation for an injury resulting in permanent impairment, whether the applicant suffered sufficient increase in the degree of permanent impairment thereby bringing section 25(4) of the Act into operation and whether any amount is payable for non-economic loss under section 27 of the Act?
Section 124(3) of the Act relevantly provides that a person is not entitled to compensation under section 24 or 25 in respect of permanent impairment being an impairment that occurred before the commencing date (1 December 1988) if:
(a)The person received compensation of a lump sum in respect of that impairment under the 1912 Act , the 1930 Act, or the 1971 Act; or
(b)The person is not entitled to receive compensation of a lump sum in respect of that impairment where the impairment commenced under the 1971 Act as in force when the impairment occurred.
At the hearing Mr Wilkins appeared for the applicant and Mr Bickford for the respondent. The documents lodged in the Tribunal pursuant to section 37 of the Administrative Appeals Tribunal Act 1975 were before the Tribunal as the T documents and further documents tendered were marked as exhibits.
Oral evidence was given by the applicant and fourteen other witnesses.
The applicant's claims are for:
(a)significant cognitive deficits giving rise to permanent cognitive and communication impairments
(b)intermittent whole person impairment resulting from epilepsy;
(c)uncontrollable epilepsy;
(d)mental distress and major depressive disorder; and
(e)personality/behavioural changes
The Evidence
10.On 3 March 1969 while a cadet at the Royal Military College, Duntroon, the applicant suffered a head injury during a boxing tournament. It seems the applicant received unsympathetic treatment from the Army and that incident eventually resulted in his hospitalization for what was described as a left temporal subdural haematoma with brain injury affecting the left temporal lobe.
11.The incident did not prevent the applicant completing his cadetship at the Military College and he graduated in December 1972.
12.The applicant was discharged from the Army on 24 January 1989 with the rank of Major and having completed 20 years service. The applicant experienced two incidents, being seizures during his service but on each occasion made a good recovery and was fit to resume his duties. Exhibit A includes documents which show the applicant to be efficient in his work and include a recommendation for promotion albeit that he was medically restricted as to duties.
13.Upon entry to the Military College and again when it was proposed that the applicant undertake flying training he was given medical and psychological examinations which he satisfied.
14.Upon discharge from the Army the applicant put some of his Army experience to good use and obtained a position of Queensland Manager for Linfox Operations relating to petroleum and dangerous goods control.
15.When Linfox sought to move him to Melbourne as a National Manager he left that employment and with his wife started a business consulting and training personnel in relation to handling dangerous goods. We were told, and accept, that his business was initially very successful until the applicant's health deteriorated.
16.While conducting his own business the applicant did a considerable amount of travelling and, on his evidence, operated at a level of activity well above the level of activity performed as an efficient officer in the Army. He said his business was "booming" until 1994.
17.The applicant said that he suffered seizures in 1980 and 1983 – they being the only incidents during his career in the Army. After discharge from the Army the first seizure suffered was, according to the applicant, in 1994 followed by further seizures over the next two years. He estimates about 20 to 30 major seizures. He did not receive medical treatment on all occasions. He had his last seizure in 1996.
18.Much was made of the applicant's fluency of speech during the hearing. Before us the applicant adopted a slow considered approach when responding to questions. That sometimes changed. He explained that he speaks slowly when in stressful conditions or when he is agitated. In response to the Tribunal's question the applicant said he spoke slowly because he finds it harder to recall his words.
19.In that regard the respondent sought to entrap the applicant by arranging for a bogus telephone call to be made to the applicant on the night before the hearing and by recording the telephone conversation. The recording is exhibit 11 in these proceedings. That recording was played several times initially to the applicant and then to medical witnesses. In the ultimate we have decided that the recording and the evidence relating to it does not assist the Tribunal in reaching its decision in this matter. The reason is that any conclusions that are open on the material are at best equivocal and of no assistance in the ultimate resolution of this case.
20.In response to the Tribunal the applicant said that he was treated with Dilantin until 1994 when he was put on Tegretol by itself. In response to Mr Bickford the applicant said he went onto Tegretol and Epilim in December 1996 after Dr Lander had tried other anticonvulsant drugs.
21.The applicant was evasive in answering questions about his business seeking to defer to his accountant in circumstances where we would consider the answers to the questions by Mr Bickford would be within the applicant's knowledge of the business.
22.It was established that the applicant is in receipt of payments under an income protection insurance policy in his favour. So far as we are concerned that fact is of minimal relevance except that the applicant relies on it to rebut any suggestion that he ceased working in the business so as to make himself eligible for compensation payments. We do not attach any weight to the fact of payments under the insurance policy.
23.The applicant's daughter gave evidence but his wife did not because, we were told, of illness. The respondent did not make an issue of the failure of the wife to give evidence and the Tribunal does not draw any adverse inference. However the respondent submitted that we should give little, if any, weight to her statement of evidence.
24.The applicant's daughter said she first became aware of her father's illness in 1994 when she was 13 years of age. She presented a different picture of her father to the impression we got from his oral evidence. She gave a picture of a somewhat explosive personality including "Dad phoned me about them (unit keys) and screamed at me down the 'phone because I hadn't taken the keys out of the car and given them back to him."
25.She noted that the applicant now spends all day reading a daily newspaper whereas he had previously devoted 1 hour to that activity. She also noted a developing slowness in articulated speech which she said was variable depending on whether the applicant was having a good or a bad day. She attributed slowness of speech to the applicant being under pressure or sometimes when he is tired.
26.Exhibit G is a statement by William Hugh Fife Duff who also gave oral evidence for the applicant. Mr Duff was Terminal Manager, Brisbane Terminal for Caltex Oil (Australia) Pty Ltd at the time the applicant was a manager for Linfox Transport. He subsequently became a consultant employed by the applicant's company. He said the applicant had performed his duties as an employee and as a lecturer for his own company to a standard of excellence until 1995 when he first noted a decline in the applicant – he was less articulate and quite vague. He gave up lecturing work at the end of 1995 asking the witness to take over that work.
27.Mr Duff said that he noted a loss of articulation and general slowing down of the applicant in 1995. He also noted that the applicant has good days and other days. The applicant's articulation is flowing on good days but on other days there is considerable hesitation in delivery of his words. Mr Duff said it was his impression that the applicant did not have memory recall problems - it was his speech that was the problem.
28.Dr W L Kelly, general practitioner, made three reports dated 8 November 1991, 22 September 1998 and 25 June 2000 to the applicant's solicitors. Dr Kelly is also a neighbour of the applicant. He said that in late 1994 he was called to the applicant's business premises for what he now considers to be an epileptic seizure. He has noted marked personality changes since that time with the loss of the previous light hearted personality. In his oral evidence Dr Kelly said the applicant had become more deliberate and slow in his speech with a tendency to temperamental outbursts. He attributed this to a slowing of the thought processes.
29.In his report of 8 November 1991 about the applicant, Dr Kelly said he had been on Tegretol for many years following the head injury while in the Army. He noted that the applicant was reluctant to give up Tegretol even though this had been recommended by Dr de Wytt. The report is, however, mainly about a back condition with there being reference to Tegretol, mainly in the context of liver function. In his oral evidence Dr Kelly confirmed that he had kept the applicant on Tegretol because of the applicant's fear of further epileptic seizures. In the light of Dr Kelly's evidence we are satisfied and find that the applicant had a continuing apprehension that he may suffer further epileptic seizures following the two incidents in the 1980s.
