The Naked Chiropractor
Insider's Guide
to Combating Quackery
and Winning the War
Against Pain

Dr. Preston H. Long

Dr. Preston H. Long is THE expert. Consumers trust Andrew Weil for reliable information about alternative medicine, Dr. Bernie Siegel for inspiring words about mind-body connection, and Dr. Dean Ornish, for practical ways to keep their hearts healthy, but who the recognized authority on back care and the limits of chiropractic medicine?

Amani Oakley's closing in the Lana Dale Lewis Inquest

THE CORONER: Ms Oakley, it's 12 o'clock. It's earlier than what we would normally take our lunch recess. I will, however, provide the option to you to either start now and we would take our lunch recess starting around 12:45 to one o'clock or we can take our lunch recess now and you may make your final submissions following lunch.

MS OAKLEY: Thank you sir. I think I'd like to start now if that's okay.

I can tell you as I turn to you now what kind of a relief it is to actually look you full in the face. All this time we've been sort of looking at each other from the side so it is, I think as all the lawyers have said, this is a moment where we get to actually look at each other for the first time through this entire inquest.

Everyone else has thanked you. I need to say beyond thanking you, the family looks to you, the jurors as a source of its hope that many of the concerns that have been raised throughout to be dealt with. I also want to take a minute to thank Dr. McLellan because it has been an extraordinary inquest and his patience has been very appreciated.

I have to say, I am going to apologize up front. I have a lot to say and I have exactly the same amount of time to say it as each of the other parties so I'm going to have to whip through things and I hope that with all of the knowledge that you have that it won't be too much of a problem.

My position here is that if you go back to the beginning and I know this has been so very long so I think part of the problem here is going back to the very beginning, you'll see that the other side's strategy, the strategy of the chiropractors throughout this inquest has been to throw whatever they can at the wall and see what sticks. There's been a lot of theories that have been thrown out at that wall and have fallen by the wayside. We've heard about the heart. We've heard about haemoconcentration, overweight, high stress from alleged sexual assaults from childhood, her husband hitting her, hit by a car four months before, fell in the shower a year before. I know you remember all these things. We're not talking about most of them now but it indicates to you the procedure here was let's see what we can throw at this. Let's see what sticks.

When all is said and done these theories put forward by the other side have crumbled. No basis in fact. No evidence to support them. Most of them nothing more than fantasies of lawyers in many instances of what can only be described as a real stretch. And of course this willingness of the chiropractic lawyers who switch to different theories, just so long as it wasn't related to the chiropractic neck manipulation injury was also seen in their experts and I'm going to show you that as we go through this. Even Mr. Schneider and you remember Mr. Schneider was here for a good long part of this inquest, made note of this fact on one occasion. Here's what he said December 12th, 2002. He said, "The only comment I make, Mr. Coroner, is that I heard Dr. Rosso change his opinion on the witness stand."

I'm going to tell you also that the evidence that I'm going to give you and that the information I'm talking to you about, I have drawn so heavily on the actual transcripts because what you heard just now for example from Mr. Paliare, I will tell you a good percentage of that is completely in error. And I'm not going to tell you just what I think of the evidence. I'm going to tell you what people said. So that you know it's not my voice that's talking to you. It's the actual evidence. I've gone through these transcripts and I'm quoting.

Mr. Foster, after we heard something like that from Mr. Schneider talking about the changing of the evidence of Dr. Rosso, and you remember Dr. Rosso. Dr. Rosso actually got in the stand and abandoned entirely the report he had made. The report he had made said it was the heart. He got on the stand, all of a sudden it was atherosclerosis. Not a word anywhere ladies and gentlemen for me to prepare, nothing. He walked into the stand, changed his entire testimony and then ­ and then he says "Well I didn't know that I needed to write another report." I mean really, I don't think you need to be an experienced expert witness to kind of figure out that when you're getting into the witness box and you already have been asked to write a report ahead of time and you've now completely changed your mind on that report, that maybe a second report is in order.

