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Transcript

Hearing: 15th January 2009, day 3

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9 PUBLIC INQUIRY INTO THE DEATH OF
10 ROBERT HAMILL
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15 Held at:
16 Interpoint
17 20-24 York Street
18 Belfast
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20 on Thursday, 15th January 2009
21 commencing at 10.30 am
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23 Day 3
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1 Thursday, 15th January 2009
2 (10.30 am)
3 MR UNDERWOOD: Sir, I propose to call Professor Crane, if
4 I may.
5 PROFESSOR JACK CRANE (called)
6 THE CHAIRMAN: Will you swear the witness, please?
7 PROFESSOR JACK CRANE (sworn)
8 THE CHAIRMAN: Do sit down, if you would like to.
9 A. Thank you.
10 Examination by MR UNDERWOOD
11 MR UNDERWOOD: Good morning, Professor. My name is
12 Ashley Underwood. I am Counsel to the Inquiry. May
13 I ask you your full name, please?
14 A. Jack Crane.
15 Q. Your professional address?
16 A. The State Pathologist Department, Institute of Forensic
17 Medicine, Grosvenor Road, Belfast.
18 Q. Thank you. Professor, we have a witness statement you
19 have helpfully signed for us, which should appear on our
20 screens at page [80215].
21 If I could have that scrolled through fairly
22 briefly, please, so we can identify it is your
23 statement, to page [80227].
24 A. Yes, it is.
25 Q. Are you content with the contents and that they are
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1 true?
2 A. Yes, I am.
3 Q. Can I go back to the first page of it, please, [80215]
4 and highlight paragraphs 2 and 3? We see you performed
5 the post mortem examination of Robert Hamill on
6 9 May 1997 in the presence, we see in paragraph 3, of
7 a number of people. We also know that you had
8 assistance from Dr Herron. Is that right?
9 A. Yes. Dr Herron was not present at the post mortem
10 examination, but subsequently I referred Mr Hamill's
11 brain to Dr Herron for a neuropathological examination.
12 Q. Thank you. Can I jump, please, to page [00954]? Is
13 this the autopsy report which you prepared?
14 A. Yes, it is. That is the first page of it.
15 Q. If we could go directly to page [00959], I want, if
16 I may, to highlight the commentary, the last half of the
17 page. In particular, I want to pick up on the first
18 substantial paragraph:
19 "Death was as a result of the head injuries which he
20 had sustained. Externally, his injuries appeared
21 trivial; there was a small area of abrasion on the left
22 side of the forehead, a bruise on the upper eyelid of
23 the left eye and a small spot of abrasion close to the
24 left nostril."
25 Then, if we go down to the next paragraph:
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1 "He had also sustained some other injuries, although
2 none of these were serious enough to have played any
3 part in his death. There was a fading bruise on the
4 front of the abdomen and some further bruising in the
5 muscles of the abdominal wall which could have been due
6 to blows during the assault. There were numerous
7 bruises on the left upper limb, particularly on the
8 forearm and hand, which could have been sustained if the
9 arm was struck whilst raised in a defensive gesture.
10 A few further bruises were located on the right upper
11 limb, but some of these were probably related to
12 injections given whilst in hospital. A fairly large
13 area of bruising overlying the right side of the pelvis
14 was due to blunt force and might have been caused by
15 a kick."
16 Now, of course, we all know that the matter which is
17 going to cause most concern is the question of the type
18 of brain injury, but leaving aside the brain injury for
19 the moment, can I just talk about the external injuries,
20 the physical signs that were present when you did the
21 examination?
22 Do they assist you to give the Inquiry any help
23 about the degree, the severity of the assault?
24 A. Certainly in the fatal assaults we would see and I have
25 dealt with in the past, we would normally expect to see
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1 a lot more in the way of external injuries.
2 However, it has to be recognised that you may have
3 a person who does appear to have very little in the way
4 of external injuries, but may have very serious internal
5 injuries, either from an assault or, for example, in
6 a road traffic accident, there may be no mark on the
7 outside of the body, yet the person could be bleeding
8 internally.
9 Normally in assault I think you might expect to see
10 more injuries, but it does not surprise me there were
11 not that many injuries.
12 Q. All right. Thank you.
13 Now I want to move on to axonal injury. Can we go
14 back to your Inquiry witness statement at page [80218],
15 please? If I pick up paragraph 13:
16 "I think the significant injury in this case was the
17 presence of diffuse axonal injury in the brain. That
18 type of injury is not one that is necessarily associated
19 with very severe external injuries because it is caused
20 by the brain being shaken about inside the cranial
21 cavity. It is possible to have a severe brain injury
22 with very little external injury. Conversely, you can
23 have quite a severe external injury but have very
24 little damage to the brain inside. It depends on
25 a number of factors ..."
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1 If we go over the page, [80219], and if I highlight
2 paragraphs 13 through to 15, please:
3 "... for example, the footwear that assailants are
4 wearing or if they are struck blows with an implement."
5 Can I ask in general, in the light of that, about
6 TDAI? What we have gathered so far from materials that
7 have been read is that this involves shearing or
8 rotational injury to parts of brain and is associated
9 with acceleration/deceleration. Is that fair
10 A. That's fair, yes.
11 Q. How much is known about it? Is it well recorded?
12 A. It is a relatively new phenomenon. Certainly, in recent
13 years, there is a lot more understanding about it.
14 I think our knowledge about it is still developing, but
15 perhaps if we take 15, 20 years ago, our knowledge of it
16 then was not terribly well understood, but we are seeing
17 more of it, and as techniques have developed for looking
18 at the brain in more detail, we are now seeing this more
19 commonly whenever we look at brains.
20 THE CHAIRMAN: When you say a relatively new phenomenon, do
21 you mean by that a phenomenon which has only relatively
22 recently been able to be observed?
23 A. That's correct. The two things that have helped that
24 are, first of all, new methods for scanning the brain
25 such as MRI scanning of the brain and also techniques in
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1 development of staining up the brain to show injury.
2 MR UNDERWOOD: You appreciate, of course, I am jumping
3 around between asking you what you found in 1997 and
4 what you now know about all sorts of things.
5 Sticking with what you now know and what you can
6 assist the Panel with on axonal injury, what is known
7 about the sort of forces, the type of forces and the
8 severity of them that are needed to cause it?
9 A. The forces that are thought to be needed to cause axonal
10 injury are very great indeed. A typical example would
11 be acceleration/deceleration injuries associated with
12 road traffic collisions. So it is that degree of force
13 that might be required to cause that.
14 In general terms, for example, a simple fall from
15 an erect posture, whilst that might be fatal -- it might
16 cause other injuries, other head injuries and be
17 fatal -- would not usually be expected to be associated
18 with diffuse axonal injury.
19 Q. I think most of the lawyers here are probably pretty
20 familiar with whiplash injuries. Can you help us with
21 the degree of severity that's needed in, say, a road
22 traffic accident to cause an axonal injury of this type
23 compared with the sort of force that would give
24 a whiplash injury?
25 A. I think it is difficult. A whiplash injury is something
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1 that's often regarded as a clinical diagnosis. People
2 seem to get whiplash injury very easily with very little
3 in the way of --
4 Q. Depending on whose fault it is, you mean?
5 A. What we do know, we are talking about significant
6 acceleration/deceleration injuries. As I say, the
7 forces that are generated when a car, perhaps moving at
8 30, 40 miles an hour, is suddenly brought to a stop and
9 impact because of collision with something else.
10 Q. We see you are talking there at the top of the page we
11 have open, that the footwear assailants are wearing may
12 be relevant. Help us with that.
13 For example, if somebody is kicked with baseball
14 shoes on rather than work boots, is it more likely that
15 soft shoes are going to cause the injury or less?
16 A. Probably less likely. The other aspect of the footwear,
17 of course, is that footwear may also leave other marks
18 and may cause other injuries, for example, lacerations
19 to the scalp. It may cause injury to the skull and so
20 forth.
21 Q. You go on to discuss in paragraphs 14 and 15 -- I don't
22 think we necessarily need to go to them -- the curiosity
23 that boxers seem not to get this. Could that possibly
24 be that a boxer will ride the punch, as it were, he will
25 be moving?
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1 A. Yes. That might be -- I mean, because their head is
2 moved, the brain is actually moving with it rather than
3 the brain suddenly being brought to a sudden stop.
4 Q. You also say in paragraph 14 in the concluding sentence:
5 "What we do know is that people who are assaulted,
6 and particularly those who are lying on the ground when
7 they were kicked, do show this injury."
8 Again, is that perhaps that, when they are lying on
9 the ground, they may be unconscious or unable to defend
10 themselves, so there is a sudden acceleration if they
11 are kicked?
12 A. That is correct. Probably we have a head that is
13 stationary and is kicked. There is suddenly a violent
14 movement within the brain, which might be rotational, it
15 might be from side to side.
16 Q. There is some reason to believe that Mr Hamill's head
17 may have been jumped on while he was on the ground. If
18 that's so, is that compatible with what we have just
19 been discussing?
20 A. Yes, it is.
21 Q. How would that mechanism work?
22 A. Because often there is -- the force is transmitted to
23 the brain, and, although the head itself might not be
24 moving very much, the force that's transmitted to the
25 brain may cause the brain inside the cranial cavity to
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1 move.
2 Q. I see. Can you help us on this at all? If somebody is
3 unconscious on the ground and is kicked, how hard does
4 the kick have to be to cause the sort of severe axonal
5 injury which you believe was the entire cause of death
6 here?
7 A. I think you have to look at it in two ways. First of
8 all, the loss of consciousness itself might have been
9 caused by the blow. It may have been caused by striking
10 the ground itself, but it might be that it is one of the
11 kicks that causes a loss of consciousness, but you are
12 talking about a significant amount of force has to be
13 applied.
14 I suppose I can maybe say this, because, as someone
15 who has dealt with people who have been assaulted and
16 who live, whilst working as a forensic medical officer,
17 lots of people are kicked in the head and seem to
18 survive. The amount of force required to cause diffuse
19 axonal injury and particularly, as I say, to cause loss
20 of consciousness from the outset needs to be severe.
21 Q. Right. All sorts of ideas are mooted about what might
22 have happened to Mr Hamill and, of course, it is one of
23 the tasks of the Inquiry to attempt to determine what
24 indeed happened.
25 Can I put one of them to you, which is the
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1 possibility that he might have been struck by a flying
2 bottle, and that that caused the axonal injury?
3 A. No, I wouldn't accept that as a cause, no.
4 Q. Because it couldn't have transmitted sufficient force?
5 A. That's correct, yes.
6 THE CHAIRMAN: When you say "not sufficient force", that
7 means insufficient force to produce the sudden and rapid
8 twisting of the brain within the skull?
9 A. That's correct, yes.
10 MR UNDERWOOD: Can I ask you about the relationship, if any,
11 between the severity of the TDAI and the extent and
12 duration of violence?
13 If we very loosely say there is a case of grade 3
14 axonal injury, very serious, does that necessarily
15 relate directly to a particular degree of violence and
16 grade 2 would necessarily relate to a lesser degree of
17 violence?
18 A. I think it is not unreasonable to conclude that the more
19 force that is applied to the head, and, along with that,
20 perhaps the more -- or the number of blows that are
21 perhaps transmitted, then obviously the more likely it
22 is that you are going to get severe axonal injury, but
23 in saying the number of blows, relatively a small number
24 of blows if sustained with a considerable amount of
25 force; in other words, if a considerable amount of force
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1 has been applied, then even a relatively small number,
2 if of sufficiently severe force, could still cause
3 severe TDAI.