30.The respondent called Mr Bruno Luigi Ribone, a pharmacist, who is employed by the pharmacy attended by the applicant. He said he had known the applicant for between 10 and 15 years. Exhibit 18 is a statement of Mr Ribone in which he states that the applicant attends the pharmacy at least once a month and sometimes on a weekly basis. He states the applicant presents as cheerful and alert. He also states that he has conversations with the applicant usually in relation to rugby league football. He says the applicant is articulate and he has not noticed long delays of up to 10 seconds in the applicant's speech.
31.We are satisfied that Mr Ribone did not find anything unusual in the way that the applicant spoke in the brief spatters of conversation that occurred between the witness and the applicant in the pharmacy.
32.Bruce Cannell was also called to give evidence by the respondent. He is a proprietor of a newsagency that delivers newspapers to the applicant's home. He described "general banter" which occurred with customers rather than conversation but eventually agreed that he had had some longer conversations with the applicant. He did not notice hesitancy in the applicant's speech patterns. Once again we are satisfied that Mr Cannell did not find anything unusual in the banter and conversations that occurred between the witness and the applicant in the Newsagency.
The Medical Evidence
33.Document T12 includes a medical summary by a medical officer in relation to the boxing incident on 3 March 1969 and a subsequent aggravation caused by a fall on 20 November 1969.
34.Following the incident on 3 March 1969 and with some delay as to diagnosis and treatment the applicant developed signs of an intracranial lesion. He was operated on through a left temporal burr-hole, an old subdural haematoma was found and evacuated.
35.He was discharged from hospital with minimal residual aphasia. He suffered further symptoms from a fall on 20 November 1969. Recovery took three months but he was eventually cleared by Professor Gye to continue his studies.
36.The applicant was reviewed by Dr Robson, a Neuro Surgeon, who made a report dated 21 August 1972 and supplementary report dated 10 September 1972 [T14]. He complained of occasional headache and difficulty with concentration. Dr Robson records the applicant as saying that he had noticed for a long time that he couldn't get the words he wanted and had trouble with reading and writing. He also thought he was a little less fluent than he had been. Dr Robson considered the burr hole "rather larger than I would have expected". Subsequent X-rays revealed a bone defect greater than 5cm in size which he thought constituted a disability. He recommended repair by cranioplasty.
37.While on leave the applicant suffered an incident of unconsciousness on 23 January 1980. He was reported to be not involved in any particular activity [T18] at the time of the incident. The discharge summary from the Prince of Wales Hospital [T20] described a grand mal seizure.
38.Following that incident the applicant was assessed for Medical classification. No restriction or reclassification was imposed [T23].
39.At that time he was seen by a Neurologist, Dr Lethlean who made a report dated 20 February 1980. He diagnosed a subarachnoid haemorrhage but no other abnormality. He said the improvement in speech had been most impressive, although he was a little slow and had to search for words, Dr Lethlean said he would, under most circumstances, pass for a person with normal speech. Dr Lethlean anticipated that resolution of the dysphasia would continue and would be complete. He expected full recovery from the incident. He suggested three months for convalescence.
40.Document T29 is a copy of a report on examination by Dr Andrews, consultant neurologist, dated 12 November 1981. Dr Andrew's diagnosed subarachnoid haemorrhage with cause unknown. He saw no causative link between the condition and the applicant's injury while boxing in (March) 1969. He thought the incident was a natural progression of a pre-existing condition.
41.Document T48 is a copy of a further report by Dr Lethlean dated 18 August 1983 following a Grand Mal seizure on 4 August 1983 which occurred five days after discharge from hospital following a successful laminectomy of the lumbar spine. Dr Lethlean could find no clear precipitating factors for the seizure but attributed the seizure as probably due to the 1969 incident but possibly the 1980 seizure.
42.Following a claim for compensation by the applicant the Commissioner for Employees' Compensation claimed a report dated April 1986 by Dr Merory, Consulting Neurologist, at the Repatriation General Hospital, Heidelberg. Dr Merory came to the following conclusion:
"In conclusion, he suffers from a very mild seizure disorder excellently controlled with Carbamazepine. His chances of having more seizures off medication, in view of the fact that e has had only two so far, is minimal, but he will be virtually eliminating this possibility by continuing his anticonvulsant medication. It is fairly definite that there is a causative link between the subdural haematoma, the seizure and "subarachnoid haemorrhage" in 1969, and the seizure suffered on 7 February 1980. The original cerebral trauma and subdural haematoma resulted in damage then and later, the seizures that he has suffered then, the CT scan appearances, and EEG findings."
43.In a report to the Director, Medical Services, dated 2 May 1986 Dr Merory said the possibility of further seizures was very low and practically negligible on medication. He said the applicant was fit for duty anywhere [T151].
44.Document T142 is a copy of a report by Dr Lander, Neurologist, dated 26 April 1996 and addressed to the applicant's solicitors. Dr Lander reported seeing the applicant on 21 December 1994, 2 March 1995, 27 June 1995, 28 November 1995, 11 December 1995 and 24 January 1996. Dr Lander reported on two incidents which she initially thought may be cardiovascular in their cause. However an MRI examination was very abnormal showing changes in the left inferior frontal and left temporal lobe due to the boxing injury. She also noted some calcification in these areas. Dr Lander concluded that the applicant's condition was increasing epilepsy with continuing intermittent epilepsy aura without evidence of tonic/clonic seizures. Dr Lander set out details of prescribed medication.
45.Dr Lander made a further report to the solicitors dated 19 August 1996 [T153]. Dr Lander noted persistent and uncontrolled epilepsy in spite of extensive trials of anticonvulsant medication. Those epileptic incidents were noted as occurring erratically without warning. There was also a problem with memory loss. Dr Lander reported a review by Dr Tomlinson, neurosurgeon and a report by Ms Anderson, neuropsychologist. She also noted that she could not give the applicant permission to drive a motor vehicle and she opined that the applicant would be unlikely to maintain his private business.
46.Dr Lander reported to the solicitors again on 16 September 1996 [T135]. She noted the applicant had a severe seizure on 8 August 1996. The applicant had agreed not to drive and that he was unable to continue running his business. The epilepsy remained uncontrolled despite medications and seizures were relatively frequent with very frequent auras.
47.Document T143 is a copy of a report by Dr Lander dated 7 April 1998 addressed to the Department of Veterans' Affairs. While the report is repetitive of the earlier reports we note the conclusion attributing the epilepsy to the serious head injury suffered in 1969 and the prognosis that the condition would remain static or perhaps slowly deteriorate with aging. In the result Dr Lander considered the applicant as being totally and permanently disabled.
48.Exhibit E is a further report by Dr Lander addressed to the applicant's solicitors and dated 9 August 2000 which is in rebuttal of reports by Dr Nothling and Dr Cameron in particular and also comments on a report of Dr Douglas. Included in Dr Lander's comments was the following:-
"It is hard now to describe just how difficult it was to clinically manage Mr Braithwaite during 1995-1998. He had undoubted and uncontrolled epilepsy; he had inappropriate and destructive outbursts in ways that were damaging to his personal reputation; and his clinical, speech and memory tests were significantly abnormal. Over the period of time from later 1998 until the present, his epilepsy and his mood have improved. When I last saw him on 27th July 2000, I commented that this was the best that I have seen him since 1994. I must stress that, to arrive at this point, he has had a great deal of pharmacological treatment and ongoing neurological and psychiatric support.
It is in this regard that I have been particularly surprised at the suggestion made especially in Dr Cameron's and Dr Nothling's reports that at least some aspects of his clinical presentation over the years have been – at best – contrived. I find the present focus on his memory tests to the exclusion of the objective clinical signs and investigations to be unhelpful.
In the early years – 1994 to 1996 – the medicolegal aspects were not in sight. Mr Braithwaite was desperately keen to maintain his work and his business. When finally the epileptic events prevented his driving, and the subsequent mood and memory changes became so intrusive as to make his continuing career impossible, Mr Braithwaite's response was one of genuine grief and loss, and was associated with a great loss of self esteem and confidence."
