JONATHON HAZELTON and CIVIL AVIATION SAFETY AUTHORITY
[2010] AATA 693
•10 September 2010
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2010] AATA 693
ADMINISTRATIVE APPEALS TRIBUNAL )
) No 2009/5517
GENERAL ADMINISTRATIVE DIVISION ) Re JONATHON HAZELTON Applicant
And
CIVIL AVIATION SAFETY AUTHORITY
Respondent
DECISION
Tribunal Honourable Dr B H McPherson CBE Deputy President,
Dr K S Levy RFD, Senior Member and
Associate Professor J B Morley RFD, MemberDate10 September 2010
PlaceBrisbane
Decision The Tribunal determines:
(1) Mr Hazelton satisfies the requirements for the issue of a class 1 and class 2 medical certificates.
(2) The matter is referred back to CASA for consideration of conditions (if any) and if so, for what period of time.
...............[Sgd]...............................
Deputy President
CATCHWORDS
CIVIL AVIATION – Class 1 and Class 2 Medical Certificate – Does Mr Hazleton satisfy the requirements for the issue of a Class 1 and Class 2 Medical Certificate – If the answer Is yes, should any restrictions or conditions be endorsed on those medical certificates – Applicant’s head injury found to be mild – A finite figure for the applicant’s absolute risk of post-traumatic epilepsy, based on the presence of his cerebral contusions cannot be calculated – Present body of scientific literature is insufficient on its own to make a determination in accordance with evidence-based medicine on the acceptability of the applicant’s current epilepsy risk to resume flying aircraft ‘with or as co-pilot’ – Sufficient clinical expertise available which is substantial enough to enable the determination of whether the applicant’s epilepsy risk is acceptably low enough to resume flying aircraft ‘with or as co-pilot’ to satisfy the standards of evidence-based medicine – Estimation of present risk to be assessed on the basis of relative risk – The 1% Rule provides an adequate estimation of an acceptable risk, and is appropriate to apply to the applicant’s case – Applicant satisfied the requirements for the issues of a Class 1 and Class 2 Medical Certificate – Matter referred back to CASA for consideration of conditions (if any) and if so, for what period.
Civil Aviation Act 1988 (Cth) ss 9, 9A
Evidence Act 1995 (Cth) ss 79, 140
Briginshaw v Briginshaw (1938) 60 CLR 336
Clark v Ryan (1960) 103 CLR 486
Darkan v R (2006) 80 ALJR 1250
Makita (Aust) Pty Ltd v Sprowles (2001) 52 NSWLR 705
Neat Holdings Pty Ltd v Karajan Holdings Pty Ltd (1992) 67 ALJR 170
Re Window and Civil Aviation Safety Authority [1999] AATA 525.
REASONS FOR DECISION
10 September 2010 Honourable Dr B H McPherson CBE Deputy President, Dr K S Levy RFD, Senior Member and
Associate Professor J B Morley RFD, MemberINTRODUCTION
1. Jonathon Hazelton, the applicant, has appealed against a determination of the Civil Aviation Safety Authority (“CASA”) to refuse to grant a Class 1 and Class 2 Medical Certificate, as is required for him to continue to engage in his occupation as an airline pilot.
2. The original decision was made and communicated to Mr Hazelton on 13 May 2009. An internal review of the decision was undertaken and was affirmed on 13 November 2009, in similar terms to the original decision.
ISSUES
3. The issues for determination are:
(a)Does Mr Hazelton satisfy the requirements for the issue of a Class 1 or Class 2 Medical Certificate?
(b) If the answer to the above is yes, should any restrictions or conditions be endorsed on those medical certificates?
EVIDENCE
4. In the hearing of this matter (in which Mr Harvey of Counsel appeared for CASA and Mr Taylor of Counsel appeared for Mr Hazleton), evidence was taken of Mr Hazelton and a number of expert doctors, including eight neurologists, and many of those doctors have specialist qualifications or knowledge in aviation medicine. Some of them have the official title of Designated Aviation Medical Examiner (“DAME”) and are authorised medical practitioners for the purpose of determining whether individual pilots meet the standards for issue of Class 1 and Class 2 medical certificates.
5. While the central issues are concerned with the details and technical assessment of the applicant’s neurological capacity and risk to be able to command a civilian aircraft, it is useful to first consider the background facts before addressing the technical medical and neurological evidence, as well as research and epidemiological evidence which the Tribunal must evaluate.
The Facts
6. Shortly put, the aetiological facts are these. Mr Hazelton is an airline captain. He is presently 40 years of age and is married with two young children. He was visiting Sydney on 1 and 2 November 2008 for a 20 year high school reunion. Following the school function, he and a school friend were returning to a hotel in the city. When passing City Hall, they were attacked from behind. The applicant gave evidence that he went to assist his friend who was attacked first and who had a slight disability, when Mr Hazleton was hit from behind. Mr Hazelton fell to the ground and hit his head on the pavement. He was then kicked in the head on the right hand side of his skull above the level of his eye. He was conveyed by ambulance to St Vincent’s Hospital in Sydney. CT scans of his brain initially revealed some bleeding into the right frontal area of his brain as a direct consequence of the assault. In the following 18 months, Mr Hazelton was the subject of medical reviews to assess his fitness to continue as a pilot. Some medical officers from CASA have expressed serious concern that Mr Hazelton may have a heightened risk of post traumatic epileptic seizure with consequential risk to human safety and that of any aircraft he might operate.
The Medical Evidence
7. A very substantial body of medical evidence has been presented to us, a great part of which requires our most detailed evaluation. We have arranged the manner by which we will consider all of it as follows:
(1) The factual background
This consists of: the material setting out the details of Mr Hazelton's head injury; his attendances at Sydney's St Vincent's Hospital and Brisbane's Mater Hospital; the findings on his four CT brain scans and two MRI brain scans; and, his two electroencephalograms.
(2) The expert evidence
This is in three main parts:
· The Radiologists' opinions on the applicant's brain scans;
· The opinions of other expert medical witnesses;
· Other expert evidence;
(3) Our consideration of the evidence.
The Factual Background
The applicant’s head injury
8. First we will collate the evidence presented to us of how Mr Hazelton sustained his head injury, and of the details of the circumstances that immediately followed, before he arrived by ambulance at St Vincent's Hospital, Sydney.
9. How he incurred his injury, and the initial succeeding events, were described by:
· Mr Hazelton, in his first statement of 23 April 2010[1], and during his evidence at the hearing; and,
· His companion that evening, Mr Martin Whiteley, in his statement received on 11 May 2010[2].
[1] Exhibit A5.
[2] Exhibit A7.
10. On 1 November 2008 the two men had attended their boarding school 20 year reunion in Sydney, at and after which Mr Hazelton estimates that he had consumed approximately twelve standard drinks[3]. In the early hours of the next morning, as they were walking along George Street to the Town Hall Railway Station to catch a train to their hotel, he and Mr Whiteley were accosted by several unknown persons. Mr Whiteley was then attacked; Mr Hazelton, on going to his aid, was struck from behind, and fell, striking the back of his head on the pavement, also to be kicked in the head[4]. Mr Whiteley stated "I did not observe any loss of consciousness by Jon", and that he "seemed to be fully aware of his surroundings, the incident and our plans to continue travelling home [to their accommodation for that night]"[5].
[3] Exhibit A5, para 7.
[4] Exhibit A5, para 8.
[5] Exhibit A7, para 7
11. They both "immediately"[6] stood up, and resumed walking to the Railway Station. However a passing bus driver had stopped, to tell them that he had called the police, whereupon they decided to wait for them. Mr Hazleton told us that when the police came, he recalls speaking to a policewoman, and then to ambulance attendants who arrived shortly after. Mr Whiteley states that Mr Hazelton was lucid as he provided his personal information to them. Mr Hazelton then was conveyed by ambulance to St Vincent's Hospital.
[6] Exhibit A5, para 9; Exhibit A7, para 4.
12. Medical documents obtained by summons from St Vincent's Hospital[7] have included a copy of the report from the Ambulance Service of New South Wales[8]. This records that the "booking" call was received at 0403 hrs on 2 November, and that the ambulance attendants arrived at the scene at 0415 hours; the entry continues:
C/T [called to] 38 yr ♂ [year-old male]. O/A [On arrival] police on scene.? Pt [Presumed patient] assaulted by unknown number of males? Pt pushed and punched, hitting occipital [sic] on pavement, now with 3 cm lac [laceration] to occipital [region] and facial swelling and contusions. O/E [On examination] pt GCS [the patient had a Glasgow coma score of] 14, [he was] amnesic for event and confused with injuries [indecipherable: possibly R/L for 'right lateral position'] pt had LOC [loss of consciousness] for unknown amount of time. Pt states [he has had] lots of ETOH [alcohol] tonight. Pt denies PMHx [past medical history of significance]. Pt stable en route [to St Vincent's Hospital). Code 3 passed.
[7] Exhibit 2.
[8] Exhibit 2, p 5.
13. This report also records that he arrived at the St Vincent's Hospital Emergency Department for triage at 0446 hrs, and that he was taken "off [the] stretcher" at 0500 hrs.
St Vincent's Hospital attendance in Sydney
14. In the St Vincent's Hospital's Emergency Department, Mr Hazelton's arrival time is recorded at 0441 hrs[9]. The intern and nursing notes, at 0445 hrs[10] and 0450 hrs[11] respectively, both have recorded the applicant's Glasgow coma score again at 14/15; and he was noted to have a right periorbital haematoma. He was described as "obviously intoxicated", with impaired coordination of all limbs, and showing two beats of bilateral nystagmus (rhythmically jerky movements) of his eyes[12]. At 0504 hrs a sample of his blood was taken for biochemical analysis, and the blood alcohol concentration was measured at 0.21 g/litre[13]; according to the applicant's oral evidence at the hearing, he had had his last alcoholic drink at about 3:00am.
[9] Exhibit 2, p 6.
[10] Exhibit 2, p 11.
[11] Exhibit 2, p 8.
[12] Exhibit 2, p 16.
[13] Exhibit 2, p 56.
15. At 0500 hrs that morning, on the Emergency Department Patient Assessment Record (triage) sheet[14], a printed box marked 'GCS<13' was ticked; we have noted this because specific reference was made to this recording during the cross examination of Dr Drane, the Senior Medical Officer for CASA[15].
[14] Exhibit 2, p 9.
[15] Transcript of Dr Drane's evidence, p 18, lines 32-37.
16. Otherwise, while Mr Hazelton was in the Emergency Department, his Glasgow coma score was consistently recorded at 14 at 0445 hrs[16], 0450 hrs[17], 0500 hrs[18], 0720 hrs[19], and 0745 hrs[20] . Thereafter, it then rose to remain at 15 (1130 hrs[21]); 1325 hrs[22] ; and 1800 hrs[23]).
[16] Exhibit 2, p 18.
[17] Exhibit 2, p 14.
[18] Exhibit 2, p 21.
[19] Exhibit 2, p 15.
[20] Exhibit 2, p 15.
[21] Exhibit 2, p 15.
[22] Exhibit 2, p 15.
[23] Exhibit 2, p 25.
17. We also have noted that, at 1400 hrs on the following day (3 November), the entry for the Ward Round of Drs Faux and Braid has recorded [24]:
GCS 14 ċ Ambos [Glasgow coma score was 14 with the Ambulance attendants] ".
[24] Exhibit 2, p 27.
However, Mr Hazelton's pertinent Glasgow coma score for that time appears 10 lines above this, in the immediately preceding Nurse's entry, as 15/15.
18. When Mr Hazelton was reviewed later on the morning of 2 November by the Emergency Department Registrar, his Glasgow coma score already had risen to 15/15, and his eye movements by now were normal[25]. He also reported impaired left hearing, and otoscopic examination revealed that bleeding had occurred behind his left tympanic membrane (eardrum). Meanwhile, a CT brain scan[26] had been performed at 0528 hrs to show two fractures of his skull, one in the base of his skull, extending longitudinally through the left temporal bone into the middle ear, and a second, minimally displaced, right orbital roof fracture. Intracranially, the scan revealed an 8 mm haemorrhagic right frontal contusion in the brain, and a possible left tentorial subdural haematoma. Because of his basal skull fracture, brain contusion, and possible subdural haematoma, later that day he was admitted into the Neurosurgical Ward[27].
[25] Exhibit 2, p 22.
[26] Exhibit 2, p 53.
[27] Exhibit 2, p 23.
19. Over the night of 2/3 November he also developed a left periorbital haematoma (bilateral "racoon's eyes"). Next morning he was seen by the plastic surgeons, who advised that his right orbital roof fracture required no attention[28]. A review CT brain scan later that morning showed "no adverse change" compared to the first scan[29]. At 1400 hrs, about 34 hours after his assault, it was recorded that he last recalled Mr Whiteley being assaulted, his memories resuming when he was in the Hospital's Emergency Department[30]; according to the times recorded in the ambulance attendants' report, this was a period of loss of memory (post-traumatic amnesia) of approximately one hour. By now he also had developed a mild left facial nerve weakness, which was diagnosed as being related to his basal skull fracture[31].