And it is kind of laughable to hear from Mr. Foster in his submissions on Monday that it was Dr. Deck who changed his theory. Oh my goodness, I have to say that's totally ironic. Dr. Deck wrote his report, in his report of December, 2001, Exhibit 17 in these proceedings. He examined all the slides. He determined, he still reaches the same conclusion as he and Dr. Pollanen originally reached, that Ms Lewis' death was caused trauma. Page seven of that report, it gives a list of 12 points setting out a number of findings that point him to the findings of trauma as the cause of death. On the stand this man innocently says, oh goodness, he says, "I've decided that of the 12 points I've given you, instead of number three being the most compelling to me to support the finding of trauma, I've decided that it's number one."

Well did we get applause from the chiropractic lawyers? Did they stand up and say this is in the highest tradition of science? That Dr. Deck upon reflection decided that the list he'd already given us, he's going to point to number one instead of number three as his most compelling. No, that was seen as a terrible occurrence, Dr. Deck changing his testimony. Where's the testimony changed? I just know in this instance your commonsense is going to prevail. Just imagine for a minute an argument you're having with your spouse. You're saying to your spouse, "I'm really angry with you. I think you show a lack of consideration and why? Because number one you went out last night and you stayed out late. Number two, you didn't phone me and tell me you were staying out late, and number three it was our anniversary yesterday." And then as you're arguing you decide that it isn't the most compelling evidence of this lack of consideration that he didn't phone you. It's that it was your anniversary last night. You changed you argument because you've now decided that the thing that you're really, really angry about is that he didn't call you as opposed to it being your anniversary? No, of course not.

On the other hand you get Dr. Pollanen, throwing his entire theory out the window and putting in a brand new one, and really with no self-respect whatsoever you have the other chiropractic experts wholesale abandoning their opinions as expressed in their reports and running after Dr. Pollanen's theory with such haste that they made serious, serious blunders that have never been made more clear that they had no idea. They didn't actually assess the evidence themselves. They were very busy supporting Dr. Pollanen. And I'm going to come back to that during the course of my submissions to you.

So all these theories thrown against the wall with the hope that something's going to stick. Of course once everyone's finished jumping ship and leaving behind all the rest of the sinking theories, the only two competing theories that are left, is that she died as a result of trauma to her neck from a chiropractic neck manipulation or did she die from atherosclerotic disease?

So okay, Mr. Oakley and I on behalf of the Lewis family, we knew the job that we had to do in this case. We knew the case we had to meet as we say in legal circles. We knew that in order to be able to succeed in convincing you, the jury, that our experts were correct that Lana Dale Lewis died as a result of stroke from trauma as opposed to any of those other theories, we needed to show you that the competing theories didn't make sense. For example, A, we needed to show you there was less than a 50 per cent chance that the heart was the source of clots. We needed to show you there was less than 50 per cent chance that the cause of the death was haemoconcentration. We needed to show you there was less than 50 per cent chance that her cause of death was from an alleged sexual incident that may have occurred more than 35 or 40 years before her death. We needed to show you there was less than a 50 per cent chance that the cause of death had anything to do with an alleged assault by her husband. We needed to show you that there was less than a 50 per cent chance that the cause of death was related to being slightly bumped by a car as she was crossing the street four months before her death. We needed to show you there was less than 50 per cent chance the cause of her death was related to a fall in the bathtub which occurred more than a year before. And finally, we needed to show you that Lana Dale Lewis did not suffer from stage six atherosclerosis.

So we set out to ask questions and put forward witnesses who could address these issues one by one and we addressed all of these theories thrown against the wall by the chiropractors' heart theory. In the end who is proposing the heart theory? Nobody. That's one that fell down.

Dr. Pollanen who was the first person to put forwards the possible heart theory, abandoned it entirely in his own testimony. He told Mr. Schneider that there was absolutely, sorry, I'm going to read this here. "It is highly unlikely that the clot originated in the heart and went into the posterior circulation."

You also heard evidence, there was suggestions that well, if there was nothing wrong with her heart why wasn't the whole heart transplanted? Why just the valves and the aortic arch? But you also heard evidence there's a reason for that and we didn't get much into it because honest to God we have so much already to cover here. But in order to transplant a whole heart, the heart must be beating at the time that it is harvested, and that wasn't the case in Lana Lewis' case. In any event, as I say to you, which of the experts is still clinging to the heart theory? Nobody.