Exhibit 13 includes a bundle of reports by Dr Lander to the General Practitioner, Dr Kelly in terms generally consistent with the reports noted above.
In her oral evidence Dr Lander described the applicant as having three kinds of seizures:-
(a)Auras – described as a sense of things not being right and referred to as a premonition;
(b)Complex partial seizures which emanate from the temporal lobe often preceded by an aura; and
(c)The more severe generalised tonicolonic seizure.
51.In her oral evidence Dr Lander stated that the applicant's condition was considerably improved. In particular the following exchange occurred while Dr Lander was being examined by Mr Wilkens.
"Q Doctor, what is his situation now as far as his epilepsy is concerned?
AAt the present time he seems to be very well-controlled, at least from the point of view of complex partial seizures and generalised tonic-clonic seizures; so, it's now two and a half years which is very good. I'm always fairly cautious about it because he's broken out once before and I think epilepsy, particularly when we know there's structural abnormality in the temporal and frontal lobe, is something that we realise we have to keep ahead of at all points. It will never be an option that he can come off treatment and any increase in the symptoms will be met with great caution. So there remains a risk – getting less admittedly – but there still remains a risk that he can still have further epilepsy, and that's a life-long risk.
QFrom your observations, what do you think his emotional state is like currently?---
AWhen I saw him just a couple of weeks ago I actually thought he was the best I'd seen him in some while. He's gone through a lot of the processes and the grieving and the losses that he's had to face. Yes, I found him considerably more composed than he has been in the past on many occasions. Mind you, he does have some ups and downs and he usually says he has good days and bad days and that's true, and I would certainly attest to that. I mean, I've seen him many, many times but, yes, he was reasonable the other day."
In her oral evidence Dr Lander did, however, discuss possible triggers for the applicant's flare up of seizures from 1994 to 1996. She listed the possible triggers as lack of sleep, stress, pressure, and consumption of alcohol at more than two drinks per day. She described the flare ups as related to the pathological sub-strate of the injuries in 1969 to 1980. It was not a new condition; Dr Lander described the flare ups as 'a new activity". She was unable to explain the activity process causing the flair ups. Dr Lander was also of the opinion that it was beyond doubt that the constancy of seizures would result in further brain damage but the applicant had not reached the circumstance of status epilepticus.
Dr Lander said that in her experience the applicant's verbal fluency was sometimes more hesitant than at other times. She attributed the variation to his well-being at the time and in particular whether he was under stress. She did say in cross-examination that the applicant can speak reasonably normal and can have a good conversation on normal things but the conversation goes round and round in circles taking time to get to the point. Dr Lander stated that the applicant would have varying difficulty with the fluency of speech depending on how he was on the day but she noted that he had always had a fairly slow and deliberate speech with some word finding difficulties and the particular environment would always be a factor as to fluency of speech.
Oral evidence was lead for the applicant from Dr Molnar, consulting psychiatrist. The applicant had been referred to Dr Molnar by Dr Lander for the purpose of treatment. With the aid of a radio nucleotide imaging recording of the applicant's brain done in 1998 (Exhibit F). Dr Molnar demonstrated decreased perfusion of the brain capillaries with oxygen and glucose from the bloodstream being denied to sections of the brain resulting in sections of the brain being malfunctional, particularly in the medial aspects of the temporal lobe and likely to be the result of uncontrolled seizures causing a continuing malfunction of that part of the brain.
Dr Molnar assessed a 50% impairment because she had reason to suspect significant suicidal ideation (Table 5.1 – Guide to the Assessment of the Degree of Permanent Impairment – "Comcare Tables").
In relation to the applicant's fluency of speech and speech patterns Dr Molnar acknowledged that the applicant would be capable of normal speech, also capable of emotional outbursts but his speech pattern was characterised by perseveration combined with difficulty of word recall.
Dr Molnar was of the opinion, based on testing in 1998, that the degree of cerebral malperfusion evident in 1998 was inconsistent with the applicant's reported abilities prior to the seizures commencing in 1994. Dr Molnar agreed that it depends on which part of the brain is malfunctioning as to how a person reacts.
Exhibit 12 is a report relating to the applicant by a psychologist (Wolfendale) in the Neurology Unit at Royal Canberra Hospital, which is undated, referring to examinations of the applicant in October 1980. The report notes:
"In January 1980 he had a sub-arachoid haemorrhage, and now complains of loss of spontaneity and fluency in verbal and written expression, restriction of vocabulary impairment of memory – particularly for names, and fatigue and loss of concentration after working three to four hours. He has also been aware of an "increase in tension". "
The psychologist administered psychometric tests and found evidence of impaired short term verbal memory, difficulty with verbal expression (written and spoken) and some impairment of spatial ability. The pattern of deficit was said to be consistent with damage to the left temporo – parietal region. Relaxation therapy was prescribed with an expressed opinion that the condition should improve.
The report is inconsistent with an earlier Medical Board examination record [T146] but in our view would tend to be more reliable because of the testing conducted.
Ms Anderson is a clinical neuropsychologist called to give evidence by the applicant. She made reports dated 28 July 1996 [T144], 19 January 1998 [T145] 9 April 1999, 2 August 2000 and 30 June 2000 (Exhibit A). Ms Anderson found a significant decline in intellectual function from his above average pre-morbid levels. In particular she noted difficulties with word finding on the verbal task tests set. She thought there was a slowing of information processing and a decline in visual memory function with a recorded severe impairment on measures of attention. She also noted a decline in general intellectual capacity between 1996 and 1998.
In her report of 30 June 2000 Ms Anderson noted inconsistency in test results which she could not explain although she did offer some possible explanations. One was the effects of medication.
In the course of oral evidence Ms Anderson said that in testing for pre-morbid intellectual function the test related right back to formal education so that the testing of the pre-morbid function was likely to reflect the applicant's functioning before the incident in 1969.
Dr Douglas is a clinical psychologist. Dr Douglas has prepared three medico-legal reports relevant to these proceedings dated 12 October 1999 (Exhibit 5), 10 January 2000 (Exhibit 6) and 3 August 2000 (Exhibit 10). She commented on the findings of Ms Anderson and also conducted her own assessment of the applicant's psychological functioning.
While Ms Anderson had noted inconsistencies in results which she was unable to explain, Dr Douglas noted the inconsistencies and opined on the basis of test results, that they reflected reduced motivation by the application in relation to the testing of cognitive functions. In her opinion:-
"the results of Ms. Anderson's 2000 assessment do cause me to alter significantly my original opinion regarding Mr Braithwaite's cognitive functioning. Thus, provision of this data does in fact provide evidence that indicates this individual has not undergone a progressive deterioration in intellectual functioning between 1996 and 2000. There is thus no evidence for a continued, ongoing decline in visuo-spatial abilities in this individual, and I would reject my prior hypothesis that there is evidence on psychometric assessment to suggest the presence of a dementia. What is noted and agreed upon (by both Ms. Anderson and myself) is the finding that Mr. Braithwaite's overall intellectual abilities have consistently fallen below the level predicted by several methods for estimating premorbid intellectual functioning. This suggests that his current intellectual abilities are below expected estimates, and the most likely explanation for this would be the 1969 injury and subsequent seizure activity. I would again stress that there is now no evidence to suggest that Mr. Braithwaite has suffered any permanent, long-term, intellectual loss over the past 4 years. His overall verbal, visuo-spatial and attentional abilities in 2000 are within the expected limits predicted by his 1996 test performance, suggesting no substantial change has occurred in these areas in the intervening time period.
