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, Member 	
Date	10 September 2010 
Place	Brisbane 
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, Member 		

INTRODUCTION
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, and during his evidence at the hearing; and,
•	His companion that evening, Mr Martin Whiteley, in his statement received on 11 May 2010.
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.  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.  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]".  
11.	They both "immediately" 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.
12.	Medical documents obtained by summons from St Vincent's Hospital have included a copy of the report from the Ambulance Service of New South Wales.  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.

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. The intern and nursing notes, at 0445 hrs and 0450 hrs 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.  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; according to the applicant's oral evidence at the hearing, he had had his last alcoholic drink at about 3:00am.  
15.	At 0500 hrs that morning, on the Emergency Department Patient Assessment Record (triage) sheet, 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. 
16.	Otherwise, while Mr Hazelton was in the Emergency Department, his Glasgow coma score was consistently recorded at 14 at 0445 hrs, 0450 hrs, 0500 hrs, 0720 hrs, and 0745 hrs .  Thereafter, it then rose to remain at 15 (1130 hrs); 1325 hrs ; and 1800 hrs).  
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 :
GCS 14 ċ Ambos [Glasgow coma score was 14 with the Ambulance attendants] ".
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.  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 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.  
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.  A review CT brain scan later that morning showed "no adverse change" compared to the first scan. 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; 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.
20.	On the following day (4 November) he still was recorded as having "no memory of events", 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".  We note that the various clinical notes' entries for that day indicate that preparations were being made for his discharge. 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.  
21.	On the following day, before leaving the Hospital, he had his third CT brain scan.  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. 
22.	At the hearing, Mr Hazelton was cross-examined on paragraphs 13, 14 and 15 of his first statement.  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.
23.	In his supplementary statement of 6 May 2010 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
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.  
25.	Attached to Mr Hazelton's supplementary statement are 20 pages of documents of his Mater Hospital attendance.  When he was seen at 1944 hrs in the Emergency Department, 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').  His physical examination otherwise was normal.  
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); 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", 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.
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; 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 ... 
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 states that he was well, and free of significant headache or further nausea or vomiting.  
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, and reads as follows:
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, provided by Drs Paul Hayes and Robert Mason, is as follows:
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:
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.
36.	His second EEG was reported on 16 December 2009 by Dr Ian Maxwell, Neurologist of Southport, as follows:
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.
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 from Professor Brian Tress, Radiologist of Royal Melbourne Hospital.
•	Letter from Dr Maurice Moriarty, Neuroradiologist of Trinity MRI, Auckland, New Zealand
•	Statement from Dr John Earwaker, Radiologist of Brisbane. 
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”.
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. At Dr Wallis’ suggestion Dr Drane had referred him to an article by Messori et al.  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.  
43.	In his second letter, 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].
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 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. 
46.	As well, a reference was made by Neurologist Dr William Wallis in his fourth report 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
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.  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."
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 and a statement; he also gave evidence in person to the hearing.
•	Associate Professor Richard Stark, Neurologist of Melbourne, who provided a report.
•	Two letters and a statement from Dr John Hastings, Neurologist of Tulsa, Oklahoma; he also provided evidence by telephone to the hearing.
•	Two statements from Dr Jeffrey Brock, Designated Aviation Medical Examiner of Robina, who also gave evidence by telephone.
•	A statement by Dr Eric Donaldson, Designated Aviation Medical Examiner of Oakey who also gave evidence in person to the hearing.
•	Two statements from Dr Robert Liddell, Designated Aviation Medical Examiner of Bicton, Western Australia.
•	A statement by Dr Sham Tak Sum, a CASA Medical Officer of Giralang, ACT.
•	Three statements 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 by Dr Tamara Bushnik, Rehabilitation Research Physician of New York.
•	Dr Allen Hauser, Neurologist of New York, gave evidence to us by telephone.
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 from Dr Alan Drane, Senior Medical Officer for CASA, who gave evidence in person.
•	A statement by Dr Pooshan Navāthé, Principal Medical Officer for CASA; he also delivered a PowerPoint presentation at the hearing.
•	Four reports and a medical note  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.
52.	As well, on file we had a report 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
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, 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.
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 is included in the Tribunal documents.
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, 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.
64.	He added that the MRI study reported by Messori et al suggested that contusions with haemosiderin entirely surrounded by gliosis carried a relatively smaller epilepsy risk.
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.
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 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.  
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.  He also had presented this only days before at an international aerospace medical conference in Phoenix, Arizona, from which he had just returned.
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  and Annegers et al 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. 
110.	However, in 1998 Annegers et al 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).  
111.	Meanwhile, 10 years earlier D'Alessandro et al 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 reported that the combination of intra and extracerebral bleeding further increased the post-traumatic epilepsy risk.
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 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.
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.
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.  The other is a more recent report by Englander et al, 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.
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 and Annegers et al 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 and Jamjoom et al, 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.  
120.	The prospectively conducted Englander et al study, 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%.  
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 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 report.  Also, Christensen et al 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.
123.	Dr Navāthé showed us that British neurosurgeon Dr John Firth has studied the original results of Jennett, 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%.
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.
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.
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.
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.
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.
133.	Although Dr Drane told us that Dr Navāthé had been directly involved in making the decision about Mr Hazelton, we heard no evidence from him concerning his assessment of Mr Hazelton's case.
Dr Alan Michael Christopher Drane, CASA Senior Medical Officer
134.	Dr Drane has been Senior Medical Officer at CASA since October 2009.  His first statement 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. 
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. 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.  
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, Englander et al and Christensen et al, but not Messori et al; 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.  
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.  
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.
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, as well as Mr Hazelton's clinical notes from St Vincent's Hospital.  As well, at the conclusion of his first statement, he had indicated that he had seen Professor Tress' reports.
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.
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.  
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.  The entry reads that Mr Hazelton:
Last recalls friend being assaulted.  Next memory [is of being] in ED [Emergency Department].
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".  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.
145.	Although Dr Drane had not seen the Mater Hospital clinical records 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 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.
146.	Mr Harvey then took him to paragraph 21 of his first statement, 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.
147.	Dr Drane said that he regarded this period of amnesia as being significant, and helpful, in making Mr Hazelton's risk assessment.
148.	In paragraphs 24 to 26 of Dr Drane's first statement, 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.
149.	He then had identified Mr Hazelton's two risks from his traumatic brain injury as cognitive impairment and/or post-traumatic epilepsy, stating that, in Mr Hazelton's case, epilepsy was the more safety relevant condition.  
150.	He analysed in detail Mr Hazelton's risks which had entailed three steps:
(a)	Categorising the type and degree of brain injury.
(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.
(c)	Determining the consequences of epilepsy.
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 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.
(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 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.
•	The Glasgow coma score is not a consistent guide to long-term post-traumatic epilepsy risk.
•	CT scan diagnosis of intracerebral bleeding within three days provides best correlation of post-traumatic epilepsy risk.
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 and Annegers et al 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.
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:
•	Clinically: the Glasgow coma score is a widely used tool, and Mr Hazelton's score was >13/15 after 30 minutes, placing him in the mild brain injury category.  From this, the following two articles estimate the resultant epilepsy incidences as: 
-	Englander et al: the post-traumatic epilepsy risk is that 8% of subjects will develop epilepsy in two years;
-	Christensen et al: the relative risk of post-traumatic epilepsy is 2.22 (2.22 times greater than in the normal population).
•	Imaging: According to both Christensen et al and Annegers et al, Mr Hazelton's right frontal contusion makes his brain injury severe.  Three studies estimate the resulting epilepsy incidences as:
-	Englander et al: for a single contusion, the post-traumatic risk is that 8.2 % of subjects will develop epilepsy in 2 years;
-	Christensen et al: the relative risk is 7.40 (7.4 times greater than in the normal population);
-	Annegers et al: the post-traumatic epilepsy risk is that 11.5% of subjects will develop epilepsy in 5 years, and their relative risk is 17.2 times greater than in the normal population over 10 years.
156.	Dr Drane went on to say that, because Mr Hazelton's assessment requires prediction of risk, the best means of stratifying the risk is required.  Current evidence suggests that CT diagnosis of intracerebral bleeding is the best discriminator, and this demonstrates that his seizure risk is above the population average for both mild and severe categories. 
157.	During his evidence-in-chief Dr Drane amplified on this point.  He made specific reference to the conclusion that Mr Hazelton has had two contusions shown on his CT scans, because the Englander et al study demonstrates a clear increase in risk of post-traumatic epilepsy in people who had multiple cerebral contusions.  
158.	Mr Harvey asked him if his aeromedical decision might be influenced by the finding of Messori et al, of an additionally increased probability of post-traumatic epilepsy when the early chronic stage follow-up MRI scans showed haemosiderin dregs incompletely enclosed by gliosis.  Dr Drane replied:
The answer to your question is almost certainly yes, but the difficulty [sic] is that while we may see that this is a factor which is perhaps protected or not protected, it’s a factor which may make it more likely that he has a seizure or less likely that he has a seizure.  We don't know, unfortunately, the long-term consequence of that ....
159.	Furthermore, Dr Drane cited six reports demonstrating that this risk of post-traumatic epilepsy has not returned to normal in less than two years, viz. Englander et al, beyond two years; D'Alessandro et al, 4-7 years; Wylie, 5 years; Jamjoom et al, nine years; Christensen et al, 10 years; and Annegers et al, 20 years. 
160.	On the other hand, during his cross-examination, Dr Drane also pointed out that the longer term studies of Annegers et al and Christensen et al show that this post-traumatic epilepsy risk decreases over time.
161.	Drs Drane and Navāthé had corresponded with Neurologist Dr John Hastings of Oklahoma for his further expert opinion, agreeing on the difficulties in relating the existing data to Mr Hazelton's case, but differing in Dr Hastings' "approach to risk".  Dr Drane addressed several matters raised by Dr Hastings in his statement:
•	He referred to Dr Hastings’ remark when discussing the problems of applying the cited studies to Mr Hazelton's case: 
....  In aerospace medicine... we are often presented with an individual with no, mild, or at most moderate TBI [traumatic brain injury] on clinical grounds and yet severe TBI on imaging grounds.  These are individuals without postconcussion syndrome, focal [neurological] deficit, or cognitive change whose disqualification is based solely on PTE [post-traumatic epilepsy] risk.  There is no scientific literature to address this 'healthier' subset of the TBI population...." 
In response, Dr Drane's comment was that, nevertheless, the literature shows distinct relevant trends.
•	Dr Hastings has asserted that Mr Hazelton's situation is not represented in the Englander et al study.  However, Dr Drane listed the entry criteria to include individuals older than 16 years, with injury from "external causes", and abnormal CT brain scan findings of intracerebral contusion within seven days of the injury.    
•	Dr Hastings, before adding that the clinical severity measures in this subset were not stated, had quoted that this Englander et al study reported "a risk of 8.2% in two years with a single contusion (higher with frontal contusion)".  Dr Drane referred to Mr Hazelton having multiple contusions, one of which was frontal, for which Englander et al found a seizure probability of 20.1%.  Furthermore, there was no sign that the number of seizures that occurred had levelled off by two years after traumatic brain injury.
•	Whereas Dr Hastings had expressed his belief that, after "16 months of seizure free observation... I believe that [Mr Hazelton's] risk of post-traumatic epilepsy is acceptably low", Dr Drane's concern was that none of the literature provides the level of confidence required by CASA regulations "to support an opinion of normal PTE (post-traumatic epilepsy) risk at one-year post injury"; and the increased risk of post-traumatic epilepsy persists for at least two years irrespective of the head injury severity, but increased when the pilot happens to have sustained an intracerebral haemorrhage.
162.	During his evidence-in-chief Dr Drane told us that CASA regarded the Englander et al study as the study most relevant to Mr Hazelton's case, because it stratified risk according to different types of cerebral contusion and their locations.  However, this study had only followed up the injured subjects for two years, yet extrapolations of the data from the Annegers et al and Christensen et al studies suggest that the increased epilepsy risk persists for up to "10 or 20 years".  Drs Drane and Hastings were agreed that the Englander et al study  had shown the "high incidence of PTE (post-traumatic epilepsy)” for the first 18 months post-injury, but Dr Drane was concerned that their data does not assist in evaluating the risk of epilepsy beyond two years.
163.	Dr Drane was questioned at length by both counsel on the question of the present magnitude of Mr Hazelton's risk of having a post-traumatic seizure.  During his evidence-in-chief, Dr Drane said that the Annegers et al and Christensen et al studies indicated that his increased risk would continue for 10 or 20 years. In response to a question from Mr Harvey, he said that Dr Hastings' estimate of Mr Hazelton's epilepsy risk of 10 times related to that of the normal population would not be "an appropriate or good standard for purposes of CASA's aeromedical decision making to accept".  When then asked what would be an acceptable level of risk, he went on to say that because "a consideration of relative risk is written into the regulation", the "paradigm” of 'the one per cent rule", as a "philosophy", "informed" the CASA medical decision-making process, although there also were other "considerations", depending upon the medical condition being discussed; he was not asked to elaborate on these.
164.	Then, when cross-examined by Mr Taylor, he was taken to the Seizure-Incidence graph, constructed from the findings on cumulative probability of post-traumatic epilepsy reported in the Englander et al study that he had included in his statement.  Dr Drane confirmed that this showed that, over two to five years following brain injury, the seizure incidence was declining further, and that this was consistent with the observations in the studies by Christensen et al and Annegers et al.  
165.	He explained that he had estimated Mr Hazelton's present risk, on the basis of calculations made by a British neurosurgeon, Dr John Firth.  Dr Wallis had provided him with a regression analysis supplied to him by Dr Firth, who he said had calculated the initial (lifetime) risk of post-traumatic epilepsy (applying at the time of injury) and the residual risk (applying to the time interval following the injury), of the 481 patients with post-traumatic epilepsy whom Professor Bryan Jennett originally had studied; Dr Wallis had included this material in his second and fourth reports.  In applying this Firth regression analysis, Dr Drane had used the data from the Englander et al study, pertaining to individuals with multiple contusions having an initial risk of post-traumatic epilepsy of 35%; with Mr Hazelton having remained seizure-free to date, his yearly percentage residual risk already had reduced to 19% at one year post-injury, and would further reduce to 14% at two years’ post-injury.  Dr Drane concluded that Mr Hazelton's current risk would lie between these two percentage figures, although he emphasised that these were statistical measures, and were "indicative ... not exact".
166.	Mr Taylor then asked him if Dr Hastings' estimate of Mr Hazelton's relative risk at the present time of about 10 times the population rate was within the 'one per cent rule', to which he replied that this is "not comparing like with like": seizure incidence is not the same as relative risk. When asked to "translate" the Firth table into relative risk, although acknowledging that the "1% Rule" is a "helpful guideline ... particularly for cardiovascular risk", Dr Drane did not "wholly accept" Dr Hastings' calculation "as yet" that Mr Hazelton satisfied the "1% Rule".  He did acknowledge that there had been an article published a few years ago suggesting that, because "the paradigms have shifted", the "1% Rule" could be relaxed to a "2% Rule".  However, he said that the decision about Mr Hazelton's medical status had been based on the calculation of his absolute risk of epilepsy, which 18 months after his injury, according to the Firth regression analysis, was 14-19%.  
167.	Still under cross-examination, he agreed that, after closely addressing evidence based medicine up to this point, this decision has to be determined by personal opinions:
So even though this is an evidence based medical assessment, opinion obviously comes into the equation?---Absolutely.  That's the critical part of evidence base, you need to know how to apply the evidence that you have, and that's been the question of this.
 	Yes.  It's not merely a matter of looking at the graphs from the literature, is it?---No.
You have to look at the graphs.  Looking at the graphs, you come to an opinion as to the risk - I'm sorry, the risk of epilepsy, but you have to use your own opinion as to how you feel that will affect air safety?---Correct. . 
 