[28] Exhibit 2, p 25.
[29] Exhibit 2, p 52.
[30] Exhibit 2, p 27.
[31] Exhibit 2, p 29.
20. On the following day (4 November) he still was recorded as having "no memory of events"[32], but no additional details were provided. He now had a troublesome headache, otherwise he was well. Meanwhile, we have noted that, on his daily Patient Assessment sheet, for each day of 2, 3 and 4 November, his Mental Health state had been consistently recorded as "alert/orientated"[33]. We note that the various clinical notes' entries for that day indicate that preparations were being made for his discharge[34]. Because of the bleeding into his left middle ear, he had been advised not to fly back to his home in Brisbane; and because of the nature of his head injuries, he also had been advised against driving for four weeks[35].
[32] Exhibit 2, p 30.
[33] Exhibit 2, p 36.
[34] Exhibit 2, pp 30-33.
[35] Exhibit 2, p 6.
21. On the following day, before leaving the Hospital, he had his third CT brain scan[36]. This also revealed no further change; the reporting radiologist included the comment, "No obvious extra-axial haemorrhages", which we assume, by inference, referred to the earlier possible tentorial subdural haematoma, as was later mentioned by Professor Tress when he reviewed Mr Hazelton's scans.
[36] Exhibit 2, p 51.
22. At the hearing, Mr Hazelton was cross-examined on paragraphs 13, 14 and 15 of his first statement[37]. In these he has stated that, apart from "a few seconds in the act of getting up" he now has "a good recollection of events which occurred during and immediately after the assault"; "a good recollection of travelling to St Vincent's Hospital in the ambulance"; and that he clearly recalls "interacting with the doctors and nurses at St Vincent's Hospital." Under cross-examination he did not change this evidence.
[37] Exhibit A5.
23. In his supplementary statement of 6 May 2010[38] Mr Hazelton related that, on his discharge on 5 November, he was driven home by his mother, during which journey he rested, and they arrived home in Brisbane on the next day. He carried with him his Discharge Summary and a CD of his brain scans, which he had been given by the medical staff at St Vincent's Hospital.
Mater Hospital attendance in Brisbane
[38] Exhibit A6.
24. Although he said that he had had recurring headaches each day following the assault, on the afternoon of Saturday 8 November, he developed a more severe headache. He then vomited twice within three hours, both times after eating food. Because his local General Practice Clinic was closed, his mother drove him to the Mater Hospital Emergency Department, where he showed to the medical staff his St Vincent Hospital Discharge Summary and CT brain scans CD. He was diagnosed with dehydration, and was given an intravenous fluid infusion[39].
[39] Exhibit A6, paras 14 to 18.
25. Attached to Mr Hazelton's supplementary statement[40] are 20 pages of documents of his Mater Hospital attendance. When he was seen at 1944 hrs in the Emergency Department[41], he had graded his level of headache pain at 2/10, and had declined pain relieving medication. The notes record that his left facial nerve weakness had increased and he now had an additional sign of his temporal bone fracture, of bruising over his left mastoid bone ('Battle's sign')[42]. His physical examination otherwise was normal.
[40] Exhibit A6, attachment JH1.
[41] Exhibit A6, attachment JH1, p 8.
[42] Exhibit A6, attachment JH1, p 9.
26. Biochemical tests performed on his blood that evening showed lower than normal levels of sodium (130 mmol/litre, normal range 135-145), chloride (93 mmol/litre, normal range 100-110), and creatinine of 58 μmol/L (normal range 64-104), but the bicarbonate level was normal at 24 mmol/litre, (normal range 22‑33)[43]; his serum osmolality was not measured. At that time he was being given intravenous fluids for his dehydration; in the Emergency Department clinical record, his doctor wrote that these biochemical results were not due to the syndrome of inappropriate antidiuretic hormone secretion, notated as "no SIADH"[44], apparently because the sodium level was not considered to be low enough for this diagnosis. Although the doctor also found "no signs of ICP [raised intracranial pressure]", he wrote up Mr Hazelton for precautionary prednisolone medication; and at 2340 hrs that evening, he was given a single oral 50 mg dose of this[45].
[43] Exhibit A6, attachment JH1, p 2.
[44] Exhibit A6, attachment JH1, p 10.
[45] Exhibit A6, attachment JH1, p 17.
27. He remained in the Emergency Department overnight for observation, pending another CT brain scan, which was performed next morning. The Radiology Registrar, Dr Phillip Law, compared this scan's features with those of Mr Hazelton's three St Vincent's Hospital scans. Dr Law's report appears in the Hospital's papers as it was amended about a year later, on 26 November 2009[46]; as well as describing the unchanged features of the applicant's skull fractures, it reads:
... The right basal frontal haemorrhagic contusion is again noted. The hyperdense central component is now less dense, consistent with expected evolution of blood products. There is a slightly larger area of low attenuation surrounding this region which in today's study measures approx. 3 cm in maximal diameter. No new intracranial haemorrhage or collection is identified. The ventricles and subarachnoid spaces are within normal limits for age. There is no shift of the midline structures and the basal cisterns are patent ...
[46] Exhibit A6, attachment JH1, pp 1 and 2.
28. We note that the sentence in this amended report "No new intracranial haemorrhage or collection is identified" appears to indicate that the only blood seen on this scan was the previously noted right basal frontal haemorrhagic contusion. We have not been given any explanation for the amending of this report.
29. Mr Hazelton was discharged that afternoon, and his Discharge Summary[47] states that he was well, and free of significant headache or further nausea or vomiting.
[47] Exhibit A6, attachment JH1, p 6.
30. His subsequent progress has been uneventful. At the hearing, he said that his facial weakness resolved after another month, and that he since has had no headaches. He has been working with Virgin as a training assistant, such as in flight simulators.
31. He also told us that, since his head injury, he has abstained from alcohol.
The applicant’s two subsequent MRI brain scans
32. Mr Hazelton later had two MRI brain scans.
33. The first was requested by Dr Barry Appleton, after he saw the applicant on 6 March 2009 for neurological opinion by referral from Dr Allan Sutch of Thornlands, the scan being performed on 10 March 2009, at St Andrew's Hospital, Brisbane, by Queensland Diagnostic Imaging. The report was provided by Dr B Clark[48], and reads as follows:
[48] Exhibit A9, attachment BA1.
Clinical Details:
Head injury November 2008 with small intracerebral haemorrhage right frontal region.
Technique:
Sagittal T1, axial T2, FLAIR, diffusion and gradient, coronal T2.
Findings:
There is a 12mm T2 high signal focus with a low signal rim at the inferior margin of the medial right frontal lobe at the floor of the anterior cranial fossa. The appearance is consistent with gliosis and a haemosiderin rim at the site of the patient's known previous haemorrhagic contusion. A further 12mm focus of gliosis at the anterior pole of the right temporal lobe is also consistent with post traumatic gliosis, although there is not [sic] evidence of old blood products in this region. On the gradient weighted imaging there is a further 6mm focus of subcortical susceptibility in the left posterior parietal lobe, likely at a site of previous haemorrhage. No susceptibility is seen elsewhere, and in particular the deep white matter is unremarkable, with no evidence of diffuse axonal or shearing injury.
There is no hydrocephalus or evidence of raised intracranial pressure. No extracerebral collection is seen.
Impression:
Gliotic change is seen at the anteroinferior right frontal lobe and anterior pole of the right temporal lobe, consistent with the sites of injury seen on the previous CT scan[sic]. Minor susceptibility in the posterior left parietal lobe is consistent with a previous site of petechial haemorrhage.
34. The second scan was ordered by Neurologist Dr Ian Maxwell, after Dr Sutch also sought his opinion on 11 December 2009, and was conducted two days later at John Flynn Hospital, Tugun. The report[49], provided by Drs Paul Hayes and Robert Mason, is as follows:
[49] Exhibit 1, ST8/17-18.
Sequences
T1 sagittal, FSE T2 fat saturation axial, FLAIR axial, gradient T2#axial, T1 axial, diffusion axial, T1 coronal of orbits and anterior coronal fossa, STIR coronal of orbits and anterior and middle cranial fossa.
History
Right orbital fracture, and left temporal bone fracture. Assaulted in Sydney. Follow up of right temporal lobe abnormality.
Findings
There is no hydrocephalus. There is no displacement of midline structures. There is no abnormal signal of deep white matter. The pons and brain stem have a normal contour and exhibit normal signal.
Each optic nerve has a normal appearance. On the coronal images no entrapment of the right inferior rectus muscle has been demonstrated.
Related to the anterior aspect of the right temporal lobe in the middle cranial fossa there is a signal abnormality which is relatively well defined measuring 10.8mm x 9.8mm. It is quite difficult to be sure whether this is intra-axial or extra-axial, but has features suggesting is extra-axial. It is of high signal on the T2 (fat sat) images and of low signal on the T1 images. This is in keeping with it being fluid. On the gradient sequence there is no indicating [sic] of blood products associated with this lesion.
Careful comparison has been made with the previous MR of 15/06/09 [sic] presented on disc. There has been absolutely no change in the size or characteristics of the lesion.
This lesion is most in keeping with an incidental arachnoid cyst, and this is a common position for an arachnoid cyst. With the lack of blood products on the gradient study a cerebral contusion would be most unlikely.
Summary
Incidental right middle cranial fossa arachnoid cyst unchanged from the previous MR of 15/06/09 [sic]. The MRI brain is otherwise normal.
The applicant's two electroencephalograms (EEGs)
35. He had his first EEG reported on 12 February 2009 by Dr Alison Reid, Neurologist of Springwood, this reading[50]:
The patient was alert and co-operative. There is a well formed and distributed 9 Hz alpha rhythm which is symmetrical and attenuates with eye opening.
Faster beta activity is seen bifrontally.
Response to hyperventilation and photic stimulation is normal.
COMMENT: This is a normal symmetrical record.
[50] Exhibit 1, T22/69.
36. His second EEG was reported on 16 December 2009 by Dr Ian Maxwell, Neurologist of Southport, as follows[51]:
REPORT
There is bilateral symmetrical 10 Hz alpha activity 30 μV in amplitude which attenuates on eye opening. There is no focal or paroxysmal activity or asymmetry in the resting record or on hyperventilation or photic stimulation.
COMMENT
Within normal limits. No asymmetry or dysrhythmic/overt epileptic features. A very stable and normal recording. No evidence of any post-traumatic changes.
[51] Exhibit 1, ST8/16.
The Expert Evidence
The Radiologists' Opinions on the Applicant's Brain Scans
37. Mr Hazelton’s CT and MRI scans collectively have been reviewed by three radiologists, and their opinions are contained in the following material:
· Three letters[52] from Professor Brian Tress, Radiologist of Royal Melbourne Hospital.
· Letter[53] from Dr Maurice Moriarty, Neuroradiologist of Trinity MRI, Auckland, New Zealand
· Statement[54] from Dr John Earwaker, Radiologist of Brisbane.
[52] Exhibits R5, R6 and R7.
[53] Exhibit R9, appendix 7.
[54] Exhibit A17.
38. These doctors were not called to give evidence at the hearing.
Professor Brian Tress
39. The only scan not studied by Professor Tress was the Mater Hospital CT scan. Of the first of the St Vincent's Hospital scans, as well as the fractures, he described “an inferior right frontal haemorrhagic region surrounded by decreased density immediately superior to the fracture, consistent with contusion and oedema." Also, he mentioned a thin layer of "Hemorrhagic density material" related to the tentorium cerebelli, possibly a subdural haematoma or subarachnoid blood. He also considered the brain's ventricles and sulci to be smaller than normal, suggesting diffuse brain swelling. In the other two subsequent CT brain scans, the tentorium cerebelli changes and diffuse brain swelling had resolved.
40. He interpreted the first MRI brain scan findings to indicate "blood breakdown products" in the right temporal pole tip, extending into the white matter, and in the inferior right medial frontal lobe. In the second MRI study, these again were seen, and were unchanged; and he referred to a third, much smaller (approximately 6 mm x 3 mm), left temporal pole defect.
41. He concluded that these findings were of three contusions, one in each temporal pole tip and the third in the right inferior frontal lobe, remarking: "These are classical sites for contusions, no matter where the point of impact”[55].
[55] Exhibit R5, p2.
42. Subsequently, in response to an e-mail from CASA Senior Medical Officer, Dr Michael Drane, and then a letter from CASA's solicitor, Professor Tress wrote two letters enlarging on these observations[56]. At Dr Wallis’ suggestion[57] Dr Drane had referred him to an article by Messori et al[58]. In the first letter, Professor Tress wrote:
Messori et al ... have further divided the haemorrhagic lesions into isolated haemosiderin deposition, haemosiderin incompletely surrounded by gliosis and haemosiderin completely surrounded by gliosis. The incompletely gliosis surrounded haemosiderin lesions were found to be the most significant of these lesions and the contusions without haemosiderin the least significant. The lesions illustrated appeared to be mainly subcortical. They did not describe any of the cortices being destroyed, as is the case with both the right temporal pole and right subfrontal lesion in Mr Hazleton [sic]. They were hampered by a lower strength magnet (1 Tesla) with thick slices and both decreased spatial resolution and susceptibility (haemorrhage) detection compared with the almost universally used 1.5 Tesla magnets and occasionally used 3 Tesla magnets ... today's 3 Tesla magnets are at least 9 times more sensitive in detecting haemorrhages. The numbers are small. Nevertheless, the prospective study does contribute useful MRI information not previously available.