It remains my opinion, based on analysis of the test date, in conjunction with performance on tests of motivation administered in the 1998, 1999 and 2000 assessments, that there is no way to accurately determine Mr. Braithwaite's memory and attentional abilities at this time. While he has consistently performed extremely poorly on these tests, the extreme variability noted on tests designed to assess similar constructs, failure to benefit from provision of recognition cues, evidence for symptom magnification on the WMS-R 1996 and 1998 test data, and failure on tests of motivation administered in both 1999 and 2000, would strongly suggest that Mr. Braithwaite's performance on tests of memory and attention be viewed as unreliable. The apparent global deficit in memory functioning indicated by Mr. Braithwaite's test performance, if viewed as accurate, would require the need to 24 hour/day managed care. It is further of note that Mr. Braithwaite's apparent inability to recall what he had for breakfast (on the morning of his assessment with Ms. Anderson in 2000), while being able to recall what he disliked about his 1999 assessment with Dr Nothling, would not be consistent with any organically based deficit in memory functioning."
(Exhibit 10)
In her oral evidence Dr Douglas, who was called to give evidence by the respondent, confirmed the conclusions in her written report set out above.
The applicant sought to discount the value of Dr Douglas' evidence on the basis that she had not administered the testing herself but relied on testing by a technician under her control. The applicant also attacked the concept of the pre-marked assessments being said to refer back to pre Duntroon time given the academic achievements of the applicant at Duntroon and service courses attended after Duntroon. Dr Douglas made it clear in response that her conclusions were based on the test results together with some reliance on the technician's observations.
Document T34 is a copy of a report by a speech therapist (Ellie Skoien) which is undated but was made following assessment of the applicant in February 1998. The applicant was referred for language assessment by Dr Molnar. She reported word finding difficulty resulting in poor expression and reduced verbal fluency. There are also auditory memory deficit problems. The deficits were said to be permanent with an adverse effect on everyday functioning actual performance of language skills being dependent on levels of fatigue and stress.
In a report to the applicant's solicitors dated 18 April 1999 Ms Skoien provided assessments of permanent impairment based on the Comcare Tables. She referred in her oral evidence to a supplementary report dated 9 August 2000 but the report was not put before the Tribunal.
In her oral evidence she said that the applicant's problem is language based rather than speech based although there is a secondary consequence for the fluency of speech. She attributed the language problem to temporal and frontal lobe damage to the brain.
In cross-examination Ms Skoien agreed that she did not test for motivation but at no stage did she form the opinion that the applicant was "putting anything on".
Dr Mackenzie, a consultant neurologist, made a medico-legal report without examination dated 6 November 1996 addressed to the applicant's solicitors. Dr Mackenzie set out a history not inconsistent with the material before this Tribunal; Dr Mackenzie responded to questions posed by the solicitors, but not set out in the report, but in particular said that the head injury sustained at Royal Military College is very likely to have been the sole cause of the epileptic condition and the other consequential problems such as cognitive impairment was said to be significant and may worsen. He did not expect medication to fully control the condition.
With the benefit of subsequent reports by Dr Douglas, Dr Cameron and Ms Skoien, Dr Mackenzie changed the conclusions in his report by a supplementary report dated 3 August 2000 addressed to the applicant's solicitors and following a conversation with Mr Bickford of counsel for the respondent. Dr Mackenzie resiled in part from his earlier opinion because of the history of no seizures after 1997. Dr Mackenzie was called for cross-examination by the respondent. He was of the opinion that slow fluency of speech was consistent with frontal lobe/temporal lobe damage but factors such as stress are relevant as to performance on the day. As to the applicant Dr Mackenzie reiterated that he had not examined the applicant. Exhibit 11 which is the taped telephone conversation was played for Dr Mackenzie and he described the applicant's speech as normal and competent and lucid.
Dr Mackenzie was asked to comment in detail on Dr Cameron's report. He was unable to do so in relation to questions that depended on there having been an examination. However, he specifically agreed with Dr Cameron that the evidence pointed to the epilepsy being related to the head injury in 1969 and the epilepsy is now under control with appropriate medication. He also agreed with Dr Cameron that the 20 major seizures in the mid 1990's were highly unlikely to have caused any permanent or deteriorating brain function.
Dr Mackenzie thought there was no ongoing impairment resulting from the seizures which occurred 1994 to 1997. He said a continuation of medication has been found which has significantly improved his epilepsy and at the same time should have stopped any effects on his cognitive function that would come directly from the seizures and that situation is likely to continue.
Exhibit 1 is a copy of a medico-legal report dated 20 April 1999 by Dr Coroneos, Neurosurgeon, and addressed to the respondent's solicitors. Dr Coroneos sets out a history taken from the applicant which generally accords with the material before this Tribunal. In a detailed report he comes to the conclusion that the incident in 1980 was not consistent with a subarachoid haemorrhage but was typical of epileptic seizure.
He was also of the opinion that the applicant experienced a left chronic subdural haematoma associated with a sub-clinical epileptic seizure in 1969 as a result of the boxing match.
Dr Coroneos was of opinion that the applicant's neurological condition was permanent prior to December 1988 with the left temporal lobe abnormality and epileptic disturbance being clearly documented and in existence.
In oral evidence Dr Coroneos said he had seen the applicant on one occasion (14 April 1999) for "about an hour". He said that he found the applicant's speech and articulation patterns as normal – same as most patients he saw. There was no evidence of dysphasia.
Dr Coroneos was of the opinion that the pattern of changes seen on the EEG's and MRI's is consistent with the injury and treatment of the applicant in 1969. He pointed out that he did not have comparable studies taken in 1969 but at least there was comparability with CT scans taken after 1969.
Dr Coroneos was in general agreement with Dr Cameron's reports. In particular, he agreed with Dr Cameron's opinion that it was highly improbable that an epileptic disturbance of 20 major seizures, as experienced by the applicant, would cause any permanent or deteriorating brain function.
Dr Coroneos also agreed in general with Dr Mackenzie. He was taken to the following comment by Dr Mackenzie:-
"He has left temporal lobe epilepsy controlled by medication. He has some cognitive impairment related to the original injury but unlikely to have been significantly worsened by subsequent events" (Exhibit 4)
and said "Yes, I think that is the most reasonable view when you consider how he presented in 1969".
In cross-examination Dr Coroneos maintained his opinion that the applicant would be able to work as a Manager but not as a Member of the Defence Force required to engage in flying. However Dr Coroneos did concede that there had been a significant change in the applicant's functioning after 1994/1996. He also conceded that there could be some disturbance caused by epilepsy which would have a detrimental effect on function.
Exhibits 2 and 3 are reports by Dr Cameron, Consultant Neurologist, dated 6 January 2000 and 6 July 2000 respectively. Both reports are addressed to the respondent's solicitor. Dr Cameron took a history which he said was very laborious because the applicant's speech was markedly slow. Dr Cameron was concerned as to inconsistency in the psycho-neurological testing results. Dr Cameron only saw the applicant on one occasion.
Dr Cameron expressed his opinion that the applicant has developed post-traumatic epilepsy as a consequence of his boxing injury. A period of epileptic instability developed in the mid 90's but this has now been controlled with appropriate medication. He also noted that there were some unexplained problems in the mid 90's which he thought were suggestive of a non-organic disturbance.
He thought that the seizures could sometimes result in some minor damage although seizures in themselves do not result in brain damage and given that the applicant only had 20 seizures underlying brain damage is not suggested in this case. No evidence of status epilepsy was present in this case, it being the most likely cause of brain damage.
In the context of the tape (Exhibit 11) which had been played to him Dr Cameron said the applicant's speech was perfectly normal to him. It was fluent, it was fast, it had content and there was no evidence of dysphasia or dysarthria. Dr Cameron said it was not the speech pattern demonstrated by the applicant at interview (p 249). He also said that the structural brain damage will stay as a permanent feature. It may get worse but it will stay as an impairment.