168.	He was taken to the conclusion of the Englander et al study:
Stratification of CT scan findings and neurosurgical procedures were the most useful findings in defining individuals at highest risk of late posttraumatic seizures.
169.	Dr Drane agreed with Mr Taylor that, apart from the image size of the contusion having to be greater than 2 pixels, i.e. the smallest single component of a CT digital image, the contusions were not graded; and the actual numbers of "multiple" contusions were not itemised; specifically, there was no identified subset of persons with only two contusions demonstrated by CT scan.  Furthermore, only 66 of the 647 subjects in the study had developed seizures, an unknown number of whom had just two contusions.  Then, from Table 1, for ages 31 to 40 the cumulative probability was 16%, for white Americans it was 11% compared to 16% for African Americans, for assaulted subjects  it was only 9.9%; and the multiple contusions subjects were not subdivided into these categories, such as into white Americans compared to African Americans.  As well, although patients with a Glasgow coma score of less than 10 were admitted into the study, it is not known how many of the multiple contusions individuals had this score.  In responding to this, Dr Drane concluded:
... Does it make sense?  Is it consistent with other studies?  And the answer is that as far as we can see it is probably the best evidence we have, although nobody will pretend it's perfect.  And we would wholly agree with the importance of reviewing it, what are the factors that are - that mitigate against the sole level of risk, what were the factors that would make it work, such as hemosiderin, lack of gliosis.  There is [sic] other factors whose importance we now recognise that we don't know the quantification of that.  So I accept your concern, but I think your deduction is incorrect, because you can just as easily say, well, he might have fallen one side as he might have fallen the other side of that group.
170.	During his cross examination, Dr Drane also explained his remark in his statement:
...  In consideration of the safety case, absence of ideal evidence is an insufficient ground to say there is no elevated risk.
He was addressing this to Dr Hastings' observation that he could not "locate" Mr Hazelton in terms of his age group in the Englander et al study.  He said:
....  But my point is that... just to say that we don't have any evidence is not sufficient to say therefore he has no risk.  To my mind, that is inconsistent.
(c)	Determining the consequences of epilepsy 
171.	This is the final stage of the risk assessment.  In his statement Dr Drane said that, with little warning, an epileptic seizure may cause the pilot to block the primary flight controls (yoke and rudder pedals) and interfere with secondary controls (throttles, flaps or undercarriage), the latter not being readily accessible to a co-pilot.  Furthermore, the confines of most cockpits would limit administering of first aid to an unconscious pilot.  A seizure affecting a solo pilot would cause complete loss of control of the aircraft.
172.	Dr Drane had evaluated that the likelihood and consequences of Mr Hazelton's risks of epilepsy "are above the acceptable level".  
173.	Under cross examination, Dr Drane confirmed for us that the "Firth Scale" estimate of 14-19% was the basis of the risk analysis determination of the "acceptability" of Mr Hazelton's epilepsy risk.  However, he could not say how this had been decided it would affect air safety, because this had been decided by Drs Tak Sum, Fitzgerald and Navāthé before he had arrived to take up his CASA appointment.  He then was asked how he would make his risk analysis assessment in terms of air safety:
Yes, all right.  And what's your experience, then, in that opinion?  I'll call it risk analysis assessment.  What is your experience in making those sorts of decisions?---Once you have identified a risk, you need to be clear about the aviation factors relating to that risk.  In this case, actually, there are particular aviation factors.  Low oxygen can increase the risk of a seizure, fatigue can certainly increase the risk of a seizure.  Those are very real entities in the aviation environment and I think it's just worth noting that these studies were all done amongst the general population, pilot population.  It's got an exposure to low oxygen and to fatigue, which I think is more than the general population.  So I think these are specific concerns which one needs to have about pilots and that would be - so we look at the aviation environment in assessing the risk.  We then look and see if there are any mitigating factors, and you're looking for mitigating factors in terms of whether you can treat the risk of epilepsy, if it was possible to have an operation that fixed it for good, no problem.  In this case, there are not any mitigating factors for the condition, unfortunately, apart from time and so then you then go and look at mitigators of the consequence, operational factors that you might be able to impose which would reduce that risk and those may be factors such as not flying over built up area as a private pilot or often multi crewing is mentioned, but I think it's not a dustbin for pilots, pilots have got their job to do 
174.	Finally, Dr Drane, in his statement, said that he had found no adequate mitigation of the risks of epilepsy to flight safety or to Mr Hazelton, and there was no reliable prediction of when Mr Hazelton might reach an acceptable level of risk.
Dr John Daniel Hastings, Neurologist
175.	Dr Hastings has been in private practice as a Neurologist since 1971, having been certified by the American Board of Medical Specialties in 1972, after two years of Army service as a Neurologist, including in South Vietnam.  He has held a Federal Aviation Administration (FAA) commercial pilot certificate since 1968, with 6000 hours of flight experience.  His relevant qualifications and appointments include:
•	Adjunct Clinical Assistant Professor in Neurology at the Oklahoma University School of Medicine, and in Aerospace Medicine at the University of Texas Medical Branch.  
•	FAA designated Aviation Medical Examiner (AME) since 1976, and a senior AME since 1981.  
•	Senior Neurological Consultant to the Federal Air Surgeon, initially appointed a Consultant in 1989.  
•	President of the Civil Aviation Medical Association 1997 to 1999, and President of the Aerospace Medical Association in 2007.
176.	He has authored or contributed to several aviation and aerospace medicine textbooks:
•	Clinical Aviation Medicine.
•	Fundamentals of Aerospace Medicine.
•	Occupational Medicine: State of the Art Reviews.  The Aviation Industry.
•	Clinical Aviation Medicine.
•	Fundamentals of Aerospace Medicine.
•	Manual of Civil Aviation Medicine.
177.	He also has delivered numerous lectures to the Civil Aviation Medical Association, and been an expert panellist at several Aerospace Medical Association scientific meetings and Transport Canada conferences.  These have been on neurological subjects, including consequences of traumatic brain injury in airmen.
178.	Dr Hasting’s detailed statement can be considered in the following sections:
(a)	The clinical and imaging features of Mr Hazleton’s traumatic brain injury;
(b)	The conflict in the medical scientific literature between clinical and imaging observations and conclusions;
(c)	The argument for a balanced evaluation of both the clinical and imaging features in Mr Hazleton’s case; 
(d)	His differing views to those of Dr Wallis.  
(a)	The clinical and imaging features of Mr Hazleton’s traumatic brain injury (paragraphs 18 to 31) 
179.	Having commenced his statement by outlining his background and experience, in paragraphs 19 to 27 Dr Hastings next summarised, from examining Mr Hazelton's medical records and reports of his brain imaging studies, the salient clinical, radiological and imaging features of his injury:
•	his altered consciousness or a lapse of awareness lasting seconds;
•	CT scan findings of right superior orbital marginal fracture with adjacent right inferior frontal 8 mm contusion, and a left basal petrous temporal bone skull fracture;
•	uneventful recovery; 
•	no residual symptoms for more than 16 months;
•	his normal EEG and COGSCREEN studies;
•	the report of his MRI scan in March 2009 of gliosis without haemosiderin in the right inferior frontal and right anterior temporal regions; and,
•	no family history of epilepsy or history of febrile seizures, previous neurological injury, or acute symptomatic seizure.
180.	When cross-examined on this, Dr Hastings was taken to the Ambulance Report record of Mr Hazelton, describing him as amnesic for the assault, and that he was confused.  He was asked if these observations modified his views about Mr Hazelton's clinical assessment, but he said that they did not, because of his recorded Glasgow coma score, post-traumatic amnesia, and blood alcohol concentration of 0.21 g/litre.  He said that he had not seen Mr Hazelton's Mater Hospital clinical notes, but had been given an account of that information verbally; this had included that a CT scan of a week following the assault showed delayed swelling around the right frontal area, for which he had been given prednisolone, but he still assessed his clinical brain injury as mild.  He also had not seen the Mater Hospital CT brain scan; however he had seen those taken at St Vincent's Hospital, as well as the two MRI scans on 10 March and 13 December.
181.	In paragraphs 28 to 31 of his statement Dr Hastings discussed the details of his assessment of the severity of Mr Hazelton's traumatic brain injury.  
182.	He opined that on clinical grounds, Mr Hazelton's transient loss or altered consciousness, no focal neurological deficit, rapid return to alertness and orientation, brief period of post-traumatic amnesia, and no early epileptic seizure, collectively satisfied the DAME (Designated Aviation Medical Examiner) Handbook criteria for a mild brain injury.
183.	In next considering the radiographic (i.e. x-rays) criteria for traumatic brain injury severity (i.e. his skull fracture), he quoted from Becker et al: "Trauma to the head causing no loss of consciousness and no evidence of focal brain injury may be inconsequential even in the presence of a linear or depressed skull fracture".  Dr Hastings remarked:
I do not believe that the skull fracture, facial weakness, or left haemotympanum in and of themselves bear upon the risk of PTE.  This is in keeping with the DAME Handbook.
184.	With regard to Mr Hazelton's imaging criteria, the CT brain scan showed an 8 mm right inferior frontal contusion, and his initial MRI scan, as well as this contusion, showed haemosiderin.  A later less powerful MRI study showed a small left medial temporal abnormality, of indeterminate significance.  He interpreted this "bleeding in brain substance", according to the CASA DAME Handbook, as a "moderate to severe" traumatic brain injury.
(b)	The conflict in the medical scientific literature between clinical and imaging observations and conclusions (paragraphs 32 to 38)
185.	He then introduced the present conflict between clinical and imaging traumatic brain injury criteria within the terminology of the DAME Handbook.
186.	With this in mind, in paragraph 32 he turned to the aeromedical issues, and set out the questions and issues that he identified to be determined for Mr Hazelton's case:
(a)	What is the risk of post-traumatic epilepsy (PTE)?
(b)	Does the risk of PTE decline with the passage of time?
(c)	When does the risk of PTE in an individual become acceptably low?
(d)	Should a risk of sudden incapacitation of 1% per year be acceptable, or should a risk of 2% be considered for multi-crew ("with or as co-pilot") aircraft operations?
(e)	When considering risk of PTE, he believed that risk should be compared to incidence of PTE in the normal population (community) not the prevalence in order to provide "meaningful comparative risk assessments" (Dr Hastings' emphasises).
187.	At paragraph 33, he surveyed the scientific literature and aeromedical regulatory policy regarding traumatic brain injury.  When giving his evidence-in-chief, he identified three phases in the development of this literature.  First, before the advent of CT imaging in the early 1970s the severity of brain injury was based upon clinical criteria.  Second, CT scanning then became a major determinant of injury severity.  Third, and in his view of utmost importance, there has been the emergence of methodological issues that renders comparability of different reported studies difficult, when they have produced wide variations in the estimation of the risk of post-traumatic epilepsy. Accordingly, although the literature can be used as a guideline, to determine a percentage risk of epilepsy in a case like Mr Hazelton's, he preferred to use evidence-based medicine.  He defined evidence-based medicine as "the best available literature combined with clinical expertise", and not the literature alone.
188.	In paragraph 33 he discussed the widespread acceptance in the literature of a correlation between the risk of post-traumatic epilepsy and the severity of traumatic brain injury.  Before CT scanning, classification of severity was based on the clinical criteria of Glasgow coma scale, post-traumatic amnesia, focal neurological deficit, and loss/alteration of consciousness, supported by radiology, such as the nature of any skull fracture present.  Dr Hastings argued that such correlation is still supported by the literature. 
189.	In paragraphs 34 and 35, he expanded on how, since the mid 1980s, CT imaging has additionally assisted traumatic brain injury assessment by demonstrating intracranial blood and other structural changes.  Particularly, intraparenchymal blood (blood within the brain substance) has been seen to be important.  Although many authors have reported a relationship of CT findings to post-traumatic epilepsy risk, it is here that the problems have appeared, of lack of comparability of reports, different 'stratification' findings, and variable correlation with clinical measures of severity, with hampering of "accurate determination of PTE (post-traumatic epilepsy) risk by imaging criteria alone":
•	Deymeer and Leviton particularly identified problems in definition, classification and ascertainment of trauma in determining post-traumatic epilepsy risk.
•	Fey pointed to the widely varying results in different reported series, from 1.9% to >30%, in incidence of late seizures, which was attributed to variability of the subject populations, especially regarding injury severity.
•	Shorvon noted that head injury severity predominantly determines post‑traumatic epilepsy risk.  
•	Beghi observed wide variabilities in seizure risk, according to population types, and injury severity including injury to brain cortex, and/or penetration of the brain's dural coating. 
•	Wylie reported 3-7% post-traumatic epilepsy risk in civilian closed head injury; a 3.6 fold increased risk was found compared to the general population, with a five year risk of about 2%.
•	In their one year study, Angeleri et al reported a 3.43 fold increased post‑traumatic epilepsy risk for a single acute phase frontal or temporal brain lesion; and an MRI of finding one-year post-injury of haemosiderin did not increase this risk.
•	In a two year study of 793 patients chosen for their high seizure risk, Temkin found most had significant trauma such as epidural or subdural haematomas, intracerebral haematoma, cortical contusion, penetrating brain injuries, early seizures following injury, Glasgow coma score of 3‑8/15 in earlier patients, and the need for surgery.
•	D’Alessandro et al studied 93 head trauma patients with CT scans within 48 hours of their injury, 49 having at least one clinical risk factor for post‑traumatic epilepsy; all of the 10 who developed seizures showed focal brain damage, more significantly related than the clinical risk factors to the development of their epilepsy.
•	Englander et al reported their study of 647 adults with various abnormal CT scan findings during the first seven days post-injury, or best GCS (Glasgow coma score) ≤ 10 during first 24 hours post-injury, followed up for 24 months until death or their first late post-traumatic seizure; stratification by CT findings and neurosurgical procedures were the most useful risk defining features. 
190.	At paragraph 36 Dr Hastings elaborated briefly on the lack of stratification in the severely injured population making up the Temkin study: patients with subdural haematomas requiring surgery had more than twice the two year risk of developing epilepsy compared to those not undergoing surgery.  In paragraph 37 he stated that, in aerospace literature and regulatory aviation policies a subject may have no severity of traumatic brain injury by clinical criteria, but is classified severe if a single subcortical contusion is present; conversely a person with clinically moderate brain injury may have no CT scan abnormality.  Under cross-examination he elaborated by saying that in some states the term "intracranial blood" is not further specified, yet others break it down to subdural or epidural haematomas, and various forms of intracranial blood.  He agreed that, by a clinical assessment, Mr Hazelton's contusion had not been disclosed; and although he had qualifications about Professor Tress' opinion that he had a third, left temporal, contusion, he accepted that Mr Hazelton had right frontal and right temporal contusions.  He also accepted that the "current operative theory" was that post-traumatic epilepsy was related to the presence of iron breakdown products of haemosiderin (from blood); however, although he accepted the observations made by Messori et al of the increased epilepsy risk influence of incomplete gliosis surrounding haemosiderin, he also took into account the opposite conclusion made by Angeleri et al.
191.	In paragraph 38 Dr Hastings pointed out that this "conflict between clinical and imaging assessment of TBI (traumatic brain injury) severity has not been resolved in the neurosurgical, neurologic, and aerospace medicine scientific communities." Aerospace medicine practitioners are often presented with individuals with moderate or milder clinical traumatic brain injury, without severe imaging traumatic brain injury.  He asserted that no scientific literature has yet addressed this "healthier" traumatic brain injury population subset.  But he said that, currently, Temkin's seizure prophylaxis studies on more severely injured individuals are used.  However, during his evidence-in-chief Dr Hastings remarked:
... the studies and the literature regarding traumatic brain injury and the risk of epilepsy can be weighted towards more severe injury because of greater societal impact and whether be it from cognitive deficit or vocal [sic i.e. focal] neurological deficit or post traumatic epilepsy and the type of population that we deal with is somewhat selective in the sense that we tend to see the healthier, if you will, traumatic brain injury patients who have no localised deficit, who has [sic] no cognitive change and who is [sic] neurologically intact and have very mild or at most moderate clinical criteria, who present themselves for recertification but yet have some CT abnormality.  So it's a selective group that has not been specifically studied in the literature, I must admit.
(c)	The argument for a balanced evaluation of both the clinical and imaging features in Mr Hazleton’s case (paragraphs 39 to 56);
192.	In paragraph 39, Dr Hastings added that, until these conflicts are resolved, he prefers to use the 1979 AMA (American Medical Association) panel 
recommendations, incorporating both brain damage extent/degree, and damage location.  
193.	In paragraphs 40 and 41 of his statement he discussed the lengthy Mayo Clinic studies by Annegers and his colleagues  He stated that, although these are often cited in aeromedical decisions involving traumatic brain injury, notably these did not represent CT based determinations; in their 1998 report the authors have said:
Brain contusion was diagnosed by computed tomography (CT) only during the last 10 years of our 50 years study, and none of the 34 patients with mild or moderate traumatic brain injuries and abnormalities on CT had seizures.
194.	Dr Hastings said that these Mayo Clinic subjects with brain contusions were diagnosed, not by CT findings, but clinically, either by focal neurological deficits or on their neurosurgical findings, neither of which circumstance applies to Mr Hazelton's case.  He returned to this point in paragraphs 53 and 54 of his statement.
195.	In paragraph 42 of his statement, Dr Hastings emphasised the importance of considering relative risk compared to absolute seizure risk.  He said that the natural epilepsy incidence in the population at large, in the usual age group of pilots (e.g. 25-55 years) generally is accepted to be about 40 seizures for every 100,000 population per year i.e. 40/100,000/year.  This means that a relative risk increase of 25 would be 1000/100,000/year - a risk of 1% per year, from which "the 1% Rule" is derived.  He pointed out that in the Annegers et al study the incidence rate of post-traumatic epileptic seizures per year was greater than 1% only for severe head‑injured patients, and was highest in the first year (our emphases).  
196.	He clarified in paragraph 43 that the application of this "1% Rule" is based on a two-pilot operation, which he stated is "a concept long in use in aeromedical disposition".  Of interest is that there have been recent calls for revision of this, to a relative risk increase of 50 for "sudden incapacitation rate" for a two-pilot operation, i.e. a doubling of the “1% Rule”.
197.	In paragraph 44, Dr Hastings lists 13 features of Mr Hazelton's case:
•	momentary alteration of consciousness/lapse of awareness (seconds);
•	no loss of consciousness;
•	no focal deficit;
•	no cognitive change;
•	no impact, immediate, or early seizure;
•	no risk factors (family history, febrile seizure, remote insult, symptomatic seizure);
•	normal EEG;
•	normal COGSCREEN;
•	a small 8 mm subfrontal contusion on acute CT imaging;
•	two small contusions (right frontal and anterior temporal based upon MRI brain imaging in a follow up study);
•	no hemosiderin on MRI imaging studies;
•	no epidural, subdural, subarachnoid or ventricular blood; and
•	the passage of 16 symptom-free, seizure-free months of follow-up post-traumatic brain injury.
198.	On these grounds, in paragraph 45, he stated that he regarded Mr Hazelton as at "an acceptably low risk of PTE (post-traumatic epilepsy) at one-year post‑injury".  He went on to specify his opinion:
Given that his activities will be restricted to 'with or as co-pilot' operations, an additional measure of safety is afforded.  I would support a risk of 2% per year, as is observed in the United Kingdom.
199.	At paragraph 46 he stated that, because Mr Hazelton's traumatic brain injury "subgroup" is not addressed by the literature, the aeromedical decision on him must be based on expert opinion.  He has added:
The existing literature reporting PTE risk with bleeding within brain substance does not allow one to identify subjects within that group who had no, mild, or moderate TBI.
200.	In paragraph 47 he confirms that he does "espouse the concept that risk of PTE relates to severity of brain injury", because this has been consistently reported in all the traumatic brain injury literature, both:
•	"old", using clinical measures of severity; and,
•	"new", using radiographic measures of severity.
201.	However, in some reports, clinically mild brain injury may be judged severe radiographically, as in Mr Hazelton's case; yet subjects with a clinically severe Glasgow coma score of ≤ 10 may have a normal CT scan.  Therefore he contended that:
... both (Dr Hastings' emphasis) clinical and imaging criteria should be considered until there is a body of literature correlating clinical and imaging criteria in determination of PTE risk in mild TBI.  I do not believe that either variable can be ignored.
202.	In paragraph 49 he commented that, in aviation risk assessment literature, he has not encountered the distinguishing of "active" from "passive" incapacitation; and he remarked that this might "embrace a more relaxed policy for passive incapacitation", and perhaps sudden incapacitation "need not be stratified".  
203.	In paragraph 50 he observed that any policy requiring a nil increase in seizure risk would then even exclude individuals with febrile seizures, yet most states allow certification for this.  This would formalise a far more exacting "0.04% rule" (based on 40/100,000/year for the general population).  Dr Hastings stated that the DAME Handbook cites a risk of 1% as acceptable.
204.	In paragraph 51, Dr Hastings dealt at length with his concern that Mr Hazelton also is not represented in the Englander et al study:
•	Mild traumatic brain injury not only was not defined, subjects like Mr Hazelton with only clinically mild injury were excluded, by the authors having studied only moderate to severe injuries, yet without describing their criteria, either clinical or radiographic, for these.
•	Although punctate haemorrhages (and subarachnoid and intraventricular haemorrhages) were studied under "other intracranial lesions", their nature and size were not defined; and they were found not to have "altered the probability by developing late posttraumatic seizure compared to individuals without such haemorrhages".
•	The article's concluding statement, that the amount of focal tissue destruction is the most important predictive factor, does not necessarily suggest that clinical assessment should be ignored.
•	Although the study reports a risk of 8.2% in two years with a single contusion (higher with frontal contusion), the report contains no clinical information about these "moderate or severe" brain injury cases. 
205.	In paragraph 52, Dr Hastings argued that, with Mr Hazelton's mild injury, he would not have been included in the Englander et al or Temkin studies' populations, which were confined to more severely injured subjects.  
206.	During his cross-examination Dr Hastings said that in these epidemiological studies, it is difficult to locate a specific individual: they study a population, not an individual, so that statistics have to be used to determine probabilities for an individual.  However, he agreed that the Englander et al study reported a risk of 8.2 per cent in two years with a single contusion, with a higher risk for two contusions, with other variable factors such as cortical and subcortical locations, and bilaterality.   Also, when asked for his views about the Englander et al study's findings about cerebral contusions influencing the post-traumatic epilepsy risk, he said:
Yes, I would state that the presence of more than one contusion elevates the risk.  I would state that having contusions elevates the risk over not having contusions.  I would state - I would agree with Dr Englander's conclusion that the two most important ingredients of the risk of determination of post-traumatic epilepsy are neurosurgical procedures, which doesn't apply here, and stratification of imaging findings.  I fully embrace that.  There's stratification of imaging findings, and, for example, Englander pointed out that not all inter-cranial [sic: intracranial] blood elevates risk.  Punctate haemorrhages didn't elevate the risk at all.  Epidural haematomas not requiring surgery didn't elevate the risk at all.  Subarachnoid blood did not elevate the risk at all.  That is the point about stratification of imaging findings that I think is important, and I think will be important in the future study of especially mild to moderate traumatic brain injury with imaging findings such as we have here.
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.
207.	However, he did not agree that, from the Englander et al study findings, about 8 per cent of patients such as Mr Hazelton developed post-traumatic epilepsy, because he did not know of the clinical characteristics of the individuals in that 8 per cent group, adding:
... I understand and accept the elevated risk factors as stated by Dr Englander and the other centres who participated in the study, and I look in those studies for a correlation between clinical criteria, such as in the Annegers study, and the CT criteria, such as in the Englander study, so that we can take out Mr Hazelton and I don't believe it can be done...
208.	In paragraphs 53 and 54, Dr Hastings returned to the point that he had made regarding the Annegers et al study and its follow up study by Annegers and Coan, that only degrees of clinical severity were addressed.  CT imaging was used to diagnose brain contusion only in the last 10 years of the 50 years' duration of this study, and none of their 34 patients with mild or moderate clinical brain injuries with CT abnormalities developed seizures.  Dr Hastings concluded at paragraph 53: 
Within the confines of this study (no CT), Mr Hazelton would be in the mild group with 0.7% cumulative five-year risk of PTE.
209.	He amplified on this at the end of paragraph 54:
This translates to 0.14% per year or 140/100,000/year, well within the 1% per year risk of sudden incapacitation.
210.	And during his examination-in-chief he confirmed his view that Mr Hazelton's epilepsy risk probably fell into less than the "1% Rule".
211.	When giving his evidence-in-chief, Dr Hastings told us that, earlier on the day of our hearing of Mr Hazelton's matter, he personally had sought to confirm that the Annegers et al study was clinically based, rather than image-based. As Dr Annegers had died some 10 years ago, he had spoken by telephone with another of the Mayo Clinic authors, Dr Hauser, with whom Dr Hastings happens also to have worked in the FAA for the past 15 years.  Dr Hauser had told him that their patients with mild to moderate clinically determined traumatic brain injuries were not reclassified according to their CT findings.
212.	When cross-examined Dr Hastings was questioned on his remark in paragraph 41:
... Annegers did not represent a CT based severity determination.
213.	Dr Hastings alluded again to the Annegers' authors' statement that CT scanning was only used in the last 10 years of the 50 years study, and that none of the 34 patients with mild or moderate traumatic brain injury and abnormalities on CT scans had seizures.  He agreed with Mr Harvey that a skull fracture would classify the injury as moderately severe.  However they had defined brain contusion either by being directly observed at surgery, or by the presence of a focal neurological deficit.  Dr Hastings quoted:
...  Brain contusion was diagnosed by computed tomography only during the last 10 years of our 50-year study, and none of the 34 patients with mild or moderate traumatic brain injuries and abnormalities on CT had seizures. 