In trying to fit Mr Hazleton's [sic] lesions into the classification, I can only conclude that both his right temporal and right frontal lesions must be in the group described as gliosis incompletely surrounding haemosiderin deposits. Because both the temporal and frontal cortices are partially destroyed and the residual damaged tissue is superficially lined by haemosiderin deposits, there is no brain tissue of any kind surrounding or forming a complete ring around the haemosiderin. The small left frontal [sic: amended in Exhibit R7 to 'small left temporal'] lesion is easier to fit in their classification. It is gliosis without haemosiderin.
I may have been a little too polite and even-handed in discussing the nature of the right temporal pole lesion. It virtually certainly is an old haemorrhagic contusion, as is the inferior right frontal lesion. The smaller left frontal [sic: amended in Exhibit R7 to 'smaller left temporal'] lesion is also most likely a contusion in which residual haemorrhage is sufficiently small that it is not detectable. The two right sided lesions are associated with gliosis, haemorrhage and cortical destruction. I agree with Dr Wallis. They have nothing to do with tiny punctate haemorrhages.
[56] Exhibits R6 and R7.
[57] Exhibit R8.
[58] Messori A et al, “Predicting Posttraumatic Epilepsy with MRI: Prospective Longitudinal Morphologic Study in Adults” (2005) 46 Epilepsia 1472; Exhibit A9, attachment BA4.
43. In his second letter[59], after correcting the typographical errors in Exhibit R6, Professor Tress added the comment:
The “right frontal and right temporal lesions fall under the classification off [sic] HG [haemosiderin dregs associated with gliosis] with IW [incomplete wall]. The left temporal lesion falls under the classification G [isolated gliosis].
[59] Exhibit R7.
Dr Maurice Moriarty
44. Dr Moriarty has provided a report on the second MRI scan. He described a 1.8 cm area of gliosis with minor associated haemosiderin in the right anteromedial temporal lobe, and a similar sized change in the right anteroinferior medial frontal lobe; and there appeared to be a 6 mm "focal parenchymal loss" in the left anteromedial temporal lobe.
45. In the fourth of his reports[60] Dr Wallis also mentioned that Dr Moriarty and he had examined CD-ROMs of Mr Hazelton's CT and MRI scans, although no report was presented.
[60] Exhibit R12, p 3.
46. As well, a reference was made by Neurologist Dr William Wallis in his fourth report[61] to "the last MR scan on 26.3.10", in which he says that Dr Maurice Moriarty has provided a report. However this has not been mentioned elsewhere, and no MRI scan of that date or its report has been included in the evidential material presented to us.
Dr John Earwaker
[61] Exhibit R12, p 3 para 2, line 8.
47. Dr Earwaker examined and reported on all four CT brain scans, and the MRI brain scans performed on 10 March and 13 December, 2009[62]. In the initial CT scan, as well as the two fractures, and their associated changes, he described "a small focal contusion on the inferior surface of the right frontal lobe", without brain swelling, subarachnoid or extra-axial blood. In the subsequent CT scans, he said that, in the right inferior frontal contusion, the focal haemorrhage was resolving, accompanied by surrounding swelling of the brain surface (cortex); and the second and third scans showed "an evolving focus of low attenuation in the right temporal pole consistent with a contusion."[63]
[62] Exhibit A17
[63] Exhibit A17, para 4, line 4.
48. He also described the first MRI brain scan to demonstrate a “lesion in the cortex of the tip of the right temporal pole”, extending into the white matter, containing haemosiderin deposits, and similar grey matter changes in the inferior right frontal lobe. There was no abnormality in the left frontal or temporal lobes. In the later MRI scan, the right temporal and inferior right frontal changes were unchanged, but consistent with evolving haemorrhagic contusions. He also mentioned an additional change, not present in the previous MRI scan, in the medial left temporal lobe, which he considered to be of uncertain significance.
Other Medical Witnesses
49. The medical witnesses for the applicant were:
· Dr Barry Appleton, Neurologist of Brisbane, with a letter[64] and a statement[65]; he also gave evidence in person to the hearing.
· Associate Professor Richard Stark, Neurologist of Melbourne, who provided a report[66].
· Two letters[67] and a statement[68] from Dr John Hastings, Neurologist of Tulsa, Oklahoma; he also provided evidence by telephone to the hearing.
· Two statements[69] from Dr Jeffrey Brock, Designated Aviation Medical Examiner of Robina, who also gave evidence by telephone.
· A statement[70] by Dr Eric Donaldson, Designated Aviation Medical Examiner of Oakey who also gave evidence in person to the hearing.
· Two statements[71] from Dr Robert Liddell, Designated Aviation Medical Examiner of Bicton, Western Australia.
· A statement[72] by Dr Sham Tak Sum, a CASA Medical Officer of Giralang, ACT.
· Three statements[73] by Dr Roderick Westerman, Physician, Neurophysiologist and Designated Aviation Medical Examiner of East Kew, Victoria; he also gave evidence by telephone.
· An e-mail comment[74] by Dr Tamara Bushnik, Rehabilitation Research Physician of New York.
· Dr Allen Hauser, Neurologist of New York, gave evidence to us by telephone.
[64] Exhibit A1
[65] Exhibit A9.
[66] Exhibit A2.
[67] Exhibits A3 and A4.
[68] Exhibit A13.
[69] Exhibits A10 and A11.
[70] Exhibit A12.
[71] Exhibits A14 and A15.
[72] Exhibit A16.
[73] Exhibits A18, A19 and A20.
[74] Exhibit A18, appendix D.
50. Both Neurologists Dr Appleton, Associate Professor Stark, and Physician and Neurophysiologist Dr Westerman, all had personally interviewed and examined Mr Hazelton.
51. The respondent's expert medical evidence was provided by:
· Two statements[75] from Dr Alan Drane, Senior Medical Officer for CASA, who gave evidence in person.
· A statement[76] by Dr Pooshan Navāthé, Principal Medical Officer for CASA; he also delivered a PowerPoint presentation[77] at the hearing.
· Four reports[78] and a medical note [79] from Dr William Wallis, Neurologist of Auckland, who also appeared at the hearing.
· Dr John Cameron, Neurologist of Brisbane, who had interviewed and examined Mr Hazelton, provided a report[80].
[75] Exhibits R2 and R3.
[76] Exhibit R4.
[77] Exhibit 3.
[78] Exhibits R8, R9, R10 and R12.
[79] Exhibit R11.
[80] Exhibit R13.
52. As well, on file we had a report[81] from Dr Ian Maxwell, Neurologist of Southport, and a Designated Aviation Medical Examiner, who also had interviewed and examined Mr Hazelton.
Dr John Cameron, Neurologist
[81] Exhibit 1, ST8/14-15.
53. Dr Cameron was the first of the Neurologists to see Mr Hazelton, this consultation being held on 14 January 2009, by referral from both his local doctor and his solicitors. His report of 16 January 2009, addressed to Dr Ian Thursgood of CASA[82], first summarised the history that he obtained of Mr Hazelton's head injury. He recorded, inter alia:
.... There was a brief period of impaired recall surrounding the event but he had sketchy recall coming about half an hour later. He can recall lying on the ground and a bus driver coming to his assistance and he can then recall being attended to by the Emergency Services and also talking to the Police.
[82] Exhibit R13; Exhibit 1, T25/72-74.
54. He listed his injuries, and the first CT brain scan findings; and remarked, "He recovered quickly." Apparently Mr Hazelton did not mention his Mater Hospital attendance to Dr Cameron.
55. He had no residual symptoms from the assault, including none suggesting any form of epileptic disturbance. He had returned to work in administration at Virgin Airways. He had no previous history of epilepsy or head injury.
56. His detailed physical examination was normal, apart from a mild left facial weakness.
57. Dr Cameron opined that Mr Hazelton probably would not resume flying for five years "because of the risk of post-traumatic epilepsy developing from his frontal lobe contusion and subdural bleed." He estimated his current post-traumatic epilepsy risk to be 20-30%, to "decrease by about 75% over the next 2 years and then gradually back to a normal risk of epilepsy … by about 5 to 7 years."
58. Dr Cameron was not called to give evidence at the hearing.
Associate Professor Richard James Stark, Neurologist
59. Associate Professor Stark of Melbourne has conducted his Neurology practice for nearly 30 years. Mr Hazelton's General Practitioner, Dr Sutch, referred him for his opinion, and Dr Stark wrote back to him on 25 June 2009; his letter[83] is included in the Tribunal documents.
[83] Exhibit 1, T13.
60. Associate Professor Stark was the third Neurologist to assess Mr Hazelton. He took a detailed history, and examined him, to find no abnormality.
61. He examined Mr Hazelton's CT scans from St Vincent's Hospital, noting "a small right frontal contusion adjacent to the fracture of the right superior orbital margin." He also inspected his MRI brain scan of March 2009, and remarked:
... this appears to show two small areas of gliosis; one in the right frontal region and one in the right anterior temporal region. I do not believe that there are any areas that I can see in which hemosiderin is present without surrounding gliosis.
62. He went on to say:
The problem he is facing that [sic] that the injury included a fracture of the right orbital roof with some contusion of the underlying cerebral cortex. The head injury was otherwise not a substantial one as there was no prolonged period of post-traumatic amnesia and no apparent loss of consciousness.
63. He then referred to an article by Englander et al[84], to make the following points:
· More than 80% of patients developing late post-traumatic epilepsy will have their first seizure in the first 12 months post-injury; more than 90% had their first fit within the first 18 months.
· The authors graded the late post-traumatic seizure risk according to a lowered initial Glasgow coma score, the occurrence of early post-traumatic seizures, and any midline shift of cerebral structures on CT scanning, none of which applied to Mr Hazelton.
· However patients with one subcortical cerebral contusion had a post-traumatic epilepsy incidence of 8.2 per cent, increasing to 25% with multiple contusions.
[84] Englander J et al, "Analyzing Risk Factors for Late Posttraumatic Seizures: a Prospective Multicenter Investigation" (2003) 84 Archives of Physical and Medical Rehabilitation 365; Exhibit 1, T1/19-27.
64. He added that the MRI study reported by Messori et al[85] suggested that contusions with haemosiderin entirely surrounded by gliosis carried a relatively smaller epilepsy risk.
[85] Messori et al, n 58.
65. From these observations, apparently on the basis of the Englander et al data for one cerebral contusion, he offered a conservative estimate that Mr Hazelton's total risk of epilepsy at the date of his injury was 8%, reducing by 80% after one year, and by 90% at 18 months, i.e. 12 months following his injury without seizures his risk would be about 1%, and significantly less than this at 18 months.
66. He also observed that it was in Mr Hazelton's favour that his flying always was performed "as or with co-pilot".
67. Associate Professor Stark also was not called to provide evidence at the hearing.
Dr Ian Cairns Maxwell, Neurologist
68. Dr Maxwell is a Neurologist who has practised at Southport, Queensland, for 30 years. He also is a Designated Aviation Medical Examiner. He was the fourth Neurologist to examine Mr Hazelton, and saw him on 11 December 2009, again at the request of Dr Sutch. His letter, a copy of which he sent to Dr David Fitzgerald of CASA, forms part of the Tribunal documents[86].
[86] Exhibit 1, ST8/14 to 15.
69. After obtaining his history, Dr Maxwell examined him and found no neurological abnormality.
70. He recorded:
There is no history of any loss of consciousness and certainly no suggestion of any retrograde or anterograde amnesia to suggest more than a mild head injury.
71. He commented that Mr Hazelton had "a very slight risk" of having an epileptic seizure in the first 12 months post-injury, which would be "dramatically reduced" at the end of that period.
72. Dr Maxwell arranged for him to have his second EEG, and his second MRI scan; the latter was performed on 13 December. Although Dr Maxwell's letter to Dr Sutch is dated 11 December, it appears that Dr Maxwell held this over, until he had taken his "latest" MRI scan to his Hospital's Neuroradiology Meeting, to discuss it with his neurologist and neurosurgeon colleagues. He told Dr Sutch that the reported incidental right temporal arachnoid cyst was considered of no clinical consequence, and his small inferior right frontal contusion was regarded as "unlikely to cause any long-term problem".
73. He opined that any risk of post-traumatic epilepsy would be "miniscule", observing that Mr Hazelton was "in a very safe operating environment where the incapacity of both the Captain and the First Officer is extremely unlikely."