4 Q. You have obviously, as you have said, had the assistance
5 of Dr Herron in the histology here and in, I gather,
6 discussions with him about the extent of TDAI here.
7 A. Yes. This is how we normally deal with these cases. We
8 work them up together. At the end of the day,
9 I produced the final report, not so much in relation to
10 the neuropathology itself, but in trying to interpret
11 the neuropathology in relation to the overall findings
12 in this case.
13 Q. In the light of all those discussions in this case and
14 in the light of everything you now know about TDAI, do
15 you still stand by the view that this was very serious
16 axonal injury?
17 A. Yes, I do, for two reasons. First of all -- and this is
18 well recognised in the literature -- if a person is
19 unconscious from the outset, having sustained their
20 injury, and remains unconscious, then the outlook is
21 very poor. It is very grave. That is an indicator that
22 the axonal injury was severe.
23 The other thing that was found is that there are
24 essentially several ways of grading the axonal injury,
25 how diffuse it is and so forth. Often what's more
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1 important is the areas of the brain that are affected.
2 In this case, the areas of the brain that were
3 affected are particularly what we call the brainstem,
4 the pons and the mid-brain. The brainstem is that part
5 of your brain that controls us. Once you damage your
6 brainstem, then the prognosis, again, is extremely poor.
7 Q. In the light of that, is there a direct causal
8 relationship between the degree of the violence and the
9 placing, as it were, of the diffuse axonal injury?
10 A. I am not aware of that. That might be something you may
11 need to put to Dr Herron. I am certainly not aware that
12 you can say that with a particular type of violence, you
13 will get diffuse axonal injury in an area like corpus
14 callosum in the brain. What we know is there are
15 particular areas of brain we tend this find this and
16 that's what we tend to look for in trauma.
17 Q. Would this be fair: you need a degree of violence to
18 produce axonal injury of any severity?
19 A. I don't wish to stop you, but I think you have to be
20 careful. Just referring to axonal injury in general,
21 you can get it from a number of causes, but if you are
22 talking about traumatic ...
23 Q. I am. I should rephrase that. I apologise.
24 Traumatic diffuse axonal injury of the type we have
25 here is necessarily associated with a high degree of
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1 violence or acceleration/deceleration?
2 A. That's correct.
3 THE CHAIRMAN: Forgive me. Mr Underwood added "or high
4 degree of acceleration/deceleration", but, as
5 I understand it, the acceleration/deceleration, even to
6 the high degree required, can be caused without actual
7 violence.
8 I mean, one can think of very hypothetical
9 situations, like someone strapped in a chair with his
10 head held firmly, but rotated violently and then in the
11 other direction. I mean, that's an unlikely scenario,
12 but it perhaps shows that the violence and the movement
13 required are not directly related.
14 A. Well, I think you are differentiating between violent
15 movements of the head, which we would still regard as
16 trauma, and injury.
17 THE CHAIRMAN: I see.
18 A. Certainly that does cause it. Work has been done on
19 primates where they have been strapped in and their head
20 has been violently, you know, rotated to show they do
21 get DAI. So whilst it may not be a blow as such, it can
22 still be a rotational cause in some other way, but we
23 would still, if you like, regard that as trauma.
24 THE CHAIRMAN: I suspect we are looking at the effect of
25 blows, are we not, Mr Underwood --
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1 MR UNDERWOOD: That seems highly likely, sir, yes.
2 THE CHAIRMAN: -- not in the other artificial ways?
3 A. Those blows in itself are causing movement of the brain.
4 MR UNDERWOOD: I don't want to bandy phrases like "bad luck"
5 about here, because this is far too tragic for that sort
6 of looseness, but would it be fair to say that it is, as
7 it were, random, if you are subjected to violence to the
8 brain of the sort that can produce this type of diffuse
9 axonal injury? It is random where that might occur in
10 the brain?
11 A. Well, you say "random". I think we do know there are
12 particular sites that occur.
13 Q. Right.
14 A. But I think in "random" you might be correct in saying
15 that if you get a lot of it in your brainstem, then that
16 is obviously -- carries a grave prognostic outlook as
17 opposed to somewhere else where it might not have such
18 severe and serious repercussions.
19 Q. Quite. Am I right in putting this -- and, again, I am
20 not trying to lead you; I am trying to evoke your
21 expertise here -- that if somebody gets diffuse axonal
22 injury, which, as it transpires, is in the brainstem and
23 therefore kills them, it is no more or less likely than
24 the same degree of violence which might have ended up
25 with the diffuse axonal injury being in another part of
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1 the brain?
2 A. Yes. I think that's fair. There is just so far I think
3 we can take these arguments, you know. I think one has
4 to be very careful. We can only assess what we see.
5 In some cases, we may see a lot of axonal injury in
6 the brainstem. In other areas, we may see it in the
7 corpus callosum. We all, if you like, react and behave
8 differently and our bodies react and behave differently.
9 Q. Does it follow from what you have been telling the Panel
10 that the same degree of violence as actually killed
11 Mr Hamill in your view might have ended up with him
12 having traumatic diffuse axonal injury in a different
13 part of the brain which would not have killed him?
14 A. Well, that is obviously a possibility, yes.
15 Q. Can I just put to you some answers you gave in
16 cross-examination at the trial of Mr Hobson, which we
17 see at page [08539]? If I pick it up -- we have numbers
18 against the lines -- at 24, if we could please highlight
19 the rest of the page, you were asked:
20 "Question: Finally, in terms of the circumstances
21 that might have given rise to this axonal injury, you
22 said that a fall accelerated by a punch could cause it.
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24 "Answer: Yes. What I said was that the view taken
25 again is that a simple fall from a person's own
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1 height -- in other words, if you fall down on to the
2 ground -- would not cause this ..."
3 Then if we go over the page, please, [08540] --
4 I don't need highlighting; I can use the whole of the
5 page:
6 "... but an accelerated fall or fall from a height
7 may be associated with diffuse axonal injury.
8 "Question: Or if one was running and fell in liquid,
9 and fell fast, could one suffer this injury?
10 "Answer: I think it is a possibility, because that
11 would be an accelerated fall.
12 "Question: Did you find a bruise at the back of the
13 scalp at the right side?
14 "Answer: I would need to refresh my memory. No,
15 there was no bruising at the back of the scalp. The
16 bruising was on each side, on the left side and the
17 right side. There was none at the back.
18 "Question: And either of those bruises might be
19 associated with the mechanism that gives rise to the
20 injury?
21 "Answer: Sorry?
22 "Question: Might either be associated with the
23 mechanism which gave rise to the injury?
24 "Answer: The bruising on the scalp indicates there
25 was a blunt force applied to the sides of the head.
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1 "Question: Which could be the head hitting
2 a surface?
3 "Answer: That is a possibility.
4 "Question: And a man running and slipping could hit
5 his head and could suffer this injury?
6 "Answer: That is a possibility.
7 "Question: Particularly a man running away in fear?
8 "Answer: Yes. That is a possibility. If someone
9 was running and fell and struck their head on the
10 ground, that diffuse axonal injury could occur."
11 That's the end of your cross-examination there.
12 I fully understand, firstly, that this was a long time
13 ago and more may be known about axonal injury now.
14 Secondly, you were giving, if I may say, fair
15 answers in the context of the standard of proof in
16 a criminal case.
17 Can I ask you what your view is now about the
18 likelihood that the injuries which you saw, which you
19 attribute Mr Hamill's death to, were caused by him
20 running or slipping and hitting his head?
21 A. Well, as you say, I think, in fairness, an accelerated
22 fall, which could occur if a person was running at
23 speed, one would have to consider that as a possibility.
24 Is that the likely scenario? In my view, it is
25 certainly considerably less likely than blows. Of
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1 course, what we had here was evidence of more than one
2 injury to the head. So it indicates that if he did fall
3 and strike his head, there must have been other force
4 applied to his head to cause the other injuries. So
5 there was more than one traumatic impact on the head.
6 Q. That's helpful. Thank you. Can I deal with other
7 possibilities now? If we go back to your statement for
8 the Inquiry at paragraph 40, which we find on
9 page [80225], if I can highlight paragraph 40, please,
10 for you, you say there:
11 "I did consider whether there was evidence of
12 hypoxic damage, but I excluded this as a cause of death.
13 Hypoxic brain injury is often associated with a very
14 swollen or oedematous brain, but this did not appear to
15 be the finding from the CT scans taken. There was no
16 neuropathological evidence of the nature which one would
17 expect to find if the brain had been deprived of oxygen
18 for a significant period such as laminar necrosis of the
19 cortex. If there had been significant starvation of
20 oxygen at the time of the injury, one would expect to
21 see clear changes in the brain develop after a week."
22 What I want to ask you about in the light of that is
23 about evidence we heard yesterday that, on arrival at
24 the Craigavon Area Hospital, the oxygen saturation was
25 measured at 75%. We were told by the clinician who
19
1 attended Mr Hamill then that that's a very low rate.
2 Can I ask you, firstly, whether you accept that's
3 a very low figure?
4 A. Yes, it is.
5 Q. Can you help us with how somebody with 75% saturation at
6 that stage would then not, a week or so later, show the
7 signs of a hypoxic injury?
8 A. Yes. Maybe I have oversimplified it in my statement.
9 There was -- and I think it is reasonable to consider
10 this -- some evidence of some hypoxic damage in the
11 brain. I think Dr Reid felt there was and Dr Herron
12 felt there was. I was not saying there was no evidence
13 of hypoxic, but if the brain is deprived of oxygen for
14 a significant period of time, and I mean deprived of
15 oxygen so no oxygen is getting to the brain for
16 a significant period of time, then irreversible changes
17 will occur in the brain. If that individual is kept
18 alive for a period of time, for example, on
19 a ventilator, then there are very significant changes,
20 very clear changes that will be seen whenever the brain
21 is examined.
22 Now those significant, well-developed changes from
23 hypoxia were not present. Obviously there were some
24 changes that were present, but if hypoxia was the main
25 cause of Mr Hamill's brain injury, if we put it -- or
20
1 brain damage, then I think we would have seen much more
2 evidence of that than was present.
3 Q. Thank you. Is it possible to conclude from what you
4 have just told us that the 75% saturation was temporary
5 or not?
6 A. Yes. I mean, I think that's reasonable. He may have
7 been breathing better initially. There may have been
8 some degree of obstruction to his breathing. Clearly,
9 when he got to hospital, I am sure the first thing they
10 would have done was to ensure that his airway was
11 properly secured, that he was given oxygen. So that
12 would be, therefore, to improve the oxygenation of the
13 brain, which is crucial in these cases.
14 THE CHAIRMAN: If there is an improvement and not too long
15 a period of starvation, then there is no permanent
16 damage?