214.	He maintained that Mr Hazelton came into this group.  He disagreed with Mr Harvey that he was saying that the Annegers findings did not apply to Mr Hazelton because his contusions were not observed at the time of surgery, simply that the Annegers' study was based on clinical features and surgical findings, and not CT findings.  Mr Harvey then quoted a similar passage from the later Annegers paper:
... Brain contusion was diagnosed by computerized tomography during only the last 10 years of our 50-year study and by clinical signs or visualization during surgery in the early years.
215.	Dr Hastings also disagreed that the later quotation in any way qualified the earlier one.  He repeated that this was what he had clarified with Dr Hauser in their conversation of earlier that day, that the entire study was done on clinical grounds.
216.	During Dr Hastings' cross-examination, one of the other medical witnesses, Neurologist Dr Wallis, who was in the hearing room, joined concurrently with Dr Hastings while he was available on the telephone.  Dr Wallis differed from Dr Hastings' interpretation of the statement that he had quoted from the Annegers et al report:
... Brain contusion was diagnosed by computed tomography (CT) only during the last 10 years of our 50-year study, and none of the 34 patients with mild or moderate traumatic brain injuries and abnormalities on CT had seizures.

217.	He disagreed that the word "abnormalities" necessarily meant that all 34 of these patients had contusions, from which Dr Hastings had concluded that the clinical features of Mr Hazelton's case included him in this group.  Dr Wallis remarked that patients with contusions in that study were not classified as mild or moderate, but as severe.  Dr Hastings repeated that, in his conversation earlier that day, Dr Hauser had confirmed that the authors of the Annegers' report had not changed any patient's classification as a result of their CT scan findings.  When Mr Taylor asked Dr Hastings if Dr Hauser might be contacted during the hearing to clarify this question, Dr Hastings agreed to assist Mr Taylor in seeking to arrange this, to which both parties agreed.
218.	Dr Wallis then referred Dr Hastings to his statement at paragraph 51, that he could not determine that Mr Hazelton situation was represented in the population of the Englander et al study.  He said that most of their subjects had had abnormal CT scans, that they were followed for two years, by which time about 8 per cent of patients with a single contusion had an epileptic fit in one year, and that their risk for epilepsy had continued for more than two years.  Dr Wallis pointed out that he had calculated from Professor Jennett's study that a patient with one contusion had a lifetime risk of about 12 per cent; thus, after two years, another 4 per cent of these patients would eventually have seizures.  For patients with multiple contusions, as Mr Hazelton had, the Englander et al study showed an even higher two year cumulative risk of 25 per cent, with a lifetime risk of more than 30 per cent, and an estimated period of more than 10 years without having a seizure to return to the same risk as for the general population.
219.	Dr Hastings responded by emphasising the difference between annual risk and lifetime or cumulative risk.  He cited the cumulative risk for every person in the general population having a single seizure in their lifetime being accepted by many authors, such as Dr Hauser, as 10 per cent; this included 3 per cent of the general population who have had febrile seizures, and about another 2 or 3 per cent who might have a single seizure in a lifetime.  However, when comparing seizure risk for aeromedical purposes, the "1% Rule" is referring to the risk of a pilot with a head injury having a seizure in one year; this is compared to the fact that any pilot without a head injury has a risk of a seizure of about 40 per 100,000 per year (40/100,000/year) or 0.4 per cent.  By contrast, he added that, with the cumulative risk of 10 per cent applying to everybody in the population, no one should fly an aeroplane because they all would exceed the "1% Rule".
220.	Dr Wallis questioned the figure of 10 per cent cumulative risk of a seizure for the normal or general population, referring to the report by Annegers et al and that by Christensen et al.  He quoted a lower figure in Western society of between 0.5 per cent and 1 per cent.  Dr Hastings pointed out that that Annegers et al report did not address the cumulative risk of epilepsy in a normal population over a lifetime, but he referred to other papers by Dr Hauser, as well as Dr Shorvon.  He suggested that this also might be discussed with Dr Hauser if he could be reached to assist our hearing.
221.	Dr Hastings asked Dr Wallis if he preferred that any pilot's risk of seizure should be that of the normal population.  Dr Wallis acknowledged that he did not regard himself a consultant in those terms, so much as a consultant neurologist to advise on the risk of an unforeseen event; and he considered Mr Hazelton's risk of suffering a seizure from his injury to be “very high”, and to continue above the risk of the general population "for a long time."  He said that it was not for him to say when Mr Hazelton would be fit to fly.  Dr Hastings then remarked that individuals with a history of febrile seizures (i.e. seizures provoked by a fever) are allowed to fly aircraft, despite their risk of having a seizure being higher than in the rest of the population.
222.	In paragraphs 55 and 56 of his statement, Dr Hastings discussed the findings of the Christensen et al study as they might pertain to Mr Hazelton's case.  This surveyed 1,605,216 persons comprising 78,572 with traumatic brain injury, of whom 1017 (1.2%) developed epilepsy.  Mr Hazelton's contusions would have placed him in this study's severe traumatic brain injury category, conferring a relative risk of 7.4, translating to 511/100,000/year, which is just over half the incidence represented by the 1% rule.  This study uses an "all age" incidence of 69/100,000/year, higher than 40/100,000/year due to the known higher incidence of epilepsy in children and those late in life, to which Dr Hastings alluded to during his cross-examination.  In paragraph 56 Dr Hastings observed that, of the 1017 subjects with traumatic brain injury, only 30 with severe injuries were older than 15 years, i.e. the number in the age group of our interest is small.  The relative risk in this older age subgroup was 12.24, translating to 856/100,000/year based on the 69/100,000/year incidence figure, yet still below the 1% figure i.e. 0.9%.
223.	However, during his evidence-in-chief, Dr Hastings expressed his reservations about the applicability to Mr Hazelton of these Christensen study findings:
•	the 30 individuals in Mr Hazelton's age group constituted too small a number to be comparable with other studies;
•	the admission criteria included patients who had moderate to severe traumatic brain injury; and,
•	severe brain injury patients were not stratified into subsets, but they included brain contusion or intracranial haemorrhage, without defining contusion, or describing its size, or if contusions were single or multiple.
224.	Under cross-examination Dr Hastings was asked:
Would you agree that the Annegers and the Christensen studies are, notwithstanding limitations of the state of the literature at the moment, the best studies available in this field at the moment?---I believe the Annegers study is the best study available in the field for clinical criteria for traumatic brain injury.  I do not believe that the Annegers study is useful at all when you attempt to apply imaging criteria to severity of traumatic brain injury, which is why Dr Hauser himself does not refer to his study when we’re talking about imaging criteria.  He refers to other authors.  So I would agree with you that the Annegers study is the best clinical study we have.  I do not believe the Christensen study is useful for studying of [sic] the private [sic: pilot]  population in traumatic brain injury, because I would have a hard time persuading someone that 30 individuals of 1.6 million studied is a sufficient number to make any generalisation.  Not only that, it's a large retrospective study and I would look to other studies that more closely examine imaging criteria, such as Englander’s and some of the others we've spoken of.  So no, I certainly don't think Christensen is applicable to the private [sic: pilot]  population in determining the risk of post-traumatic epilepsy.  I don't find that at all, sir.
225.	During his evidence-in chief Dr Hastings stated his view that an individual risk assessment should not be based on brain contusions alone.  It should consider:
•	the two "ingredients" of evidence-based medicine, available evidence and clinical expertise;
•	clinical measures of severity, such as cognitive impairment or focal neurological deficit;
•	family history of seizures, and past history of febrile seizures or previous neurological insult; and,
•	stratification of imaging findings.
226.	In paragraph 57 Dr Hastings had recorded his difference of opinion with some of Dr Wallis' comments:
•	Traumatic brain injuries' structural changes, rather than their pathophysiology, are defined by CT and MR imaging techniques.  
•	He did not state that Mr Hazelton has mild traumatic brain injury: he refers to this as being mild only on clinical grounds, whereas on imaging grounds, according to the DAME Handbook, his injury was severe.  
•	Longer term, he did accept that post-traumatic epilepsy risk beyond two years continues above that of the normal population, but his view was that this was low enough to be acceptable.
•	The authors of the Annegers et al and Christensen et al papers did not “include cerebral contusion as a mandatory criterion that classifies a head injury as severe."
•	He did not accept the Christensen et al article as being important for Mr Hazelton's case: of over 1.6 million subjects in the study population, 78,572 suffered traumatic brain injury, 1017 (1.2%) of whom suffered seizures, and the maximum age of subjects was 25 years.  Only 30 individuals with severe brain injury were older than 15 years, and their clinical characteristics were not described.
227.	In paragraph 58 Dr Hastings discussed the role of haemosiderin in causing post-traumatic epilepsy, remarking that this is still under consideration.  Although the study by Messori et al of 135 patients with mild to deep coma found haemosiderin incompletely surrounded by gliosis to be an important risk determinant, Angeleri et al did not at one year post injury.
228.	At paragraph 59 Dr Hastings concluded that Mr Hazelton's post-traumatic epilepsy risk is acceptably low.  He based this opinion on:
•	the clinical features of his injury;
•	his imaging findings;
•	16 months without seizures developing;
•	consideration of the 1% rule; and,
•	his interpretation of the existing literature. 
229.	In Dr Hastings' view, Mr Hazelton warranted “airman medical certification” at this time.  He went on to state:
A 2% rule applied to a 'with or as co-pilot' limitation would allow an additional measure of protection, since acceptable incidence would be doubled.  Acceptable risk of 1% per year translates to an incidence of 1000/100,000/yr and 2% translates to 2000/100,000/year.  I believe that Mr Hazelton's risk falls within these boundaries.
Dr William Allen Hauser, Neurologist
230.	Dr Hauser of New York is Professor of Neurology at Columbia University. We already had been well informed by both Dr Hastings and Dr Wallis of Dr Hauser's eminent reputation in the USA in the field of epilepsy, as author and co-author of many original papers over many years on various aspects of the subject.  In particular, he had been a senior co-author with the late Dr Annegers in the 1998 Mayo Clinic report; and, he had been the study neurologist, identified as WAH, in their 2000 report.  Also Dr Hastings had advised us that he had been associated with Dr Hauser in the past 15 years in advising the Federal Aviation Administration.  
231.	Dr Hauser had kindly made himself available at very short notice to give evidence by telephone, after Mr Taylor, with Dr Hastings' aid, had contacted him to seek his assistance in clarifying the questions of difference of view that had been canvassed between Dr Hastings and Dr Wallis during Dr Hastings' cross‑examination.  Dr Hastings also was included in the telephone linkup; and Dr Wallis was present in the hearing room.
232.	On his examination-in-chief, Dr Hauser first was asked about the severity of brain injury classification of the subjects in the last 10 years of the study who had CT scans who were mentioned in the 1998 report.  Dr Hauser answered that, on that initial assessment, as stated in that report these patients were not reclassified if their CT scans had been abnormal.  He also confirmed that, for that report, all of the subjects were classified on their clinical features.  This was a univariate analysis, from which direct comparisons were being made with a population to determine an incidence rate ratio.  Their subsequent analysis of the study data was multivariate, searching for additional risk factors, such as epidural, subdural, and intracerebral haemorrhages.
233.	Mr Taylor then put to Dr Hauser the second question, of the incidence of epileptic seizures in the population in general.  He referred him to one of his co‑authored publications, and quoted from the summary abstract at its commencement:
The cumulative incidence of epilepsy to age 74 was 3 per cent, of all unprovoked seizures was 4.1 per cent and of any convulsive disorder was 10 per cent.  
234.	Dr Hauser confirmed that that statement was correct for the data in that paper.  He added that the cumulative incidence for epilepsy in the general population probably is higher than those figures, because they were based on a 40 or 50 years' incidence rate.  A cumulative incidence of epilepsy of 3 per cent that applies up to the age of 75 increases to about 4 per cent up to the age of 85, although those details were not included in that publication.
235.	Under cross-examination Dr Hauser told us that, in the second, multivariate, analysis, they found that some of the previously important clinical features, notably varying durations of loss of consciousness, or occurrence of early epileptic seizures, were not particularly significant; but the presence of subdural or intracerebral blood was, including contusions.  In answer to a question from Mr Harvey, he said that they did not analyse any varying effects of locations of the blood in different brain regions.  He remarked that the iron present in the blood's haemoglobin was a very potent "epileptogenic agent".  He was aware that recurrent seizures in experimental animals had been induced by iron injected into the brain cortex.  He was not familiar with the findings of Messori et al of the apparent higher post-traumatic epilepsy risks with MRI scan findings of incomplete gliotic enclosure of haemosiderin remnants, but commented that the hypothesis and assumptions seemed reasonable.
236.	Dr Hastings asked Dr Hauser if he was correctly interpreting the 1998 report if he said that the 34 patients with abnormal CT scans did not have their severity of injury reclassified because of their CT scan findings; and that that study was largely clinical, with later studies emphasising the CT scan findings as criteria for severity.  Dr Hauser affirmed both of these interpretations.  He added that, without him having immediate access to those records, he could not state what abnormalities had been shown on those CT scans.
237.	After Dr Hauser was excused, we asked Dr Hastings some questions about the "1% Rule".  Dr Hastings affirmed that this translates to an incidence of 1000 sudden incapacitations for 100,000 patients per year.  This compares to an incidence figure for the age group of interest for pilots, from past estimations by Dr Hauser, to be 35 to 40 per 100,000 per year; and Dr Hastings had chosen to take the higher figure.  From this, a relative risk of 25 times that of the normal population based on the figure of 40 provides the one per cent figure.  When asked for his estimate of Mr Hazelton's risk of seizure, he again said that, based on Mr Hazelton's clinical criteria combined with his CT and MR scan findings, it could be as much as 10 times that of the normal pilot population, that is, 10 times 40 per 100,000 per year (or 400 per 100,000 per year, or 0.40 per cent), less than half of the one per cent rule.
Dr Donald Barry Appleton, Neurologist
238.	After several years attending as a Neurologist at the Royal Brisbane and Royal Children's Hospital, Dr Appleton commenced practice in Neurology in 1973. Currently he is a staff member of the Neurosciences Department of the Royal Children's Hospital. He has published numerous original articles in neurological scientific literature, including on epilepsy.  From 1979 to 2001 he also was Consultant Neurologist for the Australian Defence Force.  As well he was the Principal Reserve Medical Officer Queensland for the RAAF for the last 11 years of that service, to retire with the rank of Group Captain.  Throughout his Australian Defence Force career he had considerable experience assessing the fitness of pilots to fly.
239.	Dr Appleton, the second Neurologist to see Mr Hazelton, had had a neurological consultation with him on 6 March 2009 at the request of his general practitioner, Dr Sutch, to whom Dr Appleton had written a report.  Available for this consultation, he had "documentation of his injury", noting from Mr Whiteley's statement that Mr Hazelton had not lost consciousness and that he was "quite lucid immediately after"; and he also had the results from Mr Hazelton's CT scans from St Vincent's Hospital, Dr Cameron's report, and Dr Reid's EEG report.  He observed that Mr Hazelton had had no subsequent memory or temperamental problems, and no seizure.  Dr Appleton told us at the hearing that, at that point, Mr Hazelton had not mentioned his Mater Hospital attendance, but he later had learned of it, and had seen the report of the CT brain scan performed there.
240.	He found his physical examination to be normal, with no residual facial weakness.
241.	He requested an MRI brain scan at St Andrew's Hospital in Brisbane which "showed a small area of gliosis in the right frontal region and another in the anterior pole of the right temporal lobe", but with no other significant abnormality.
242.	Because of his skull fracture and "history of loss of consciousness" he had estimated Mr Hazelton's seizure risk at 0.7% in one year and 1.6% in five years, this being higher if the EEG is not normal.
243.	He cited three reports from the literature.  Guidelines derived from a report in 2001 by the US Department of Transportation in conjunction with the Federal Aviation Administration suggest that "for severe traumatic brain injury there should be at least 1 year recovery period and the condition considered stable by the attending physician.”  In 2004 Johnston and O'Brien discussed various grounding periods depending upon duration of post-traumatic amnesia, but Dr Appleton found that Mr Hazelton had had no post-traumatic amnesia.  He also considered that the relevance to Mr Hazelton's case, of the study by Messori et al predicting post‑traumatic epilepsy with MRI scans, was limited by the small number of patients in this group.
244.	He observed that, according to Federal Aviation Administration Guidelines, Mr Hazelton appeared to be eligible to return to flying after one year, particularly in a multi crew environment; he supported that consideration.
245.	In his statement Dr Appleton amplified on these observations.  He quoted Adams and Victor in their widely respected Neurology textbook Principles of Neurology, who concluded that with a skull fracture and a history of loss of consciousness, the seizure risk is 0.7% in one year and 1.6% in five years.
246.	For Mr Hazelton's case he then reviewed two authorities, the CASR, Part 67, subpart 67.C, 67.145 and 67.155, and the Designated Aviation Medical Examiner's Handbook, Medical Aspects, 2.5 Neurology, 2.5.2 Nervous System Standard - CASR Part 67.  By referring again to the US Department of Transportation and Federal Aviation Administration report in 2001, he confirmed his view that Mr Hazelton would be eligible under Federal Aviation Administration rules to return to flying, in a multi crew environment, after one year; and his opinion was that he satisfied the criteria in regulation 67.150 of the CASR to hold a Class 1 medical certificate "with or as a co-pilot".
247.	He then addressed Dr Drane's statement, noting that he relied on research articles on head injuries and post-traumatic epilepsy.  He pointed out: "The underlying difficulty with heavy reliance on research articles is that there are no universally accepted definitions of the severity of a traumatic brain injury."  By the criteria used by Englander et al, the applicant's Glasgow coma score of 13-15 and his single CT contusion lesion, his injury would be "mild".  These authors added that 80% of seizures occur in the first year and 90% occur within 18 months post injury, with seizure-risk onset diminishing "rapidly" after the first year.  The Christensen authors had acknowledged these definition problems, stating, "clinical discrimination between different types of brain injury is difficult and the definitions vary between countries." Taking specific points of Dr Drane's:
•	With regard to his cognitive function, Mr Hazelton's psychometric assessment showed no cognitive impairment, and his MRI scan showed no axonal injury changes as described by Mittl.
•	He opined that Mr Hazelton's risk was "very low" of suffering a seizure in flight to prevent a co-pilot from controlling the aircraft.
•	He disagreed that his right orbital roof fracture and right inferior frontal contusion were consistent with "severe" injury, this requiring a Glasgow coma score of less than 10.
•	He disagreed that his early intracerebral bleeding correlated with his post-traumatic epilepsy risk, opining that, according to Messori et al the MRI is "much more effective with haemosiderin deposits", his post-traumatic epilepsy probability appearing to be "relatively low".
248.	On Mr Hazleton’s likelihood of experiencing post-traumatic epilepsy, as Dr Drane discussed, Dr Appleton observed two points.  First, the population-based cohort study by Christensen et al indicates a doubled post-traumatic epilepsy risk for mild brain injury, but also considered that the difficulty in grading brain injury severity may have resulted in "mild brain injury" patients actually having more severe injury, resulting in overestimated epilepsy risk.  Second, in their population-based study Annegers et al thought that this seizure risk may be "artificially high" because of more accurate ascertainment in the injury cohort than the general population.  Also, not one of their 34 patients with "mild or moderate traumatic brain injuries and abnormalities on CT had seizures."
•	Mr Hazelton had only one of the contusion injuries, and not in the parietal region, as listed by Dr Drane, and therefore according to Englander his risk of post-traumatic epilepsy is low.
•	His post-traumatic epilepsy risk for his "mild" brain injury (Glasgow coma score 13/15) is not 8% in two years, as cited from Englander et al, which is a study of "moderate to severe traumatic brain injury".  He opined that the Adams and Victor conclusions were the more relevant.  His right frontal contusion did not place the applicant in the "severe" category.
•	Although his seizure frequency risk will not be reduced to normal population levels within two years, this is insufficient grounds to conclude he was unfit for Class 1 and Class 2 medical certificate.
249.	Addressing Dr Wallis' statement, Dr Appleton disagreed that Mr Hazelton's contusion makes his case "severe" according to Annegers.  The more recent article by Maas "states that the traditional approaches to the classification of clinical severity are the subject of debate and that translating the basic research remains a challenge."  According to the Maas scales, the applicant's Glasgow coma score indicates "mild" injury, and his structural changes amount to "mild to moderate".
250.	In his evidence-in-chief at the hearing, Dr Appleton emphasised that the contemporary literature on post-traumatic epilepsy recognises that the grading of the severity of head injuries is very difficult, due to different definitions adopted by different authors, based on both clinical and imaging grounds.  He regarded as important that a balance of these two should be found, as mentioned in the recent Maas article, from the European and American Brain Trauma Consortia.
251.	He went on to say that it is difficult to make a firm statement about Mr Hazelton's present risk of developing post-traumatic epilepsy, except that most literature says that, by 18 months, 90 per cent of people who are going to have a seizure will have had it.  Also, more recent literature has suggested that the risk of a seizure occurring later than that is proportionate to the extent of the injury in volume.  
252.	He disagreed with Dr Drane's estimate that Mr Hazelton's absolute risk of epilepsy at the time of his injury was 35 per cent, referring to it as a "blanket statement" not taking the extent of his trauma into account.  In his opinion, by referring to the Englander study, an 8 per cent risk over two years was a reasonable starting point for a "moderate" injury; this study was based on CT scan findings, included multiple contusions.  Mr Hazelton's initial CT scan showed only one contusion, although his later MRI scans showed a second smaller one; and in the Englander study, they also may have found second lesions if their subjects also had had MRI scans.
253.	He had seen the second and third CT scans performed at St Vincent's Hospital, but not the first, which was said to have shown diffuse brain swelling. 
This had resolved on the second scan.  He noted that the Mater Hospital scan of a week later had shown "localised swelling, which was not unexpected, but the ventricles and the basal cisterns were normal and without distortion. He had seen one contusion on the Sydney scans, but the MRI scans initially showed two small areas each about 8 mm in extent, with possibly a later third small area.
254.	Under cross-examination, he told us that he had seen the reports of the Mater Hospital CT scan of both Dr Law and Dr Earwaker only the day before this hearing.  
255.	He confirmed that, in the annexure to his statement of the section from the Adams and Victor textbook, for his opinion regarding Mr Hazelton's epilepsy risks, he had relied on several of the authors' citations.  There was a reference to the earliest report of the Annegers study from the Mayo Clinic.  Another was:
... Approximately 6 months after injury, half the patients who will develop epilepsy have had their first attack, and by the end of 2 years the figure rises to 80 percent..."