74. Dr Maxwell did not give evidence at the hearing.
Dr Pooshan Dattatraya Navāthé, Principal Medical Officer for CASA
75. Dr Navāthé has been a specialist in Aerospace Medicine for 22 years, and has worked as an occupational physician for most of his professional working life in the military, and subsequently in his regulatory positions. After 10 months as Senior Medical Officer with CASA, he has been the Principal Medical Officer since December 2008. Before that he was a Senior Medical Officer at the Civil Aviation Authority of New Zealand for seven years, following 22 years as a medical officer with the Indian Air Force. He has held Professorial appointments, and been Head, of the Department of Aviation Safety and Crew Performance, Human Factors Division, at the Institute of Aerospace Medicine in India. He continues in the appointment of Senior Lecturer and Course Director for Aviation Medicine at the University of Otago.
76. In his statement[87] he summarises his in-cockpit flying experience as "in excess of 1200 hrs in helicopters, 750 hrs in military transports, and 50 hrs of fast jets (fighters)." He has listed 28 publications in Aviation Medicine peer-reviewed journals.
[87] Exhibit R4, appendix B.
77. In his statement he began by introducing aviation medicine as:
... the branch of medicine concerned with human capacity to safely and effectively perform complex tasks in the potentially hostile aviation working environment.
78. He stated that, worldwide, most civil aviation regulatory medical practice consists of assessing professional and non-professional pilots and air traffic controllers against defined medical standards. Currently there are four full-time aviation medicine specialist practitioners in the Australian civil aviation industry, all working with CASA. About another half-dozen full-time practitioners are employed in the Australian Defence Force. As well, a large number of practitioners throughout Australia work part-time as Designated Aviation Medical Examiners (DAMEs), having completed a CASA approved course.
79. He next outlined aviation medicine's regulation. Internationally the International Civil Aviation Organisation (ICAO) includes in its functions the adoption of international standards and practices pertaining to air navigation, and the registration of aircraft and certification of personnel such as flight crew. ICAO medical provisions for licensing aviation personnel include those for issuing commercial and airline pilot licences. The standards to be applied generally have been implemented in Australian law.
80. Domestically, the Australian civil aviation medical certification system is governed by the Civil Aviation Act 1988 (Cth) ("the Act"), the Civil Aviation Regulations 1988 (Cth), and the Civil Aviation Safety Regulations 1998 (Cth) (“the CASR”). Medical certificates are subject to differing maximum validity periods; the usual maximum is four years, and it is very unusual for it to be less than three months. Currently over 35,000 pilot licences and air traffic controller licences are on issue from CASA, 5700 being for commercial pilots. Approximately 42,000 Australian civil aviation medical certificates were issued during the past 12 months, some 8500 being first-time certifications. The 700 DAMEs and the CASA Office of Aviation Medical staff are directly involved in these certifications.
81. He then expanded on the "System of Regulatory Aviation Medicine in Australia", in three sections:
A. Regulatory Medical Decision-Making:
82. CASA Office of Aviation Medicine (AvMed) develops and administers medical standards to licence holders in air transport, general aviation and air-traffic control operations, in accordance with Civil Aviation Safety Regulations. CASA also prepares guidance material and advice. As well it:
· appoints, oversees and educates DAMEs; and,
· provides expert aviation medicine regulatory advice.
83. Complex medical cases are determined by consensus on a collective collegial basis by the AvMed medical officers. Wherever possible, their decisions are evidence based on appropriate medical and scientific research literature, with consultation with appropriate specialists. Medical evidence is often imperfect, but not necessarily ignored by CASA if it can be applied reasonably.
84. Any aviation medical certification system involves acceptance of the existence of medical risk, and risk management is a fundamental function of CASA medical officers, who seek a balance between safety and excessive restriction. Any certificate applicant with a medical condition has the risk assessed, as well as the effectiveness and reliability of its risk mitigation efforts. The terms "safety‑relevant" and "likely" are used in Australian civil aviation medical legislation. "Safety-relevant" is applied to medical conditions; and "likely" assumes importance when judging that a condition "is not likely to endanger the safety of air navigation".
85. Numerical criteria are used to estimate if a medical condition impairs an applicant's capabilities to a "safety-relevant" extent, defining a boundary which is ultimately based on judging if there is a real and substantial (and not trivial) risk to air navigation safety.
B. Consulting Clinical Specialists:
86. Specialists are regularly consulted regarding diagnosis or prognosis for medical conditions. When conflicting opinions are obtained, such as when an applicant in a disputed decision engages clinical specialists, CASA has to weigh the various opinions, in the context of each specialist's experience and expertise in aviation medicine and medical certification decision-making.
C. Making Decisions:
87. Sometimes AvMed decisions have to be made on imperfect or contradictory medical history or information. The clinical consultant specialist provides one of many components in this decision process, including to identify if the condition is safety-relevant and its prognosis - vital in the decision process. However the certification decision requires different information, expertise and skill set.
88. When new information is received after a decision is made, the decision is reviewed, resulting in such outcomes as:
· decision reversal;
· further information is sought;
· a different decision; and,
· no change.
Regulatory decisions are not permanent.
89. Applicants who do not meet medical standards cause the most difficult decisions, of making judgment of the "extent to which (the applicant) does not meet the standard is not likely to endanger the safety of air navigation". This requires:
· knowledge of the standards;
· knowledge of the extent to which the applicant varies from these standards;
· understanding air safety navigation;
· understanding the effect on air safety navigation of medical conditions;
· understanding which mitigators are available;
· understanding the extent to which mitigators are effective.
90. Only an individual who clearly understands the standards as defined by "safety-relevance" can decide whether a person meets the standards, because this is more of a judgment than a determination. This can only be informed by a high level of clinical competence, with understanding of concepts of aviation safety, its compromising by medical conditions, and possible mitigations of these.
91. The appropriate consultant to express a definitive opinion or make an operative decision must have either all of the competencies, or draw upon them as needed. The Australasian Faculty of Occupational and Environmental Medicine describes Occupational Medicine as:
... a medical specialty where highly-trained specialists focus on the effects of work on health and (conversely) health on work. It understands the full range of workplace and environmental hazards (chemical, physical, biological & psychosocial), associated risks of exposure to such hazards, and how these may cause an adverse impact on biological health, such as injury or illness. It covers all occupational/work groupings, and understands the nature of such work in terms of inherent task requirements, environment, and human ergonomics (Dr Navāthé's emphases).
92. Occupational physicians in aviation medicine meet five of the six competencies needed for aeromedical decision-making, perhaps with adequate clinical expertise also in some areas, but it is common for the occupational physician to seek the expertise of the relevant clinical specialist in making a specific decision.
93. However, there is a significant "disconnect" between the occupational and the clinical perspectives. A clinician's decision is based on the best long-term outcome for the patient, and the accepted level of risk is based at that which does not unduly compromise the individual's day-to-day life. Conversely, the prime occupational health issues are the effects of the individual's condition and its treatment on work safety. The accepted risk level is based on the safety of the individual and of others in the workplace. Such decisions may be of limited duration (1 to 4 years), placing a short-term viewpoint on the issues.
94. Next there is the dealing with uncertainty, defined as "a state of having limited knowledge where it is impossible to exactly describe existing state or future outcomes". Medicine is an uncertain science; different medical practitioners may conclude differently from the same information. In the latter case the opinions can be "benchmarked" against evidence in peer-reviewed literature; but when a diagnosis cannot be formed, a risk management decision becomes obligatory, based on the constellation of symptoms and other available clinical information.
95. When clinical information, investigations, and specialist opinions do not lead to an unequivocal diagnosis, sometimes nothing more can be done than issuing a certificate. Unless CASA can be satisfied that issuing a medical certificate will not adversely affect air safety navigation, CASA has no ability to do so.
96. The paramount factors in regulatory aeromedical decision-making are identified in section 9A of the Act, which states:
In exercising its powers and performing its functions, CASA must regard the safety of air navigation as the most important consideration.
This holds primacy over any other relevant considerations, including an individual's rights.
97. At the hearing, Dr Navāthé commenced his evidence-in-chief by giving us a PowerPoint presentation on Aeromedical Decision-Making in Cases of Traumatic Head Injury[88]. He also had presented this only days before at an international aerospace medical conference in Phoenix, Arizona, from which he had just returned.
[88] Exhibit 3.
98. He began by referring to section 180 of Part 67 of the CASR, which sets out the two circumstances by which, following an incident such as a head injury, a medical certificate should be issued: either if the applicant meets the relevant medical standard; or, if not, the extent to which the standard is not met, the applicant is not likely to endanger the safety of his/her navigation.
99. With regard to head injury, four possible outcomes constitute potential dangers viz cognitive impairment, post-traumatic epilepsy, focal neurological sequelae, and (other) late complications. The first two of these are the most important.
100. Cognitive impairment is measurable, but may be difficult to evaluate because pilots generally have above-average cognitive capabilities. Testing of this after an injury may show that the pilot meets population parameters, but this does not necessarily indicate that he/she is no worse since the subject injury; and only one or two airlines perform "baseline" neurocognitive testing on their pilots when they first employ them.
101. Focal neurological sequelae can occur if part of the brain is damaged. In their various forms these are relatively straightforward, because they are overt, and are readily detected on neurological examination. These, and late neurological sequelae, do not apply to Mr Hazelton's case.
102. However, any possibility of post-traumatic epilepsy constitutes a real risk. At the recent international aerospace medical conference, Dr Hastings presented a case of a pilot who had a tonic-clonic seizure in the cockpit. His foot hit the rudder pedal so hard that he fractured his ankle, with the risk of a disastrous inappropriate control input.
103. Yet the measurement of the risk of developing post-traumatic epilepsy is not easy. First, it entails estimations, derived from evidence-based medicine, of such statistical measurables as incidence and prevalence data of post-traumatic epilepsy. Second, the CASA medical officers look for aeromedical factors that could change the likelihood of a seizure-induced aviation; for example, Mr Hazelton has completely stopped taking alcohol, which reduces the risk. On the other hand, hypoxia (oxygen lack) from flying at higher amplitude increases the epileptic potential.
104. The next question to be examined is that of the acceptable level of risk for aviation purposes. Here the aviation medicine paradigms of the so-called "1% Rule", "2% Rule" can be used. However, if the person does not meet the acceptable risk, the CASA staff attempt to manage the risk by managing likelihood.
105. Risk is a function of consequence and likelihood. In other words, how likely is it that something will happen; and if that happens, what are its consequences? Both of these questions are considered in deciding how much risk is acceptable, and at CASA the likelihood is managed by these processes.
106. With some situations intervention, such as with medication, is possible. However, for post-traumatic epilepsy, there is nothing else to be done than to wait for a particular period of time to pass to allow the risk to diminish to an acceptable level.
107. If CASA is not satisfied that the person's risk is acceptable, they then try to manage its consequences. With Mr Hazelton, this is the place of considering "with or as co-pilot" certification; and there are numerous other ways in which the consequences of this situation can be limited.
108. The next step is to consider the severity of the subject head injury. This is because the head injury severity directly influences the risk of post-traumatic epilepsy. For this, the peer-reviewed medical scientific literature on post-traumatic epilepsy is consulted.
109. Earlier reported studies such as Jennett[89] and Annegers et al[90] used clinical features to classify head injuries into three categories, mild, moderate and severe. For example, if the associated post-traumatic amnesia or loss of consciousness lasted for less than half an hour, or there were no persisting neurological signs or no skull fracture, the head injury was classed as mild. Loss of consciousness or duration of post-traumatic amnesia for more than half an hour but less than 24 hours, or non-depressed skull fracture, constituted a moderate injury. Longer amnesic or unconscious periods than 24 hours, brain injuries such as intra or extracerebral haematomas, depressed skull fracture, persisting neurological signs, or an early epileptic seizure within one week of the injury, automatically marked the injury as severe.
[89] Jennett B, Epilepsy after Non-Missile Head Injuries (2nd ed, William Heinemann, London, 1975).
[90] Annegers JF, Grabow JD et al, "Seizures after Head Trauma: a Population Study" (1980) 30 Neurology 683.
110. However, in 1998 Annegers et al[91] reported their completed 50 year study in Minnesota for 4500 people, and this showed no clear relationship between these clinical features and risk of post-traumatic epilepsy; but there was a clear correlation with bleeding either around the brain (extracerebral) or within it (intracerebral).
[91] Annegers JF, Hauser WA et al, "A Population-Based Study of Seizures after Traumatic Brain Injuries" (1998) 338 New England Journal of Medicine 20; Exhibit 1, T1 folios 14-18.
111. Meanwhile, 10 years earlier D'Alessandro et al[92] had shown, in 220 individuals, that bleeding into the brain was an independent variable: all subjects with intracerebral bleeding shown on their CT brain scans developed post-traumatic epilepsy, whereas none with normal CT scans did. Three years later Jamjoom et al[93] reported that the combination of intra and extracerebral bleeding further increased the post-traumatic epilepsy risk.
[92] D'Alessandro R, Ferrara R et al, "Computed Tomographic Scans in Post-Traumatic Epilepsy" (1988) 45 Archives of Neurology 42.