Haemoconcentration was another ridiculous theory that held no water once examined. Frankly as well given the limitations placed the family's expert witnesses in supposedly testifying in areas that they were not qualified to testifying in it's amazing to recall the theory of haemoconcentration was put forward by Dr. Moulton and by the way, he's an orthopaedic surgeon. He is not, as you heard from Mr. Paliare, a neurologist. He has no expertise at haematology or conditions such as haemoconcentration since such conditions have nothing to do with what he did. Hopefully you recall what happened when Dr. Moulton was cross-examined by me on that theory. He admitted that (A), haemoconcentration was a condition whereby a person had too many cells in their bloodstream, those cells being white cells, red cells, and platelets. He also admitted, (B), Ms Lewis' cell counts were perfectly normal; (C), He admitted haemoglobin is not a cell but is a substance found within red cells and so an elevated haemoglobin level cannot form the basis for a theory that a person has haemoconcentration. He also admitted that, (D), he knew that people who smoked tended to have elevated haemoglobin levels.

Every other witness who has been examined on this theory has confirmed Ms Lewis did not have haemoconcentration. So there goes that theory.

As for the theory put forward by Mr. Danson that high stress levels from an alleged childhood sexual assault, I have to say this theory was nothing short of obscene. You'll notice that you heard no evidence, no evidence for this from any expert witness at all. The only evidence you heard about this was from Mr. Danson and you've heard the Coroner tell you repeatedly that us lawyers, we can't give you that evidence.

There is no question that a lawyer has a duty to his or her client to represent them the best way they can. But they also have a duty to the judicial system to not turn proceedings into a circus. By throwing in entirely unfounded theories that an alleged childhood assault had anything whatsoever to do with Lana Lewis' death at age 45, Mr. Danson deliberately and cruelly smeared the reputation of the Lewis family, not to mention violating the requirement of the legal system to not identifying victims of sexual assault unless they want to be identified.

In any case, I am certain that you will find that there was no basis laid for such an absurd theory. No experts adopted the theory and as a result the pain inflicted on the family was inflicted without any solid expert foundation and therefore for no good reason. Such a tactic by Mr. Danson could only have been directed at hurting as the family without any experts to back it, it had no chance of succeeding.

Pretty much the same kinds of things can be said about suggestions made by Mr. Danson and Mr. Foster that Jim Sweeney hit Lana Dale Lewis and this is what resulted in her death. Great theory but once again smear the reputation of the family. Only one small problem again. No evidence. Not only that, but look at the ridiculousness of the theory in the big picture. We saw the letters Jim Sweeney wrote to the Coroner's office asking that his wife's death be investigated. Mr. Foster and Mr. Danson suggested that Mr. Sweeney had a guilty conscience in adding in one of his letters that he was prepared to take a lie detector test. At first glance, it certainly appeared unusual to say that, but his explanation is that he thought all options were going to be examined by a circle of experts by the Coroner's office and he wanted to let them know he would cooperate every way he thought possible.

Mr. Danson, in his submissions, suggests that Jim Sweeney saying that he would take a lie detector is like a deer caught in the headlights, a confession of guilt. The only guilt Jim Sweeney had was being stupid enough to recommend that his wife attend a the chiropractor for treatment of migraine headaches.

Thinking about it for a minute, the Coroner's office had done absolutely nothing in terms of investigating Lana's death as far as Jim Sweeney knew. At the time that he wrote those letters, pushing the Coroner's office to investigate, the Coroner's office had not been in contact with him at all, or given him any information to suggest to him that an investigation was underway. So what you're being asked to believe here is in a situation where Jim Sweeney had guilt about his involvement in his wife's death allegedly, he is the one that pushed the Coroner's office to investigate? He is the one that called and wrote letters saying what's going on? Please investigate? Does that make sense?

What you're going to hear from me, is I'm going to tell you over and over again that whenever possible look for hard evidence that is not open to different interpretations by anyone. As far as I'm concerned if you're not convinced by what Mr. Sweeney said, that he didn't hit his wife, and that didn't cause her death, look at the hard evidence. It's easy. If Jim Sweeney hit her, the obvious thing to expect is there would be bruises on her body, both in her neck area and other places on her body if the two of them were involved in some kind of physical altercation. You heard evidence from various witnesses including Dr. Dhanani that if someone were to attend an emergency complaining about neck pain it would be an obvious that that an examining doctor would look to a neck to see if there was bruising and would definitely note it if there was. There's no bruising on her neck. It's not noted in the emerg records and it's not noted by the way in about five other places.