He confirmed that this observation was irrespective of the injuries' severities, 
256.	Dr Appleton also pointed to another citation later in that same paragraph: 
•	For the less severely injured (mainly closed-head injuries), patients reach 75 percent certainty of seizure-freedom in 2-6 months, 90 percent in 12‑17 months, and 95 percent in 21-25 months; and,
•	The same "assurance periods" for severe (penetrating) brain wounds were found to be one year, two years, and three years.  

257.	He said that these observations form the basis of his opinion that Mr Hazelton's epilepsy risk is acceptably low.  He had attempted to take "a balanced approach between clinical and imaging".  From this he was putting him at the "mild to moderate" level of the Annegers 1998 study, in which 34 cases with CT scan abnormalities had no seizures over 10 years.
258.	There followed this exchange:
Just tell us, if you wouldn't mind, how you've gone about that balancing exercise?---Okay.  First of all, he has had or had at the time, a quick recovery.  If this were a severe injury I would have expected perhaps he would have worsened over the next 48 hours, not improved.  So on that grounds [sic] alone, I think this would indicate it’s a less severe injury.  I looked also further at the literature, and where there has been a more severe and diffuse injury, this will often show up later on MR scans, and I refer particularly to an article by Mittel [sic: Mittl], which describes diffuse axonal injury findings, where the injury is severe.  These were not present on the sophisticated MR scan that Mr Hazelton had.  So that's another ground for supporting that this was not as severe a head injury as has been suggested.
All right, and did you take into account the views of Professor Brian Tress?---I have.
And you see that he had identified, in particular, two contusions with a possible third contusion?---Yes, I have.
And that didn't affect the weight that you gave to the radiological evidence that you base your opinions on; is that right?---I think those lesions that he described might be seen in anybody that perhaps has had a concussion from a football or a rugby injury, where there has been a rapid acceleration-deceleration of the brain within the skull, so- - -
So to focus more directly on my question, the analysis that Professor Tress gave of the radiological scans taken at St Vincent's Hospital and at the Mater Hospital, did not affect the conclusion that you had already come to, as to where the particular severity of this injury should lie?---I would have expected, if it were a severe injury, that there would have been evidence of diffuse axonal injury, which there was not.
All right, and because there was not that particular feature, you are able then to essentially acknowledge Professor Tress's reports of course, but?---Exactly.
- - - to then?---Yes.  I don't disagree with what he said, but I'm just saying that I don't think it necessarily concludes that this was a severe head injury .
259.	Dr Appleton affirmed that, in his balancing process, he had taken into account Mr Hazelton's clinical features, his presentation to him at his consultation in March 2009, and his Glasgow coma score in which he also considered any loss of consciousness; and, from the St Vincent's Hospital records, he concluded that there was no significant evidence that he had had post-traumatic amnesia.
260.	In response to a question from the Deputy President, Dr Appleton remarked that he did not consider that intracranial bleeding necessarily indicates a severe head injury, because it sometimes can be caused by mild trauma.  He would term it "a significant injury, but not necessarily severe".
William Eduardo Wallis, Neurologist
261.	After three years of service in the United States Air Force as a Neurologist in West Germany, Dr Wallis has practised in Auckland since 1972, initially as a full-time Neurologist in the Auckland Hospital, then commencing private practice in 1974.  His 25 presentations by invitation to learned societies have included four on aeromedical issues of head injury and post-traumatic epilepsy.  He also was Principal Neurology Teacher to the Civil Aviation Authority Aviation Neurology Course in 2002 and 2003. His Curriculum Vitae lists 31 original publications, eight on epilepsy and its treatment; and three were on the subject of medical fitness to fly:
•	Fitness of Aviators Following Head Injuries, Report Prepared for New Zealand Ministry of Transport, Aviation Division, 1983.
•	A Proposal for Revision of Civil Aviation Authority Medical Manual.  Head Injuries and Post-Traumatic Epilepsy in Pilots, Civil Aviation Authority Manual 2002, revised 2003.
•	Ischaemic Cerebrovascular Disease and Medical Fitness to Fly, Report for Civil Aviation Authority, 2007.
262.	As well as his Curriculum Vitae, Dr Wallis provided four reports.  
263.	His first report was a letter of 8 March 2010 to Drs Navāthé and Drane.  He disagreed with the opinions of:
•	Drs Maxwell and Hastings on the "mild or minor" classification of Mr Hazelton's head injury; 
•	Dr Stark's estimate of his risk of post-traumatic epilepsy of eight per cent, reducing by 90 per cent in two years;
•	Dr Appleton's selection of the literature and his cited figures; 
264.	Apart from Dr Cameron's estimation of the rate of residual post-traumatic epilepsy risk decline, he agreed with his opinion.  He stated his view that Mr Hazelton's head injury should be classified as severe, because of his skull fracture, cerebral contusions, brain swelling, and blood in the tentorium region.  Although confident about the clarity of the CT scan results, he suggested that Professor Tress review the MR scans, particularly with reference to the article by Messori et al.
265.	His second document dated 30 March 2010 was a provisional report to Dr Navāthé.  He had not yet seen for himself Mr Hazelton's hospital records or CT brain scans, but had had the opportunity to review numerous other documents.  From these he addressed:
1.	The clinical and radiological features of Mr Hazelton's head injury.
266.	From the material that he already had seen, he summarised the information about Mr Hazelton's head injury, as multiple head blows in an assault, without loss of consciousness, and about half an hour of "patchy post-traumatic confusion or amnesia".  He was admitted to Sydney's St Vincent's Hospital for three days, and developed facial bruising, left facial weakness, and left haemotympanum.  His Glasgow coma scale was said to be 13. His CT scans on 2, 3 and 5 November showed a longitudinal left petrous temporal skull fracture with associated left temporomandibular soft tissue surgical emphysema, a comminuted right supraorbital fracture, brain swelling, an 8 mm right inferior frontal contusion above the longitudinal fracture, and blood in the tentorial region which quickly resolved, as did the brain swelling.  Tests of cognitive function were normal, and he had no seizure.  MR scans were performed, the first on either 10 March or 15 June 2009, the second on 13 December 2009.  Dr Wallis had no report of the first scan, but noted the second mentioned no sign of brain trauma, but a possible right temporal arachnoid cyst, there being no changes seen since the first scan.  
267.	Dr Wallis referred to Professor Tress' opinion on the CT and MRI scans, and his different interpretations of the MRI scans to those of the reporting radiologists, of right and left temporal lobe contre coup contusions in addition to the right frontal contusion.  Professor Tress had further reviewed the MRI films, and confirmed that haemosiderin dregs, incompletely surrounded by gliosis, were present in the right frontal and right temporal lesions, such as reported by Messori et al  as predictors of post-traumatic epilepsy. However, Dr Wallis remarked that "the role of MRI scans for predicting PTE remains problematical."  
268.	Dr Wallis himself also had reviewed the CD-ROMs of the CT and MRI scans with Auckland Neuroradiologist Dr Maurice Moriarty.  The images of the CT scans that they had seen at that point had been taken with the equipment set to show only the bone changes; but they agreed with Professor Tress' conclusions about the MRI scans.  Dr Wallis had not reviewed Mr Hazelton's EEGs, adding: "Some but not all authorities regard the EEG as not particularly useful in the prediction of the risk of post-traumatic epilepsy".
2.	Dr Wallis' assessments of Mr Hazelton's head injury's severity and his risk of post-traumatic epilepsy
269.	He cited references indicating that the risk of post-traumatic epilepsy increases with the severity of the head injury; and asserted that Mr Hazelton's injury was severe.  He remarked that proposed definitions of "minor head injuries" were unsatisfactory, most being based only on clinical features without brain imaging, thereby running "the risk of seriously underestimating severe and occasionally fatal traumatic brain damage", such as an epidural haematoma.  He referred to a report by Servadei et al, that about 6 to 10 per cent of patients classified with minor head injury will have an intracranial haematoma. Dr Wallis stated that CT brain imaging had "revolutionized the urgent evaluation of head injury", and predicting post-traumatic epilepsy. 
270.	Dr Wallis cited the Annegers et al and Christensen et al reports as the "most important modern papers on the long-term epidemiology of PTE (post‑traumatic epilepsy)".  Studies show that blood in the brain raises the risk of epilepsy.  D’Alessandro et al report that cerebral contusion increases the risk of post-traumatic epilepsy irrespective of clinical features such as post-traumatic amnesia or early epilepsy, yet if the CT scan is normal epilepsy rarely occurs.
271.	He said that the data from Englander et al shows that, with a single cerebral contusion, the epilepsy risk after two years is 8.2 per cent; for multiple contusions it is 25.2 per cent.  Dr Wallis then posed two questions:
(1)	Is the risk now near that in the normal population?
(2)	If not, how long will it take to reach that in the normal population?
3.	Dr Wallis' assessment of the decline Mr Hazelton's post-traumatic epilepsy risk since his injury
272.	Dr Wallis disagreed with the opinions that Mr Hazelton's risk of post-traumatic epilepsy has declined sufficiently now to be considered insignificant.
273.	The decline in the risk, although rapid in the first two years, does not plateau for many years, sometimes for longer than 10 years.  Two important elements of this are:
(a)	The yearly cumulative per cent increase in the incidence of post-traumatic epilepsy
The cumulative per cent is the proportion of patients who develop epilepsy who have experienced its onset at given points of time e.g. one year, two years, three years etc.
(b)	The difference between initial risk and residual risk in head-injured subjects
The initial risk is the proportion of the injured patients who ultimately are going to develop epilepsy.  Calculated by both investigations and clinical criteria at the time of injury, it also is the lifetime risk.  Jennett calculated the initial risk of 1000 consecutive head-injured patients by studying their progress, of whom 480 developed epilepsy; this initial risk varied from 6 per cent to 60 per cent depending on each patient's injury's severity.  
274.	As time passes without epilepsy developing, the residual risk of a head-injured patient diminishes proportionally as the cumulative risk increases.  For different injury severity cohorts, the cohort's residual risk was calculated at any given year after the injury.  Dr Wallis presented two Tables and a Figure of yearly increase in incidence of post-traumatic epilepsy, and a regression analysis of initial to residual risk of post-traumatic epilepsy, from Jennett's patients' data.  He stated that this material had been derived, and provided to Dr Wallis, by the British neurosurgeon, Dr John Firth.
275.	Englander et al found that 8.2 per cent of patients with a single contusion developed epilepsy by two years, this being the period over which the study was conducted.  Because Jennett found that 69 per cent of his patients who developed epilepsy had suffered their first seizure by two years, this meant that about another 30 per cent of this Englander et al group were still to develop their epilepsy.  By reference to the Firth figures, this single contusion group on the Englander et al figures has an initial or lifetime risk approaching 12 per cent; and by two years about 8 per cent of them have developed their epilepsy.
276.	The point that Dr Wallis was making was that if 8 per cent of patients had developed epilepsy two years post-injury, those remaining epilepsy-free had a continuing residual epilepsy risk for many years before reaching the expected risk of a single seizure which prevails in the general population.
277.	On the other hand, unlike Jennett, the Annegers et al and Christensen et al studies used comparative risk calculations i.e. comparing the risk of developing post-traumatic epilepsy to that in the general population.
278.	By referring to both the Annegers et al and Christensen et al criteria, Dr Wallis stated that Mr Hazelton's injury was severe because of his contusion.  By taking a Figure from the Annegers et al paper Dr Wallis concluded that Mr Hazelton's risk of post-traumatic epilepsy would continue for 10 or more years.  Alternatively, from the Christensen et al paper, although Mr Hazelton's risk would plateau in about four years, it would never reach the normal control group in 10 years.
279.	From this material, by accepting the Englander et al data for a single contusion, Dr Wallis concluded: 
(1)	Mr Hazelton's initial or lifetime post-traumatic epilepsy risk when injured was conservatively estimated at 12 per cent. 
(2)	By 2 years after the injury, some 8 per cent of patients such as Mr Hazelton had developed epilepsy, leaving a residual risk of 4 per cent still to develop it.
(3)	By 2 years post-injury, with this residual risk of 4 per cent, he would reach the expected risk in the general population by about 6 to 7 years post-injury.
280.	Dr Wallis ended this report with three observations which he considered might render these estimates as unduly optimistic:
•	In the Englander et al series, more than half of the 177 single contusion patients were lost to follow up.
•	Mr Hazelton's severe category of head injury by the Annegers et al and Christensen et al criteria carried considerably higher initial and residual risks of post-traumatic epilepsy than on the Englander et al figures.
•	The Englander et al, Annegers et al and D'Alessandro et al studies on contusions did not take into account the incomplete gliosis surrounding haemosiderin remnants discussed by Messori et al.
281.	To this report, Dr Wallis also attached a copy of the letter to him of 26 March 2010 from Dr Moriarty.
282.	His third report was a letter of 16 April 2010 to Dr Navāthé, with his observations about Mr Hazelton's St Vincent's Hospital records and CT scan CD‑ROMs.  He described now having examined the latter with Dr Moriarty, and reported their view that these showed a second, right temporal, lesion, which they considered to be in the same site as the contusion shown on the later MR scans.  He also provided his summary of the relevant parts of Mr Hazelton's Hospital records.
283.	The fourth report, dated 11 May 2010, again was addressed to Dr Navāthé.  It was based on his second report, but amplified by additional information that Dr Wallis subsequently had received.  Again he used the same headings as in his second report.
1.	The clinical and radiological features of Mr Hazelton's head injury.
284.	Dr Wallis had compiled this after receiving copies of the Hospital notes from both Sydney's St Vincent's Hospital and Brisbane's Mater Hospital, to incorporate their salient features in this report.  He estimated Mr Hazelton's duration of post‑traumatic amnesia as 30 to 45 minutes, possibly slightly longer, with brief retrograde amnesia.  He noted his Glasgow coma score was variously recorded at 14 and 15, with one entry of < 13 at 5 a.m. on 2 November.
285.	On his Mater Hospital admission on 8 November, he commented on Mr Hazelton's low serum sodium level, remarking "although not commented upon, [this] could have been related to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) related to the head injury;" however this overlooks the notation in the clinical notes "No SIADH".  He noted the findings on Mr Hazelton's further CT brain scan on 9 November, showing "that the swelling around the previously noted right frontal contusion had increased in size (his emphasis), when compared to the previous CT scans at St Vincent's Hospital, to around 3 cm."  He observed that his treatment with "prednisone" was "presumably because of the increased swelling around the contusion."
286.	He also took note of Dr Earwaker's reports of Mr Hazelton's four CT scan and two MR scans, and that he also concluded that he had two contusions, in the right frontal and right temporal lobes, both being also visible on the Mater Hospital CT Scan of 9 November.
2.	Dr Wallis' assessment of Mr Hazelton's head injury's severity and his risk of post-traumatic epilepsy
287.	He enlarged on his point that a clinically "minor" injury may be misleading in such an instance as an epidural haematoma, which would rely on early CT brain imaging for life-saving detection, and citing the tragic instance in Québec of the celebrity Natasha Richardson of the Redgrave family.
288.	In discussing the important modern papers of long-term epidemiology of post‑traumatic epilepsy, he added the Annegers 2000 report to the Annegers 1998 paper.  He then discussed the differences of opinions between Dr Hastings and himself.
289.	First, he referred to their differing interpretations of the quotations from the 1998 and the 2000 papers that he and Dr Hastings subsequently had debated during Dr Hastings' cross-examination at the hearing, and as already noted above:
Brain contusion was diagnosed by computed tomography (CT) only during the last 10 years of our 50-year study, and none of the 34 patients with mild or moderate traumatic brain injuries and abnormalities on CT had seizures.
Brain contusion was diagnosed by computerized tomography during only the last 10 years of our 50-year study and by clinical signs or visualization during surgery in the early years.