[93] Jamjoom AB et al, "Epilepsy Related to Traumatic Extradural Haematomas" (1991) 302 British Medical Journal 448.
112. To satisfy evidence-based medicine standards, there has been much discussion about the relatively small numbers in these studies of subjects with post‑traumatic epilepsy. Then, last year, from Denmark, Christensen et al[94] published their study of 1.6 million people from 1977 to 2002, of whom some 78,000 had traumatic brain injury; and they had followed them for 10 years. They identified that the relative risk of post-traumatic epilepsy was increased seven times in the subjects who had intracranial bleeding. The large numbers of persons in this study conferred a high level of confidence on these results.
[94] Christensen J et al, "Long-Term Risk of Epilepsy after Traumatic Brain Injury in Children and Young Adults: a Population-Based Cohort Study" (2009) 373 Lancet 1105; Exhibit 1, T1 folios 6-13.
113. When blood is present in the brain, it haemolyses or breaks down, and releases iron as ferrous ions. Research has shown that, through formation of hydrogen peroxide, oxygen, and hydroxylase in brain tissue, these cause what is called a lipid peroxidation injury; and in the brain, by affecting the DNA of the nerve cells, this change predisposes to epileptic seizures.
114. Thus, the evidence is compelling that traumatic bleeding into the brain, rather more than other risk factors, is the key to whether post-traumatic epilepsy will follow a head injury.
115. This means that the paradigms of risk assessment must be changed, to re‑classify any head injury of a person applying for an aviation medical certificate, according to:
· The factors affecting aviation risk.
· Initial risk estimates.
· How the risk changes over time.
116. If a person reports a traumatic brain injury, the assessing CASA medical officers first ask if the person has sustained a cognitive defect. If so, in the aviation setting, the person has to wait for cognition to return to normal before being considered for a medical certificate. However, if cognition has been unaffected, attention turns to the risk of post-traumatic epilepsy. If imaging was not performed, the person's head injury is classified according to Jennett's clinical criteria[95].
[95] Jennett, n 89.
117. If a CT brain scan has been performed, the person's head injury classification is based on a paradigm from two studies, one being that of Annegers et al[96]. The other is a more recent report by Englander et al[97], which followed up, for a limited period of two years, 647 head-injured subjects either with abnormal CT brain scans, or clinically more severe head injuries; they also found that the presence of bleeding into the brain was a significant risk factor.
[96] Annegers, Hauser et al, n 91.
[97] Englander et al, n 84.
118. If the person has not had a CT brain scan, but has had an MRI brain scan, the assessment of the aviation risk is not clear, simply because, as yet, insufficient studies have been published to allow confident application of the findings to this risk analysis exercise.
119. So, with the present information available, the first question to ask is, what is the initial risk? However, referring to the results of Jennett[98] and Annegers et al[99] for bleeding inside the head (extracerebral and/or intracerebral) raises difficulties, because these two studies obtained differing risk figures for both extracerebral bleeding, and intracerebral bleeding, although they accord fairly closely for a combination of the two. Although other differing figures again have been reported by D'Alessandro et al[100] and Jamjoom et al[101], they also show that combined intracerebral and extracerebral bleeding indicate a higher initial risk of post-traumatic epilepsy than all other form of bleeding alone.
[98] Jennett n 89.
[99] Annegers, Hauser et al, n 91.
[100] D'Alessandro , Ferrara et al, n 92.
[101] Jamjoom et al, n 93.
120. The prospectively conducted Englander et al study[102], although limited by its two year duration, found that with a single cerebral contusion the initial risk is about 12%, but rises for multiple contusions to about 30%.
[102] Englander et al, n 84.
121. Therefore the classification of head injury severity is simply based around the answers to the questions:
· Has bleeding occurred into the brain?
· Where has the bleeding occurred?
· How many contusions are there?
122. Knowing the initial risk, assessing CASA medical staff next want to know when that risk will decay to a number which can be regarded as acceptable. The Annegers et al report[103] has used a measure called standardised incidence ratios, which approximates to relative risks. Dr Navāthé had charted on a graph the Annegers et al figures obtained for probability (in percentage) for developing post-traumatic epilepsy, against the number of years elapsed since the injury, with three separately plotted lines for mild, moderate, and severe head injuries. For severe head injuries, i.e. bleeding in the brain, the line does not flatten out until about 20 years post-injury. Similar results are obtained by doing the same charting for the figures from the Englander et al[104] report. Also, Christensen et al[105] have constructed their own relative risk graph over a 10 year period, at the end of which time, for severe head injuries, the relative risk is still about five times greater than normal.
[103] Annegers, Hauser et al, n 91.
[104] Englander et al, n 84.
[105] Christensen et al, n 94.
123. Dr Navāthé showed us that British neurosurgeon Dr John Firth has studied the original results of Jennett[106], of more than 1000 head-injured subjects of whom 481 developed post-traumatic epilepsy; from this data Dr Firth had created a regression equation which informs at what age post-injury the residual epilepsy risk would be. His calculation has shown that, for one contusion, the initial post‑traumatic epilepsy risk is about 12%, reducing at one year to between 5% and 7%, and at two years it is between 3% and 5%. However, for multiple contusions, the initial risk is between 30% and 35%, at one year 16% to 19%, and at two years 12% to 14%.
[106] Jennett n 89.
124. Accordingly, when making aeromedical decisions of post-traumatic epilepsy risk, three matters must be examined.
125. The first is the initial risk, which is the risk of post-traumatic epilepsy that applies when the injury is first sustained. Attention is directed at whether bleeding has occurred inside the head, and whether it is located inside or outside the brain. If it has bled into the brain, it then is established whether there are one or more contusions. From this the initial risk number is identified.
126. The second is the rate of decay of this risk number, using Firth's regression analysis.
127. The third is to determine from this when the risk has fallen to an acceptable level.
128. At the conclusion of the PowerPoint presentation, when Mr Harvey asked Dr Navāthé about possibly intervening with preventive anti-epileptic medication, he replied that in medical practice this has not been found to be beneficial; as well, the medications can have unacceptable side-effects. Also, he confirmed that the literature consistently describes an initial relatively high risk of developing epilepsy, tailing off over a number of years; and the recent studies are attempting to quantify that tailing off period[107].
[107] Transcript of Dr Navāthé's evidence, page 10, line 12 to page 12, line 36.
129. He also affirmed that he regards the CT scan findings as more relevant than those of MRI scans, but also agreed that if both types of scan have been performed, he would be interested in the results of both. Nevertheless, he regarded the literature on CT scan results as being currently more robust than for the MRI scan[108].
[108] Transcript of Dr Navāthé's evidence, page 11, line 38 to page 13, line 19.
130. He was asked by the Deputy President about his use of the term "likelihood". He affirmed that he distinguished between a possibility and a likelihood. He explained that what he meant by "likely" is not necessarily what he meant by "likelihood"; he would choose "likely" for "a real, substantial risk", but he would not necessarily be meaning "likelihood". By likelihood, he was referring to the concept of the possibility, or chance, that an event will occur. He did not consider the extent of the brain damage or injury, in working out whether something was likely or not[109].
[109] Transcript of Dr Navāthé's evidence, p 12, line 26 to p 14, line 8.
131. Mr Harvey also asked him about the "1% Rule", and if the International Civil Aviation Organisation supports the application of this in aeromedical decision making. He answered that the Organisation, which represents 189 nations, has avoided doing this, although some jurisdictions, such as Europe and Canada, are making attempts to quantify risk numbers[110].
[110] Transcript of Dr Navāthé's evidence, p 16, lines 20 to 30.
132. When cross-examined, he said that, for a commercial pilot seeking certification, he would be "looking at" an acceptable absolute risk in the range of 2‑2.5%. However, he had not yet discussed in his evidence how he had made the decision about Mr Hazelton's absolute risk of epilepsy[111].
[111] Transcript of Dr Navāthé's evidence, p 17, lines 19 to 43.
133. Although Dr Drane told us that Dr Navāthé had been directly involved in making the decision about Mr Hazelton[112], we heard no evidence from him concerning his assessment of Mr Hazelton's case.
Dr Alan Michael Christopher Drane, CASA Senior Medical Officer
[112] Transcript of Dr Drane's evidence, p 21, line 44 to p 24, line 24; Exhibit 1, ST2, ST3 and ST4.
134. Dr Drane has been Senior Medical Officer at CASA since October 2009. His first statement[113] informed us that he previously had worked as Medical Officer at Emirates Airlines since 2007, his responsibilities included complex aeromedical assessments; and before that he had been a Medical Officer for four years with the Civil Aviation Authority of New Zealand. His tertiary educational qualifications include a Masters degree in Aviation Medicine, and a Postgraduate Certificate of Aeromedical Retrieval, both from the University of Otago[114].
[113] Exhibit R2, paras 2 and 3.
[114] Exhibit R2, para 7.
135. When giving his evidence-in-chief, Dr Drane outlined how he had been involved Mr Hazelton's case. This had been examined under CASA's 'Complex Case Management' procedure, of which there are records of several discussions[115]. He explained that these had taken place between the other CASA Medical Officers before he had commenced his appointment with CASA. Dr Drane said that he then had been asked to comment because of his previous experience in dealing with head injuries with flight crew with Emirates Airlines[116].
[115] Exhibit 1, ST1-ST5/1-6.
[116] Transcript of Dr Drane's evidence, p 2, lines 25 to 31.
136. Under cross-examination he told us that, before coming to Australia to commence work with CASA last October, he already had read the papers by Annegers et al[117], Englander et al[118] and Christensen et al[119], but not Messori et al[120]; and he agreed that although it had been he who had signed the document that went to Mr Hazelton, he had not made the decision[121].
[117] Annegers, Hauser et al, n 91.
[118] Englander, et al, n 84.
[119] Christensen et al, n 94.
[120] Messori et al, n 58; Transcript of Dr Drane's evidence, p 16, lines 1-13.
[121] Transcript of Dr Drane's evidence, p 15, lines 14-16.
137. Also under cross-examination Dr Drane said that the decision about Mr Hazelton already had been made between the other three medical officers, Drs Navāthé, Fitzgerald and Tak Sum; of these, Dr Tak Sum had opined that Mr Hazelton's risk was acceptable[122].
[122] Transcript of Dr Drane's evidence, p 15, lines 5-19.
138. During his prior appointment with the Civil Aviation Authority in New Zealand between 2003 and 2007 he had known Dr Navāthé; and he also had known that Dr Wallis' advice sometimes was sought by that Authority[123].
[123] Transcript of Dr Drane's evidence, p 15, lines 39-47.
139. During his evidence-in-chief Dr Drane had told us that he had obtained his information on Mr Hazelton's case from the sources listed in his first statement[124], as well as Mr Hazelton's clinical notes from St Vincent's Hospital[125]. As well, at the conclusion of his first statement[126], he had indicated that he had seen Professor Tress' reports[127].
[124] Exhibit R2, para 19.
[125] Exhibit 2; Transcript of Dr Drane's evidence, p 2, lines 40 to 47.
[126] Exhibit R2, paras 48 and 49.
[127] Exhibits R5, R6 and R7.
140. From all of this material, he had summarised Mr Hazelton's case in paragraphs 20 to 23 of his first statement. In assessing the severity of his head injury, he had paid particular attention to two types of evidence in this information recorded in the first few hours and days, "clinical" and "radiological"; by "clinical" he meant that derived by various doctors who had examined Mr Hazelton, and by "radiological" he was referring to the information obtained from his various brain scans[128].
[128] Transcript of Dr Drane's evidence, p 3, lines 12 to 15.
141. The two items of clinical information of interest to him were whether Mr Hazelton had lost consciousness, and to what extent he had had post-traumatic amnesia. Dr Drane remarked that Mr Hazelton's Glasgow coma score of 14 recorded in the ambulance report was merely a "small reduction" below the "totally normal" level of 15, but he also noted that he had been described as confused, "amnesic to the event" and was said to have lost consciousness for an unknown period of time. In Dr Drane's view, any loss of consciousness could not have been simply attributable to alcohol, for, if it had been, the alcohol effects would also have prevented him from having been able to remember all that he had recalled prior to the event[129].
[129] Transcript of Dr Drane's evidence, p 3, line 20 to p 5, line 25.
142. He then was taken by Mr Harvey to the record of the Ward Round conducted at 1400 hrs on 3 November by Drs Faux and Braid[130]. The entry reads that Mr Hazelton:
Last recalls friend being assaulted. Next memory [is of being] in ED [Emergency Department][131].
[130] Transcript of Dr Drane's evidence, p 5, line 9.
[131] Exhibit 2 p 27.
143. As we observed above, this indicates that, at this point, 34 hours after his head injury, Mr Hazelton still was suffering a period of post-traumatic amnesia of about one hour.
144. Mr Harvey then referred Dr Drane to Mr Hazelton's Glasgow coma score that day (3 November) still being 14, to which Dr Drane responded that this indicated that he was still not "back to normal"[132]. However, we already have noted that this observation was based on a reference to an earlier Glasgow coma score of Mr Hazelton's when he was still in the care of the ambulance attendants[133].