17 A. That's correct, yes.
18 MR UNDERWOOD: Now -- I am so sorry, I will wait for pens.
19 I want to come in the end to the vexed, but perhaps,
20 in the end, not important question of Neuroleptic
21 Malignant Syndrome.
22 You and Dr Lawler I think have to agree to disagree
23 about this, but can I put some of this to you to see
24 what help we can get for the Panel? If we look in your
25 statement at page [80222], paragraph 28, you say:
21
1 "Specifically we considered the possibility of
2 Malignant Neuroleptic Syndrome and I was in discussion
3 and correspondence with Dr Herron as to whether this was
4 the cause of death or the head injury alone. Factors
5 which pointed to NMS were the fact that the patient had
6 a head injury, he had a spiked temperature and he had
7 been given Chlorpromazine. At the time of the autopsy,
8 I was not aware of the results for the CK tests showing
9 924 per litre, but that level of CK is not especially
10 elevated. A raised CK level is not unusual where
11 a patient has undergone physical trauma. I would have
12 expected a far higher level of CK, in the thousands, in
13 a case involving NMS."
14 Going over, if we may, [80223]:
15 "29. The reasons I ruled out NMS include the
16 absence of damage to the kidneys, where NMS would have
17 caused casts of myoglobin, but none were present. I did
18 special stains on the kidney to look for muscle damage,
19 but there was none. There were no casts identified
20 within the tubules. There was an absence of damage to
21 the liver with no necrosis evident. There was no
22 rigidity in the muscles, which is a notable symptom of
23 NMS. Neither were there the changes to the brain which
24 would normally be associated with NMS, such as necrosis,
25 particularly in the cerebellum. We specifically looked
22
1 for all of the changes that you get in this syndrome.
2 It was in my view a possibility and one that we needed
3 to consider. All of the typical markers that are
4 associated with the syndrome were not found and that is
5 why I excluded it as being a cause of death."
6 In the face of that, can I put this suggestion to
7 you: that if the NMS had a very rapid onset, is it
8 possible that those indicators you had looked for there
9 could not yet have had time to be found?
10 A. That certainly is a possibility, but then one has to
11 consider then, what was the mechanism of death? The
12 mechanism of death in Malignant Neuroleptic Syndrome is
13 often liver failure, it is often renal failure. It is
14 often the changes in the brain you get associated with
15 it.
16 It is not a condition that comes on very rapidly and
17 causes death very rapidly. I think, with respect to
18 Dr Lawler and Dr Reid, what neither of them addressed --
19 and I think this is what's crucial -- was the fact that
20 Mr Hamill was unconscious from the time of incident,
21 from the time he was admitted to hospital until his
22 death.
23 Now, clearly, that could not fit, in my view, within
24 NMS, because clearly there had been brain damage from
25 the outset and it wasn't something that he was doing
23
1 well and then suddenly developed this. As I say, we did
2 consider it. We don't -- I suppose I am not ruling out
3 completely that there was an element of it or it might
4 have been developing, but I'm ruling it out as the cause
5 of his death.
6 Q. If I just ask you a more general question about NMS,
7 again how well-chronicled is that?
8 A. It is a very uncommon condition. I certainly, as
9 a pathologist, have only come across relatively few
10 cases. Dr Herron, I think did have some cases, and
11 I think he may have written those up, but it is a very
12 uncommon condition.
13 I was dealing with another case, actually, in the
14 courts earlier in the week and I consulted with one of
15 my retired consultant neurosurgeons about how commonly
16 he had seen it in patients who were given
17 Chlorpromazine. In his experience, and he is now
18 retired, he had never come across a case of it in
19 a patient he had treated with a head injury.
20 Certainly my experience is it is extremely uncommon.
21 Q. Can I ask you to, as it were, suspend your disbelief for
22 a minute about the NMS? If you are wrong and if, in
23 fact, there was a head injury which was then, as it
24 were, overtaken by NMS, would that change your view
25 about the severity of the axonal injury?
24
1 A. No, it wouldn't, because the staining of the brain still
2 showed up the axonal injury. So I don't think that one
3 can simply put that aside and say, "Well, that wasn't
4 important", even if there was.
5 Q. So even if Mr Hamill did develop this reaction to
6 Chlorpromazine and even if that, in fact, killed him,
7 your view is he would have died from the axonal injury
8 in any event, is it?
9 A. Yes. The view I take is that his prognosis was poor
10 from the outset.
11 Q. That's very helpful. Thank you. One last possibility
12 I need to ask you about is at paragraph 43, which we
13 find on page [80226]. If I can highlight paragraph 43,
14 please.
15 This paragraph concerns your treatment of a police
16 file note. I am not interested in the police file note
17 or what it may say about any views of yours. What I am
18 interested in is that you deal here with septicaemia.
19 If we see in the middle of the paragraph that the file
20 note had made a reference to septicaemia and you say
21 that reflects a misinterpretation of your words.
22 Can I ask you more about septicaemia, please?
23 Obviously you considered it --
24 A. Yes, I did.
25 Q. -- and obviously excluded it. Can I ask you what signs
25
1 there might have been, or reason there might have been,
2 for considering septicaemia and why you excluded it in
3 the end?
4 A. The reason why it was a possibility was, first of all,
5 here was a patient in an intensive care unit being
6 ventilated. Hospitals are extremely unhealthy places,
7 especially for unconscious patients and they pick up all
8 sorts of bugs. Many patients die from an infection they
9 have incurred because they are perhaps compromised in
10 some way, such as being unconscious, absence of cough
11 reflex and so forth.
12 Secondly, Mr Hamill had a spiky temperature. That's
13 an indication there may be underlying infection there.
14 So it was considered. What one normally does in those
15 circumstances then is to look for evidence of
16 septicaemia.
17 Essentially, there are two things one looks for.
18 There may be changes in the internal organs to indicate
19 that there is a source of infection. There might be
20 pneumonia. There might be evidence of infection
21 elsewhere in the body. One can see those either grossly
22 or microscopically and they were not present.
23 The other thing one did was to take samples from
24 a number of the organs. They are then sent to the
25 laboratory for culture. So, for example, if you have
26
1 a sore throat, the doctor might take a swab. At post
2 mortem we do the same thing.
3 Now, the difficulty is, with post mortem
4 bacteriology, it is not terribly reliable for a number
5 of reasons, but my view was that the organisms that we
6 did grow were probably not significant, and I think
7 probably the other pathologist, doctor, I think probably
8 agreed they were not significant. So I came to the
9 conclusion that septicaemia was not a factor in
10 Mr Hamill's death.
11 MR UNDERWOOD: Thank you very much.
12 Professor, there is one other area I need to ask you
13 about and that's the length of time between the autopsy
14 and the arrival of your report. Can I just run through
15 the events, please? If we go to [80216], we see in
16 paragraph 5, as you have told us, the brain was
17 submitted for neuropathology. As part of an autopsy you
18 examine the scalp, the skull, etc:
19 "But, after that, the brain is taken out and is
20 fixed by immersion in formaldehyde for a period of at least
21 6 weeks. Once fixed, the brain is given to a
22 neuropathologist for examination."
23 Can you help us with the dates here or not?
24 A. I can't, because it is not usually me that actually
25 physically takes the brain to neuropathology. It is
27
1 kept in the mortuary or in my laboratory. Whenever we
2 think it is ready for examination, it is taken over by
3 my staff.
4 Q. Presumably, the amount of time it might take to fix in
5 formaldehyde might vary?
6 A. It does, yes. Anything between usually five to eight
7 weeks. The longer it is in formaldehyde, the better fix
8 it is. So I'm afraid I don't have a definite indication
9 of when it was sent to Dr Herron.
10 Q. Dr Herron tells us that he tends to section the brain in
11 your presence. Do you recall that happening here?
12 A. Yes. Again, I can't remember the date, but what happens
13 is that there is a mutually convenient time whenever
14 Dr Herron is available and whenever I am available.
15 What we do is, I come over and we examine the brain
16 together. The brain is cut. So that's the usual
17 procedure.
18 Q. Can I ask you to look at page [31862]? This is
19 a document that was not addressed to us. You may know
20 nothing about it. Can I ask you your comments on it?
21 Can I highlight the lower half, please? This is
22 a letter from the Assistant Director of the Director of
23 Public Prosecutions Office to the resident magistrate,
24 dated 27th October 1997. What he says is:
25 "On the afternoon of 21 October, I telephoned to
28
1 Professor Crane. My specific purpose in doing so was to
2 obtain up-to-date information from him on the position
3 regarding his completion of the report and when it was
4 likely that it would be available to this office.
5 I know that you are aware that I have communicated
6 previously with Professor Crane on this issue."
7 What the author there seems to be suggesting is
8 that, prior to 21st October, he had been, to put it in
9 the vernacular, chasing you for the report. Is that --
10 A. Yes. This is fairly typical of the lawyers who expect
11 us to produce reports within days. These things take as
12 long as they take. They are not rushed in any way.
13 With the greatest respect, we produce our reports
14 a lot quicker than legal and judicial proceedings take,
15 and I take great exception to constantly being harassed
16 by either the police or lawyers looking for the report.
17 If they want a proper and detailed report, they have to
18 wait for it. Neuropathology does take a considerable
19 period of time to do.
20 I should also say the neuropathology is done out of
21 goodwill by Dr Herron and his colleagues. They are not
22 paid for doing it. They are employed to deal with
23 living patients in the health service. They provide
24 this service as a courtesy to us.
25 Q. I want to come to that in a minute, if I may. Can
29
1 I move on to the next paragraph:
2 " Professor Crane informed me that the
3 neuropathology department had requested further
4 information from him and that, subject to the provision
5 of that information, all examinations would be complete.
6 Professor Crane thus hoped to have the post mortem
7 report completed in the very near future ..."
8 Is that right, that the neuropathology department
9 had requested something from you at that stage?
10 A. Well, they must have. I can't remember what it was.
11 What I suspect it might have been is more clinical
12 information, because Dr Herron would only have
13 relatively scant information that I might have been
14 provided with at the time of the autopsy.
15 What I do, in completion of my report, is obtain the
16 hospital records to look at those in more detail. So it
17 may have been that that's what Dr Herron was requiring.
18 Q. I understand. So your position then, is it, is you do
19 reports as quickly as is feasible, and that, in this
20 case, because the brain had to be fixed, that took
21 a period? We don't know how long that period was,
22 because the matter was not in your hands. Then we come
23 to the point that the necessary intervention of the
24 neuropathologist was on a voluntary basis.
25 A. That's correct.
30
1 Q. Is that still the system?
2 A. Yes, it is.
3 Q. So the position is, is it, that while, as in this case,
4 six people were in custody for six months, one is
5 depending on the goodwill of people acting voluntarily
6 to fit into their busy diaries the work that's required
7 to produce the necessary report?
8 A. Yes, and that tends to be the practice throughout the
9 United Kingdom. As far as I know, there is only one
10 forensic neuropathologist in the UK, Professor Whitwell.
11 I should also say that my understanding is that the
12 report from Dr Herron was obtained round about
13 27th October. That was my --
14 Q. Indeed it was.
15 A. My report was then completed the first week in November.
16 Q. Nobody is suggesting that once the neuropathology report
17 was in, there was any delay.
18 That deals with all the questions I wanted to ask
19 the Professor. I am very grateful, Professor. I don't
20 know whether, in the course of that, anything else has
21 emerged which anybody would either like me to ask or,
22 more economically, simply ask you, sir, to ask
23 themselves.
24 MR ADAIR: Sir, I wonder might I be permitted to ask just
25 a few questions?
31
1 I had mentioned to Mr Underwood a number of issues
2 which he has attempted to deal with, but arising out of
3 the answers, might I be permitted to did just a few
4 questions.