Dr Cameron also reiterated his view that the seizures experienced by the applicant would not be sufficient to have caused additional brain damage, although he did say that dysfunctional brain tissue may result in the vicinity of the focus of the seizure. He also said that the presence of minimal speech disturbance (dysphasia) on testing although he doubted that the applicant was dysphasic. He also doubted that it was correct to say that the applicant suffered 20 major seizures.
Dr Cameron thought that it was conceivable that the applicant suffered some deterioration in the brain function from the 1994-1996 seizures although he preferred the view that little, if any, damage occurred. Dr Cameron said the history indicated "One major seizure and a few simple seizures".
Dr Cameron seemed to prefer an explanation for the applicant's condition as being founded in depression and psychological factors. In explanation he said that the head injury is static – it hasn't changed and in fact the applicant's condition has improved in more recent times.
The respondent also called Dr Nothling, Consultant Psychiatrist, to give evidence. Following examination Dr Nothling provided the respondent with medico-legal reports dated 28 October 1999 (Exhibit 5), 12 January 2000 (Exhibit 6), 27 January 2000 (Exhibit 7) and after further examination of the applicant a report dated 7 August 2000 (Exhibits 9 and 21). Dr Nothling also supplied copies of raw test data to the respondent under cover of his letter dated 3 June 2000 (Exhibit 8).
Dr Nothling noted markedly slow speech. He also noted that testing by Dr Douglas had found that the applicant's overall level of intellectual functioning apparently falls in the low average range, but estimates of pre-morbid functioning were within the high average range.
Dr Nothling noted Dr Douglas' findings about inconsistent test results suggesting a lack of motivation in the 1999 testing so that an assessment of current cognitive function was not possible. In his report dated 12 January 2000 (Exhibit 6) Dr Nothling said, it was not possible to determine his actual degree of cognitive impairment at that time due to the strong evidence for the influence of reduced motivational levels in the 1999 assessment.
In a further report dated 27 January 2000 (Exhibit 7) Dr Nothling, after considering Dr Cameron's report, went a step further and distinguished the poor performance on testing as not related to the original head injury. The probable explanation being poor motivation to perform at his true level on those tests, being conscious factors unrelated to the original injury.
Dr Nothling conducted another examination on 4 August 2000. He concluded that the applicant had not suffered from any progressive deterioration in intellectual functioning between 1996 and 2000. Rather he thought there had been an improvement not consistent with dementia. Further, the speech pattern at interview was not consistent with traumatic brain injury and not consistent with major depressive disorder. Nor did he find evidence to diagnose a personality disorder (Exhibit 9).
In oral evidence Dr Nothling confirmed that the exhibited speech pattern was inconsistent both with the reported brain damage and also inconsistent with depression. He said that the testing showed an improvement in IQ in 2000 which is inconsistent with ongoing dementia which only gets worse. There has not been a decline in cognitive abilities. Further Dr Nothling was of the opinion that there was no evidence of personality disorder.
In response to Mr Bickford, Dr Nothling said that in his opinion the applicant was capable of performing work as he had prior to 1994.
In so far as the applicant sought to attack Dr Nothling's credit, we are not satisfied that anything arose in the course of his evidence which would cause us to discount Dr Nothling's evidence so as to give it less weight on the grounds of bias or partiality.
The evidence of Dr Nothling satisfied us that the applicant was a reluctant participant at the examinations by Dr Nothling and we are also satisfied that the applicant's conduct at the examinations, including the testing, was not frank and open but was contrived with a view to manipulating a particular outcome for the applicant's benefit.
In response to a question from the Tribunal Dr Nothling said that periods of depression were likely during the period that the epilepsy was unstable. If there had been some depressive condition in the past Dr Nothling said that the applicant does not now have a diagnosable condition.
The Applicant's SubmissionsThe applicant's claim is for compensation for permanent impairment and for non-economic loss under sections 24 and 27 of the Safety Rehabilitation and Compensation Act 1988 ("the Act").
The applicant relies in particular on the evidence of Drs Lander, Molnar, Ms Anderson and Ms Skoien. The essence of his case is that there was no or minimal impairment of neurological functions prior to the seizures that occurred in the 1994 to 1997 period while the cause of the present impairment is clearly the boxing accident in 1969. To some extent the applicant's condition has been exacerbated by treatment for the accepted conditions so that exacerbation is causally connected to the 1969 injury.
He also says that there has not been a general worsening of the condition over the years but a severe exacerbation from 1994 resulting from a new permanent impairment. This is made clear by the fact of his being fit for Army service until discharge in 1989, the fact of his subsequent satisfactory employment with Linfox leading to offered promotion and the fact of the successful conduct of a business up to 1994. In each of these periods of employment and self employment the applicant was a high achiever and he was not impaired to any significant degree by the head injury in 1969. The fact that he was a high achiever contradicts any suggestion of malingering. Further the evidence of Ms Skoien, speech therapist, contradicted such a suggestion.
The Respondent's Case
The question is whether the applicant suffered a further or new permanent impairment on the proper construction of section 124 of the Act after 1 December 1988.
The applicant's credit is in issue here. The evidence shows that the applicant's claimed lack of fluency of speech before the Tribunal is inconsistent with his normal cognitive functioning and the applicant has deliberately attempted to obfuscate and create the impression of a disability which does not exist. The respondent sought to support this submission in various ways. In particular counsel referred to the cross-examination of the applicant at pages 52-57 of the transcript relating to a claim for compensation made on 13 March 1989 (T68) being a claim for compensation in respect of grand mal seizure and subarachnoid haemorrhage. As the applicant acknowledged liability for these conditions had been accepted while he was a serving officer. The applicant expanded the claim to include:
Permanent epilepsy as a result of the Subdural Haematoma.
On permanent medication due to epilepsy. This affects my home and work life through side effects of medication, ie often tired, drowsy, short tempered, aggressive, etc.
Loss of short term memory.
Continual reduction in ability to communicate, oral and written.
Complete loss of senses of taste and smell.
Being prohibited from participating in contact sports from 1969, especially rugby and boxing.
Frequent headaches.
Continual soreness and sensitivity around large burr hole in left temporal region. The burr hole has never been closed.
Continual jolt or twitch down left side of face.
Difficulty and pain in opening mouth (especially at the dentist), and often when chewing food.
Military career, postings and promotion affected by medical downgrading as a result of injuries, and side effects of drugs.
Stigma caused by epilepsy within the community resulting in difficulty getting a job and either non-acceptance or significant premium loading in obtaining life insurance and loans. This has a considerable effect on the security and future of my family.
As a direct result of my injuries, my wife has refused to have any more children in case I should die prematurely leaving her with a young, large family to support without adequate means. My wife suffers continual stress unsure of when and where I could have the next fit or injury, or if I will come out of it alive. This causes continued friction and tension within the family unit. In particular this is of great anguish and frustration to me as the cause is completely out of my control.
The respondent says that the applicant's statement is corroborated by, inter alia, the report of Dr Merory, Consulting Neurologist, in April 1986.
The applicant's memory function is better than he asserts. The respondent also submitted that the applicant is now deriving weekly compensation and insurance payments comparable in amount to his income from business in earlier years so that the applicant's assertion of being on "pension peanuts" had no basis in fact.
The respondent submits that the applicant does not suffer any permanent psychiatric condition.
ConsiderationThere is no dispute that the respondent is liable for compensation in relation to the head injury which occurred in 1969 and was probably exacerbated in 1980. Those injuries have been well recognised and no issue arises in relation to the fact of the injuries.