September the 1st, which is the day that she went to the hospital, on page 529, there are diagrams and you'll see them if you look at the records in your deliberations. There are little stick figures, or little silhouettes of a body and they are found routinely throughout the hospital record. What they say is skin, on the one side here and it's got boxes for intact, abrasion, laceration, bruising, lash, ulceration, redness, swelling, raise, removed and so on. And under skin on September the 1st when she entered in hospital it says "intact." The box for bruising is not ticked off. That's what you call hard evidence.

So we don't need to believe Jim Sweeney or not. Take a look at the hospital records and just in case there's a possibility that it was missed in emerg, take a look at the other pages where her condition for bruising is noted on September the 3rd. So that's second day in or third day she's in hospital. Page 539 of the record it shows there is a bruise, right loin from the angiogram. So there it is, it's actually X'd onto the little diagram I showed you on the right loin area, it says bruising.

September the 4th, again she's examined for bruising. Page 549 of the records, again the right groin bruise is shown. Then September 10th, when she comes back to hospital, page 540, I apologize, 450 again the bruise on the right loin is noted. Nothing else. And September the 10th again on another page 483 it says they checked for bruising, none found.

Then of course there is the actual autopsy record where the body was examined. The body was examined so thoroughly that you will see and the exhibit I believe is 16 that in the notes she has a bandage in the middle finger of one of her hands. So ladies and gentlemen if there was bruising you better believe it would have been picked up either in hospital in the many days she'd been examined or on autopsy, wouldn't it?

Don't forget she went to see Dr. Knapp in the interim between the hospital visits. She told Dr. Knapp in the past about altercations she'd had with her husband. Why wouldn't she now? Why if that were the cause of the problem wouldn't she have said to Dr. Knapp, "Jim did it again. He hit me." There you go. And Dr. Knapp in fact indicated he would have expected that. She was not the kind of woman who wouldn't have told him.

So how does any fair-minded lawyer continue putting this theory forward knowing the pain it's going to cause the family? Common decency ought to prevail when there's no evidence of any kind of supported theory that will be devastating to a man who still blames himself entirely for being the one who told his wife to see the chiropractor. Just another theory that the chiropractors threw against the wall hoping something would stick.

With this theory like the previous one though, I think there was a hope that not only might some of the theory stick to the wall and maybe muddy up the waters, but they were also hoping that negative feelings might be generated against the family. Chiropractic lawyers want to whisper to you, this man beats his wife. This woman's father sexually abused her as a child. Shocking. Whatever the chiropractor did couldn't have been that bad. And I want to remind you that Mr. Danson never did abandon this theory. As late as Dr. Whitwell, Mr. Danson suggested to her that there was abuse from the husband and so in terms of what we were talking about with Dr. Whitwell the only thing that Dr. Whitwell would have had any interest in is if that abuse was known to have occurred around the time of death. The other evidence, things like being bumped by a car and falling in a bathtub, well I think they were so unsupportable that they were abandoned without much of a fight.

So after leaving all these other theories pooling on the ground at the base of the wall with nothing sticking to that wall, we now come down to the theory of atherosclerosis having caused Ms Lewis' death. This is harder to dislodge off the wall but it is dislodged once you carefully look at the evidence that we've heard at this inquest.

As I take you through the evidence I'm going to ask you to keep in mind the timing of events at this inquest. I'll point out to you what I mean as we go through the evidence but for now I need you to keep in mind different theories emerge at different times.

We heard from a number of neuropathologists, pathologists and pathology witnesses who felt there was evidence of trauma in the slides they examined. The witnesses who thought they saw trauma in the slides they examined are, Dr. Pollanen originally, Dr. Deck, Dr. Whitwell, Dr. Fornasier, Dr. Richardson. The pathology witnesses who felt the slides did not show trauma, Dr. Pollanen, finally, Dr. Rhodes and Dr. Ramsay.