[132] Transcript of Dr Drane's evidence, p 5, line 33 to p 7, line 3.
[133] Exhibit 2, p 27.
145. Although Dr Drane had not seen the Mater Hospital clinical records[134] until only a few weeks before this hearing, he had found that these contained no information that had any "impact" on their CASA decision. However, he had noted that Mr Hazelton's CT brain scan that was performed in that hospital, of just one week post-injury, had shown a "slightly larger area of low attenuation" surrounding the right basal frontal contusion[135] than "one would naturally expect"; and this indicated that he was still suffering neurological effects of his blow to the head, including that Mr Hazelton's vomiting and headache were "very characteristic" of "cerebral irritation after such an injury". He opined that Mr Hazelton was still suffering "the after effects of a bad blow to the head" for which he was treated with "prednisone", to reduce swelling in brain tissue[136].
[134] Exhibit A6, attachment JH1.
[135] Exhibit A6, attachment JH1, p 1.
[136] Transcript of Dr Drane's evidence, p 7, line 44 to p 9, line 27.
146. Mr Harvey then took him to paragraph 21 of his first statement[137], where he referred to Mr Hazelton's consultation, some 10 weeks after his assault, with Dr Cameron, and where he had stated:
... Dr Cameron describes the applicant as having a 'brief period of impaired recall surrounding the event but he had sketchy recall coming about half an hour later. He can recall lying on the ground and a bus driver coming to his assistance and he can then recall being attended to by the Emergency Services and also talking to the Police.
[137] Exhibit R2.
147. Dr Drane said that he regarded this period of amnesia as being significant, and helpful, in making Mr Hazelton's risk assessment[138].
[138] Transcript of Dr Drane's evidence, p 9, lines 10 to 21.
148. In paragraphs 24 to 26 of Dr Drane's first statement[139], he had introduced the process of his Risk Assessment for Mr Hazelton's case, in which he followed the AS/NZS 4360.2009 risk assessment standard, specifically addressing the potential aeromedical risks of either sudden or subtle pilot incapacitation. This involved three basic steps:
1. Identifying the risks;
2. Analysing the risks; and,
3. Evaluating the risks.
[139] Exhibit R2.
149. He then had identified Mr Hazelton's two risks from his traumatic brain injury as cognitive impairment and/or post-traumatic epilepsy[140], stating that, in Mr Hazelton's case, epilepsy was the more safety relevant condition[141].
[140] Exhibit R2, paras 27 and 28.
[141] Exhibit R2, para 30.
150. He analysed in detail Mr Hazelton's risks[142] which had entailed three steps:
(a) Categorising the type and degree of brain injury[143].
(b)Determining the likelihood of post-traumatic epilepsy and cognitive impairment; despite the recent major impact of technological scanning in the care of the brain-injured patient, this has not yet amassed sufficient literature for comprehensive evidence-based decision-making, and risk determination may have to rely on the lesser level of evidence, of expert opinion[144].
(c) Determining the consequences of epilepsy[145].
[142] Exhibit R2, para 29.
[143] Exhibit R2, para 31.
[144] Exhibit R2, paras 32 to 36.
[145] Exhibit R2, paras 37 to 41.
151. Taking these in sequence:
(a)Categorising the brain injury
152. Attempting to categorise Mr Hazelton's traumatic brain injury according to relevant published studies poses difficulties because it provides two differing classifications:
· his basal skull fracture and post-traumatic amnesia of seconds or minutes (< 30 minutes) are consistent with mild traumatic brain injury; but,
· according to the criteria used in the Christensen[146] studies, his CT scan imaging finding of an 8 mm right inferior frontal contusion in conjunction with his right orbital roof fracture is consistent with severe traumatic brain injury[147].
[146] Christensen et al, n 94; Annegers, Hauser et al, n 91.
[147] Transcript of Dr Drane's evidence, p 10, lines 19-24.
(b)Determining the likelihood of post-traumatic epilepsy
153. This involves complicated considerations. Dr Drane summarised the salient elements of four available reported studies:
· Reviews differ in using clinical signs and/or imaging in diagnosing and categorising mild or severe traumatic brain injury; in older studies, such as by Annegers et al[148] where surgery was not performed on patients without significant clinical signs, the risk of post-traumatic epilepsy in these mild injuries may have been overestimated because the true severity of the underlying brain injury may not have been recognised without scanning neuroimaging being available.
· Duration of hospital stay is not associated with post-traumatic epilepsy risk[149].
· The Glasgow coma score is not a consistent guide to long-term post-traumatic epilepsy risk[150].
· CT scan diagnosis of intracerebral bleeding within three days provides best correlation of post-traumatic epilepsy risk[151].
[148] Annegers, Hauser et al, n 91.
[149] Christensen et al, n 94.
[150] Englander et al, n 84.
[151] D'Alessandro , Ferrara et al, n 92.
154. Dr Drane stated that it is difficult to apply some of these studies' findings to Mr Hazelton's situation because modern use of CT and MRI imaging now provides a more immediate visualisation of the degree of brain injury. Furthermore, many studies have not followed the consequences of brain injury, which may persist many years, for long enough. However certain important trends are:
· Duration of increased post-traumatic epilepsy risk: after this risk is maximal in the first year, it slowly declines, but few studies which included CT imaging have continued for long enough follow up; Christensen et al[152] and Annegers et al[153] show that for both mild and severe traumatic brain injuries, the risks of post-traumatic epilepsy remain raised for at least 10 years.
· Degree of injury: post-traumatic epilepsy risk increases with greater damage to the brain, such as multiple brain contusions, dural penetration, foreign body penetration of the brain, multiple operations, subdural haematoma evacuation, and midline shift greater than 5 mm[154].
[152] Christensen et al, 94.
[153] Annegers, Hauser et al, n 91.
[154] Englander et al, n 84.
155. Applying these studies' findings to Mr Hazelton's case, Dr Drane said that his post-traumatic epilepsy risk may be evaluated both on his clinical and brain scan (CT and MRI) features; more recent studies have relied increasingly on the scans (advanced imaging), which have been found to be much more reliable indicators of traumatic brain injury. Comparing the two approaches:
450. Dr Hastings has practised as a Neurologist for nearly 40 years, is Adjunct Clinical Assistant Professor in Aerospace Medicine at the University Of Texas Medical Branch, has been a senior FAA designated Aviation Medical Examiner for nearly 30 years, is Senior Neurological Consultant to the Federal Air Surgeon, and in the past 10 years has authored or contributed on neurological subjects to six aviation and aerospace textbook publications[576]. As Dr Drane told us when giving his oral evidence, Dr Hastings was consulted by the CASA medical staff on Mr Hazelton's case, and in evidence we have documents of their correspondence exchanges[577].
[576] Exhibit A3, paras 1 to 17.
[577] Exhibit 1, T9, ST7, and ST10.
451. Dr Appleton, now in neurological practice for almost 40 years, is known nationally and overseas for his numerous contributions to the neurological literature, including on epilepsy. He retired nine years ago, with the rank of Group Captain, as Principal Reserve Medical Officer Queensland with the Australian Defence Force after 22 years of service. One of his frequent responsibilities was assessing the fitness of pilots to fly[578].
[578] Exhibit A1, paras 1 to 4; Transcript of Dr Wallis' evidence, p 28, lines 6 to 11, p 65, lines 33 to 34.
452. Various important contents of their evidence were supported by other Neurologists and neurological specialists i.e. Dr Hauser, Dr Westerman, Associate Professor Stark and Dr Maxwell.
453. Dr Wallis also is a very experienced Neurologist of 30 years standing; and it is clear to us that he has made himself closely familiar with the literature on post‑traumatic epilepsy. From this, he presented the respondent's case for using absolute risk calculations from the data from the Annegers, Englander and Christensen reports. However, under cross-examination, in conceding that the figures which he had used were not absolute, but guides, he has disarmed his argument[579]. Furthermore, he was not familiar with Dr Hauser's work on the general population's lifetime risk of suffering an epileptic seizure; and he was uncertain about distinguishing prospective from retrospective studies.
[579] Transcript of Dr Wallis' evidence, p 28, lines 6 to 11, p 65, lines 33 to 34.
454. Moreover, although Dr Wallis has advised the New Zealand Civil Aviation Authority, his aeromedical experience does not match Dr Hastings' or Dr Appleton's. During his conjoint evidence with Dr Hastings, he acknowledged that he did not regard himself as a consultant on a pilot's risk of having a seizure, or when Mr Hazelton would be fit to fly[580]; and under cross-examination he remarked that he did not wish to involve himself in questions of aviation safety[581].
[580] Transcript of Dr Hastings' evidence, p 34, line 45 to p 36, line 4.
[581] Transcript of Dr Wallis' evidence, p 21, lines 3 and 4.
455. As well, at times Dr Wallis' expert testimony was encumbered with advocacy.
456. The respondent's other Neurologist, Dr Cameron, is of very high standing in his specialty; but we have already remarked that he also was not invited to comment on the literature, and he was not called to give evidence at the hearing.
457. In addition, all aspects of aviation navigation safety in Mr Hazelton's case in the evidence of Drs Appleton and Hastings were supported by the aviation medicine
experts, Drs Brock, Donaldson, Liddell, and Sham Tak Sum. Their opinions were disputed only by Dr Drane, who had relied on calculations provided to him by Dr Wallis; Dr Navāthé gave us no evidence about Mr Hazelton's case.
458. In presenting their evidence against the adequacy of the scientific literature alone, Drs Hastings and Appleton have demonstrated their commanding intellectual grasp of it, and their clear perception of its significant limitations. Notable instances are:
· Dr Hastings identified that the Annegers et al[582] reports of the 50 year Mayo Clinic study were clinical studies rather than imaging; Dr Hauser in his evidence clarified that the CT imaging component was only incorporated in the later Annegers and Coan report, for which he was the study neurologist (WAH)[583].
· Dr Appleton questioned the applicability of the Englander et al[584] findings to Mr Hazelton, because they had been based on individuals with clinically moderate to severe brain injury, and he contended that their conclusions should not be applied to his case. Likewise Dr Hastings expressed several concerns: that although this report identifies the influential importance of the presence of cerebral contusions on post-traumatic epilepsy risk, it does so only in terms of "single" and "multiple" (as distinct from "two") contusions; that, as already noted, it included too small a sample of only 12 subjects in Mr Hazelton's age group who developed late post-traumatic epilepsy; and that there were other contusion variables recorded which have not been addressed in the evidence presented to us, such as whether they were bilateral or unilateral, without clinical details.
· Again, as Dr Hastings has pointed out to us, the Christensen et al study included only 30 individuals of Mr Hazelton's age group i.e. too small a sample size. Also Dr Appleton commented that these authors acknowledged that some patients diagnosed with mild brain injury might actually suffer more severe injury leading to an overestimated risk of epilepsy.
[582] Annegers, Grabow et al, n 90; Annegers, Hauser et al, n 91.
[583] Annegers and Coan, n 254 at 454.
[584] Englander, et al, n 84.
459. Further to these, in the Christensen et al study we have noted several conflicting sets of relative risk figures, any of which might be applied to Mr Hazelton's case. One instance depends on whether Mr Hazelton might be included either in the skull fractures group, or in the severe head injury group because of his contusions. For Mr Hazelton's duration of hospital admission of three days, for severe head injury the relative risk was 4.82, compared to only 1.77 for skull fractures[585].
[585] Christensen et al, n 94 at 1108, table 3.
460. Then, when these two alternative sets of figures are linked to Mr Hazelton's negative family history, on which we have heard no evidence at all, these authors have tabulated that, on the one hand, for severe head injuries, individuals with no family history had nearly eight times less an adjusted comparative risk (1.00) compared to those with a family history (7.81)[586]. This contrasted with their observations that subjects with skull fractures and no family history had less than half the risk of developing epilepsy (1.00) compared to those with a family history (2.28)[587].
[586] Christensen et al, n 94 at 1108, table 4.
[587] Christensen et al, n 94 at 1108, table 4.
461. Hence, we are persuaded that these conflicting figures, taken on their own, cannot be utilised for the individual circumstances of Mr Hazelton's case. The inadequacies for our purposes of this otherwise very comprehensive study were summed up in this report's accompanying editorial[588]:
Christensen and co-workers' investigation is of commendable size and completeness, with an advanced statistical design - as such, it should be accepted as the reference study in the field. This is not to say that there are not methodological criticisms. There are issues inherent in the study design: the diagnosis of epilepsy and the classification of severity of trauma are based on registry data, with all the inaccuracy that this implies; no attempt is made to distinguish between immediate, early, and late epilepsy although these categories have important clinical implications; previously identified risk factors for post-traumatic epilepsy, such as the presence of dural tear, intracranial haemorrhage, and early seizures (<1 week) were not investigated; and no data are provided about the type or severity of the epilepsy.
[588] Shorvon and Neligan, n 403.