5 THE CHAIRMAN: Yes. Very well.
6 Cross-examination by MR ADAIR
7 MR ADAIR: Professor Crane, just to clarify the axonal
8 injury and cause of axonal injury, my understanding,
9 just going first of all to acceleration and
10 deceleration, is that it is the severity of the force
11 which causes potentially the axonal injury?
12 A. Yes, that's correct.
13 Q. Am I right in saying that a fall, an accelerated fall,
14 can cause axonal injury?
15 A. Yes, it can.
16 Q. By the term "accelerated fall", would that include
17 a fall as a result of a blow or punch?
18 A. Yes.
19 Q. Again I am very conscious, Professor, that very often
20 when I am cross-examining, we are dealing with
21 possibilities in a criminal trial. We are attempting
22 here, as you will appreciate, to deal with likelihoods
23 and to ascertain the truth, so, is it a perfectly
24 reasonable scenario that the axonal injury could well
25 have been caused by a blow when Mr Hamill then fell to
32
1 the ground?
2 A. Yes, it is certainly a possibility.
3 THE CHAIRMAN: You mean a blow received in the impact of
4 falling on the ground?
5 MR ADAIR: I was just going to ask, "Is it a combination of
6 the two or is it the blow itself?", as a subsequent
7 question, sir.
8 Is the cause of the axonal injury a combination of
9 the blow and the fall on the ground causing a sort of
10 the contre-coup or is it the blow or the impact with the
11 ground?
12 A. I think the contre-coup injury you mentioned is
13 a separate issue. So if we leave that out.
14 The blow itself, so, for example, if somebody gives
15 us a punch, theoretically that can cause rotational
16 effects in the brain, but what I was saying in answer is
17 that, strangely enough, we don't see this terribly
18 commonly in boxers. So probably what is happening in
19 relation to the accelerated fall to the ground is that
20 the brain is moving. There is both rotational and
21 forward/backward movement, but it is the sudden
22 deceleration of the brain as it impacts on the ground
23 that might then account for the fact that we are seeing
24 axonal injury in those cases.
25 Q. So when one is dealing with likelihoods, as we are
33
1 really in this, subject to anything the Panel may say,
2 is it a reasonable proposition that the axonal injury
3 may well have been caused by a blow to the ground?
4 A. Well, yes, I think that's a possibility. I think one
5 has to look, though, at other aspects of the case. So,
6 for example, to take your scenario of a punch, the
7 person falling backwards and striking his head on the
8 ground, what we might expect to find under those
9 circumstances is bruising to the back of the head,
10 an underlying skull fracture at the back of the head and
11 evidence of contre-coup injury to the front of the
12 brain, because that's where it occurs.
13 Of course, we looked for all those and none of those
14 were present.
15 Q. I think there was an injury to the back of the head.
16 I don't think it is mentioned in --
17 A. Clinically, he was -- a nurse had mentioned there was
18 a cut to the back of the head. Now, at post mortem
19 there was not any injury. So if it had healed, it was
20 not present. There was still no bruising to the back of
21 the head.
22 I can't exclude injury to the back of the head
23 completely, but I think that if we are talking about
24 an accelerated fall from a punch sufficient to cause
25 DAI, I think I might have expected to see some of the
34
1 other findings that I have mentioned, bruising, perhaps
2 a skull fracture, perhaps contre-coup injury to the
3 front of the brain.
4 Q. Just again so we are all clear about it, do you regard
5 that then as a possibility rather than a likelihood?
6 A. I think that's a possibility. I think it is less likely
7 than perhaps blows, which I think were directed probably
8 to the side of the head.
9 Q. Yes. Again then, is it the position that the more
10 likely scenario is that the axonal injury was caused as
11 a result of severe kicking to the head?
12 A. Well, it has to be caused by blows to the head. I don't
13 know whether it was kicks or by an implement or anything
14 else, but certainly --
15 Q. If I phrase it another way then, is it more likely then
16 that the axonal injury was caused as a result of
17 a number of blows to the head, whether standing or lying
18 down?
19 A. Yes. I think the most likely is the blows were
20 inflicted whilst he was on the ground and the head was
21 moving.
22 Q. So that's the most likely scenario?
23 A. Yes, that's my opinion, yes.
24 Q. My understanding also is that it could be one or two
25 severe kicks to the head that caused the injuries you
35
1 found on the head?
2 A. Yes. I think, as I said, it depends on the force of the
3 blows and obviously the more blows there are, then the
4 more likely they may be to get injured.
5 Q. When you are looking at the nature of this injury, it is
6 severity rather than a sustained attack that determines
7 the injury; in other words, one severe kick could have
8 caused this axonal injury?
9 A. Yes.
10 Q. That's perfectly reasonable.
11 You have often described sometimes, Professor Crane,
12 where people have described kicking a head like a rugby
13 ball. So a kick like that, it's a perfectly reasonable
14 proposition that one kick such as that could have caused
15 the axonal injury you found?
16 A. Yes, it could.
17 Q. There was nothing that you found on the head to indicate
18 that there were or was a sustained kicking of the head?
19 A. Well, what we found was that there were areas of
20 bruising on both sides of the head. There was also
21 evidence of an injury to the left front of the head, the
22 left frontal area, which was associated with
23 an underlying fracture of the skull. So we have
24 injuries in three separate areas that I found.
25 Q. Does that suggest the possibility, then, of three kicks?
36
1 A. Well, it suggests the possibility of either three blows
2 or three contacts. For example, one could have been
3 sustained if Mr Hamill had fallen to the ground. That's
4 a possibility.
5 Q. So we are absolutely clear, the findings do not indicate
6 in relation to the head anything more than possibly two
7 kicks or possibly three kicks? One can't say with any
8 certainty that there were more than two or three kicks
9 to the head?
10 A. I think that's right. I think in answer to counsel
11 earlier I think I said we often see people being
12 assaulted with a lot more injuries than Mr Hamill.
13 Q. Obviously that could be done in seconds?
14 A. Yes, it could.
15 Q. Finally, Professor Crane, it is apparent from what you
16 have said, but the other injuries on the body, leaving
17 aside the head, I think were relatively minor?
18 A. Yes, they were. These were injuries essentially to the
19 skin. These were bruising not associated with any
20 underlying damage either to the ribs or internal organs.
21 Q. There was nothing in the nature of those injuries to
22 indicate a prolonged or sustained attack?
23 A. Well, there were a number of injuries and they could
24 have been caused by a number of blows, as I indicated.
25 I think one has to say, you know, what does one regard
37
1 as a sustained attack? I mean, there were other
2 injuries. I have documented them. They could have been
3 caused by a number of blows.
4 MR ADAIR: Thank you.
5 Thank you very much, sir.
6 Questions from THE REV BARONESS KATHLEEN RICHARDSON
7 REV. BARONESS KATHLEEN RICHARDSON: Professor Crane, if the
8 injuries had been caused by an accelerated fall, would
9 you have expected to see more bruising, for example, on
10 shoulders, hips, as well?
11 A. Not necessarily, no.
12 MR McGRORY: Sir, I would have one issue.
13 THE CHAIRMAN: Very well.
14 Cross-examination by MR MCGRORY
15 MR McGRORY: Professor Crane, would the type of footwear
16 worn by somebody kicking a person lying on the ground
17 have an effect on the outer manifestation of the
18 injuries?
19 A. Yes, it may do. If a person is wearing what we might
20 call, you know, heavy footwear, like boots, or Dr Marten
21 shoes or those things, they will often be associated
22 with cuts to the scalp, cuts to the skin and may be
23 associated with more localised injury, whereas, if
24 a person is wearing, for example -- if we say trainers
25 or something like that, they may not be associated with
38
1 the same degree, you know, of external injury.
2 Q. So if some people were wearing trainers, and they were
3 involved in a more sustained attack, it would be correct
4 to say that there might not have been as many physical
5 manifestations of the attack?
6 A. Yes. There might not be as many external injuries.
7 Q. Yes.
8 A. Although even with kicks with trainers, you might have
9 expected, if there were multiple kicks of force, to see
10 a lot more bruising on the undersurface of the skull and
11 there was not a considerable amount there. There was
12 some on both sides, but you might have expected -- you
13 know, if they were really concerted blows, even with
14 trainers.
15 MR McGRORY: Yes. Thank you.
16 MS DINSMORE: Might I put one question to Professor Crane?
17 THE CHAIRMAN: Yes.
18 Cross-examination by MS DINSMORE
19 MS DINSMORE: Professor Crane, should Mr Hamill have
20 sustained a blow to the head by being struck by
21 a bottle, could that possibly, that type of force,
22 contribute to the injury within the brain and the nature
23 of the fall which Mr Hamill sustained, if that happened?
24 A. In my view probably not, no.
25 Q. Why do you say that, Professor?
39
1 A. Struck by a bottle certainly could have caused an injury
2 to the skin or the scalp. It might have caused him to
3 fall, but my view is I don't think it would have
4 generated sufficient force, the so-called accelerated
5 fall, I think, to have cause diffuse axonal brain
6 injury. Simply being struck by a bottle that was thrown
7 would not, in my opinion, be sufficient.
8 Q. Would that depend, of course, on the measure of force
9 with which one was struck by that bottle?
10 A. I think, of course, that's true.
11 MS DINSMORE: Thank you very much.
12 MR UNDERWOOD: I have nothing arising out of that.
13 Questions from THE CHAIRMAN
14 THE CHAIRMAN: Presumably, Professor Crane, if you consider
15 the person lying on the ground, then a boot is a more
16 effective way, or a kick, to inflict injury than having
17 to stoop to punch?
18 A. Yes. I think that's right. I think that punching
19 a person whilst they are on the ground probably -- it is
20 difficult probably to generate sufficient force simply
21 from a punch to cause injury. I mean, we think forces
22 are considerable here, but I think probably just a punch
23 on its own or a number of punches on their own might not
24 be sufficient.
25 THE CHAIRMAN: Thank you.
40
1 MR UNDERWOOD: Thank you very much. I think that's the
2 entirety of the questioning. I am very grateful,
3 Professor. Thank you very much for coming.
4 THE CHAIRMAN: Thank you, Professor.
5 A. Thank you very much.
6 (The witness withdrew)
7 MR UNDERWOOD: Sir, I am very grateful for the cooperation
8 of all my learned friends, who gave me a number of
9 lines of questioning to put to the Professor, which led
10 us to dealing with him very quickly, which leads me to
11 the embarrassment of saying that we have the one other
12 witness scheduled for today, who is Dr Herron, who was
13 scheduled for 2 o'clock. Very kindly, he has moved that
14 forward. He is available at 11.50. May I suggest that
15 we rise until then?
16 THE CHAIRMAN: Yes. Very well. 11.50 am.
17 (11.25 am)
18 (A short break)
19 (11.50 am)
20 MR UNDERWOOD: Sir, I call Dr Herron.
21 DR BRIAN HERRON (called)
22 A. Shall I sit?
23 THE CHAIRMAN: Just take the oath and then do sit down.
24 DR BRIAN HERRON (sworn)
25 THE CHAIRMAN: Do sit down.
41
1 Examination by MR UNDERWOOD
2 MR UNDERWOOD: Doctor, my name is Ashley Underwood. I am
3 Counsel to the Inquiry. At least initially I will be
4 asking the questions, but it is the Panel that is going
5 to need to hear the answers.
6 May I ask your full name?
7 A. My name is Brian Herron.
8 Q. Your professional address?
9 A. Royal Victoria Hospital, Belfast.
10 Q. Doctor, can I thank you, first of all, for coming out of
11 schedule. It is very much appreciated.