Dr Wallis was concerned by Dr Hastings' inference that the 34 patients who had CT scans and no seizures all had had cerebral contusions.
290.	Second, he disagreed with Dr Hastings' opinion that the Christensen et al study was not applicable to Mr Hazelton, because most of the population was younger than him.  He went on to point out that these studies show that the risk of post-traumatic epilepsy in this study actually increased with each increment of 5 years of age.  He added by quoting Dr Simon Shorvon's editorial remark on the Christensen et al paper "... it should be accepted as the reference study in the field".
3.	Dr Wallis' assessment of the decline of Mr Hazelton's post-traumatic epilepsy risk since his injury.
291.	The only material that Dr Wallis added to this section was the data from the Englander et al report of patients with multiple contusions, who had a cumulative probability of post-traumatic epilepsy of 25.2 per cent at two years, compared to 8.2 per cent at the same time for only a single contusion.  He interpreted this to indicate that, by applying the Jennett regression analysis figures, this would result in an initial post-traumatic epilepsy risk of about 35 per cent, and a residual risk at two years of 14 per cent, taking more than 10 years for the residual risk to reach to that of the general population.
292.	When giving his evidence at the hearing, Dr Wallis first took us through a PowerPoint presentation of some of Mr Hazelton's CT and MRI images, of which we were provided with six print outs.  These consisted of:
•	a single axial (horizontal) view of his second St Vincent's Hospital CT scan, performed without contrast, of 3 November 2008, demonstrating the inferior right frontal contusion; neither anterior temporal region was included in this view: (Dr Wallis told us that this was the only scan that could be extracted from the CD of the St Vincent's Hospital scans);
•	two axial (horizontal) scanning views of his Mater Hospital CT studies, performed without contrast, of 9 November 2008 showing resolution of the frontal contusion with the surrounding region of localised swelling, as well as suspicion of an anterior right temporal contusion; no definite abnormality was apparent in the anterior left temporal region; and,
•	three horizontal scanning views of his MRI studies of 13 December 2009, taken consecutively and in parallel, in descending order, through the occipital horns of the lateral ventricles, the upper midbrain, and the lower midbrain, to depict the localised inferior right frontal and anterior right temporal brain changes residual to the original contusions.
293.	In his evidence-in chief, Dr Wallis stated that he disagreed strongly that, in assessing a person's risk of post-traumatic epilepsy, both the clinical findings and the radiological findings should be taken into account.  He again referred to the overlooking of Natasha Richardson's fatal epidural haematoma resulting from a clinically mild injury, without a CT scan having been performed, as being one reason for his view that clinical evaluation is less helpful in assessing head injuries than thought years ago. 
 
294.	He went on to say that CT and MRI imaging provided better information, and that was a reason for Mr Hazelton having four CT scans.  He said that, if he had seen Mr Hazelton with his "raccoon eyes" but with a laceration on the back of his head, and then looked in his ear to see blood behind the ear drum, he would have known clinically that he had a skull fracture.  From clinical experience, because he knew that people with skull fractures sometimes have associated brain problems, he would have requested an emergency CT scan; and his doctors had repeated his scans to make sure that he was not developing a surgical problem, of a clot between his skull and his brain (epidural or subdural haematoma).  Then, a week later, because of his late deterioration, he had had another scan at the Mater Hospital, which showed that the swelling around the contusion had increased in size from one centimetre to three centimetres.  He said that this explained his headache and his vomiting, as well as showing no serious cause for his worsening facial weakness.  Therefore Mr Hazelton's doctors at the Mater Hospital gave him a drug to reduce his brain swelling, but were able to send him home.  He stated that these features illustrate the importance of CT imaging in patients who have head injuries.
295.	Mr Harvey asked him how he became involved in neurological aspects of aeromedical decision-making.  He described an extraordinary case in which he had been involved in 1986.  A professional pilot had been admitted into hospital after suffering a head injury with a skull fracture, with a facial weakness.  After two days he signed himself out against medical advice.  Because of the New Zealand Accident Compensation Corporation's policy of returning injured persons to work as soon as possible, he was reviewed by a Neurologist who declared that he was fit to resume work.  Six or seven months after his injury he was flying a small aircraft, without a co-pilot, with three or four passengers.  After reaching an appropriate altitude to turn on the automatic pilot, he suffered a generalised epileptic seizure.  One of the passengers had a private pilot's licence, and took the controls, and radioed Auckland airport.  The airport staff obtained a doctor, who advised him over the radio to wait until the pilot had regained consciousness, and then recovered sufficiently to bring the aircraft back to safety.  Dr Wallis later was asked to see the pilot, and arranged his CT scan, which showed a single temporal lobe lesion, with evidence of an old contusion.  On reviewing the pilot's original head injury notes,
the presence of a skull fracture had been recorded.   It now is required of any New Zealand pilot who suffers a head injury in the Annegers moderate category, of either a fractured skull or post-traumatic amnesia of more than half an hour, to see a Neurologist.  The Neurologist then must review the pilot's notes and x-rays personally, with a Neuroradiologist's opinion also if necessary, to determine the pilots risk of developing post-traumatic epilepsy.
296.	When asked about applying the medical literature to a case like Mr Hazelton's, he stated that the data from the literature should be used, which is called evidence based medicine.  He stated:
... if there is a good literature, you should rely on the literature, not to the exclusion of everything else, but you should - you should know the literature and you should be able to apply the literature, and you should be able to understand the details of the literature if you are giving an opinion or seeing a patient regarding a specific problem such as this ....

297.	He then restated his opinion:
... in my opinion, and it is only my opinion, radiology is the single most important thing in assessment of a situation like this, regardless of what the clinical picture is.  Once somebody ends up in hospital with evidence of a head injury, without the radiology, it is almost impossible to predict the risk of post-traumatic epilepsy" .

298.	Mr Harvey then asked him:
There are also comments that it is difficult to locate Mr Hazelton precisely in the literature relevant to PTE; what you say about that?---Well, it depends if you want to locate him or do not want to locate him.  I mean, if you do not want to locate him, you can find all these little exceptions, and I think you alluded to this about the red-headed person with the green eyes who smokes 15 cigarettes a day, and so forth.  You know, you cannot locate somebody like that in a study showing that smoking causes cancer.  Well, it is impossible to locate individuals and there are studies like this.  All you can do is analyse the studies and to have a sense of proportion as to what it means.

299.	Dr Wallis then was asked several questions about the Englander et al study.  He said that the Tables that he had provided in his second and fourth reports were from the Jennett series, applying the Englander et al data, show that the post-traumatic epilepsy risk, after being highest in the initial stages after injury, continues for over 10 years; the Englander et al study itself could not demonstrate this because it was terminated after only two years.  He added that he was "astonished" that Dr Bushnik, a co-author of the Englander et al report, had given an opinion that Mr Hazelton's risk is now around one per cent.  
300.	However the Englander et al study suggests the important influence on the post-traumatic epilepsy risk of blood, such as contusions, in the brain, as observed also by Dr Hauser in his evidence.  Dr Wallis said that the Englander et al study probably is the first that has correlated the number of contusions with the epilepsy risk; however this, as in other studies, has not provided information about any effects of the size of contusions.  
301.	He disagreed with Dr Hastings about there being a conflict between the findings on the one hand of Messori et al and Angeleri et al on the other, regarding the protective effect of a gliotic wall surrounding hemosiderin in the brain.  He explained that the Messori et al study was simply a continuation of a study of the same group of patients that had been commenced by Angeleri and colleagues.  However, as he had said in his reports, he regarded the interpretation of MRI imaging in assessing post-traumatic epilepsy risk as still being problematical, because the amount of literature on the subject is still small.
302.	Mr Harvey asked Dr Wallis to explain how the concepts of absolute risk and relative risk might apply to Mr Hazelton's case.  He began his answer by saying that absolute risk pertains to a baby, at birth, having a 10 per cent risk if it lives until 75 that it will have a seizure.  Relative risk is taking a condition that predisposes an individual to an outcome, and then comparing it to somebody who does not have that condition; for example, having a high blood pressure is a relative risk to developing a stroke or heart attack compared to someone with a normal blood pressure, from which the relative risk of high blood pressure is calculated compared to a control population.  The Englander et al study is deficient in this respect, by having no control group for comparison, in contrast to the important Christensen et al and Annegers et al studies.  
303.	He referred to Figure 1 of the Annegers et al study, charting the cumulative probability of unprovoked post-traumatic seizures year-by-year, with four lines, three being for mild, moderate and severe categories of traumatic brain injury.  The fourth, for the general population showed a straight line commencing at zero, rising gradually over the 30 years of the recording period; he said that a person in this population aged 20 years, by the time they reach 50 years, would have a cumulative percentage risk of about one or two per cent. He said:
This is why I objected so strongly to the idea that all of us have a 10 per cent risk of epileptic seizure; we don't, actually.  It depends on what stage of your life you're at.  If you're a baby it might be in a lifetime, but if you take a control group, match - matching the patients who have had injuries, you can see it's very low.
304.	Still addressing Figure 1 of the Annegers et al paper, Dr Wallis continued to compare first the graph line for mild injuries, with no skull fracture and less than half an hour of post-traumatic amnesia, as being almost the same as the control group's; the moderate injury graph slowly rose higher, in which Mr Hazelton may have been included without his contusion.  However, the third graph was for severe head injury patients, with post-traumatic amnesia more than 24 hours, focal neurological signs, or contusion demonstrated at surgery; and this rose much more steeply above the others.  He went on:
And this is where the disagreement occurred as to whether this study took contusion in to account.  The study says that they used CT scan [sic] to diagnose contusion.  We have heard that that didn't make any difference, that if somebody had a contusion and was in the mild category, it was left in the mild category.  That's not quite right actually, because when this - these groups of patient [sic] were subject to what is called multivariate analysis, where they took all different things in to account: how long someone was unconscious, whether there was a fracture, whether the person already had epilepsy and so forth, and also bleeding inside the brain or bleeding outside the brain.  What this analysis showed – if you use CT imaging – is that that’s the most powerful predictor, whether you have blood inside your brain and outside your brain.  And if you have it in combination - if you have both - it is even higher.
305.	He went on to say that CT imaging results were taken into account in the multivariate analysis, to show that bleeding in the brain was an independent variable, so that an apparent minor injury with bleeding "is not good in terms of post-traumatic epilepsy."  He then returned to refer to relative risk, and concluded:
I am not a statistician - but as a general rule if the relative risk is above two, most of us pay some attention to it.
306.	On his cross-examination, Mr Taylor alluded to Dr Wallis' account of the 1986 incident involving the New Zealand pilot; and he referred to the evidence from Dr Westerman, that in 35 years he has known of no seizure incident in any two pilot operation, with similar evidence by Dr Brock.  Dr Wallis remarked that he did not have the expertise to comment about two pilot or one pilot operations. 
307.	They then discussed Dr Wallis' calculation by extrapolation of Mr Hazelton's absolute risk of post-traumatic epilepsy of 12 per cent, which he said was based on assuming that he had only one contusion.  He had reconsidered this when, on the review of the scan images by the Radiologists, Mr Hazelton's MRI scan was described as showing two contusions, although he added that he was reluctant to place strong emphasis on MRI findings.  Nevertheless, he did not agree that Mr Hazelton would have been in the one contusion category in the Englander et al series.  He acknowledged that he had not examined Mr Hazelton, but stated that all that he was required to do was to examine his scans.
308.	Mr Taylor referred to Dr Bushnik agreeing with Dr Stark's calculation of Mr Hazelton's epilepsy risk:
You have not examined Mr Hazelton, have you?---No.
But on your view you don't have to do because all you have to do is look at the scans?---Yes, I think that's true.  You don't have to if you - if the person has been examined by a competent neurologist who say [sic] he's got a normal neurological examination - I have no reason to disagree with that.  I don't think that I would find anything useful examining Mr Hazelton.  No, I don't think it's - I agree that he's got a normal neurological examination.  I just disagree with the opinions of some people who - about his risk of post-traumatic epilepsy.  That's the only disagreement.
Well, there are a number of opinions that disagree - - -?---Mm.
- - - obviously, because we had those doctors called here, and we also have some statements from doctors who have not been called for cross-examination.  We also have, as you said before, the co-author of the Englander Report agreeing with Dr Stark?---Well, you mean - - -
Well, agreeing with his - - -?---That's Dr Bushnik you're talking about?
Yes, Dr Bushnik?---Well, I think it's astonishing that she would send - give an opinion in an email about somebody she knows nothing about and make a statement that, at the end of - - -
She did have Dr Tress's radiology, though?----No, she didn't have it.  All she had was - she didn't review the - she's not even a medical doctor, she's a PhD, and if you look at - you see she's a PhD, and she has not taken into account the difference between initial risk and residual risk, or the evolution of it.  She's assumed that everybody in the Englander trial who had an epileptic fit would have had it by two years, and that's a gross mistake, I think.
She's been incorrect about her use of her own - - - ?---Yes.
- - - scale?---I think she has.
Yes, all right?---And she's not the only one, I think".
309.	Dr Wallis told Mr Taylor that, although he has reviewed the literature with colleagues at medical meetings, and published papers about epilepsy, he had not published any personal research, nor put to peer review, his view that to provide his opinions to the New Zealand Civil Aviation Authority, it was only necessary for him to examine the radiology of the patient.  He said that this was "a very widely held opinion" by neurologists familiar with the literature, because it predicted post‑traumatic epilepsy.
310.	Mr Taylor then took Dr Wallis to the Christensen et al article.  First, Dr Wallis disagreed with the suggestion that, although it utilised medical records, this was a retrospective study.  Dr Wallis suggested that Mr Hazelton's case was represented in the severe brain injury category, at age ≥ 15 years in Table 2; this sets out the age of the patients at their first admission with brain injury and relative risk of epilepsy, of whom there were 30 in number.  The authors calculated an adjusted relative risk of 12.24.  Then Dr Wallis was taken to Table 3, listing the duration of the patients' first hospital stay with brain injury with their relative risk of epilepsy, of whom 24 persons were in hospital 1-6 days, with a relative risk of 4.82.  Table 4 showed the influence of a positive family history of epilepsy, conferring a higher risk.  Mr Taylor quoted the authors' remark:
Patients with head injury may be followed more closely than the general population, which might increase the completeness and overestimate the relative risk of epilepsy after brain injury.  However effect in this bias is likely to decrease over time.
311.	Dr Wallis agreed that such tables, as with those in such studies as Annegers et al and Englander et al, can only be used as a guide.  However, although conceding that such figures could not be used as "absolute", he disagreed that if the literature alone could not provide the answer, clinical details would have to be used.
312.	Mr Taylor then quoted from Englander et al:
Recently, Annegers et al retrospectively analysed risk factors for late posttraumatic seizure in a large sample of individuals with TBI in Olmstead County, MN.  Unfortunately, the inherent limitations in a retrospective review and the relative homogeneity of the study population (i.e., rural Minnesota) prevents broad generalization of the results of this investigation.
313.	Dr Wallis also disagreed that the Annegers et al study was retrospective; he said that, although information had been collected from the Mayo Clinic records and then continued, it was "probably more prospective, than retrospective".
314.	Mr Taylor then brought Dr Wallis back to his calculation of Mr Hazelton's risk of post-traumatic epilepsy:
Right.  You haven't calculated relative risk in [sic] a yearly basis, have you?---In Mr Hazelton?
On a yearly basis, yes?---I could if you - if you want to do that we could do that, yes.
Because that’s what Dr Hastings did, didn’t he?  He says ---?---No.  We can do that if you would like to do it.  
When you're calculating the one per cent rule, you use yearly risk?---Well, I don't want to get into the one per cent rule if you don't mind, because it's not something that I'm an expert in.  I can tell you what the yearly risk is or residual risk is if you want.  If you want to look at page 6, table 2 and table 3 (Exhibit R12), I can tell you that, yes.
Yes.  All right?---Do you want to do that or - - -
Yes?---All right.  Well, first of all if you assume that he has a risk of eight per cent post-traumatic epilepsy in their [sic] lifetime and that after two years close to 70 per cent of people would have had epileptic seizures, then you can pick the initial lifetime risk as 12 per cent, because once 70 per cent have had seizures, then you have a residual risk which is lower.  So if the risk is, let's say, just between 10 and six per cent to begin with, at one year between five and three per cent, and two years between three and two per cent, three years 2.5 to 1.5 per cent, and at four years it becomes one per cent which is very close to that of the general population.
Yes?---But if you take 25 per cent and 70 per cent have had seizures within two years, then the initial risk is more like 35 per cent.  And, then, at one year 19 per cent, two years 14 and so forth, and you see it never quite gets there.  It never quite gets to one.  It just depends where in the table you want to go, but - and I'm not saying this table is absolutely accurate.  It is a guide.
And because I think before, when you were discussing the 10 per cent lifetime epileptic risk, you said that that's not a relative risk?---That's an absolute risk.
That's an absolute risk?---At birth, when you're just born - the day you're born, and compared to the day you die, that's what that means.
But, then, you didn't want to use that 10 per cent, did you?---Sorry?
You wanted to go to the one per cent risk?---Well, it's not relevant.  We're not talking about Mr Hazelton's risk of epilepsy when he was [sic].  We're talking about his risk of epilepsy at his age compared to a comparable population of people.  That's what we're talking [sic].  We're not talking about a lifetime risk of a baby.  And we're not talking about febrile seizures and things of that sort.  We're talking about what the risk of epilepsy is after a specific point in your lifetime.  And that's where you can use this sort of data.
All right?---But to say that's - and that's where you have to have control groups.  And this is - if you go back to - if you go back to the figures in the Annegers trial, you can see that the control group doesn't get to 10 per cent in 30 years.  It [sic] sort of one or two per cent, something like that.  To say that people in this room have a 10 per cent chance of having an epileptic seizure between now and when we die is mistaken. 