462. We had many other references cited to us during the hearing, but none of these were of the large scale epidemiological nature as these three, particularly with Englander et al[589] and, to a less extent, Christensen et al[590] directing attention to imaging observations.
[589] Englander et al, n 84.
[590] Christensen et al, n 94.
463. As well as CT imaging, we have had several references during the hearing to two published reports of MRI studies, by Angeleri et al[591] and Messori et al[592]. Dr Wallis has pointed out that the second of these was simply an extension in time of the first study. They have examined 135 adult head-injured patients, with varying head injuries' severities, including differing levels of coma for a total period of up to five years, of whom 20 developed post-traumatic epilepsy. They observed the extent to which gliosis (which is the brain tissue's repair process following injury) surrounding the haemoglobin-iron remnants of blood, modifies the post-traumatic epilepsy risk. As Dr Appleton has pointed out, the number of individuals in this study is too small to enable us to draw any conclusions for Mr Hazelton's case. This is even without taking into account the fact that Mr Hazelton suffered no level of coma.
[591] Angeleri et al, n 240.
[592] Messori et al, n 58.
464. Toward the end of his cross examination, Mr Harvey asked Dr Hastings:
Yes. I mean, all you're suggesting is that there's a lot of room for further work to be done in this field?---Indeed I do, yes[593] .
[593] Transcript of Dr Hastings evidence, p 21, lines 13 to 28.
465. In this respect, although it is evident that the medical scientific literature to date lacks sufficient reports of MRI technology applications to Mr Hazelton's problem, Dr Appleton appended a copy of a recently published article[594], whose authors discuss the expanding scope of imaging procedures for traumatic brain injury. They review various forms of MRI neuroimaging, of both structural and functional changes, as well as PET scanning, and magnetic encephalography. With the emergence of these increasingly sophisticated technologies, there would appear to be ample prospects for helpful neuro-imaging developments in this field in the not too distant future.
[594] Metting et al, n 370; Exhibit A9, attachment BA9.
466. We also note that Dr Westerman has made a suggestion, regarding which he said he has corresponded with Dr Hastings that CASA AvMed might collaborate with US FAA and CAA of Canada in a neuro-epidemiological research project into the type of problem that Mr Hazelton's case presents[595].
[595] Exhibit A20, para 20; Sackett et al, n 504.
467. Determination: We find that the present body of scientific literature is insufficient on its own from which to make a determination, in accordance with evidence-based medicine as defined by Sackett et al[596], on the acceptability or otherwise of Mr Hazelton's current epilepsy risk to resume flying aircraft "with or as co-pilot".
(4) The determination of whether Mr Hazelton's epilepsy risk is acceptably low enough to resume flying aircraft "with or as co-pilot" should be a balanced decision involving both clinical and imaging criteria.
[596] Sackett et al, n 504.
468. This proposition accords with the definition of evidence-based medicine enunciated by Sackett et al[597], that it is the "integration of best research evidence with clinical expertise and patient values." Accordingly, it becomes our task to evaluate whether the necessary clinical expertise is available in this matter to provide this "balanced decision" in a manner to satisfy the standards of evidence-based medicine.
[597] Sackett et al, n 504.
469. We already have just outlined our reasons, on the grounds of their qualifications and clinical expertise, for preferring the neurological opinions of Drs Hastings and Appleton. Both of them have argued convincingly for this balanced opinion approach.
470. Furthermore, they are supported unequivocally in this view by six other expert medical witnesses, each with extensive experience in aviation medicine:
· Dr Jeffrey Brock who graduated in medicine almost 30 years ago, is a qualified military (Army) pilot, with extensive domestic and international flying experience, and is a CASA Designated Aviation Medical Examiner (DAME). In 1998 he completed 2½ years as Acting Director of Aviation Medicine for CASA; and he has been Senior Medical Officer for the Civil Aviation Authority (CAA) of New Zealand. For the past 20 years he has been Consultant Adviser in Aviation Medicine to the Australian Defence Force, consecutively to the Army, the Health Service, the Surgeon General, the Air Forces Commander, and the joint Health Commander[598] As well as his statement, he gave oral evidence to the hearing.
· Dr Eric Donaldson has practised medicine for more than 45 years, is a qualified Army pilot, and served 20 years with the Army before retiring as Colonel in 1989. He then was appointed Director of Medical Services with Qantas, a position he held for 10 years. He has since taught as Adjunct Professor at Griffith University, and is Senior Aviation Medical Officer at the RAAF Institute of Aviation Medicine. He is an Honorary Life Member of the Society of the United States Army Flight Surgeons, and of the Aviation Medical Society of Australia and New Zealand[599]. He also gave oral evidence to the hearing.
· Dr Robert Liddell qualified in medicine nearly 40 years ago, is a DAME, and for six years was company doctor for the United Kingdom airline Dan Air with whom he flew 2400 hours as a Boeing 727 first officer, and still holds an Airline Transport Pilot's Licence and a current Command Instrument Rating. He was the Director of Aviation Medicine of CASA from 1988 until 1996. He set up the first Australian Course in Aviation Medicine Training for doctors at Monash University, and is an Academician of the International Academy of Aerospace Medicine[600].
· Dr Ian Maxwell is a Neurologist who has practised at Southport in Queensland for 30 years. He holds a Private Pilot Licence, and is a DAME. He saw Mr Hazelton at the request of his General Practitioner, Dr Sutch, and his letter appears in the Tribunal documents[601].
· Dr Sham Tak Sum is a medical graduate of some 35 years, holds a Private Pilot Licence, Multi-Engine Command Instrument Rating, and previously was a DAME for four years. He has since been a Medical Officer with CASA for more than 20 years. He was a full-time Medical Officer for 7 years with the RAAF, with whom he continues as a Specialist Reserve Medical Officer[602].
· Dr Roderick Westerman is a Physician and Neurophysiologist, graduating 55 years ago, and is a DAME. As Associate Professor in Physiology at Monash University, he helped initiate and then coordinate for 12 years the course for the Australian Certificate of Civil Aviation Medicine. He is Adjunct Professor in Postgraduate Medicine at Edith Cowan University, where he coordinates and examines in the Postgraduate Certificate in Aviation Medicine. He has been an Associate Member of the Australian and New Zealand Association of Neurologists for 25 years, and has published more than 125 scientific papers and edited four books on neurophysiological and occupational medicine topics[603].
[598] Exhibit A10, paras 2 to 8.
[599] Exhibit A12, paras 2 to 18.
[600] Exhibit A14, paras 2 to 17.
[601] Exhibit 1, ST8.
[602] Exhibit A16, paras 2 to 7.
[603] Exhibit A18, paras 1 to 10.
471. We are persuaded that, for the determination of this matter, we have available a sufficiently impressive collective body of clinical expertise in this field of aviation medicine.
472. Determination: We conclude that we have available sufficient clinical expertise, which is substantial enough to enable the determination of whether Mr Hazelton's epilepsy risk is acceptably low enough to resume flying aircraft "with or as co-pilot", to be a balanced decision involving both clinical and imaging criteria; and, that this decision would satisfy the standards of evidence-based medicine.
(5)The estimation of Mr Hazelton's present risk of developing epilepsy should be made on the basis of relative risk.
473. From all the foregoing, we accept Dr Hastings' argument, as he puts it in his statement, that relative risk calculation is much more readily applicable to this aeromedical decision than absolute risk[604]; and, throughout this aspect of his evidence, he consistently has referred to the use of the "1% Rule" for sudden incapacitation, with possible modification to a "2% Rule" for multi crew.
[604] Exhibit A13, para 32(e).
474. He is supported, without exception or qualification, by all six of the Designated Aviation Medical Examiners whose names and credentials appear above.
475. Furthermore, we have noted that, prior to Dr Drane's arrival at CASA, and eight months after Mr Hazelton sustained his injury, there was a division of opinion among the then three members of the CASA medical staff. Dr Sham Tak Sum favoured him flying "multi crew", referring to the 2% recommendation made by Dr Evans, who we note to be the Chief of Aviation Medicine of the International Civil Aviation Organisation[605]; Dr Fitzgerald favoured his recertification at 18 months. However, the decision against him was made on the grounds of Dr Navāthé's concerns about his post-traumatic epilepsy risk due to the CT demonstration of his contusion[606]. Dr Drane informed us during his cross-examination that the risk analysis of the "acceptability" or otherwise of Mr Hazelton's epilepsy risk had been collectively decided by Drs Sham Tak Sum, Fitzgerald and Navāthé, before he had arrived to take up his CASA appointment[607].
[605] Exhibit A16, para 14; Mitchell and Evans, n 206.
[606] Exhibit 1, ST3.
[607] Transcript of Dr Drane's evidence, p 22, lines 11-21 and p 24, lines 23-24.
476. In addition, several witnesses have testified regarding the possible consequences of "active incapacitation" of Mr Hazelton during a flight, caused by him having an epileptic seizure. There have been two elements to this consideration.
477. The first addresses the question which concerned Dr Drane in his risk assessment of Mr Hazelton[608], of how the remaining pilot manages to retain control of the aircraft in the event of the colleague on the flight deck being incapacitated by a seizure:
· Mr Peter Macmillan is a Flying Operations Inspector with CASA, and has nearly 45 years' experience as a pilot, having flown with the Australian Army Aviation Regiment, Ansett Airlines, Condor, and SilkAir. He gave oral evidence to us and also provided a statement[609]. He has said that a two pilot crew requirement on aircraft is due to the demands of flying and that it cannot be met safely by one pilot; and incapacitation of one leaves the remaining pilot to perform the work of two. As well, he was concerned about the difficult consequences of an incapacitated pilot inadvertently affecting the aircraft controls, especially in a critical stage of the flight such as early in the take-off or late in the landing.
· Mr Andrew Bauer is a Line Operations Manager with Virgin Blue Airlines who has provided a statement[610]. He has said that the airline operates Boeing 737 and Embraer aircraft only, designed to operate with a flight crew of two pilots, with dual controls so that the other pilot can fully control the aircraft in all phases of flight, with duplication of all instrumentation.
· In his second statement, Dr Westerman disagreed with a number of Mr Macmillan's observations. He remarked that the "inbuilt automated systems" of the multicrew aircraft that we are considering enable them to be "very safely flown by one pilot in the event that one is incapacitated"[611]; and that structural damage to controls is prevented by automatic high‑speed cut-off systems[612].
· In his second statement[613] Dr Brock has addressed Mr Macmillan's concerns, referring to the assistance that can be rendered by other crew members such as flight attendants, and lack of hindrance of the other pilot in assuming and retaining control of the flight, even should the incapacitated pilot still be fitting.
· Dr Liddell also has referred to Mr Macmillan's statement in his own second statement[614]. He has described how, for this contingency, the modern training of a pilot consists of the procedure of the engaging of the autopilot, calling a cabin attendant to the flight deck, and either securing the incapacitated pilot in the seat or removing the pilot to commence first aid[615].
[608] Exhibit R2 paras 37 to 41.
[609] Exhibit R14.
[610] Exhibit A8.
[611] Exhibit A19, para 10.
[612] Exhibit A19, para 16.
[613] Exhibit A11, para 3.
[614] Exhibit A15, paras 4 to 14.
[615] Exhibit A15, para 12.
478. Second, there is the question of the likelihood of an aircraft accident resulting from a pilot suffering a seizure on a multicrew flight deck in flight.
· Dr Donaldson attested[616] that there has been no recorded aircraft accident in the English speaking world in pilot airline operations, caused by a pilot's incapacity, in the past 35 years. He also said that he has searched the literature extensively, and found no instance of an accident in a two pilot airline operation caused by a flight crew member suffering an epileptic fit[617]. He also has observed flight simulator trials, and has described:
[616] Exhibit A12, para 26.
[617] Exhibit A12, para 57.
I used a well schooled pilot demonstrating tonic and clonic stages of a seizure very close to touch down and lift off (which are the critical stages of flight). The simulator trials demonstrate that the most dangerous situation appears to be the sustained sudden extension of one leg in contact with the rudder. The simulator trials have demonstrated that, even in the most critical stages of flight, it is a matter of mere seconds of the flight where the aircraft is not recoverable. Given that:-
a. only a small percentage of seizures would present as the sustained sudden extension of one leg in contact with the rudder; and
b. the proficiency of the second pilot
the risk of an accident is most unlikely[618].
· Dr Westerman confirmed[619] that simulator training sessions, for many years, have included dramatic incapacitations and sudden failures, and all pilots must undergo such simulator training twice each year. He also referred to the absence of aircraft accidents using risk assessment models based on the "1% Rule" [620].
· In his second statement Dr Liddell[621] has described the research performed in 1984 by Dr Chapman of British Caledonian Airways, to which Dr Donaldson also alluded in his evidence, on his company's airline pilots in the company's jet aircraft simulator:
Over 1300 closely observed simulator exercises using two protocols (sudden obvious and sudden subtle incapacitation) to the handling pilot at a critical stage of flight were flown. The simulator instructing pilot graded the performance of the remaining pilot to assess whether the aircraft was operated in a safe manner until it had landed. Using this research, Chapman was able to show that the risk of catastrophic failure (losing the aircraft) when one pilot was incapacitated was a rare event which could on the basis of his research be given a statistical probability. The research found that the chance of an accident occurring should one pilot become incapacitated at a critical stage of flight was 0.2%.[622].