12 You have kindly signed a witness statement for us,
13 which we can find on our screens. It is page [80435].
14 If I can ask you to look at the screen rather than
15 a hard copy, then everybody will be, as it were, on the
16 same page.
17 A. Yes.
18 Q. Can I highlight paragraph 2, please?
19 A. Yes.
20 Q. We see you are a neuropathologist. Presently you are
21 a consultant at the RVH. You give your qualifications
22 there. You are also a general pathologist, we see, and
23 you run the adult autopsy service for the majority of
24 the hospitals in Belfast.
25 We know also you prepared a report, which we see at
42
1 page [31395]. I would like to take you through this, if
2 I may, starting -- if I could magnify the last half the
3 page -- the second half, I should say:
4 "Histology.
5 "Sections were taken", this is of Mr Hamill's brain,
6 "from the right and left frontal lobes, corpus callosum,
7 left and right hippocampi, hypothalamus, cerebellum,
8 midbrain and pons."
9 Then you describe what you found in each of those
10 "Frontal lobe: examination of the sections from the
11 right and left frontal lobes show the presence of white
12 matter contusions."
13 Can you explain that to us?
14 A. A contusion, in layman's terms, is a bruise. Contusions
15 in the brain are of many different types. If you have
16 a bruise on the surface of the brain, it usually tells
17 you there is a particular mechanism to that injury.
18 If you have contusion in the white matter of the
19 brain, it tells you that there is a different sort of
20 injury or mechanism of injury present. Really, it means
21 there has been disruption of the normal tissue deep in
22 the brain.
23 Q. We will come on to axonal injury, but is this associated
24 with axonal injury?
25 A. It is a condition that is associated with axonal injury.
43
1 Q. Thank you. You go on to say:
2 "This is associated with tissue necrosis ..."
3 "Necrosis" just means the death of tissue, doesn't
4 it?
5 A. Yes.
6 Q. "... and a macrophage reaction."
7 Can you help us with that?
8 A. When you have an injury of any sort, the brain or the
9 skin or the bone reacts in a particular way. When you
10 have damage to the tissue of the brain, the cells that
11 are damaged are absorbed by inflammatory cells. These
12 inflammatory cells are called macrophages. The
13 macrophage reaction tells us there has been time for
14 a tissue reaction to occur.
15 Q. I am jumping ahead a little about axonal injury.
16 Where one has axonal injury, is it the shearing of
17 the axons which cause the difficulty or is it the
18 macrophage reaction itself?
19 A. It is the -- it is a very complicated question. I will
20 try to make it as easy as possible.
21 An axon is like the wire that comes from your
22 switch. When you have an acceleration or deceleration
23 of the brain, the wire gets stretched. It doesn't get
24 broken, it gets stretched. That allows for other
25 chemicals to get into the axon and, subsequently, the
44
1 axon becomes ruptured.
2 So it is the axon and axonal damage that is the main
3 problem for these people. The axons carry the messages
4 from the nerve cell bodies to other parts of the brain.
5 So when you break the wire or you break the axon, those
6 signals can't disseminate.
7 Q. Is it right to say, then, that axonal injury itself,
8 because it stretches the axon, will not disrupt the
9 messages, but it is the reaction which allows other
10 chemicals to get in which disrupts them?
11 A. It is the entrance of the other chemicals into the axon.
12 An axon is a tube through which signals flow. When you
13 stretch the axon by an acceleration or deceleration, the
14 wall of the tube gets stretched and calcium gets into
15 the tube. Calcium blocks all the normal chemical
16 reactions within this tube and stops the flow of signal
17 and chemicals within the tube.
18 Q. Thank you. Going back to what you found in the frontal
19 lobe, you say:
20 "Surrounding this there is extensive diffuse axonal
21 damage. There is no evidence of hypoxic/ischaemic
22 necrosis of the adjacent cortex. There is no
23 meningoencephalitis."
24 What is the significance of those findings in
25 a frontal lobe, and how, as it were, dangerous to
45
1 somebody's existence is such a set of findings?
2 A. I think you have to put this into the whole context of
3 what a neuropathologist does and how a neuropathologist
4 is involved in a case.
5 We knew the clinical history of Mr Robert Hamill.
6 The role of the neuropathologist is slightly different
7 now from it was in 1997, but the role of the
8 neuropathologist is to help the forensic pathologist,
9 Professor Crane in this case, to come to a conclusion.
10 There would have been a number of possible
11 conditions that could have caused Mr Hamill's
12 presentation to hospital and his subsequent death.
13 A lot of the remarks that are present in a report are to
14 exclude some of the possibilities and suggestions that
15 might have caused his unconsciousness. So you would
16 quite often put in negative findings to help -- for
17 example, if he had a skull fracture, a skull fracture is
18 a portal of entry for infection. Infection can cause
19 unconsciousness in meningitis or encephalitis.
20 So one of the things that can cause a patient to be
21 unconscious after an injury is meningitis or
22 encephalitis. There is a relative negative finding in
23 that case.
24 Q. All right, but the positive findings you have there, the
25 white matter contusions, tissue necrosis, macrophage
46
1 reaction, extensive diffuse axonal injury in the frontal
2 lobe of the brain, are they fatal?
3 A. It can be. It implies -- this matter of reaction
4 implies that this is a diffuse pattern of brain injury.
5 Now, the brain, relative to other organs, is a large
6 organ. It maybe weighs -- in this case, it was about
7 1,500 grams. So you have to be selective in the areas
8 of tissue that you examine under the microscope. You
9 cannot examine all of it, otherwise you would never get
10 anything else done. So you must be selective in what
11 you examine.
12 The frontal lobe is just an example of an area of
13 brain that has been damaged. It is of no specific
14 interest to point out that it is in the frontal lobe.
15 Q. Okay:
16 "Corpus callosum: examination shows diffuse axonal
17 damage."
18 Nothing I need to ask you about that I think, except
19 that you don't use the word "extensive" there in the way
20 you do in relation to the frontal lobe and, indeed, the
21 left internal capsule. Is that deliberate?
22 A. No, it is not deliberate.
23 Q. Right. Jumping down then to the hypothalamus. That is
24 deep in the brain, is it not?
25 A. The hypothalamus, if you go behind the eyes, you have
47
1 a gland called the pituitary gland. Above that is
2 a minor organ called the hypothalamus. It measures
3 maybe 1 centimetre cubed and is present on either side.
4 The hypothalamus, however, is very important. It
5 runs all our hormones. It is responsible for running
6 all our glands. It is the commander of all our
7 endocrine organs, but also, it is the part of the brain
8 that controls temperature.
9 It was mentioned specifically in this case possibly
10 for clinical reasons.
11 Q. You found there axonal damage. Again, is there anything
12 deliberate about the absence of an adjective?
13 A. Well, it is only -- it is an organ that is only about
14 1 centimetre cubed. There is nothing significant about
15 that or the inclusion of it.
16 Q. How significant is axonal damage in a hypothalamus?
17 A. In this case, it could be particularly significant,
18 given the various opinions that were offered
19 subsequently to my report.
20 It is debated in this case how Mr Hamill ultimately
21 died. I am sure we will come to this. One of the
22 questions was whether or not he had a very rare
23 condition called Malignant Neuroleptic Syndrome, where
24 one of the features of Malignant Neuroleptic Syndrome is
25 the presence of high temperature.
48
1 A high temperature can occur in an unconscious or
2 semi-conscious patient for many reasons. Malignant
3 Neuroleptic Syndrome would be one of the rarest reasons
4 to cause that; infection would be the most common
5 reason.
6 Also, a head injury that affects the area of the
7 brain that controls temperature -- and in this case it
8 is affected -- would be one of the reasons why someone
9 might develop a high temperature after injury, and
10 that's well-recognised.
11 Q. That's helpful, thank you.
12 Can we go over to page [31396] and highlight that,
13 please? You say:
14 "Midbrain: examination shows diffuse axonal damage.
15 There is no secondary brain stem haemorrhage. The
16 substantia nigra shows no evidence of degenerative
17 change.
18 "Pons: examination shows the features of severe
19 diffuse axonal damage.
20 "Cerebellum: examination shows no evidence of
21 cortical necrosis. The Purkinje cells are preserved.
22 A small gliotic scar is present in the white matter."
23 "Comment:
24 "In summary, the predominant finding in case is the
25 severe diffuse axonal damage. Diffuse axonal damage is
49
1 thought to be due to interruption of movement of
2 cytoplasm through axons with subsequent accumulation of
3 axonal material seen on H&E examination as small
4 eosinophilic bulbs. In this case it was distributed
5 throughout the deep white matter, corpus callosum and
6 brain stem. This pattern of damage is consistent with
7 being caused by trauma. It is indicative of a severe
8 head injury."
9 I know that you have read since you wrote this
10 a good deal of critique by Dr Lawler and others. Does
11 this remain your view, or have you changed it?
12 A. It remains my view.
13 Q. Thank you. Can you just help us while we are on this
14 document with the dates; 7th August, and
15 29th October 1997?
16 A. I can try and answer that to the best of my ability.
17 Our secretaries, when they are typing reports, will date
18 when they type reports. I am assuming those are
19 secretarial dates. Going back through my notes of the
20 case, it seems that 7/8/97 would have been when what we
21 call the macroscopic description was prepared. That's
22 when we look at the brain and examine the brain without
23 any microscope to look at injuries, and the second date
24 is most likely when the histology, which is the
25 microscopic examination that you have just read out,
50
1 would have been prepared.
2 Q. Thank you. If we go back to your witness statement, at
3 paragraph 21, which we find on page [80443], you assist
4 us by giving us some reference to publications, in
5 particular in the second sentence:
6 "In a study of 2000, 'only the severest
7 acceleration/deceleration forces with or without
8 deceleration caused diffuse axonal injury extending down
9 into the brainstem.'"
10 What I want to discern is how much you may be able
11 to assist with the relationship between diffuse axonal
12 injury of this sort and, as it were, the violence of the
13 event that caused it.
14 Can I ask you, first of all, whether you have done
15 any more work or had any more experience of diffuse
16 axonal injury since you did the work on this in 1997?
17 A. The interpretation of diffuse axonal injury is very
18 current in neuropathology and especially in quite a lot
19 of homicide trials that I would be involved in. The
20 literature in 1997 was beginning to develop and there
21 have been numerous publications since then. It is
22 something with which I am familiar on a weekly basis and
23 would -- it has been debated in numerous court cases
24 that I have been involved in.
25 Q. Thank you. Can you help us then in general? We have
51
1 already been told, as you pointed out here, that this
2 type of axonal injury is generally associated with
3 severe acceleration/deceleration. We have been told,
4 for example, that it is the sort of thing you might get
5 in a car accident, where you come to a very sudden halt.
6 Is that right?
7 A. The most common scenario is exactly as you say. There
8 are a lot of physical factors involved and one of the
9 factors involved is the speed of deceleration as well as
10 the force of the deceleration.
11 We would normally see it in people who have been in
12 road traffic accidents, quite often in people who fall
13 down stairs, but it is hotly debated as to whether or not
14 you can get it in certain other scenarios. Some people
15 think you can; some people think you can't. There is
16 a lot of debate about it.
17 Q. What about, for example, a shaken baby? Would a shaken
18 baby get it?