Dr Roderick Alan Westerman, Physician and Neurophysiologist
315.	Dr Westerman is a Physician and Neurophysiologist.  After qualifying in medicine at the University of Adelaide in 1954, he obtained his PhD at the Australian National University in 1961, thereafter to practise as a Neurophysiologist as well as a Physician.  When Associate Professor in Physiology at Monash University, he initiated that University's course for the Australian Certificate of Civil Aviation Medicine, then to coordinate and run this course for 12 years.  Subsequently he was appointed Adjunct Professor in Postgraduate Medicine at Edith Cowan University, where he has coordinated and examined in the Postgraduate Certificate in Aviation Medicine.  He is a Designated Aviation Medical Examiner, as well as an Associate Member of the Australian and New Zealand Association of Neurologists, and a member of the International Brain Research Organisation and the Australasian Society of Aerospace Medicine; recently he has been elected to the International Academy of AeroSpace Medicine.  He has published more than 125 scientific papers, and edited four books all on neurophysiological and occupational medicine topics.  
316.	He has provided three statements; attached to his first statement are four appendices:
•	Appendix A was his report of the Memory Monitoring System (CogHealth) test that he administered to Mr Hazelton on 25 June 2009.  His interpretation of the results reads:
Higher than average performance for age, and a clearly very stable state with almost identical performances between two serial tests administered immediately after a practice test.
•	Appendix B was his report of 1 July 2009 to Dr Eric Donaldson and Dr Alan Sutch of his consultation, examination, and cognitive assessment that he had conducted on Mr Hazelton.
•	Appendix C comprised copies of Associate Professor Stark's reports that he had forwarded to Dr Tamara Bushnik, and her reply.
•	Appendix D was his letter of 16 April 2010 to Dr Bushnik requesting her critique of Associate Professor Stark's report.
317.	In his first statement, after listing the documents regarding Mr Hazelton's case to which he had referred during his comprehensive assessment of him, Dr Westerman first categorised his head injury as clinically mild.  He contrasted this to Dr Drane's assessment as severe, because of the presence of his inferior right frontal cerebral contusion.  However, he contended that both "radiographic assessment (CT and MRI)" and clinical assessment should be used, as had been argued by Associate Professor Stark; and for this reason he had sought the opinion of Dr Bushnik, the senior co-author of the Englander et al report to which Associate Professor Stark had referred.
318.	He then identified the two incapacitation risks arising from Mr Hazelton's head injury, of either subtle incapacitation (such as neurological, psychiatric, psychomotor or cognitive disturbances) or suddenly incapacitation, mainly from post-traumatic epilepsy; and referred to his Appendix A findings as confirming Mr Hazelton's "completely normal" cognitive functions.
319.	With regard to Mr Hazelton's risk of developing post-traumatic epilepsy, he quoted the statement of Annegers et al, that this risk varied greatly according to the severity of the injury and the time since the injury.  He recorded his agreement with "aviation neurologists" Drs Appleton, Stark and Hastings, that, on clinical and imaging data, by 18 months post injury without seizures, he would meet the medical standard according to the criteria in Regulation 67.150 of the CASR.  He averaged their post-traumatic epilepsy risk estimates at between 0.7-0.8% at 18 months post‑injury, noting that all four of them had used the criteria employed by Englander et al, regarded by the CASA medical staff as the "most seminal paper".
320.	To this he added reference to Dr Eric Donaldson's opinion, noting his extensive experience in aviation medicine, and that he had used the "1% Rule", which had been used in the past by CASA for risk assessment.  Dr Westerman's view was that the currently conservative CASA approach reflected the military background of their senior medical personnel.  He illustrated this by referring to the different non-flying periods required of head-injured pilots of five years for the United States Air Force compared to one year for the Federal Aviation Authority.
321.	He considered that the evidence-based paradigm, as advocated by Dr Navāthé in his statement, lacked sufficient evidentiary support.  He stated that, although using the "1% Rule", the United Kingdom Civil Aviation Authority has had no reported aircraft accidents, adding that "active incapacitation" to which the CASA medical officers have referred has not been a source of any accidents in any two pilot regular public transport airline operations throughout the world.
322.	His second statement addressed Mr Macmillan's observations in his statement, about the difficulties he envisaged that a second pilot would experience, in taking over command of an aircraft from a pilot who was suddenly incapacitated by an epileptic fit.  Dr Westerman referred to his own experience in training DAMEs, both in simulators and on aircraft flight decks.  After disagreeing with the contents of Mr MacMillan's paragraphs 14, 15, 17, 20, and 21 he stated:
Thus, in summarising my observations and surveillance described above, all Pilots holding Class 1 licences and medical certificates who are flying regular Public transport operations for airlines must undergo recurrent simulator training of 3½-4 hours sessions usually spread over two days, and occurring at least every 6 months (twice per year).  These always include various simulated failures as well as subtle and sudden incapacitations.  The pilots being tested are specifically trained to take over, put on autopilot, push back seats, lock controls, restrain the incapacitated pilot (if needed) by seat belt tightening, and perform all the safety manoeuvres to ensure that the incapacitated pilot does not interfere with the safe control of the aircraft (his emphasis).
323.	Because of Mr Macmillan's concerns about high cockpit workload in multicrew aircraft, Dr Westerman had re-administered further Cogstate tests on Mr Hazelton on 7 May 2010, again with satisfactory results, and the comment that he was "above average on all the subtests".
324.	Dr Westerman's third statement refers to Dr Drane's third statement.  He disagreed with Dr Drane's interpretations of several details recorded in Mr Hazelton's clinical notes from St Vincent's and Mater Hospitals, pertaining to his post-traumatic amnesia, to the effects of his blood alcohol level of 0.21 g/litre, and to the reason for his attending the Mater Hospital.  He also discussed the prognostic significance of him not suffering any immediate impact epileptic seizure.  He attached a copy of a letter from British neurosurgeon Dr John Firth, of 15 October 2008 to Dr David Fitzgerald of CASA, commenting about Mr John Keith Torr, whose case was the subject of previous Tribunal proceedings. 
325.	In his evidence to the hearing by telephone, Dr Westerman provided more detail on the matters that he had raised in his statement.
Dr Tamara Bushnik, Rehabilitation Specialist
326.	Dr Bushnik is Director of Research in the Department of Rehabilitation Medicine of the Rusk Institute for Rehabilitation in New York; and she was the senior co-author of the report by Englander et al.
327.	On 16 April 2010 Dr Westerman sent her an e-mail, with an attached copy of Associate Professor Stark's report, seeking her comment.  She responded by e‑mail on 29 April:
I am writing to respond to your request to review the information that you sent me concerning Jonathan Hazelton and the estimates of post-traumatic epilepsy (PTE) occurrence provided by Dr Richard Stark.  Based upon the article by Englander et al, as well as the provided reports, Dr Stark's estimate of an annualized 1% risk of PTE after 12 months and a less than 1% (0.8%) chance of PTE 18 months after the injury are reasonable and may be conservative since Mr Hazelton appeared to experience an injury without any of the other prognostic risk factors.
I noted that the 18 mnth [sic] anniversary of Mr Hazelton's injury has already passed - during this time, he has remained PTE-free, as well as symptom-free, and is abstaining from risky behaviours that might increase the risk of PTE.  Thus, the probability of Mr Hazelton experiencing PTE as [sic] this point is understandably lower.
Please be aware that this area of prognosis is a difficult one and that any estimates are based on best available knowledge.
328.	It was pointed out by Dr Wallis during his cross-examination that Dr Bushnik did not have available Professor Tress' report of Mr Hazelton's CT brain scans.
Dr Eric Donaldson, Occupational Aviation Medicine Specialist
329.	Dr Donaldson is a Designated Aviation Medical Examiner, a qualified Army Pilot, a Fellow of the Aerospace Medical Association, a Fellow of the Royal Aeronautical Society, and a Fellow of the Faculty of Occupational and Environmental Medicine.  He is a Past President and Honorary Life Member of the Aviation Medical Society of Australia and New Zealand, and a Past President of the International Academy of Aviation and Space Medicine; he is also an Honorary Life Member of the Society of United States Army Flight Surgeons.  He served 20 years in the Australian Regular Army, retiring in 1989 as Colonel, to be Director of Medical Services with Qantas for 10 years.  He then took up a teaching position, now as Adjunct Professor, at Griffith University, and is recognised as a Senior Aviation Medical Officer by the Commanding Officer of the RAAF Institute of Aviation Medicine.
330.	He has stated:
In the last 35 years there are no recorded aircraft accidents in the English-speaking world in two pilot airline operations due to the incapacity of a pilot thus applying a more rigorous application of medical standards to regulate pilot fitness is unlikely to influence the overall safety of two pilot airline operations.
331.	He next has specified the five steps of the risk assessment and management process.
332.	The first is to establish the context of the risk, this being, in Mr Hazelton's case, that of Regular Public Transport two pilot airline operations.
333.	The second is to identify the risk of an accident, which, in Mr Hazelton's case, entails estimating his risk of experiencing a post-traumatic seizure.  This requires assessment by those medical specialists who manage head injuries and their sequelae, and who are familiar with the literature in this field.
334.	He then set out his approach to performing the third and fourth steps, of analysing and evaluating the risk, under the headings:
(a)	the "1% Rule";
(b)	the risk of an accident (incapacitation versus engineering/mechanical failure);
(c)	individual considerations; and,
(d)	active incapacitation.
335.	He explained that the "1% Rule" has been the yardstick for medical decisions on certification for many years in the United Kingdom.  Its rationale is that a pilot's risk of incapacitation of 1% per year (one in 100) can be equated to 1 per million per flight because:
(a)		There are approximately 10,000 hours in one year.
(b)	The average flight time was estimated at one hour, of which no more than 10% was regarded as critical.
(c)		This makes the risk 1 in 10 million per flight.
336.	He stated that this does not consider the role of a second pilot, particularly in mitigating accident risk, which has been closely studied.  He referred to the work in 1984 of the former Medical Director of British Caledonian Airways Ltd, Dr Chapman, who has shown that the second pilot should recover all but one in one hundred threatened crashes due to the first pilot's incapacitation at a critical stage of flight.  Thus a pilot with a 1% risk of incapacitation in any given year, in a two crew operation, equates to a risk of one in 1000 million per hour of flight in two pilot aircraft operations.
337.	It is acknowledged that the risk of in-flight failure of a vital component of the aircraft is accepted by the travelling public; and, for a two engine public transport aircraft, this has been calculated at more than five times the risk of human failure due to pilot incapacitation in a two pilot operation.  This means that, by the "1% Rule" safety standard, the pilot is considerably safer than the aircraft.
338.	In addition, individual consideration to Mr Hazelton's flying duties should be given.  The average flight time for his airline is much greater than one hour, which impacts significantly on the underlying mathematical basis of the "1% Rule", of which no more than 10% is regard as critical.  Thus, this critical period is substantially less than that incorporated in the "1% Rule".
339.	Dr Donaldson stated that, with the current simulator training provided by Virgin Airlines, a pilot is not permitted to fly until demonstrating proficiency in recovering an aircraft at a critical phase of flight from the command pilot's incapacitation.  A number of very experienced simulator instructors have reported that, in more than 1000 tests, there has been 100% co-pilot success rate in recovering the aircraft.  Dr Donaldson remarked:
When these figures are interpolated into the calculation used to derive the "1% Rule", the risk of an accident is lessened by an order of magnitude.
340.	He further stated that, notwithstanding the adult average annual incidence rate of seizures from all causes being 0.05% per year, none of the reported seizures in two pilot airline operations have led to an accident.
341.	An additional step in analysing and evaluating the risk arises from CASA medical officers' concern over the CASA concept of "active incapacitation".  This has been represented in simulator trials in the highly dangerous situation, of a pilot in a seizure suddenly extending the leg in contact with the rudder pedal.  Dr Donaldson reported 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".  He has concluded:
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