The pathologists and neuropathologists who felt that the cause of death was trauma, pointed to a number of things to support their position and I'm going to come back to the issue of trauma but I first want to deal with the atherosclerotic theory. If you remember the first witness to put the atherosclerotic theory forward it was Dr. Michael Pollanen. Remember the tons of information you were given to justify this theory? As I recollect we've heard from all manner of witnesses who supported the theory that atherosclerosis killed Lana Dale Lewis and all of them took great pains to point that to you. Not the presence of atherosclerosis ladies and gentlemen. In fact we were told that the presence of atherosclerosis was pretty normal in everybody and atherosclerosis begins to make its appearance as early as age nine. It wasn't the presence that was emphasized to you over and over again. Instead in the case of Lana Dale Lewis the important thing to note about her atherosclerosis was it was severe and if you recall we were also told what severe meant. Let's go back to Dr. Pollanen for this.

Dr. Pollanen spoke about six stages of atherosclerosis. The sixth stages as set out by the American Heart Association. Remember all that talk about stages. And he got the stages and he told us was from Robins. The pathological base of the disease that prevents the addition and he quotes the Bible of pathology and he says it was basic text that all pathology students are familiar with and have read and all pathologists are familiar with as well. And he described atherosclerosis in this way, and I'm quoting.

"Atherosclerotic process involves and is very complicated but essentially involves the deposition of certain types of material and cells within the artery such that the artery becomes clogged off or occluded. There are certain risks for ­ risk factors for that process but essentially it culminates in what the American Heart Association has classified as six different lesions. Stage one and I just draw your attention to this diagramŠ" and this is Dr. Pollanen speaking, he is looking at the chart now, "Šand this shows stage one, two, three, four, five and six. Obviously six is the end stage. Type one lesion is the initial stage and this is generally correlated with other observations such as early onset in general terms as well as clinical correlation.

So basically you have six stages. In the first decade of life the changes are minor consisting of small accumulations of fat, we call them fatty streaks, on the surface of the artery. And by the fourth decade, that's in the 40s essentially, if you're going to develop atherosclerotic disease what happens isŠ" and listen carefully to this "Šthe plaque becomes what we call complicated."

That's Dr. Pollanen telling you what to look for in plaque.

"But there wasn't a high degree of what we call stenosisŠ" this is another area, another quote. Dr. Pollanen is talking about what he's seeing and what he's expecting.

"The arteries are blocked by atherosclerosis. It's sub-occlusive. It's calcific, which means that calcium was being deposited into the wall of the artery as part of the disease process."

Another thing to look for, calcium in the walls and he says,

"If you remember back to the diagram I showed a table. The atherosclerotic process occurs over, over a period of time, years, and the end stage includes mineralization or deposition of calcium within the wall of the artery and that is a generative feature of this disease."

Dr. Pollanen is answering questions from Mr. Schneider at this point. So Dr. Pollanen testified he looked for characteristics of stage six atherosclerosis and said that he found those characteristics in Lana Dale Lewis' plaque. Here's what he said he found. He said he found calcification. He said he found pre-aneurismal changes. He said he found ectasia. He said he found impingement on the lumen and he said he found neo-angiogensis and haemorrhage of the plaque. That's why he then said to Mr. Schneider, "I saw those things and I'm saying because I found those things she had stage six atherosclerosis."

So even Dr. Pollanen and you're going to hear this echoed over and over, said to you it's not the presence of atherosclerosis, it's the characteristics and he lists what he says were the characteristics he said he found.

I'd like to ask you because you now know so much about this process. Early on when we were hearing from Dr. Pollanen and Dr. Deck, we took their word for whatever they saw under that microscope. You said you saw calcification? Guess it was there. We just took their word. But we know now so much more and I'm now going to ask you to critically evaluate whether or not those findings actually were there.

So there's a common theme that we've heard from every single person who told us about pathology, neuropathology and several of the neurologists as well, and that is, except for Dr. Ramsay, they all said to you in order to determine if atherosclerosis killed Lana Dale Lewis we must determine how severe her atherosclerosis was. As you could see, through this inquest, it was highly unusual to have a meeting of the minds on just about anything but they met on that. Except for Dr. Ramsay.

Now, if you think back, what you will realize is that different experts use different language to describe this common theme. Dr. Pollanen talked about stage six atherosclerosis. Dr. Richardson determined that whether the plaque was safe or a vulnerable plaque and whether the plaque stenosed or closed down the lumen of the artery or the opening in the artery.