[618] Exhibit A12, para 58.
[619] Exhibit A19, paras 14 and 20.
[620] Exhibit A18, paras 17(e) and 17(f).
[621] Exhibit A15, para 7.
[622] Chapman, n 489.
479. In addition, Dr Donaldson informed us that there have been cases of a pilot having an epileptic fit in flight, but they were due to hypoxia or brain tumours. He said that, in single pilot cases, they had not survived; however he was aware of the instance in New Zealand that Dr Wallis had described, of the aircraft landing safely after the pilot had recovered from a post-traumatic seizure[623]. However he had not found any instance of a pilot in a multicrew airline operation having a post-traumatic epileptic seizure[624]. This evidence was not challenged.
[623] Transcript of Dr Wallis' evidence, p 49, line 35 to p 50, line 20.
[624] Transcript of Dr Donaldson's evidence, p 5, lines 16 to 25.
480. Furthermore, Dr Brock stated that, in all of his career, he had never seen or known of a report of a pilot's "active inactivation"[625]; Dr Liddell stated that there have
been no accidents reported due to pilot incapacitation since the present restricted licensing was accepted 25 years ago by the International Civil Aviation Organisation[626]; and Dr Westerman stated that, despite a comprehensive search, no multicrew aircraft accident or serious incident due to epileptic seizure has been found[627]. Again, none of this evidence was disputed.
[625] Exhibit A10, para 12(h).
[626] Exhibit A15, para 10.
[627] Exhibit A19, para 21.
481. From this evidence we are satisfied that:
· The probability of a pilot having an epileptic seizure at a critical stage in flight is exceptionally low, in view of all of the precautionary measures taken against this occurring.
· In such an event, because of systematic pilot simulated training, the risk of an accident is most unlikely.
482. On the information provided to us, because of its widespread acceptance in the aviation medicine community, the salient precautionary measure to be taken against Mr Hazelton suffering an in-flight seizure in a two-pilot aircraft is to establish that his risk of having a post-traumatic epileptic seizure satisfies the "1% Rule".
483. Determination: We decide that the estimation of Mr Hazelton's present risk of developing epilepsy should be made, as have CASA determinations in earlier years, on the basis of relative risk.
(6)An estimation of relative risk which satisfies the "1% Rule" of Mr Hazelton's risk of developing epilepsy also satisfies an "acceptable risk".
484. We have been informed that the "1% Rule" has been deemed to satisfy an "acceptable risk" by other highly esteemed aviation regulatory bodies, such as the Federal Aviation Administration in the United States of America and the Civil Aviation Administration in the United Kingdom.
485. After Dr Hauser had finished giving his evidence to us, we asked Dr Hastings some questions about the "1% Rule". Dr Hastings explained that he takes the
epileptic seizure incidence figure for the age group of interest for pilots, from estimations made by Dr Hauser, to be 35 to 40 per 100,000 per year, of which Dr Hastings chose to take the higher figure. From this, a relative risk of 25 times that of this "normal pilot population", based on the figure of 40, provides the one per cent figure.
486. For Mr Hazelton, Dr Hastings confirmed that, at this time 18 months post-injury, based on his clinical criteria combined with his imaging findings, it could be as much as 10 times that of the normal population. That would be 10 times 40 per 100,000 per year (or 400 per 100,000 per year, or 0.40 per cent), or less than half of the one per cent rule[628].
[628] Transcript of Dr Hastings evidence, p 12, line 6 to p 14, line 32.
487. We also note again that, in paragraphs 55 and 56 of his statement[629], Dr Hastings had turned his attention to this by examining the Christensen et al[630] data. This he did provisionally, because during his examination-in-chief he has detailed his reservations about the difficulties of applying this material to Mr Hazelton's case; this is because of the small number of 30 subjects represented in this study in Mr Hazelton's age group, the inclusion of patients with moderate to severe traumatic brain injury, and the non-stratification of the severe brain injury persons[631]. With these caveats, Dr Hastings hypothetically placed Mr Hazelton into this study's severe traumatic brain injury category. This conferred a relative risk of 7.4, which translated to 511/100,000/year, which is a little more than half the incidence represented by the "1% Rule" at 0.5%. Furthermore, on narrowing attention to Mr Hazelton's very small age subgroup in this series, the relative risk for them was higher at 12.24, translating to 856/100,000/year, yet still just below the "1% Rule" at 0.9%. These calculations were partly "slanted", being based on this study's higher "all age" epilepsy incidence of 69/100,000/year, in comparison to the 40/100,000/year incidence for the pilots' age group that is used in the "1% Rule".
[629] Exhibit A13.
[630] Christensen et al, n 94.
[631] Transcript of Dr Hastings' evidence, p 3, line 43 to p 6, line 26.
488. We are persuaded that Dr Hastings' calculations that Mr Hazelton's risk is of the order of 1% is conservative but appropriate.
489. We also are satisfied that this is an acceptable risk for him to fly multicrew.
490. Determination: The "1% Rule" provides an adequate estimation of an acceptable risk, and is appropriate to apply to Mr Hazelton's case.
Does Mr Hazelton have a “Safety Relevant” Condition?
491. In answering this question, we must apply the evidence and the principles relating to expert evidence. We must consider also the question of whether Mr Hazelton is “likely” to have a reduced capacity, or conversely, whether he is “likely” to have an increased risk of post-traumatic epilepsy if permitted to fly an aircraft again. In that context, it has been held that the word “likely” means “a substantial or real and not remote chance”[632]. The word “likely” seems always (correctly in our view) to have been treated by the Courts synonymously with “probable”. More recently, the word “probable” was held by the High Court to mean “a real possibility or chance”[633].
[632] Window and Civil Aviation Safety Authority [1999] AATA 525.
[633] Darkan v R (2006) 80 ALJR 1250.
492. At the outset, we considered the credit of the applicant as some earlier medical evidence obtained from Mater Hospital records was only disclosed to his medical advisers at a late stage of proceedings. We have accepted his evidence that there has been no seizure or other sequelae since his original brain trauma. In the circumstances, we have accepted him as a witness of truth.
493. From the enormous expertise which has been presented, the statistical evidence from empirical studies and imaging studies alone are not sufficiently persuasive for the respondent’s arguments to succeed. Despite the published levels of statistical significance, the basis of comparing the results of different studies were problematical in assessing the likelihood of risk for Mr Hazleton’s case.
494. The applicant provided supplementary submissions about the weight to be given to Dr Cameron’s evidence. The respondent objected. The matters canvassed went beyond the purpose of the invitation for further submissions and we have not drawn any adverse inference of the sort described in Jones v Dunkel (1959) 101 CLR 298 given that eight neurologists from Australia and overseas were subsequently consulted and who provided detailed and more current opinions.
495. As stated earlier, we find that ‘relative risk’ is the appropriate measure to be adopted (as opposed to absolute risk). That relative risk, to be indicative of “a safety relevant” condition, must reduce or be likely to reduce Mr Hazelton’s capacity to perform his role as a pilot. After over 18 months since the accident, the only remarkable clinical evidence of the applicant has been some brain swelling in the day or two immediately after the accident and that seems to be accepted by some of the experts as insignificant in view of its nature and the proximity to the accident. Mr Hazelton has had no post-traumatic epilepsy in this first 18 months which is a critical factor when assessed against the empirical evidence which demonstrates that those who have an epileptic seizure within one month of the initial trauma, are at significant risk of having a later recurrence. For example, based on one set of figures in the Christensen et al[634] study, patients with no family history of epilepsy (and Mr Hazelton is one who fits within that category) have nearly 8 times less risk than those patients who do have such a family history.
[634] Christensen et al, n 94.
496. Having considered the conflicting evidence, we find that the risk of post-traumatic epilepsy for Mr Hazleton is well within the acceptable medical criteria for the aviation industry. We have taken account of all of the evidence and appropriately given weight to the factors affecting the disputed facts. In determining what are acceptable limits or tolerances in this case, we reject the oral evidence of Dr Wallis and Dr Drane and the written evidence of Dr Navāthé. We have accepted and placed considerable weight on the expert opinions of Dr Hastings and Dr Appleton, in particular. We have done so on the basis of a demonstrated clinical experience, industry expertise, and analyses of and currency with the professional literature. The assessment of the medical evidence of Mr Hazleton against all of the evidence and using the “1% Rule”, explained in clear terms by Dr Hastings, was of assistance to the Tribunal. Dr Appleton was comprehensive in his assessment of neurological functions and also took account of other relevant factors such as neuropsychological assessment of Mr Hazleton. In addition, both doctors had a similar balancing
approach to weighing the evidence, taking account of the difficulty in relying specifically on the epidemiological evidence. Both Dr Hastings and Dr Appleton provided evidence which assisted the Tribunal in terms of the principles set out in Makita (Aust) Pty Ltd v Sprowles (2001) 52 NSWLR 705.
497. We noted also the 11 December 2009 report[635] of Dr Ian Maxwell, a DAME, who opined, after discussing the case with other neurologists and neurosurgeons, that it was unlikely that Mr Hazelton would have any long term deficits. The evidence given by Dr Brock, Dr Donaldson and Dr Liddell was likewise, of considerable force. We regarded the evidence of these doctors also as objective and balanced in their evaluations.
[635] Exhibit 1, ST8/14 to 15.
498. In giving appropriate weight to the evidence in dealing with the ultimate issues, we have balanced the grave consequences of potential for loss of lives as well as loss of a huge value of assets (and consequential costs) if such was occasioned by a pilot with risk of post-traumatic epilepsy being granted a medical certificate under the Regulations. We also balanced against those risks, the entitlement of a relatively young man in the applicant’s circumstances and in light of the medical opinions of his likely risk against imprecise objective criteria, to enjoy his professional skills and career and to provide for his family. The fact that the aircraft he is licensed to fly are co-piloted was also taken into account in making this determination.
499. We have found that the evidence shows that there is no direct evidence that Mr Hazleton has a reduced capacity. But we must also consider the evidence as to whether he is “likely” to have reduced capacity.
500. We find from the clinical and epidemiological evidence, Mr Hazelton’s virtually uneventful history since the accident (particularly in relation to the absence of post‑traumatic epilepsy in that period), there appears to be a preponderance of weight pointing to an “inherent unlikelihood” of post-traumatic epilepsy for the applicant[636]. In so concluding we note in a complementary way, that the respondent’s case was not uniformly robust. In particular, we placed weight adversely for the respondent on the fact that three of the doctors, the Principal Medical Officer, Dr Navāthé and the medical officer Dr Drane, and Dr Wallis from his New Zealand consultancy, who had worked together previously had inconsistent opinions with other doctors from within CASA and with external expert opinion, and we were not satisfied that all of the views of those doctors were objective assessments. We considered Dr Drane’s evidence, who had the benefit of the opinion of Dr Hastings, the United States specialist, but we found Dr Drane seemed unduly influenced by Dr Navāthé’s opinion.
[636] The test in Briginshawv Briginshaw (1938) 60 CLR 336.
501. We noted in particular, in July 2009 (8 months after Mr Hazleton’s assault incident), email evidence of the strong views taken by Dr Sham Tak Sum and the more moderate views of Dr Fitzgerald, both of whom are employed by CASA. Clearly, Dr Sham Tak Sum and Dr Fitzgerald would have been sympathetic to re‑licensing Mr Hazelton, but those views seemed to have been minimised by the other medical officers at CASA and that evidence is at odds with Dr Navāthé’s written statement.
502. Consistently with those findings which are based on the whole of the evidence, we also find that Mr Hazelton is less likely to have a reduced capacity for operating effectively as an airline pilot. Therefore, we answer the issues for determination as follows:
(1)Mr Hazelton satisfies the requirements for the issue of a Class 1 and Class 2 medical certificates.
(2)The matter is referred back to CASA for consideration of conditions (if any) and if so, for what period of time.
I certify that the 502 preceding paragraphs are a true copy of the reasons for the decision herein of Honourable Dr B H McPherson CBE Deputy President, Dr K S Levy RFD, Senior Member and Associate Professor J B Morley RFD, Member
Signed: .....................[Sgd]........................................................
Kate Slack, Research AssociateDate/s of Hearing 17, 18 and 19 May 2010
Date of Decision 10 September 2010
Counsel for the Applicant Michael Taylor
Solicitor for the Applicant Tracey Jessie, Flower & Hart Solicitors
Counsel for the Respondent Ian Harvey
Solicitor for the Respondent Tanya Canny, Principal Lawyer
[368] Servadei F, Teasdale G and Merry G, "Defining Acute Mild Head Injury in Adults: A Proposal Based on Prognostic Factors, Diagnosis and Management" (2001) 18 Journal of Neurotrauma 657.
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