342.	 The final step in the risk assessment and management process is how to modify the risk.  This can be done by CASA directing that Mr Hazelton flies only "as or with a co-pilot": not only does this reduce the accident risk, but it mandates the pilot who has such a certificate to advise the second pilot of this restriction on his licence and the possible risk, thereby alerting the second pilot.
343.	Dr Donaldson concluded his statement by remarking that he believed Mr Hazelton's risk of being involved in an accident due to a seizure to be "miniscule", and much below the risk of an accident caused by aircraft mechanical failure.  He added that, when he was the Medical Director of Qantas, he would have accepted him with his medical history, with the licence restriction of "as or with a co‑pilot".
344.	During his evidence-in-chief at the hearing, he was taken to his statement which the individual pilot considerations involved in analysing and evaluating the risk:
In Australia, pilots have a right to be assessed as individuals and there is a distinction between the absolute risk of incapacitation in the cockpit and the attributable risk of post traumatic seizure.  The absolute risk of incapacitation in the cockpit is the significant figure
345.	He explained that the commonness cause of acute pilot incapacitation in flight is severe gastrointestinal pain; but the most significant medical risk was a heart attack.  In estimating a pilot's total risk of incapacitation, what is taken into most account is a pilot's heart condition.  Although epileptic fits are included in the series of incapacitations, and do happen, in his literature search he found no instance of a fit in a two-pilot airline transport episode having caused an accident.  He said that, in Dr Hastings' case that Dr Navāthé had mentioned in his Powerpoint presentation, in which the pilot, during an epileptic seizure, struck his foot so hard on the rudder pedal to break his ankle, the two pilot aircraft nevertheless was landed safely.
346.	The Deputy President suggested to him that, in the possible instance of both pilots being killed, it would not be known if one had had a fit and interfered with the other.  Dr Donaldson replied that, in cases when a single pilot had had a fit, they have not survived; and they have ascertained the cause by looking at the pilot's medical history to find that the pilot has not supplied information about an epilepsy history.  He went on:
... But fits happen, no question.  I haven't found any fits in a regular airline operation that we attribute to post-accident epilepsy.  The fits are normally – the ones that I can find are attributed to hypoxia or brain tumours.  There are a whole series of initial fits of a presentation of epilepsy.  But I know that - I think there was a case in New Zealand where it seems likely that the cause could have been a post-epileptic - a post-traumatic seizure.
THE D.  PRESIDENT: And was that a multiple-pilot aircraft or not?---Well, it landed successfully, so I'm not sure whether it was the person that was actually sitting in the cockpit that took over or whether in fact it was an airline operation.
347.	Then, during his cross-examination Dr Donaldson was asked:
But is there not a circumstance in which with epilepsy, there would be a partial or incomplete epilepsy and that, in itself, would not be readily apparent to the - - -?---Like a subtle incapacitation, yes.  Except that the - you know, in the cockpit they now have a series of required questions and responses, and when the aircraft is in a critical phase if the required response is not given then it automatically – the second pilot takes command.  And this is certainly within 500 feet off the ground.
348.	Dr Donaldson acknowledged that he himself had not examined Mr Hazelton.  In forming his opinion about Mr Hazelton's case, he had relied on the reports of Neurologists Drs Hastings, Appleton and Cameron in the Tribunal documents. He later also had seen Professor Stark's report. However he had not seen those from Professor Tress or Dr Wallis.
Dr Jeffrey Robert Brock, Physician
349.	Dr Brock has practised as a Physician since qualifying in medicine nearly 30 years ago, and has postgraduate qualifications in Occupational Medicine and Aviation Medicine.  He is a qualified military (Army) pilot and a Designated Aviation Medical Examiner.  He was the Acting Director of Aviation Medicine for CASA for 2½ years, and has worked with the Civil Aviation Authority of New Zealand.  For more than 20 years he has been the Consultant Adviser in Aviation Medicine to the Director General Army Health Services, the Director General Defence Health Service, the Surgeon General Australian Defence Force, the Army Forces Commander, and now the Joint Health Commander. He has provided two statements.
350.	In paragraph 10 of his first statement he has listed the material that he studied in forming his opinion expressed in his statement.  This included the reports of Neurologists Associate Professor Stark, Drs Hastings, Appleton, Cameron, and Dr Wallis, as well as Professor Tress.
351.	In paragraph 12 he opined that Mr Hazelton's risk of post-traumatic epilepsy was of the order of 1%, which is acceptably low to satisfy the criteria in Regulation 67.150 of the CASR to satisfy medical standard 1, sufficient for him to be granted a Class 1 Medical Certificate; and that he is not suffering safety-relevant effects of a head injury.  He specified that his flying activities should be restricted to "with or as co-pilot" operations.  He stated that he was not at any real risk of "an episode of active incapacitation", remarking:
I have never seen a report of active incapacitation in my aviation career and have never had any professional or military pilot report such an occurrence to me or my aviation medicine contemporaries.
352.	He also stated:
Given the research evidence and opinion presented on his risk of PTE, there is a very compelling case for CASA to re-issue Jon with a Class 1 and 2 Medical Certificate, and for CASA to still feel confident that it has done its utmost to establish risk.  I do not believe that CASA could, or would, be considered reckless for re-certifying him at this time, given the broad weight of opinion supporting such a decision.
353.	In his second statement he referred to the statements by Dr Drane, Mr Macmillan and Dr Westerman, and the report by Dr Firth of 15 October 2008 to Dr Fitzgerald regarding Mr John Keith Torr.
354.	He devoted paragraph 3 to observations answering concerns expressed by Mr Macmillan, of the difficulties dealing with a fitting pilot on the flight deck.  He said that other crew members, such as cabin attendants, can render assistance; that during the extraction of an incapacitated pilot, the other pilot can still retain full flight control; and that the involuntary movements of an epileptic seizure would not impose undue difficulties on the attempts of other crew members to assist.  However, he also said that "conventionally designed transport aircraft such as the Boeing fleet" do not have a facility, like the Airbus, by which, if a pilot is incapacitated, one set of controls immediately can be de-activated.
355.	In paragraph 4, he contrasted Dr Firth's remark "It is important to treat the man not the scan" with Dr Wallis's approach "to treat the scan and not the man" (Dr Brock's words); and in paragraph 7 he advocated Dr Firth's approach.
356.	Under cross-examination at the hearing, referring to paragraph 15 in his first statement, Dr Brock confirmed his view that numerical assessments of a pilot's risk are rarely determinative, because clinical judgment is often imprecise; and that annual review of risk can be appropriate.  He agreed that new technologies can assist in being more precise.
357.	The evening before, he had received from the respondent some material that he had not previously seen, such as the clinical notes from the Mater Hospital, Dr Earwaker's report and Dr Wallis' fourth report.  However his opinion regarding Mr Hazelton's risk of post-traumatic epilepsy remained as recorded in his first statement; and he said:
I don't believe there's sufficient evidence there yet to absolutely and rigidly apply the criteria that Dr Wallis puts in his report to apply that rigidly to Mr Hazelton or anyone else at the present time.
358.	When re-examined Dr Brock confirmed that he disagreed with Dr Wallis' approach, of choosing to calculate absolute risk, based on the literature.  In his opinion, as Dr Hastings has propounded, clinical findings should be taken into account as well as the CT findings.
Dr Robert William Liddell, Medical Practitioner
359.	Dr Liddell has practised medicine for nearly 40 years, is an airline pilot, and a Designated Aviation Medical Examiner.  His aviation career began with the Western Australian section of the Royal Flying Doctor Service, of which he became Medical Director, and later President; and he currently is a Board member.  After six years as company Doctor to the British airline Dan Air, during which he flew as a pilot more than 2400 hours on Boeing 727 aircraft, he returned in 1988 to Australia to be CASA Director of Aviation Medicine for the next eight years.  He is an Academician of the International Academy of Aerospace Medicine, and was a former President of the Aviation Medicine Society. He has prepared two statements.
360.	In his first statement he has briefly reviewed some of his initiatives in aviation medicine.
361.	His second statement has addressed that of Mr Macmillan, and he has taken Mr Macmillan's three main points.
362.	First, Dr Liddell stated that, because modern aircraft are highly automated, although they are designed to be operated by two pilots, it has been demonstrated many times that one pilot can safely operate the aircraft if the other is incapacitated.
363.	Second, with regard to pilot incapacity degrading safety, Dr Liddell provided information about the research conducted in 1984 by Dr Chapman of British Caledonian Airways.  With the company's airline pilots in the company's jet aircraft simulator, he conducted 1300 exercises using two sudden incapacitation protocols, obvious, and subtle, of the handling pilot at a critical stage of flight.  He had shown that the risk of losing the aircraft in these circumstances was 0.2%.
364.	Subsequently the International Civil Aviation Authority accepted the concept of a medical certification restricted to the pilot operating "as or with co-pilot".  Taking the level of the statistical risk target for safety as an observed airline accident rate at 1 per one million flight hours, the level of risk incapacitation for a pilot in a two crew aircraft has been accepted at 1 per cent per year or less.  Dr Liddell stated:
This has been rigorously tested since that time and worldwide licensing authorities have not found reason to change this risk level....  There have been no accidents as a result of incapacitation of a person having this restriction since its inception 25 years ago.
365.	Mr Macmillan's third man point referred to a pilot's in-flight incapacitation from an epileptic seizure.  Dr Liddell stated that the greater concern has been with subtle incapacitation, such as a stroke, or partial seizure, but these are readily dealt with on the flight deck when recognised by the other pilot.  As for the more severe grand mal epileptic fit, although physically intimidating, he remarked: 
The shaking is usually of low amplitude almost like a tremor... [unlikely] to either disconnect the auto pilot or result in interference with the controls".
366.	Dr Liddell observed that Mr Macmillan would not have been "privy" to the "enormous amount of research and statistical work that went into the International Civil Aviation Authority supporting a restricted medical certificate in the 1980s".
367.	Dr Liddell was not called to give evidence at the hearing.
Dr Sham Tak Sum, CASA Medical Officer 
368.	Having been a Medical Officer with CASA since 1989, Dr Sham Tak Sum previously was a full-time Medical Officer with the RAAF from 1979 to 1986, and was a Designated Aviation Medical Examiner.  He continues as a Specialist Reserve Medical Officer with the RAAF and holds a Private Pilot Licence.  He has provided a statement.
369.	He has opined that Mr Hazelton should be granted a Class 1 Medical Certificate and a Class 2 Medical Certificate, with the risk mitigating factor being the restriction that he flies "as or with co-pilot".
370.	He stated:
It is essential that we take into account clinical data, imaging data, expert opinion and statistical information with emphasis on the quality of each of these different type [sic] of data.  By data I mean the inputs from each of these sources.  After evaluating the quality of each data set then a balance has to be struck amongst the total.
371.	Dr Sham Tak Sum was not called to give evidence at the hearing.
Other Expert Evidence
Andrew Douglas Bauer, Line Operations Manager for Virgin Blue Airlines
372.	Captain Bauer, Line Operations Manager for Virgin Blue Airlines, had prepared a statement.
373.	He stated that the only aircraft operated by Virgin Blue Airlines are Boeing 737 and Embraer, both operated by two pilots.  Their cockpits have dual controls for all primary control functions, and either pilot can fully control aircraft in all phases of flight.  All other controls and switches required for normal or emergency circumstances are accessible to both pilots, and all instrumentation is duplicated for either pilot.  
374.	He observed that, if Mr Hazelton should resume flying with Virgin Blue Airlines, it will always be "as or with a co-pilot".
375.	Captain Bauer was not required to give oral evidence at the hearing.
Peter Campbell Macmillan, CASA Flying Operations Inspector
376.	Mr Macmillan has been a Flying Operations Inspector with CASA for 10 years.  His flying career began in 1967 as a charter pilot and flight instructor with the Royal Queensland Aero Club, during part of which time he was conscripted into National Service, and became a pilot in 1 Army Aviation Regiment.  In 1970 he commenced a 20 year career flying with Ansett Airlines, and then went on to work for two years with Condor (a charter company owned by Lufthansa), before moving to SilkAir (Singapore) from 1992 to 2000.  He has held a professional pilot licence since 1967.
377.	In his present role he has a number of responsibilities: assessing applications for, and conducting surveillance of, operators, "Approved Persons" and key personnel; testing pilots regarding relevant licences and rating; investigating and initiating action regarding incidents, complaints or other reports; and checking procedures, facilities and services.
378.	He prepared a statement in response to statements made by Captain Bauer and Mr Hazelton.  He addressed three main points.
379.	First, according to the Civil Aviation Regulations 1988 (CAR), the Embraer E190 and Boeing 737 aircraft can be operated only by two appropriately qualified pilots.  This indicates that the demands of flying these aircraft cannot safely be met by one pilot.
380.	Second, incapacitation of a pilot reduces the safety margins of operating these high-capacity aircraft, particularly during critical phases of flight such as takeoff and landing.
381.	Third, although pilots are trained to detect passive incapacitation, he was not aware of specific training for more active incapacitation which might cause interference with flight controls, particularly if the pilot had to be disentangled from the controls, or to counteract uncommanded control inputs via the yoke or rudder pedals.  This especially applied to critical stages of flight.
382.	In his evidence-in-chief at the hearing, he said that he knew of no instance of an epileptic seizure causing a pilot's incapacitation since incapacitation training was introduced.  Under cross-examination, he could not say to what extent a pilot incapacitation might reduce the safety margins of operating the aircraft.  He acknowledged that Virgin Blue had never had an instance of the other pilot being unable to deal with a pilot's incapacitation. 
CONSIDERATION
383.	The relevant statutory law is governed by the Act.  Section 9 of the Act outlines CASA’s regulatory oversight function, including its safety related functions. Section 9A(1) provides that “… CASA must regard the safety of air navigation as the most important consideration”.
384.	Those responsibilities are amplified further in the CASR:
Regulation 67.010	
…
“medically significant condition” includes “any illness or injury” or “any bodily infirmity, defect or incapacity”
Regulation 67.015
“…a medically significant condition is safety relevant if it reduces, or is likely to reduce, the ability of someone who has it to exercise a privilege conferred or to be conferred, or perform a duty imposed or to be imposed, by a licence that he or she holds …”
Regulation 67.150
This regulation provides the criteria for medical certificate 1.  Relevantly, the Table in this Regulation provides:
1.1	To hold a certificate, a person must have no safety relevant condition which produces a risk of incapacitation from an injury.
…
1.7	A person must have no established medical history or clinical diagnosis of epilepsy.
1.8	Is not suffering from safety related-effects of a head injury or neurosurgical procedure.

Regulation 67.155
	This regulation refers to the criteria for a medical certificate 2.  It has the same criteria as for medical certificate 1.  Given their virtually identical content, it appears that the only distinction between medical certificates 1 and 2 is that a holder of medical certificate 1 has no restrictions whereas a holder of a  medical certificate 2 requires a pilot to fly with a co-pilot.
Regulation 67.180
CASA must issue a medical certificate only, where an applicant does not meet the relevant medical standard, where “the extent to which he or she does not meet the standard is not likely to endanger the safety of air navigation” (Reg 67.180(2)(e)(ii)). (emphasis added).
385.	Once a pilot does not have a current medical certificate appropriate for the licence issued, that person must not perform a duty authorised by the license.
386.	In assessing the issues for determination, it is not in dispute that Mr Hazelton suffered a “medically significant condition”. But is it a “safety relevant” condition?  This requires an assessment of whether the applicant’s condition, in the light of all of the evidence from the time of the injury to its present state of development, has reduced or is likely to reduce Mr Hazelton’s capacity to operate an aircraft and specifically, whether any likelihood of post-traumatic epilepsy (PTE) is within acceptable limits.
Is Mr Hazelton “likely” to have reduced capacity? 
387.	This question depends on the standard of proof required and the admissibility or weight of expert evidence, of which the latter governs almost all the issues in dispute.
The Standard of Proof
388.	The standard of proof in civil matters is prescribed by s 140 of the Evidence Act 1995 (Cth).  Subsection (1) of s 140 requires us to find the applicant’s case proved if we are satisfied on the balance of probabilities.  Subsection (2) shows the type of considerations which are relevant for us to reach a conclusion on the balance of probabilities:
(a)	The nature of the cause of action and defence; and
(b)	the nature of the subject matter of the proceeding; and
(c)	the gravity of the matters alleged.
389.	Where an allegation is very serious in nature, the strength of evidence required to establish that matter on the balance of probabilities will need to be more cogent.  The High Court of Australia in that case also referred with approval, to the earlier High Court case of Briginshaw v Briginshaw (1938) 60 CLR 336 where Dixon J had said:
…The seriousness of an allegation made, the inherent unlikelihood of an occurrence of a given description, or the gravity of the consequences flowing from a particular finding are considerations which must affect the answer to the question whether the issue has been proved…
390.	But in Briginshaw’s case, the famous words of Dixon J about the standard of proof are also pertinent to determining the differences in the complex evidence in this case.  His Honour said:
The truth is that, when the law requires the proof of any fact, the tribunal must feel an actual persuasion of its occurrence or existence before it can be found.  It cannot be found as a result of a mere mechanical comparison of probabilities independently of any belief in its reality.
The Law Relating to Expert Evidence
391.	Expert evidence is only admissible where the common knowledge rule does not apply. That means that the Tribunal would not, in its ordinary experience, be likely to be able to assess the evidence without technical assistance or specialist opinion. 
392.	This has now been given statutory effect in s 79 of the Evidence Act 1995 (Cth).  That section provides that for expert opinion to be admissible, there must be a body of “specialised knowledge” and witnesses providing opinions must be accepted as being appropriately qualified. We accept the field of neurology as being an area of “specialised knowledge”. Also, all of the medically qualified witnesses are accepted as experts in the field of knowledge in this matter, whether as a DAME or otherwise.  But critically, the law requires that they must also persuade the Tribunal that their opinions are relevant to the facts in issue and how inferences can be drawn reliably from their evidence to assist the Tribunal in deciding the ultimate issues. 
The Expert Evidence Considered
393.	From the medical evidence presented to us, we are presented with the task of conducting a systematic review of the medical scientific literature, with the guidance of the medical experts.  We must first examine the subject of post-traumatic epilepsy arising from traumatic brain injury, as it applies to the particular circumstances of Mr Hazelton's case, of a head-injured individual who has made a complete recovery, and who has not yet had an epileptic seizure.  Moreover, when it became evident during the hearing that the presence of blood in his brain resulting from his injury, (his cerebral contusions), was a significant post-traumatic epilepsy risk, this feature became a crucial factor for us to take into consideration.  Then we must determine if his residual risk of post-traumatic epilepsy, now 18 months following his head injury, has declined sufficiently to be considered as an acceptable risk, for him to be granted a medical certificate to resume flying as an airline pilot.  Of all of the evidence that we have had presented to us regarding Mr Hazleton’s case, none has been concerned with any other form of flying than "as or with co-pilot". 
394.	We accept the arguments from both parties that our determination of the medical facts of this matter will be derived, wherever possible, from the best available medical scientific evidence.  Therefore, to borrow the expression used frequently by the expert medical witnesses, wherever possible we shall rely on evidence-based medicine.  There are various definitions of "evidence-based medicine"; and for our purposes, we take one which is widely accepted, of Sackett et al, "the integration of best research evidence with clinical expertise and patient values."  
395.	This requires that the material in the medical evidence that we accept must have been obtained by that which is recognised throughout the medical community as the scientific method; and, in Mr Hazelton's case this demands that the standard of the reports that we accept as evidence is that they have been properly documented in peer-reviewed journals for critical scrutiny by the medical scientific
community. This also has the effect that, by utilising this evidence-based medicine approach, the standard of proof to which we have aspired is as close to certainty as possible.
396.	However, when this is not attainable on the reports alone, we then must rely on those expert medical witnesses in whose experience and expertise we have confidence.  This is still consistent with the above definition that we have adopted of "evidence-based medicine".  
397.	As will become evident, and as embodied in the above definition of evidence-based medicine, this has meant that the expert medical evidence we have heard has been of two types, viz examination of that medical scientific literature which addresses post-traumatic epilepsy, and relevant expert medical opinions.  The medical opinions that we have heard regarding post-traumatic epilepsy have been from Neurologists; and, those regarding the influence of the risk of post‑traumatic epilepsy on flying two pilot aircrafts have been from aviation medicine experts.
398.	The contest between the parties has been whether our determination of Mr Hazelton's fitness to fly should be confined exclusively to considering the medical scientific literature, with particular reference to his head trauma having caused bleeding into his brain in the form of contusion (as shown on imaging), or should be balanced by also considering his clinical features.
399.	It is appropriate to remark that, of the very substantial body of this literature to which we have been taken, several reports have been the most prominent viz Annegers et al (1980), Annegers et al (1998), Annegers and Croan, Englander et al and Christensen et al.  
400.	The medical witnesses who have taken us to most of this literature have been Drs Appleton, Drane, Hastings, Hauser, Stark, Wallis and Westerman, all but one of
whom have given their evidence to us in person.  These doctors also have provided their expert medical opinions, as have all of the other doctors, the majority of whom also have given us oral evidence.  Inevitably, with so many doctors, there have been differences in opinion or interpretation of different reports in the literature, and of different selected passages in the reports.  Thus it has fallen to us to exercise our judgment in the weighting of such conflicting views, and de jure to give our reasons.
401.	We begin our evaluation of the medical evidence by identifying those medical facts and contentions, and their supporting evidence, which the parties do not dispute.  We then shall turn to examine those matters that are in dispute, and outline how we have resolved our determinations on them.
Medical facts and contentions not in dispute
(1)	The clinical, radiological (x-ray) and imaging features of Mr Hazelton's injury
402.	At about 4 a.m. on 2 November 2008, Mr Hazelton and his companion Mr Whiteley were attacked in George Street, Sydney, by an unknown number of assailants.  Mr Hazelton sustained two skull fractures, with the consequences of transient brain swelling (cerebral oedema), a temporary blood accumulation in the left middle ear (haemotympanum), and a temporary lower motor neurone left facial nerve weakness.  He also sustained at least one haemorrhagic brain bruise (cerebral contusion), of about 8 mm in diameter, located in the inferior right frontal region.  This first was shown on a CT brain scan performed about 1½ hours after the assault, when he was taken to St Vincent's Hospital.  
403.	That Hospital's reporting radiologist Dr Nicholas also described changes suggesting other blood accumulation inside Mr Hazelton's head, in the region of the left tentorium cerebelli (i.e. between the inferior surface of the left cerebral hemisphere's occipital lobe at the back of the brain, and the superior surface of the underlying left cerebellar hemisphere).  Professor Tress also reported these appearances when he subsequently reviewed this and Mr Hazelton's other St Vincent's Hospital CT brain scans, as well as his two MRI brain scans.  However this blood accumulation was seen to have dispersed on Mr Hazelton's second scan another two days later, and is considered to have been insignificant.  
404.	For this information we have relied on the evidence of Mr Hazelton, Mr Whiteley, our examination of the clinical notes from St Vincent's Hospital, and reports from Radiologist Professor Tress and Dr Earwaker.
(2)	Mr Hazelton made an uneventful recovery from the effects of his head injury.
405.	The evidentiary material from Mr Hazelton, the Mater Hospital clinical notes, Dr Cameron's report and Dr Appleton's report all record that, apart from daily headaches for at least a week following his head injury, and two brief bouts of vomiting one afternoon, one week after his injury, Mr Hazelton made an uneventful and complete recovery from all effects of his head injury.
(3)	 Mr Hazelton has had no epileptic seizure.
406.	From Mr Hazelton's evidence, and from records of his subsequent consultations with Neurologists Dr Cameron, Dr Appleton, and Associate Professor Stark, and Physician and Neurophysiologist Dr Westerman, he has had no epileptic seizure following his head injury.
(4)	Mr Hazelton has suffered no cognitive effects from his head injury.
407.	Two subsequent tests of Mr Hazelton's cognitive functions, conducted by Dr Westerman, were normal.
(5)	In his head injury Mr Hazelton sustained two cerebral contusions.
408.	The Hospital radiologists reporting Mr Hazelton's CT scans, three at St Vincent's Hospital, and one at the Mater Hospital, all described one cerebral contusion, in the inferior right frontal region.  In Dr Wallis' report of 11 May 2010 he refers to examining the St Vincent's Hospital CT scans with Dr Moriarty, and that they considered that these showed evidence of a second contusion in the right temporal lobe.  Dr Earwaker also concluded, from his examination of these CT scans, that this second contusion was visible on the second and third of these scans.  
409.	Dr Moriarty reported only on the second MRI scan, whereas Professor Tress and Dr Earwaker each reported on both of them; all three Radiologists described this right temporal contusion on these MRI scans, as well as the anterior right inferior frontal contusion.
410.	We have noted that the report presented to us of Mr Hazelton's CT brain scan in the Mater Hospital, prepared by Dr Law, was as amended more than a year later.  We have been given no explanation for this.
411.	Bearing in mind that the presence of cerebral contusions, including their number, became recognised as an important factor in considering Mr Hazelton's risk of developing post-traumatic epilepsy, we put on record our concern that we did not have the benefit of the attendance of one or more of the Radiologists to give evidence at the hearing.
412.	Professor Tress and Dr Moriarty also tentatively raised the possibility of a third contusion in the anterior left temporal region, but Dr Earwaker did not.  This was not prosecuted further.
413.	Accordingly, for the purposes of our hearing, there has been no dispute that, in suffering his head injury, Mr Hazelton sustained two cerebral contusions, in the inferior right frontal and anterior right temporal regions.  
(6)	The presence of cerebral contusions increases the risk of post-traumatic epilepsy.
414.	Medical expert witnesses provided by both parties have all agreed that there is a substantial body of evidence to conclude that, if a cerebral contusion forms part of a traumatic brain injury, it additionally increases the risk of post-traumatic epilepsy; and that this risk further increases with more than one contusion.  The presence of contusions as significant risk factors has been well demonstrated in the report published in 2003 by Englander et al.  In a prospective study lasting for two years they followed 647 subjects with traumatic brain injury, who were admitted to trauma centres within 24 hours of their injury during which time they all had CT brain scans performed within the first seven days.  403 had one or more cerebral contusions demonstrated, of whom 56 (14%) later developed seizures. 10 of these 56 epilepsy subjects had a single contusion, providing a relative risk of epilepsy at 24 months of 1.38 times more than the general population; this compared to the remaining 46 individuals with multiple contusions, whose relative risk was about three and a half times greater, at 4.97 times that of the general population.  The authors of this report have not specified how many persons in this multiple contusions group had 2, 3, or even more of them.
(7)	According to imaging criteria, Mr Hazelton had a severe head injury. 
415.	In giving us their evidence, expert medical witnesses Drs Hastings, Appleton, Wallis and Drane, all have accepted that Mr Hazelton's two cerebral contusions shown on his CT and MRI brain scans satisfy the criteria used by Englander et al for severe head injury.  No other witness disagreed with this.
(8)	Mr Hazelton has an increased risk of developing epilepsy, declining with time.
416.	Mr Hazelton has an increased risk compared to the general population of developing epilepsy as a result of his injury, although this risk is continuing to decline.  We have been presented with numerous medical references supporting this, with no contradicting evidence.  During this hearing, we have been repeatedly referred, by expert medical witnesses for both parties, to several reports, and in particular to those by Annegers et al, Englander et al and Christensen et al.  There was vigorous debate between the parties about the rate at which the risk continues to decline, but there has been no argument that the risk is declining.
(9)	 Mr Hazelton has resumed non-flying duties and has abstained from alcohol since his injury.
417.	Mr Hazelton has given unchallenged evidence that he has resumed non-flying duties with Virgin and has abstained from alcohol since his injury. 
(10)	In all other respects Mr Hazelton is medically fit to resume flying.
418.	Having abstained from alcohol and remained seizure-free for 18 months since his injury, an inherent and unchallenged assumption attending all the evidence that we have examined is that, in all other respects, Mr Hazelton is medically fit to resume flying.
Medical facts and contentions in dispute
419.	The medical facts and contentions in dispute, and our determinations in relation to each of those, are:
(1)	According to clinical criteria, Mr Hazelton had a mild head injury. 
420.	As we already have seen, although there is no dispute that Mr Hazelton's cerebral contusions, by imaging definition, classify his head injury as severe, all of the doctors testifying on Mr Hazelton's behalf have commented that, by applying clinical criteria, his head injury was mild.  In their statements, and when giving their oral evidence, all of the expert medical witnesses have pointed to the difficulties in the medical literature which arise from differing clinical definitions of the severity of injury, and disparities between the clinical and imaging classifications of severity.  When attempts are made to correlate the clinical and imaging findings in a case of post-traumatic epilepsy, as Dr Hastings has put it:
The conflict between clinical and imaging assessment of TBI severity has not been resolved in the neurosurgical, neurologic, and aerospace medicine scientific communities.
  