There is also no issue that the injuries caused post trauma epilepsy, there being a history of occasional seizures from 1969.
We have to consider whether there has been a marked deterioration in the permanent impairment, being an increase in the degree of impairment of 10% or more (s 24(4)). Alternatively a new permanent impairment occurred after 1 December 1988 thereby avoiding the operation of section 124(4) of the Act.
The issues confronting the Tribunal have been considered by the Federal Court in:
Blackman v ATC (1990) 12 AAR 11
Brennan v Comcare (1994) 19 AAR 542
Comcare v Levett (1995) 38 ALD 518
Comcare v West (1998) 50 ALD 712In Blackman the claimant applicant had retired from Commonwealth employment in 1960 on grounds of being medically unfit due to hypertension and anxiety being war caused disabilities. In November 1988 the applicant was diagnosed as having mesothelioma which was held to have been contributed to by the applicant's Commonwealth employment. The applicant argued that although there was only one disease, and therefore one injury as defined, if the impairment has worsened substantially after 1 December 1988 then that worsening in itself constituted an impairment occurring after the commencing date.
That proposition was rejected by the Court. It said at page 14:-
"The natural reading of "impairment …….that occurred before the commencement date" is such as to cover the case in which there is but a single impairment, which came into existence before (1 December 1988) and thereafter fluctuated in intensity but generally worsened". The Court found that the applicant was not entitled to compensation under sections 24 and 25 in respect of his permanent impairment because it came into existence before December 1988."
In Brennan v Comcare (1994) 19 AAR 542 the claimant sought compensation for back injuries suffered prior to 1 December 1988 but stabilised following an operation after 1 December 1988. This Tribunal, as then constituted, found in favour of the applicant claimant on the basis that the injury was sustained after 1 December 1988. That decision was set aside by Neaves J. The applicant appealed to the Full Court which dismissed the appeal.
Gummow J noted at 557 that there was no direct legislative guidance given, in relation to the concept of "permanent impairment", as to the effect of the expression in section 124(3), "occurred before the commencing date". His Honour said that there are at least three steps involved:-
(a)has there been an injury before the commencement date (1 December 1988):
(b)has the injury resulted in impairment; and
(c)is that impairment permanent?
Section 24 does not rule out more than one impairment resulting from an injury. At page 557-8 Gummow J referred to the decision in Blackman and agreed with Burchett J that caution was needed in so far as Blackmansuggests that a variation of the degree of impairment cannot be treated as a new impairment ie a fluctuation in intensity with general worsening is not a new impairment.
Changes in degree of permanent impairment are not determinative of whether there is a new permanent impairment (Gummow J at 558).
At page 548 Burchett J expressed the opinion that the dicta in Blackman, would not stand in the way of the Tribunal finding that a "significant development had occurred resulting in impairment which was a new impairment.
A further refinement, which illustrated the problem with the reasoning in Blackman, occurred in the Full Court's decision in Comcare v Levett (1995) 38 ALD 518. In that case the Tribunal had found that the claimant had suffered an injury resulting in impairment before 1 December 1988 but the impairment had not become permanent until after that date. Section 124(3) did not therefore operate to prevent the operation of section 24 on the circumstances of the case, as the Tribunal had found. The Full Court clearly distinguished the date of impairment from the date of permanent impairment so that if the latter occurred after 1 December 1988, notwithstanding that relevant impairment occurred prior to that date, then section 24 was satisfied and section 124(3) did not operate to deny entitlement.
In Comcare v West (1998) 50 ALD 712 the Federal Court divided over the relevance of the time of impairment and time of permanent impairment. There had been a significant worsening of the claimant's lumbar spine condition after 1 December 1988. The Tribunal had held that the claimant was entitled to a lump sum payment for permanent impairment on the basis that the permanent impairment at 1 December 1988 had been assessed at 10% but this had increased to 20% after that date. The question at issue was whether this significant increase was a new permanent impairment.
Heerey J said it was not and there was no entitlement post 1 December 1988. O'Connor and Merkel JJ for reasons expressed by Merkel J also upheld the appeal, but remitted the matter to the Tribunal to make further findings of fact. However, in doing so there Honours refused to follow Blackman. In particular at page 729 Merkel J said:
" A loss of the entitlement conferred under ss 24 and 25 by reason of s 124(3) only occurs when the permanent impairment the subject of the claim is the permanent impairment that the employee suffered as at 1 December 1988. On my reasoning, and that of Burchett J in Brennan, where a change in a permanent impairment occurring after the commencement date is such that, quantitatively and qualitatively, it is properly to be characterised as a further or new impairment occurring after the commencing date it is compensable by a lump sum payment under ss 24 and 25. That conclusion is consistent with the language used and with the statutory policy to be discerned from ss 24, 25 and 124 of providing benefits to workers in respect of a further permanent impairment that occurs after the commencing day irrespective of whether the injury that resulted in the impairment occurred before or after the commencing day. It also avoids capricious and arbitrary outcomes under workers' compensation legislation, which is of a remedial nature and should be construed liberally: see Brennan at FCR 559 and the cases there referred to.
I have had the advantage of reading the reasons of Heerey J. The essential difference between his Honour's approach and the one which I have adopted is that I have concluded that it is not appropriate to characterise the relevant permanent impairment solely by reference to a loss of use or malfunction of part of the body or bodily system or function without regard to the nature and extent of the loss of use or malfunction. In my view the nature and extent of the loss of use or malfunction is critical to determining whether an impairment has changed to such an extent that it is a further or new impairment. His Honour's conclusion must treat a slight loss of use of a limb which progresses to a total loss of use as the same permanent impairment. For the reasons set out above I do not accept that that is so.
However, in reaching my conclusion, I do not disagree with the conclusion in Blackman that gradual worsening does not result in a series of separate or further impairments. Inevitably, questions of fact and degree are involved in making a qualitative assessment as to whether, in a particular case, the permanent impairment existing as at 1 December 1988 has deteriorated to an extent that it is properly to be characterised as a further or different impairment to that which existed at the commencement date. When that question is answered in the affirmative an entitlement to lump sum compensation arises under ss 24 and 25 which is not precluded by s 124(3)."In the present case we are satisfied, on the basis of the material before us, that the applicant suffered trauma to the brain in 1969 which resulted in post trauma epilepsy. That condition was the subject of treatment on a continuing basis from 1969. Liability for compensation was admitted and the applicant is in receipt of incapacity payments.
We are satisfied and find that the post traumatic epilepsy was and is a permanent condition. It became a permanent condition either ab initio or at least since 1980 and constituted an impairment, as defined, from that time.
We are also satisfied that the permanent condition became unstable in 1994 resulting in an exacerbation of the pre-existing condition and Dr Lander had to change medication to eventually stabilise the condition. That was, in our view, a temporary exacerbation of the condition notwithstanding that a period of more than three years was required to stabilise the condition.
The question then arises as to whether the applicant suffered further injury because of the exacerbation of the pre-existing condition resulting in a new impairment. On the material before us we have come to the conclusion that there was no significant further injury demonstrated on the evidence.
In that regard we formed an adverse impression of the applicant in relation to his evidence which we have concluded must also reflect on histories given to the medical specialists. We have come to the view that the evidence of the applicant was contrived. We do not accept that his fluency of speech in giving his evidence was frank. It was inconsistent with independent evidence about his speech. In coming to that conclusion we have preferred the evidence of witnesses before the Tribunal but have given little weight to the evidence in so far as it relates to the recorded telephone conversation (Exhibit 11).
Taking the medical evidence into account we are not satisfied that the applicant suffered a new permanent impairment after 1 December 1988.