19 A. A shaken baby gets diffuse axonal injury for a different
20 reason. A baby that is shaken -- again, this is one of
21 the most controversial areas of forensic
22 neuropathology -- has a pattern of injuries. One is
23 damage to the eye. One is a subdural haemorrhage, which
24 is a bleed over the surface of the brain. The brain
25 swells.
52
1 If your brain swells to a certain extent, the blood
2 can't circulate through the brain. So the axons, which
3 are the tubes in the main functioning areas of the
4 brain, because the blood does not get through, they lose
5 their blood supply and it is because of the loss of
6 blood supply, rather than a stretching injury, that they
7 get diffuse axonal injury. It is a different type of
8 diffuse axonal injury.
9 Q. So the degree of violence in shaking a baby to death is
10 not sufficient to cause the sort of diffuse axonal
11 injury that we have here?
12 A. I think you have to be very careful in comparing
13 a baby's brain to an adult's brain. They will react
14 differently. They have different structures involved.
15 They have different neck muscles. I would be very
16 cautious about comparing the two.
17 Q. Thank you. If that's not a helpful comparison, it is
18 good to know that. Thank you.
19 Moving then to the application of violence to
20 somebody with the result that they have the sort of
21 diffuse axonal injury that we are talking about here,
22 can you help us with what's known about the degree of
23 violence and the extent of it, duration?
24 A. Yes. What is known -- there is a very helpful paper by
25 Jenny Geddes -- that might actually be the paper I am
53
1 referring to here -- that has rehearsed different
2 scenarios in which people have traumatic diffuse axonal
3 injury.
4 There is no doubt you get it in car crashes. There
5 is no doubt you get it in falls from a height. It is
6 debated as to whether or not you can get it, for
7 instance, from a single kick to the head.
8 It is -- there is no doubt that it has been
9 described by Professor Graham in his large series in
10 cases of assault, but like a lot of these cases of
11 assault pre-CCTV, the witness evidence is not
12 necessarily taken as fact. So while they are caused by
13 assault, the exact mechanism is not known.
14 One of the theories is that it could be caused by
15 an accelerated fall; for instance, a punch to the
16 unprotected head with an accelerated motion to the
17 ground. It is one of the theories.
18 Boxers don't get it, but maybe that's because they
19 have such strong musculature of the neck that they are
20 able to protect their head from punches. There is no
21 doubt it has been caused by assault from a standing
22 position to a fall, but the precise mechanism is
23 slightly debated on that.
24 Q. So you say there is a debate about whether a single kick
25 can do it. Does that mean there are two views about
54
1 this or there is simply no comment?
2 A. In Dr Geddes' paper, she suggests that the physical
3 mechanisms, as far as I remember, aren't enough with
4 a kick, but other neuropathologists have described cases
5 where they think it has been caused by a kick or kicks
6 to the head.
7 Q. So more than one kick?
8 A. Again, it would have been helpful, I suppose, if I had
9 known -- I mean, my report is 46 paragraphs long -- to
10 know on what specific aspect of the evidence you were
11 going to rehearse and I could have brought the papers
12 with me to be absolutely clear about that, but it is
13 debated whether kick or kicks to the head can cause --
14 Q. Doctor, this is not a viva. We are grateful for any
15 help you give us. Please don't think I am being
16 critical if I push the boundaries of what you know.
17 A. Well, I can conclude it is debated that a kick to the
18 head can cause this type of injury.
19 Q. Can you help us about whether somebody being struck by
20 a flying bottle could, as a result of that, have the
21 type of injury that you are finding here?
22 A. I would be very surprised if the patient remained
23 standing, that that kind of force could cause
24 a traumatic axonal injury that could kill a patient. If
25 the person fell to the ground following that, it is
55
1 possible.
2 Q. What I think might help the Panel is to get some concept
3 of the degree of violence that the literature tells us
4 is necessary to produce this. So if somebody were lying
5 on the ground and they were kicked, would it have to be
6 a kick like kicking a rugby ball, for example?
7 A. You are asking questions and it is my duty to this trial
8 to let you know that this is controversial and not
9 everybody accepts each of the theories.
10 It is thought that a simple fall to the ground and
11 banging your head will not cause enough axonal damage to
12 cause you to die. So it would have to be a force
13 greater than a simple fall and hitting your head on the
14 ground.
15 Q. You told us that sometimes falling downstairs is
16 associated with this.
17 A. Yes.
18 Q. A simple trip and fall?
19 A. A simple drunk fall, Friday night, on the stairs is
20 a common cause of this.
21 THE CHAIRMAN: Is that just a fall and one bang or a bump,
22 bump, bump as the person goes down the stairs?
23 A. I mean, that will be an accelerated motion towards the
24 ground. In Belfast in particular, in certain areas of
25 Belfast you have very steep staircases and you have
56
1 tiled floors. So you have an accelerated motion with no
2 protection down the stairwell and nothing to stop you
3 from hitting the ground, especially if you are drunk, at
4 the end, and an acceleration/deceleration movement.
5 MR UNDERWOOD: So the sort of speed --
6 A. It doesn't have to be from the top of the stairs either.
7 Q. Thank you.
8 I want to ask you now about the location in the
9 brain of areas of diffuse axonal injury and the degree
10 of violence.
11 We looked, when we saw your report, at the way you
12 had taken sections from different parts of the brain.
13 You told me that I shouldn't draw conclusions from any
14 one part of those, but does the location of diffuse
15 axonal injury in a particular part of the brain give you
16 any indication of how the injury was caused?
17 A. It does, I think. David Graham, Professor Graham, who
18 is the leader in all this research, had a series of
19 cases -- I think, from memory, about 118 -- that he
20 examined in Glasgow. He was able to say how likely
21 possibly you were to die or live, depending on the grade
22 of the axonal damage and its location in the brain, and
23 other factors.
24 In this particular case I thought the axonal damage
25 was in many areas of the brain, particularly in areas --
57
1 and we come back to the quote that's in paragraph 21 --
2 the brainstem and very low in the brainstem, and if you
3 go by that quote, only the severest
4 acceleration/deceleration forces caused diffuse axonal
5 injury extending down to the brainstem and the axonal
6 injury did extend down into the brainstem in this case.
7 Q. The fact it goes that deep is an indicator of how far
8 the assault or insult was?
9 A. How severe the injury, yes, yes.
10 Q. Can I take you to -- in fact, don't worry. I will leave
11 you there for the moment on that page.
12 Can I ask you about Neuroleptic Malignant Syndrome?
13 Would it be fair to summarise what you have said in your
14 statement that you don't rule anything out definitively
15 in terms of NMS, but you think it is highly unlikely
16 here to be a mechanism?
17 A. Neuroleptic Malignant Syndrome is a rare condition that
18 has only been recognised to any great extent in the last
19 20 or 30 years. It is a condition that occurs as
20 an idiosyncratic and unexpected reaction to certain
21 types of medication.
22 Now, in 1997, there were very few cases reported in
23 the literature as to the pathology of this. Since 1997,
24 there have been loads of papers written about it. It is
25 a condition that is manifested by the patient developing
58
1 a very high temperature and a thing called autonomic
2 instability, where your heart rate will change and you
3 may sweat a lot. Those were two of the features present
4 in Mr Hamill that were part of that syndrome. So we
5 considered whether or not we thought Neuroleptic
6 Malignant Syndrome was present and Professor Crane and
7 I debated this at length.
8 I think to put it into context -- and it has
9 possibly been suggested in the subsequent reports that
10 maybe we did not think about it -- there was another
11 patient in the Royal in the same year, and I don't want
12 to give a name for confidentiality reasons, whom I did
13 diagnose Neuroleptic Malignant Syndrome in. So it is
14 something I am very aware of.
15 I treated a patient previous to this case, as
16 a junior doctor, who developed Neuroleptic Malignant
17 Syndrome and died. I had written a series -- and
18 presented a series of cases in a paper to the British
19 Neuropathological Society describing the pathology of
20 Neuroleptic Malignant Syndrome. At that stage, that was
21 the largest series I think in world literature. So we
22 were very aware of this diagnosis and we considered it.
23 The reasons that I didn't think this syndrome was
24 present -- the main reason was I felt that the brain
25 pathology in itself was to explain everything that had
59
1 happened.
2 There is no controversy, I think, between all the
3 expert witnesses that this patient had a traumatic brain
4 injury. Everything is accepted. The grading of it is
5 debated by one of the authors, and two of them suggest
6 the possibility of Neuroleptic Malignant Syndrome as
7 being what has caused his death at the end.
8 I felt that the -- medics always like to look for
9 one diagnosis rather than two. I felt there was enough
10 pathology in the brain to explain everything that
11 happened to Mr Hamill.
12 The other reasons why I didn't think there was
13 enough to make the diagnosis of Neuroleptic Malignant
14 Syndrome was he lacked a lot of features I had seen in
15 my case series.
16 One of the particular features of Neuroleptic
17 Malignant Syndrome clinically is an almost inability to
18 bend the patient's arms and legs. You know what the
19 signs of meningitis are besides the rash; you get
20 a stiffening of the arms. The patient I had looked
21 after, as a junior doctor, was so stiff you could not
22 actually -- they call it lead pipe rigidity. I am not
23 aware that that was present in Mr Hamill's case. The
24 temperature can be explained by damage to the
25 hypothalamus.
60
1 Dr Lawler suggests we did not know about the
2 creatinine kinase result until after the post mortem.
3 That would not have swayed me either way. Creatinine
4 kinase is an enzyme that is present in muscle.
5 In the cases I had written up of NMS, the enzyme
6 level in the blood was in the order of 50,000 to 60,000.
7 In the case of Mr Hamill, it was about 900, 970,
8 something like that.
9 There are numerous papers that describe the causes
10 of creatinine kinase and one of those is assault or
11 injections in the hospital. So everything could be
12 explained by his brain injury and his management in the
13 hospital environment to explain all the symptoms that
14 others think may be Neuroleptic Malignant Syndrome.
15 But this is a rare disease. There may be a spectrum
16 we don't know about. For that reason, I don't like to
17 absolutely exclude it being part of the diagnosis.
18 Q. That's helpful. Thank you. Can I just ask you one
19 thing arising out of that? You say that the axonal
20 damage is sufficient to explain the death. Can you help
21 us with how it explains the sudden deterioration?
22 A. No. I think that is still a difficult issue in this
23 case. There are various ways that I can suggest, but
24 I don't think I could be conclusive.
25 Also, you must remember what the role of
61
1 a neuropathologist is in the overall context of the
2 case. We look at a very specific aspect of the
3 pathology. We look at the brain pathology. The
4 forensic pathologist collects all the data, all the
5 toxicology, all the reports from the whole system and
6 puts it together.
7 For instance, if Professor Crane had found
8 a pneumonia, that would have explained the death, but --
9 Q. So, as it were, outside your realm?
10 A. Yes, but in the context of the brain pathology, diffuse
11 axonal injury is not a static process. It is a dynamic
12 process. As I mentioned to you at the start, the axons
13 are not broken at the start, but, because of secondary
14 chemical actions, they break.
15 Now, most people with a severe diffuse axonal injury
16 die because they get pneumonia, because they are
17 unconscious in hospital. In this case it is possible,
18 but only possible, that the ongoing dynamic process of
19 the axonal injury could have caused, for instance,
20 a cardiac arrest, an arrhythmia, a respiratory arrest,
21 but that's not definite.