421.	Earlier in his statement, Dr Hastings specified that Mr Hazelton's transient loss or alteration of consciousness, no focal neurological deficit, rapid return to alertness and orientation, and post-traumatic amnesia of less than one hour, all satisfy the criteria for Mild Brain Injury in the Designated Aviation Medical Examiner's (DAME) Handbook (Version 3.0, December 2003).  Furthermore, Dr Westerman, in his first statement, has referred to the World Health Organisation definition of mild traumatic brain injury: this requires one or more features of confusion or disorientation, loss of consciousness for less than 30 minutes, a Glasgow coma score of 13-15/15 at 30 minutes or more post-injury, post-traumatic amnesia for less than 24 hours, or other transient neurological abnormalities.  In his first statement, Dr Drane referred to Mr Hazelton's "transient lapse of awareness" being "significantly less than loss of consciousness for 30 minutes", and that that was consistent with the Christensen et al definition of  mild brain injury.
422.	On the other hand, in Dr Wallis' fourth report, he asserted that Mr Hazelton's head injury was severe.  He also expressed dissatisfaction with the various clinical definitions of mild or minor head injury; in his Appendix he briefly set out the differing clinical rating scales used in the Annegers reports, and by Christensen et al in using the American Congress of Rehabilitation Medicine definition.  However, he went on to illustrate this problem with clinical classification, by referring to the crucial fact that a clinically mild head injury, without imaging, may be complicated by the potentially fatal traumatic complication of an epidural haematoma, and he cited a widely reported tragic instance which occurred in Québec last year.  We acknowledge the point that he has sought to make; but we take issue with his inappropriately likening a different (acute, non-resolved) head injury complicated by a very different clinical outcome, of death, to that which occupies our attention in Mr Hazelton's case.  Here we are concerned with a significantly delayed outcome, of late post-traumatic epilepsy, from a head injury which otherwise has completely resolved.
423.	Determination:  At this point, we accept that by using clinical criteria alone, Mr Hazelton's head injury was mild; but, we also accept that disparities arise when attempts are made to compare these with imaging criteria, and we shall return to this shortly. 
(2)	The finite quantum of Mr Hazelton's present risk of post-traumatic epilepsy, based on the presence of his cerebral contusions, can be calculated in terms of absolute risk.
424.	This has been contended by Drs Wallis, Navāthé and Drane.
425.	Drs Appleton, Drane, Hastings and Wallis were all agreed that the report of the Englander et al series was the most relevant to Mr Hazelton's case; and these authors have provided figures for both absolute and relative risks.  However, Drs Appleton and Hastings, although unequivocally acknowledging the value of the Englander et al report, opposed the view of Drs Drane and Wallis that only the data from this study could be applied to Mr Hazelton's case in accordance with evidence-based medicine.
426.	In addition, to attain CASA's intention, if possible, that the decision for Mr Hazelton's case might be evidence-based, Dr Wallis strongly preferred the calculation of Mr Hazelton's absolute risk of post-traumatic epilepsy to that of his relative risk.  Absolute risk indicates the probability of a person experiencing an outcome, in this case post-traumatic epilepsy, during a specific period, expressed either as a figure between 0 to 1, or as a percentage i.e. up to 100%.  
427.	On the other hand, Dr Hastings consistently and vigorously has supported the use of relative risk calculations.  He favours this because, by contrast to absolute risk, it provides a figure giving the proportional increase of a particular outcome between two groups.  For our purposes this is comparing the risks of developing epilepsy between head-injured individuals on the one hand, and the general population on the other, with specific reference to individuals of Mr Hazelton's age group.  Dr Hastings has pointed out that it is relative risk that is customarily used in aeromedical decision-making, commonly in the form of the so-called "1% Rule" for sudden incapacitation.  
428.	Five aviation medicine experts, viz Drs Brock, Donaldson, Hastings Liddell and Westerman have informed us how the "1% Rule" has been devised in aviation medicine to assist the assessment of the risk of a pilot's incapacitation, and have told us that it has been widely used throughout the international aviation medicine community; this evidence has not been challenged.  It sets the standard for the risk of pilot incapacitation to be equivalent to or less than one per cent per year, which is accepted as a component of the overall target risk of fatal accidents of 0.1 to 0.5 per million hours that the pilot flies.  This results in an estimation of the risk of a pilot's incapacitation at 1 in 10 million per hour of flight.  
429.	For the purposes of Mr Hazelton's case, this is calculated by comparing his estimated risk of epilepsy relative to that for individuals in the population at large in his age group, to see if this increases the risk of his incapacitation by a seizure when piloting to above the 1% level.
430.	One of Dr Wallis' concerns was that the "1% Rule" incorporated, for the general population, a cumulative lifetime risk of an epileptic seizure calculated at 10%; he considered that this was too high.  During the hearing of Dr Hauser's evidence we had this clarified, when Dr Hauser was taken to a statement in one of his personal publications:
The cumulative incidence of epilepsy to age 74 was 3 per cent, of all unprovoked seizures was 4.1 per cent and of any convulsive disorder was 10 per cent.

431.	Dr Hauser confirmed that this was correct for the data in that paper, covering a 40 to 50 years lifetime period, the figure being a little higher for 75 years. 
432.	During his evidence-in-chief Dr Drane also confirmed that "there is a consideration of relative risk written into the [CASA] regulation".  Nevertheless, he had calculated Mr Hazelton's present risk of post-traumatic epilepsy from figures provided from Dr Wallis' fourth report, which Dr Wallis had received from British neurosurgeon Dr John Firth.  We have been told that Dr Firth had constructed regression analysis figures of initial (lifetime) absolute risk of post-traumatic epilepsy for the 481 subjects with epilepsy in Professor Jennett's series of more than 1000 consecutive head-injured patients.  
433.	Dr Wallis then had applied these to data from the Englander et al report for their 226 patients with multiple contusions, of whom 46 had developed epilepsy.  For these, after the two years' duration of the follow up period of their study, they had calculated a cumulative probability of 25.2%.  From this, by then using a table of the yearly cumulative percentage increase in incidence of post-traumatic epilepsy, Dr Wallis had calculated that these "multiple contusions" patients had had an initial post-traumatic epilepsy risk of 35%.  He explained that the initial risk of each individual is that of them developing post-traumatic epilepsy later in their lifetimes, which immediately came into effect at the point of sustaining their head injuries; and this, as we have already noted, is a gradually declining risk ("residual risk") as time passes without them yet having suffered a seizure.
434.	Dr Firth's figures indicated that, at one year post-injury without an epileptic seizure having yet occurred, a 35% initial post-traumatic epilepsy risk had fallen to 19%, and at two years to 14%.  Accordingly, Dr Wallis had estimated that Mr Hazelton's absolute risk, now 18 months after his injury, was lying between these two figures.  It was these figures that Dr Drane had used as the basis for concluding that Mr Hazelton's risk was not acceptable.
435.	We have several problems with this complex collection of figures:
(a)	The Englander et al study, although specifically examining the influence of the presence of cerebral contusions on post-traumatic epilepsy risk, does so only in terms of "single" and "multiple" (as distinct from "two") contusions.  We have no information from this study about whether or not individuals with more than two contusions were found to have a significantly higher epilepsy risk than those with only two contusions. To assume that there is no significant difference in risk for patients with two contusions compared to more than two is inconsistent with the rigorous requirements of evidence-based medicine. 
(b)	For Mr Hazelton's relevant age group of 31-40 years, this study had a "sample size" of 151 subjects, of whom only 18 developed late post‑traumatic epilepsy.  This is too small a sample to be acceptable for evidence-based medicine.
(c)	Subjects such as Mr Hazelton with unilateral (unnumbered) contusions had only half the risk of developing epilepsy compared to those with bilateral (unnumbered) contusions; 81 of 258 (32%) in the lower risk unilateral group had multiple contusions, of whom an unknown number had two contusions. This is a variable which, in the evidence presented to us, has not been accommodated to satisfy evidence-based medicine standards.
(d)	We recognise Dr Firth as a distinguished British neurosurgeon who is held in high regard in the international aviation medicine community; (Dr Westerman has referred to his contributions in two of his statements).  However, Dr Wallis has given no reference for the source of Dr Firth’s regression analysis calculations, or any evidence that they have been published for international peer-review scrutiny.  This is so despite the Tribunal’s additional research efforts enlisting the assistance of highly skilled and competent librarians.  Without such information about it, we cannot accept this material as satisfying the requirements for evidence-based medicine..
436.	In short, we find that this absolute risk calculation could not be effected to satisfy the necessarily rigorous standards of evidence-based medicine.  Indeed, under cross-examination, Dr Wallis conceded that the figures that he had calculated were not "absolutely accurate", but "a guide”; and during his examination-in-chief he said that he is "not a statistician".
437.	Turning to the other studies presented to us, none of them can provide us with calculations of the absolute risk of post-traumatic epilepsy of subjects whose CT scans have shown two contusions, with no other abnormalities.  In particular, the other two main studies to which we repeatedly have been taken  were Annegers et al and Christensen et al:
•	In the Annegers et al study, as Dr Hastings pointed out, CT scans were used only in the last 10 years, and we were informed by both Dr Hastings and Dr Hauser that no patients with "CT abnormalities" developed post‑traumatic epilepsy.
•	Although the authors of Christensen et al indicated that CT scans were used on subjects in their series, they have provided no information on actual subject numbers, or categorisation of findings, including contusions.
438.	Hence, on examining the material and findings in these studies, we must prefer the carefully considered opinions of Drs Hastings and Appleton about the use of them for Mr Hazelton's case.  Although we already have accepted that Mr Hazelton's risk of developing post-traumatic epilepsy is increased, and will remain so for some time, it is apparent to us that, on the evidence presented to us at this hearing, in absolute terms, his risk cannot be quantified.
439.	Determination: A finite figure for Mr Hazelton's absolute risk of post-traumatic epilepsy, based on the presence of his cerebral contusions, cannot be calculated from the scientific literature presented to us as currently available on imaging reports.
(3)	The present body of scientific literature, on its own, provides sufficient data to enable a determination to be made, from evidence-based medicine, on whether Mr Hazelton has an acceptable current epilepsy risk for him to resume flying aircraft "with or as co-pilot". 
440.	Although it is clear to us that, because of his traumatic brain injury, Mr Hazelton has a higher risk of developing epilepsy than that of someone in his age group in the general population, the question to decide is whether or not his prevailing risk is low enough, or "acceptable", for him to resume flying multicrew passenger aircraft.  
441.	Furthermore, all of the attention during our hearing of this matter has been directed to his medical fitness to fly, not solo, but "with or as co-pilot".
442.	We have found that, from the present body of scientific literature on imaging, on its own, the specific quantum of Mr Hazelton's absolute risk of post-traumatic epilepsy cannot be calculated.  Therefore we now examine what can be accomplished by using relative risk, again considering only Mr Hazelton's imaging features, as contended by Drs Wallis and Drane.  
443.	We have heard from Dr Hastings that relative risk estimations are widely accepted by aeromedical decision-makers, having the distinct advantage of calculating the comparative risk of one individual with that of the general population; the CASA doctors have not disputed this. 
444.	This brings us to the pivotal point of our deliberative process in this matter.  As we already have just seen in our immediately preceding determination, we are confronted by the conclusion that the evidence-based medical scientific literature alone cannot provide us with our solution to Mr Hazelton's case.  Therefore, as argued by Dr Hastings, and in accord with the definition of evidence-based medicine given by Sackett et al, we now must integrate the best medical literature evidence that we have examined with the clinical expertise available to us.  And it is transparently clear that the relevant clinical expertise that we primarily must use, in deciding Mr Hazelton's risk of post-traumatic epilepsy, is that of the Neurologists who have been consulted on all of the elements of Mr Hazelton's case. 
445.	We have had evidence presented to us from eight neurological specialists.  However, five of them have been able to assist us only to limited extents with their neurological opinions. Dr Cameron and Dr Maxwell were not invited to comment on the medical scientific literature available on post-traumatic epilepsy; and they were not requested to give evidence at the hearing. Dr Hauser was called only to clarify certain questions that had arisen about some of the evidence; and he had not been asked to assess Mr Hazelton's case.  Associate Professor Stark, like Drs Cameron and Maxwell, had examined Mr Hazelton, but has addressed only the Englander et al and the Messori et al reports; and, because he did not have the benefit of the information of the Radiologists' reviews of Mr Hazelton's CT and MRI brain scans, he has considered Mr Hazelton's case on the basis of having only one cerebral contusion.  Dr Westerman, although highly qualified, as is Dr Cameron, does not practise clinically as a Neurologist.
446.	Therefore, because each of them has comprehensively examined the medical scientific literature on post-traumatic epilepsy, we come to consider the neurological opinions about Mr Hazelton's case of Drs Appleton, Hastings and Wallis.
447.	Inherent in our determination against absolute risk being calculable on Mr Hazelton's imaging data has been our preference for the opinions of Drs Hastings and Appleton, that they cannot be applied on their own without taking his clinical features also into account.  We also prefer their opinions on this question of using relative risk.
448.	In preferring the opinions of Neurologists Drs Hastings and Appleton, we first observe that we have been persuaded by their cogent presentations of the details of Mr Hazelton's case, and their judicious selection of the material relevant to it contained in the very large body of contemporary scientific literature on post‑traumatic epilepsy. Dr Hastings' statement impressed us as a scholarly and masterful document of review of the present state of knowledge; and Dr Appleton's was a thoughtfully penetrating exploration of the subject.  When giving their evidence at the hearing, both doctors showed calm and measured objectivity, and their evaluations were models of expert testimony.  
449.	We also have taken into account the very substantial experience and qualifications of Drs Hastings and Appleton on those aspects of post-traumatic epilepsy that pertain to the safety of air navigation. 
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.  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.
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. 
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.  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.  
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; and under cross-examination he remarked that he did not wish to involve himself in questions of aviation safety.  
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 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).
•	Dr Appleton questioned the applicability of the Englander et al 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. 
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.  
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).  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).  
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:
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.

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 and, to a less extent, Christensen et al directing attention to imaging observations.
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 and Messori et al.  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.
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 .

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, 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.
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.
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, 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.
468.	This proposition accords with the definition of evidence-based medicine enunciated by Sackett et al, 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.
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 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.  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.
•	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.
•	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.  
•	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.
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; 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.
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; 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. 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.  
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, 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.  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.  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"; and that structural damage to controls is prevented by automatic high‑speed cut-off systems.
•	In his second statement 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.  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.
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 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.  He also has observed flight simulator trials, and has described:
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.
•	Dr Westerman confirmed 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" .
•	In his second statement Dr Liddell 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%..  

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.  However he had not found any instance of a pilot in a multicrew airline operation having a post-traumatic epileptic seizure.  This evidence was not challenged.
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"; 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; and Dr Westerman stated that, despite a comprehensive search, no multicrew aircraft accident or serious incident due to epileptic seizure has been found.  Again, none of this evidence was disputed.
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.
487.	We also note again that, in paragraphs 55 and 56 of his statement, Dr Hastings had turned his attention to this by examining the Christensen et al 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.  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".
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”.  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”.
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 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. 
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 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.
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. 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.
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 Associate

Date/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