The consequence is that the applicant is not entitled within the terms of sections 24 and 25 of the Act in respect of his permanent impairment because it came into existence before 1 December 1988. There was no entitlement to payment of a lump sum for such a permanent impairment prior to 1 December 1988.
As to the claim for depressive illness with personality disorder we have come to the view that the evidence of Dr Nothling and Dr Lander is decisive in this aspect. Dr Lander is of the view that there has been a substantial improvement in the applicant – a view inconsistent with dementia noted by Dr Molnar. We have also noted that Dr Douglas, in her assessment of the psychological tests stated that the apparent global deficit in memory functioning indicated by those tests, if viewed as accurate, would require need for 24 hours per day managed care. That view is inconsistent with the evidence before us as to the applicant's day to day functioning.
More importantly we have already noted that the applicant has presented a contrived history to the Tribunal and to at least some of the medical reporters. Dr Molnar has described major depressive disorder caused by the exacerbation of the epilepsy in 1994. We are faced with that diagnosis by the treating psychiatrist and the opposing view of Dr Nothling who considered the history and presentation to be inconsistent with depressive illness.
Our dissatisfaction with the applicant's evidence leads us to the conclusion that we should accept Dr Nothling's opinion that there is not a diagnosable depressive illness.
For these reasons we are satisfied that both decisions under review should be affirmed. There will be no order for costs.
I certify that the 133 preceding paragraphs are a true copy of the reasons for the decision herein of Mr K L Beddoe, (Senior Member) and Dr KP Kennedy, OBE, (Member)
Signed: .....................................................................................
AssociateDate/s of Hearing 9-17 August 2000
Date of Decision 21 February 2001
Counsel for the Applicant Mr Wilkins
Solicitor for the Applicant Mr McMurran
Counsel for the Respondent Mr Bickford
Solicitor for the Respondent Ms Tyszkiewicz
DISSENTING DECISION OF MISS A M BRENNAN (MEMBER)
A summary of all the evidence and an outline of the matters to be decided before the Tribunal have already been outlined in the majority decision and need not be repeated here. It remains for me to explain the reasons for my decision, namely that the permanent impairment existing as at 1988 has changed boundaries since 1994 because additional elements of a medical social and psychological nature have become part of the constellation of factors which represent Mr Braithwaite's condition.
Essentially I found the evidence provided by the witnesses called by the applicant to be more convincing and rigorous than that provided by the witnesses who were called to give evidence by the respondent. The witnesses called by the applicant had grappled with his medical, psychological, social and vocational problems over a matter of years and this longer historical perspective gave depth and understanding of the applicant's difficulties and dysfunctions. This understanding was not available from the other witnesses who were primarily clinical witnesses who had been consulted for assessment purposes.
Witnesses called by the Applicant
The witnesses called by the applicant all regarded the onset of the major epileptic condition in 1994-96 and its sequelae of increased cognitive impairment, depression and personality disorder as a tragic event in his life because he was forced to cease work and many of his social relationships were impaired. Moreover they indicated that to date Mr Braithwaite has not been able to regain anything like the momentum or successful life he had enjoyed prior to him suffering from the medical conditions during the 1994-96 period.
In my opinion Dr C Lander was a key witness in this case. She has been Mr Braithwaite's primary physician since 1994 and is a highly respected specialist in neurology. She has had to diagnose and re-evaluate her diagnoses over a period of six years and while Dr Lander recognised that Mr Braithwaite's condition had improved over these years, she was cautious about making any future predictions. When giving evidence Dr Lander said:
"I'm always fairly cautious about it (epilepsy) because he's broken out once before and I think epilepsy, particularly when we know there's structural abnormality in the temporal and frontal lobe, is something that we realise we have to keep ahead of at all points. It will never be an option that he can come off treatment and any increase in the symptoms will be met with great caution So there remains a risk – getting less admittedly – but there still remains a risk that he can still have further epilepsy, and that's a life long risk" (transcript page 114)
When writing a report in 1999 about Mr Braithwaite's underlying pathophysiology she said:
"The underlying pathophysiology of Mr Braithwaite's organic brain syndrome relates to the following factors: structural brain injury in 1969; boxing injury; 1980 subarachnoid haemorrhage, increasing partial and secondarily generalised epilepsy.
The underlying substrata for this pathology is organic brain injury and consequent epilepsy as listed above. … However as time progressed his neural cells that were injured previously continued to degenerate and decline in function. This process reaches a critical point at which function is seen to be significantly impaired. In Mr Braithwaite's case this occurred in the mid-1990's when his functional capacity went from being able to cope and compensate for his various disabilities to being functionally unable to cope with his deficits." (transcript pages 122-123 Exhibit 3C)
When Dr Lander was cross examined on these opinions by Mr Bickford, Dr Lander recognised that the underlying substrata for Mr Braithwaite's condition as far as his epilepsy was concerned was his organic brain injury but she was of the opinion that in the 1994-96 period he did develop new activity in his brain. In evidence she said:
"I can't tell you the pathophysiology … that's occurring, but something is occurring there that has made it unstable where it hasn't been – it has been stable to this point, and then for some reason it's not stable." (transcript page123)
In Dr Lander's opinion, Mr Braithwaite's depression was circumstantial to the whole change in his life affairs that resulted from his unstable epileptic condition in the mid 1990's.
When I asked Dr Lander if the constellation of factors which constituted Mr Braithwaite's condition in 1994 onwards was different from the constellation of factors she envisaged his condition comprised prior to the late 1980's she replied "It's a constellation with much more embroidered on to it … the degree would not trace equally over it" (transcript page 135).
When any of witnesses called by the applicant were questioned about credibility issues relative to Mr Braithwaite the answers were given within the context of clinical issues and problems.
For instance, when Ms Anderson, a clinical neuropsychologist, was asked in evidence about Mr Braithwaite's motivation and the fact that some of his tests were not completed and were invalid, she said:
"In Mr Braithwaite's case, specifically, he reports having good and bad days and on the most recent occasion that I saw him, I saw him over two occasions, one of those days he was alert and very responsive on the second day he was having a lot more difficulty actually performing the tests and so on and that was the day that I had the invalid test." (transcript pages 91-92)
Ms Anderson went on to explain that on the second day Mr Braithwaite fell asleep on the desk and she concluded that medication levels or seizure activity could have contributed to his responses on this occasion.
When Dr Lander was asked about Mr Braithwaite's motivation to get back to work she said in evidence:
"… I think he very much always wanted to keep working in his old job. The difficulty is he couldn't do his old job. He couldn't function up front and he couldn't drive. So effectively – and I think that's still true now – I don't see how he could do his old job. Even putting aside the memory arguments, if we were to say he could start his old job to-morrow, he's still got the problem, okay, he may be able to drive but what happens if he has a seizure in three months time. It's a very precarious situation … and add to that the memory problems and, then, the catastrophic reactions when he gets irritated which have been a problem as well." (transcript page 119)
Witnesses called by the Respondent
As noted earlier the doctors called by the respondent to give evidence had had brief contacts with Mr Braithwaite. Doctors Cameron and Coroneos each saw Mr Braithwaite on one occasion, Dr Nothling had two consultations and Doctor Mackenzie gave his opinions on the basis of reports and had not had a consultation with Mr Braithwaite.
An outline of the evidence given by these doctors is in the majority report. This evidence reveals a number of conflicting opinions between these doctors and between these doctors and Mr Braithwaite's treating physicians, namely Doctors Lander and Molnar (psychiatrist).
For instance Dr Cameron preferred an explanation for Mr Braithwaite's condition as being founded in depression and psychological factors. Dr. Nothling found no evidence of depression, personality disorder or speech pattens consistent with brain damage. In Dr Nothling's opinion Mr Braithwaite was capable of performing work as he had prior to 1994.