22 Q. So the actual instant, as it were, cause of death is
23 unknown. Is that right?
24 A. I think that's -- according to my reading of
25 Professor Crane and the other evidence in this case,
62
1 yes.
2 Q. Can I ask you about one other possibility which has been
3 suggested, which is hypoxia? You deal with this in
4 paragraph 34 of your statement to us, which we find at
5 page [80447]. If I could highlight paragraph 34,
6 please. You are here dealing with something that
7 Dr Reid has concluded about hypoxia. In the second
8 sentence you say:
9 "I agree that there was perhaps hypoxic/ischaemic
10 change on or around the time of death and that this did
11 not have an effect earlier on."
12 You go on to deal with Dr Reid giving a statistical
13 statement that hypoxia contributed to worsening the
14 initial brain injury by less than one third:
15 "I do not know of any literature or any mechanism
16 that would allow me to make a statement like that.
17 There was some terminal neuronal damage that could have
18 multi-factorial causes: it could have been
19 seizure related or hypoxic/ischaemic related. To be
20 clear, for the reasons I have already stated, my view is
21 that the hypoxia/ischaemia was not related to
22 Mr Hamill's initial condition."
23 Can I tease that out a bit? We have been told that
24 the oxygen saturation of Mr Hamill when he arrived at
25 Craigavon Hospital was 70%. Can you comment on what
63
1 that tells us?
2 A. I can't comment on that statistic because it is not
3 something I deal with on a day-to-day basis, but I will
4 try to clear this issue to the understanding of
5 everybody.
6 Hypoxia means there is not enough oxygen in your
7 blood. If you were allowed to do experiments where you
8 could put a patient on a ventilator and keep their heart
9 going and remove their oxygen, they wouldn't come to any
10 significant damage. There has to be a loss of blood
11 flow as well. The hypoxia per se does not do long-term
12 damage. That's when I have put "the hypoxic/ischaemic
13 change". Ischaemic change is lack of blood flow. So it
14 is the combination of those things you would typically
15 get after a cardiac arrest.
16 The brain reacts in a stereotypic way to
17 hypoxic/ischaemic damage. It causes a particular change
18 that we see under the microscope to the nerve cells.
19 There was a change to the nerve cells that probably
20 happened in the day or so before his death that could
21 have a number of causes, but what we needed to address
22 was the cause of this man, Mr Hamill's, initial
23 presentation.
24 The pattern of injury to the brain showed that there
25 was no hypoxic/ischaemic damage that would have occurred
64
1 at the time of admission to hospital and that was not
2 the cause of his unconsciousness and that was not the
3 cause of his axonal damage. If it had been, then the
4 brain would have an 11-day reaction to that, and it
5 didn't.
6 Q. That's quite clear, is it?
7 A. I think it is accepted by all the authors, yes.
8 Q. Thank you. One final area I need to ask you about is
9 the sequence of events by which the eventual post mortem
10 report was produced about six months after the death
11 here. Can I attempt to establish with you the
12 chronology?
13 We know in this case that the brain was fixed in
14 formaldehyde. In due course, sections were taken. You
15 looked at those sections. You gave your report, as we
16 have seen, to Professor Crane and he produced his
17 report. He couldn't help us with the dates when the
18 brain went for fixing and came out of fixing.
19 You help us at page [80437], the third bullet point
20 on the page, if I can highlight that paragraph:
21 "The small pieces of tissue began processing in my
22 laboratory on 25/7/97 and were initially
23 available for me on 6/8/97."
24 Now, do you know why it took until 25th July 1997
25 for you to get the small pieces of tissue in your
65
1 laboratory?
2 A. That wouldn't be unusual. As I said in
3 a paragraph before that, it takes a certain amount of
4 time for the brain to fix in the formalin.
5 If you examine it, especially if there has been
6 brain swelling, the formalin does not penetrate into the
7 centre of the brain. If you examine it too fast or too
8 early, you will get erroneous results. Quite often we
9 wait for three months before we examine a brain. In
10 this case, I think -- was it -- I am not sure how long
11 it was.
12 Q. It is about two and a half months.
13 A. That wouldn't be unusual. You have to also remember
14 a number of other things here. For continuity of
15 evidence, the various people involved had to be there
16 and that's something we are very strict about in
17 Belfast. You also have to remember that this is fitted
18 into an NHS job. I am employed by the Royal Victoria
19 Hospital to be an NHS consultant, not to be -- I don't
20 work for the NIO or the State pathologist. So there are
21 a number of factors, but the main factor is you can't
22 examine these things too quickly, otherwise you will get
23 a bad result.
24 Q. So it would be perfectly ordinary, for good scientific
25 reasons then, to wait two to three months after --
66
1 A. Oh, completely.
2 Q. Thank you. We have you then looking at it on
3 6th August 1997, which you may recall is the day before
4 the first date we see on your report. So, is that
5 likely to have a relationship with that date,
6 7th August?
7 A. Sorry. Can you ask that question again?
8 Q. Sorry. You say there that the small pieces of tissue
9 were initially available for you on 6th August. We see
10 the first typed date on your report of 7th August.
11 Is there any reason, do you think, that that date
12 would have arisen there?
13 A. I can't see 7th August on the screen.
14 Q. We can find it again by all means. It is [31396].
15 That's the first typed date on your report?
16 A. Yes. What I think happened was we examined the date
17 and, the next day, the initial sections became available
18 for me to look at and they were looked at the next day.
19 Q. Thank you. Then going back, if I may, to [80437], the
20 final two bullet points on the page, you say:
21 "When asked as an expert for a report, the expert
22 must be allowed to access the relevant medical
23 literature; otherwise the report may be deficient.
24 "At the time of reporting this case there was
25 a dearth of literature on Neuroleptic Malignant Syndrome
67
1 and a burgeoning literature on diffuse axonal injury."
2 Is this a case where you had to do research?
3 A. Oh, completely, yes. This was one of the most -- and
4 I think subsequently it has been shown to be a very
5 difficult case, otherwise we would not be here --
6 I might not be here today.
7 The two conditions that were considered here,
8 diffuse axonal injury, traumatic diffuse axonal injury
9 and Neuroleptic Malignant Syndrome are extremely
10 controversial, because a lot of -- well, the first one
11 is very controversial because a lot of trials depend on
12 its interpretation. The literature was expanding on it
13 at that time.
14 Neuroleptic Malignant Syndrome was such a rare
15 condition and, because it was considered a possible
16 diagnosis in this case, a consultant or an expert would
17 be considered deficient in his report if he did not read
18 all the available information on these conditions.
19 So it takes time to get hold of these papers. It is
20 not like now where you can flick the Internet and read
21 everything. Quite often you would have to send to the
22 British Library or get it off your friends in Glasgow or
23 whatever. It takes a long time to get these things
24 together to give an accurate report.
25 Q. If we go over the page to [80438], the second bullet
68
1 point, you tell us:
2 "Despite all of these factors", you have just
3 described, "my report was ready about 3 months after the
4 brain dissection, which is in very good time considering
5 the points discussed above. My report was typed on
6 29/10/97 and I can think of no mechanism by
7 which a proper report could have been safely prepared
8 any quicker."
9 You just told us there is a large distinction to be
10 drawn between the accessibility of the learning, as it
11 were, pre-Internet in 1997 and the accessibility of the
12 learning now.
13 If the conditions for this report were replicated
14 now and you were able to use Internet technology, would
15 the report be quicker?
16 A. No, I don't think so. This is only a small selection of
17 what goes on in the background. You may get the
18 impression that all I do is report one case and it is
19 sitting on my desk for three months. I think we have
20 70 cases referred to us from the NIO this year. All the
21 non-stabbing, non-shooting homicides in Northern Ireland
22 are looked at by two neuropathologists. We also have
23 full-time jobs for the Health Service. We do this as
24 an extra and it is fitted into our time. We try to be
25 as quick about these cases as possible, but that's only
69
1 one factor.
2 The other factor is there is an awful lot of coming
3 and going with a case in its preparation. As I say, the
4 slides first arrived with me. Then they went for more
5 work. Then they come back. Then they went for more
6 work. Then you consider something else. You talk to --
7 you are a surgeon and you talk to the State pathologist.
8 This is a very dynamic process.
9 Unless you are sure you have everything you need,
10 whether it be the literature, whether it be the extra
11 sections, and the special stains and things, we do take
12 three or four weeks at a time. Then you get them back.
13 Then you decide you need more. So if I were doing this
14 again, I don't know it would happen any faster.
15 Q. Thank you. If we go to page [80436], there is a bullet
16 point three from the bottom where you say:
17 "In this current year I will be asked for advice on
18 approximately 70 forensic cases from Northern Ireland."
19 As you have just told us:
20 "The majority of these cases involve complex
21 neurological disorders, suspicious deaths or murders."
22 You go on later to say that most cases take at least
23 ten hours to finish and that one took about 55 hours,
24 never mind the court time.
25 That's the system, is it, by which all
70
1 neuropathological reports are produced in
2 Northern Ireland; that it relies on your good offices,
3 your goodwill?
4 A. There are two of us.
5 Q. Between you to do 550 hours -- 700 hours?
6 A. This would be an exception, that it would take 55 hours.
7 That was a case in London that I had timed. So that was
8 the statistics I had on a time sheet. That was
9 a complex murder case. Most cases will take a couple of
10 days per case.
11 Q. If you take the average that you have given us there of
12 at least ten hours to finish times 70 case, that is
13 700 hours a year, between two of you, on top of your
14 cases?
15 A. No, each.
16 Q. Voluntarily, without a contract?
17 A. No funding or pay.
18 Q. That's still the situation with no proposals for change,
19 is it?
20 A. Well, it is still the situation. There are so few --
21 I think -- I am asked about once a week -- I get a phone
22 call or e-mail, "Please, could you help us to prepare
23 a defence report for such and such a person in
24 Huddersfield, in Birmingham, in London?", because there
25 are no forensic neuropathologists who can do it. There
71
1 are about half a dozen in the whole of the
2 United Kingdom who have the expertise to do this.
3 It is something that we are particularly interested
4 in and we have trained to do over the last 20 years, but
5 it is because there are so few that that is the system.
6 As far as I know, all bar one works for the NHS.
7 Q. So it all does it for nothing?
8 A. I don't know. I am sure they don't in England.
9 THE CHAIRMAN: How many are there in Northern Ireland?
10 A. Two.
11 THE CHAIRMAN: Just two.
12 A. I suspect if we decided not to do this, I don't think --
13 I can't imagine that the State pathologist's department
14 would get their work done, because if they were to send
15 it to Scotland, that would take a lot of time and be
16 extremely expensive.
17 MR UNDERWOOD: Doctor, thank you very much. It may be that
18 others have questions they either wish to put themselves
19 or through me. That's a matter for the Chairman.
20 Perhaps you would wait there for the moment, please.
21 MR ADAIR: I would like to ask about two brief matters, sir,
22 if I may, please.
23 THE CHAIRMAN: Yes.
24 Cross-examination by MR ADAIR
25 MR ADAIR: In relation to the last point you were being
72
1 asked about, about the availability of
2 neuropathologists, from your own knowledge, does the
3 same position pertain in the rest of the UK in relation
4 to the availability and time that it takes to prepare
5 reports?
6 A. I can't answer that, but -- I can't answer that too
7 accurately, because I don't know, but the way things
8 work in England is the forensic pathologists are like
9 barristers and they have sets and they work
10 independently.