Dr Coroneos said that the left temporal lobe abnormality and epileptic disturbance was clearly documented and in existence and was of the opinion that Mr Braithwaite's neurological condition was permanent prior to December 1988.
In cross examination Dr Coroneos maintained his opinion that the applicant would be able to work as a manager but not as a member of the Defence Force required to engage in flying. However, Dr Coroneos did concede that there had been a significant change in the applicant's functioning after 1994/196. He also conceded that there could be some disturbance caused by epilepsy which would have a detrimental effect on function (majority decision, paragraph 84).
Dr Mackenzie thought there was no ongoing impairment resulting from the seizures which occurred 1994 to 1997. He said a continuation of medication has been found which has significantly improved his epilepsy and at the same time should have stopped any effects on his cognitive functions that would come directly from the seizures and that situation is likely to continue (majority decision, paragraph 76).
The difficulty in my view with much of this evidence is that it was presented within narrow conceptual frameworks and these narrow frameworks left the way open for some of Mr Braithwaite's behaviour to be construed in terms of credibility issues.
For instance, when Mr Braithwaite had an outburst with his GP, Dr Kelly, in the mid 1990's it was noted as a clinical sign of his condition. When on the other hand Mr Braithwaite had an angry outburst with Dr Cameron in December 1999 the incident became an occasion to make judgments about Mr Braithwaite's potential for different rates of speech. This angry outburst with Dr Cameron was consistent with Dr Lander's opinion that Mr Braithwaite could have catastrophic reactions when he got irritated. This problem which appeared to emerge after 1994 is one which has implications for future work, relationships and general social functioning.
Dr Nothling's assessment focussed mainly on tests for motivation. This assessment did not include any detailed analysis of what the psychological, social and vocational consequences of Mr Braithwaite's 1994-98 medical episodes were for him.
I find it difficult to accept Dr Nothling's argument that it was not relevant for him to have information about Mr Braithwaite's treatment by Dr Molnar. Further, why was Mr Braithwaite reluctant to reveal any details about Dr Molnar's treatment to Dr Nothling? If Mr Braithwaite had been "motivated" to enhance the presentation of his disabilities then the information about his treatment from Dr Molnar would have done that.
In Dr Nothling's opinion Mr Braithwaite would be able to resume his former active life if he stopped fabricating disabilities yet this opinion does not fit with the reality of Mr Braithwaite's situation. He is still being strongly supported and treated by Dr Lander and Dr Molnar, he does not have approval to drive and he has exhibited aggressive behaviour over recent times.
From the evidence it appears that Doctors Nothling and Cameron formed an independent assessment team and on the basis of a few brief contacts formed opinions which were in many respects in marked contrast to those held by Mr Braithwaite's treating doctors.
Dr Nothling proposed that treating psychiatrists are often too identified with their patients to give an objective assessment. He suggested that in medico-legal matters independent psychiatrists who see people purely for the purpose of an assessment are more likely to provide an objective assessment (transcript pages 347-348). This proposal may have some merit in certain situations but in Mr Braithwaite's case his disease/condition becomes manifest at different times and under different circumstances and is not likely to be observed or understood in its entirety over short time periods.
In a report by Dr Lander addressed to the applicant's solicitors and dated 9 August, 2000 (Exhibit E) she refutes aspects of reports by Dr Nothling and Dr Cameron. Dr Lander's report includes the following statements:
"It is hard now to describe just how difficult it was to clinically manage Mr Braithwaite during 1995-1998. He had undoubted and uncontrolled epilepsy; he had inappropriate and destructive outbursts in ways that were damaging to his personal reputation; and his clinical, speech and memory tests were significantly abnormal. Over the period of time from later 1998 until the present, his epilepsy and his mood have improved. When I last saw him on 27th July 2000, I commented that this was the best that I have seen him since 1994. I must stress that, to arrive at this point, he has had a great deal of pharmacological treatment and ongoing neurological and psychiatric support.
It is in this regard that I have been particularly surprised at the suggestion made especially in Dr Cameron's and Dr Nothling's reports that at least some aspects of his clinical presentation over the years have been – at best – contrived. I find the present focus on his memory tests to the exclusion of the objective clinical signs and investigations to be unhelpful.
In the early years – 1994 to 1996 – the medicolegal aspects were not in sight. Mr Braithwaite was desperately keen to maintain his work and his business. When finally the epileptic events prevent his driving, and the subsequent mood and memory changes became so intrusive as to make his continuing career impossible, Mr Braithwaite's response was one of genuine grief and loss, and was associated with a great loss of self esteem and confidence."
…
Dr Nothling seems to accept that Mr Braithwaite's epilepsy is real yet Dr Nothing also trivialises the reality of his catastrophic disorder. He does not consider what the psychological consequences of this condition are for Mr Braithwaite. I find it curious that Dr Nothling has not applied himself to these psychological and psychosocial problems faced by a man who has, until recently, been able to manage in a hectic business world and who has now been obliged by circumstances beyond his control to adapt to a different way of life."
Consideration
I accept paragraphs 110-125 inclusive of the majority decision.
I am satisfied that the permanent condition became unstable in 1994 resulting in an exacerbation of the pre-existing condition. However, at this time Dr Lander had a difficult time in providing clinical management as she had to attend not only to his pharmacological treatment over a three year period for his uncontrolled epilepsy but also to Mr Braithwaite's family, social, vocational and psychological/psychiatric problems which emerged as a result of his unstable condition.
Although Dr Lander said that Mr Braithwaite's epilepsy and mood have improved since 1998 she never indicated that his overall level of functioning had achieved anything like his pre 1994 levels. She was cautious in making predictions about his future employment prospects and other functional capacities. Further, Mr Braithwaite is still receiving support and treatment from Dr Lander and his psychiatrist, Dr Molnar.
In my lay opinion, Mr Braithwaite did not present during the hearing as a person who would be able to resume an executive type position in the business world or a responsible position in the Defence Forces. From 1969 to 1994 Mr Braithwaite suffered from a number of epileptic seizures of varying intensity and on each occasion he was able to recover from these episodes and resume responsible work and maintain a high level of social functioning. What happened in 1994-1996 appeared to be an assault on his whole person from which he is slowly improving with intensive clinical management.
On the available evidence I formed the opinion that Mr Braithwaite's patterns of speech and other irregularities in his behaviour and responses had to do with his constellation of medical psychological conditions and medications than any motivation to create the impression of disabilities which do not exist. Further it is significant to note that prior to 1994 Mr Braithwaite dealt with his medical problems in a constructive way and showed no signs throughout his Army career of being preoccupied with health issues, compensation or fabricating medical conditions.
I therefore find that the permanent impairment which existed as at 1 December, 1988 has deteriorated since 1995 to an extent that it is now properly characterised as a further or expanded impairment. As Dr Lander said in evidence, the permanent impairment of the late 1980's now has "much more embroidered on to it" (transcript page 135). Attached as "Appendix A" is Dr Lander's assessments of the "Percentage Permanent Impairments" referrable to Mr Braithwaite on the dates 1/12/88 and 16/3/99.
On the basis of my conclusion Mr Braithwaite is entitled to lump sum compensation under The Safety Rehabilitation and Compensation Act 1988 as ss 24 and 25 would not be precluded by s 124(3).
I certify that the 33 preceding paragraphs are a true copy of the reasons for the decision herein of Miss AM Brennan, AM (Member)
Signed: .....................................................................................
AssociateDate/s of Hearing 9-17 August 2000
Date of Decision 21 February 2001
Counsel for the Applicant Mr Wilkins
Solicitor for the Applicant Mr McMurran
Counsel for the Respondent Mr Bickford
Solicitor for the Respondent Ms Tyszkiewicz
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