11 In Northern Ireland they work for the NIO through
12 Queen's, as far as I know. So, for instance, there is
13 a death in Birmingham, a murder in Birmingham. The
14 forensic pathologist or -- I think they are called
15 something else over there; Home Office pathologists
16 maybe -- will do the PM. He will get the police to
17 organise the neuropathology report and distribute the
18 tissues and pay for it.
19 Three months is an average turn-around time that we
20 would expect to do an examination in, but with more
21 complex cases it is going to be longer.
22 Q. If I might say so, Dr Herron, I am not suggesting -- it
23 is a matter for the Panel ultimately -- that you and
24 your colleague don't do everything that you possibly can
25 within a reasonable time, but it might help the Panel --
73
1 have you any suggestions as to how the system might be
2 improved?
3 A. You may want to train a forensic neuropathologist, set
4 up a lab and provide the millions of pounds that would
5 do that. I can't think of any other way.
6 Q. Okay.
7 THE CHAIRMAN: Do you get many cases coming from the
8 mainland because they can't find the people there?
9 A. I get asked about once a week.
10 THE CHAIRMAN: From the mainland?
11 A. Yes. About once a week, at the minute, I get an e-mail.
12 THE CHAIRMAN: To what extent do you think that is dependent
13 or caused by the shortage of people in England or
14 Scotland or Wales, or on your own particular reputation?
15 That's rather an embarrassing question.
16 A. I suspect it is not my reputation; it is my
17 availability. On a website or something they find my
18 name from somewhere. People train as doctors, then
19 as -- well, I trained strictly -- all my training is
20 through neurosurgery, neurology, neuroscience and
21 through neuropathology, that way.
22 You may have one or two in each major town or city.
23 So there may be 30 or 40 in the whole of the United
24 Kingdom. Most of them will have other interests. It
25 might be -- most of my work, my NHS work, is diagnosing
74
1 and managing the patients in Northern Ireland with brain
2 tumours. That's the day-to-day work of
3 a neuropathologist, or muscle disease, children with
4 muscular dystrophy. That's what we do.
5 I have developed an interest, because of our links
6 with the State pathologist department, in forensic
7 neuropathology, and there is only maybe a quarter of the
8 neuropathologists -- I can't give you an accurate
9 number -- of those 30 or 40, who have the expertise and
10 the interest.
11 So when there is a murder in England -- ten years
12 ago, the court would have accepted the word of the
13 forensic pathologist, but now the court is allowed to
14 ask for other experts to give opinions, and I am often
15 asked by the defence to provide a report for their
16 clients in London or elsewhere in England.
17 I think it is because there are so few people that
18 they come to me, not because of my reputation.
19 MR ADAIR: I wonder if I might ask just one matter in
20 relation to the diffuse axonal injury?
21 You had said there was no doubt from the literature,
22 and, I think, from your own experience, that it has been
23 caused by an assault from a standing position to a fall,
24 but the precise mechanism is slightly debated.
25 A. It is debated, yes.
75
1 Q. I think you said about that scenario that the precise
2 mechanism is slightly debated.
3 You also said there was a debate as to whether
4 a kick or kicks can cause the diffuse axonal injury.
5 A. That's correct.
6 Q. Now, I am not trying to pick out words -- and correct me
7 if I have misinterpreted this -- but does that mean that
8 it is more likely to be caused by a blow and accelerated
9 fall than by a kick or kicks?
10 A. I can't answer that accurately. I can't answer which is
11 more likely, because the mechanism isn't known for sure.
12 Q. So the debate goes on in relation to both mechanisms?
13 A. Yes.
14 Q. Does the literature or your own experience determine
15 that one mechanism or another is more likely?
16 A. Because it is not known for sure, that question can't be
17 answered, in my opinion.
18 MR ADAIR: Okay. Thank you.
19 Cross-examination by MR MCGRORY
20 MR McGRORY: I have two quite discrete questions, Dr Herron.
21 If, in a scenario where the victim in an assault
22 falls unconscious very quickly, either because of a fall
23 following a punch and a knock on the head in the course
24 of that, or because of a kick, there are subsequent
25 kicks to the head, would the fact that the victim is
76
1 already unconscious render the onset of diffuse axonal
2 injury more likely?
3 A. It really depends on the state of the victim. Because
4 boxers don't get this injury, it may be because they are
5 prepared and their neck muscles -- now, this is slightly
6 controversial as well -- are tight. So they don't have
7 the amount of acceleration or deceleration.
8 I suppose if there was an unprotected neck rather
9 than a neck with lots of muscle spasm and tightness,
10 that would make the accelerations following a kick more
11 severe. That's just from simple physics, not from any
12 neuropathological knowledge. If you are not able to
13 protect the movement of the head, and if you are
14 unconscious, obviously you wouldn't be able to protect
15 it.
16 Q. Are you aware in this case that there was little sign of
17 any defensive injuries on the victim?
18 A. I wouldn't have got too concerned with the external
19 injuries in this particular case, so I don't know that
20 I would have known that at the time.
21 Q. I have one further question for you, Dr Herron, and that
22 is, if a victim like this on the ground was kicked by
23 someone who was highly trained in a martial art which
24 concentrates on the art of attack by kicking, would you
25 agree that it would be more likely to cause more serious
77
1 injury?
2 A. Because it is too controversial as to whether or not --
3 the mechanism -- I will give you a background to the
4 physics of it.
5 It is the rotation of the head that causes the
6 damage, and the movement of the brain within the skull.
7 The brain is not tightly fixed to the skull. So when,
8 for instance, a motorbike hits a wall, the helmet and
9 head stop and the brain moves and that stretches the
10 axons. So the greater the degree of acceleration and
11 the particular type of acceleration, which way the head
12 moves, makes it more likely that the axonal damage will
13 occur.
14 So by simple physics, the greater the acceleration
15 or deceleration, the greater the likelihood of the axons
16 being stretched, and I think that's the best I can do to
17 answer your question.
18 If you are suggesting that a particular impact
19 causes a greater acceleration, then I could say it is
20 more likely to cause damage than a lesser acceleration.
21 MR McGRORY: Thank you, doctor.
22 MS DINSMORE: I have no questions, Mr Chairman.
23 MR UNDERWOOD: Nothing arising from me, sir.
24 Questions from THE CHAIRMAN
25 THE CHAIRMAN: It seems, from what you have told us, that it
78
1 is not easy to draw an equation between the amount of
2 axonal damage with the vigour of the attack upon the
3 head.
4 A. I think that's right, yes.
5 THE CHAIRMAN: The other thing --
6 A. Well, no. Let me, because -- I did draw a comparison
7 between the degree of acceleration and the degree of
8 axonal damage. Vigour of an attack is something that --
9 I am not too sure about what exactly each of those words
10 means, because there could be different parts of
11 an attack.
12 THE CHAIRMAN: Yes. The same blow struck in a different way
13 to a different part of the head may cause varying
14 degrees of acceleration?
15 A. Yes, that's right.
16 THE CHAIRMAN: So to that extent, it is not easy to draw
17 an equation between the amount of axonal damage and what
18 had to have caused it?
19 A. The acceleration isn't the only factor and there are
20 other factors involved. Yes, that's right.
21 THE CHAIRMAN: Thank you. Just on a different matter, it
22 may be almost impossible to answer this, but I don't
23 know if you can help us. To what extent does the
24 shortage of doctors with your discipline cause delay in
25 criminal investigations?
79
1 A. I can't answer that. We report things as best and as
2 fast and as accurately as we can. We could report
3 things faster, but I don't think they would be as
4 accurate.
5 If there were more neuropathologists -- it is not
6 just the doctors, the infrastructure. Very much of what
7 we do is dependent on a whole system behind us,
8 including senior scientists in a laboratory, secretarial
9 staff, a building to house us. So just getting more
10 neuropathologists will not necessarily speed things up.
11 Q. You have to have the back-up as well?
12 A. You have to have all the infrastructure.
13 Q. Do you find you either can't take on a case or you will
14 take it on, but it has to wait because you are dealing
15 with other matters?
16 A. We have a lot of things happening in our jobs, and if
17 I didn't work for the Health Service, I suppose, and had
18 a laboratory dedicated to my neuropathology service,
19 I think things might happen faster, yes.
20 THE CHAIRMAN: Thank you very much.
21 Questions from REV. BARONESS KATHLEEN RICHARDSON
22 REV. BARONESS KATHLEEN RICHARDSON: May I ask a question
23 that might sound rather silly?
24 Is the damage to the brain caused more by its own
25 skull than by anything outside hitting it? It is the
80
1 impact that moves it rather than the force of the blow?
2 A. I can answer that question in a slightly different way.
3 In belted, front-seat passengers or drivers, you do not
4 necessarily have an impact to the skull. If you
5 decelerate your car, if your car crashes and you are
6 belted, you still get this injury. So there doesn't
7 have to be an impact to the skull. It is the movement
8 of the skull -- of the brain inside the skull and its
9 acceleration and deceleration relevant to a static
10 state.
11 REV. BARONESS KATHLEEN RICHARDSON: Thank you.
12 MR UNDERWOOD: I think that concludes the doctor's evidence.
13 THE CHAIRMAN: Thank you. Thank you very much.
14 MR UNDERWOOD: Thank you, Doctor.
15 (The witness withdrew)
16 MR UNDERWOOD: That concludes the evidence for today.
17 Again, I apologise for running out of witnesses. We do,
18 I know, have the familiarisation exercise this evening.
19 I know that legal representatives will be keen to know
20 the details of the mechanics of that. I will deal with
21 that with the Inquiry staff in due course, if I may, but
22 so far as the public side of the Inquiry goes, I have
23 nothing else to offer you today, I am afraid.
24 THE CHAIRMAN: We can do with an eclipse of the sun to bring
25 on the view sooner. Yes. Very well. About how long do
81
1 you think tomorrow's proceedings will last? Perhaps it
2 is easier now to get a view on that.
3 MR UNDERWOOD: It is much easier now. Assuming that I can
4 get both the nurses and Dr Lawler here in the morning,
5 I apprehend, with the speed and efficiency with which
6 everybody is working, it is possible we will finish by
7 1 o'clock.
8 THE CHAIRMAN: I see. Thank you very much.
9 10.30 tomorrow morning.
10 (12.50 pm)
11 (The hearing adjourned until 10.30 tomorrow morning)
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1 I N D E X
2
3
3 PROFESSOR JACK CRANE (sworn) ..................... 1
4 Examination by MR UNDERWOOD ............... 1
4 Cross-examination by MR ADAIR ............. 31
5 Questions from THE REV BARONESS KATHLEEN .. 37
5 RICHARDSON
6 Cross-examination by MR MCGRORY ........... 37
6 Cross-examination by MS DINSMORE .......... 38
7 Questions from THE CHAIRMAN ............... 39
7
8 DR BRIAN HERRON (sworn) .......................... 40
8 Examination by MR UNDERWOOD ............... 41
9 Cross-examination by MR ADAIR ............. 71
9 Cross-examination by MR MCGRORY ........... 75
10 Questions from THE CHAIRMAN ............... 77
10 Questions from REV. BARONESS KATHLEEN ..... 79
11 RICHARDSON
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Robert Hamill Inquiry

Witness Timetable

Transcripts

Transcript

Hearing: 15th January 2009, day 3