In a few minutes I'm going to show you, despite using this different terminology ßeveryone's really saying the same thing. They were all saying: were the characteristics of atherosclerosis seen in Lana Dale Lewis' arteries consistent with a woman in her mid-40s dieing from atherosclerosis. There were slight variations on the same theme. For example, Dr. Pollanen looked at it this way. Were the characteristics of atherosclerosis consistent with stage six atherosclerosis and therefore responsible for the death? Dr. Richardson would put it this way: Were the characteristics of the atherosclerosis consistent with vulnerable plaque and therefore responsible for her death?

The only expert we've heard from who said the characteristics of atherosclerotic plaque were not important was Dr. Ramsay. Dr. Ramsay told us the specific characteristics of the plaque were not in issue for him at all. He told us it was sufficient for him to simply see the plaque next to the thrombus and he would then equate the presence of thrombus to that plaque and call it a day.

Ladies and gentlemen I'm going to ask you that you completely reject the position of Dr. Ramsay. Here's one of those issues of timing that I flagged for you early on. Dr. Ramsay appeared after all the pathology experts of the family were finished and after I had cross-examined Dr. Rhodes and showed that supposedly key findings made by Dr. Pollanen to support that atherosclerosis was stage six and severe were not actually present in the slides. Dr. Ramsay was even allowed to testify after Dr. Whitwell who rejected all of Dr. Pollanen's supposed findings that were meant to support a conclusion that atherosclerosis was severe. So after all that, we suddenly hear from a new expert of Mr. Danson. An expert who very conveniently now says, don't worry that all the supposed indications of severe atherosclerosis have now been shown to be non-existent. The final witness is brought in to save Mr. Danson's atherosclerosis theory by now saying that the characteristics of plaque don't matter a wit. He very simplistically says if atherosclerosis is there and next to a thrombus that's good enough for me. Let's everyone go home now.

You know, I don't know about you but I find it really hard to believe that Dr. Ramsay was the only one of the all the neuropathologists and pathologists that we heard from in this inquest who knew what was going on. Dr. Ramsay actually said something that helped us here. He said look for areas of agreement. And ladies and gentlemen one of the key areas of agreement on experts on both sides of this debate is that they all testified that they needed to assess the characteristics of atherosclerotic plaques as seen in Ms Lewis' arteries in order to determine the severity of the atherosclerosis. We all know that the experts do not agree on their conclusions but there is equally no question that all the experts, except for Dr. Ramsay, testified that they needed to look at the characteristics of atherosclerosis, not merely the fact that it was present.

So Dr. Ramsay suggested, look for those areas where the experts come together and I suggest to you the following experts came together to say the nature and characteristics of the atherosclerosis need to be determined: Dr. Deck, Dr. Pollanen, Dr. Richardson, Dr. Fornasier, Dr. Cheung, Dr. Rhodes, Dr. Whitwell, and Dr. Rathbone, all of them said the same thing. No one, except for Dr. Ramsay is sitting in the camp that suggests that those characteristics are unimportant and only the proximity to the thrombus is important.

On that basis I think it makes sense to reject Dr. Ramsay as the odd person out on that. Once you reject his position that leaves us with a need to look over the evidence and determine what we know about the severity. If the experts only needed to find evidence of atherosclerosis and then they could all pack it in, well there really wouldn't have been any controversy because they all saw it so it's not that they didn't see it, they saw it.

I want to caution you on what they're asking you to accept here. If you were to accept the proposition that just looking at a body and finding evidence of disease process then you can just go home, what you would basically be saying is that someone who has evidence of some other disease process in their body would never be found to have died from some other cause other than the disease process that they already have. That's clearly absurd. No body, except maybe the bodies of young children, is free of all disease processes and this is what has been so disturbing about this inquest. The chiropractic community seems to be saying to you that unless you have a perfectly healthy individual who is the perfect weight, who eats right and doesn't smoke and who is young enough they don't have appreciable atherosclerosis in their body, you can't conclude that a chiropractic neck manipulation was responsible for the death. And I say to you that the knowledge of what disease process may be found in a body and the assessment of whether that disease process killed the person or some external force killed the person is what pathologists and neuropathologists do all the time.

For example, you may have heard a story on the news just last week about a very large black man who was beaten by police in Chicago and he died. Most of the police beating was caught on video. The man who was beaten weighed 350 pounds. On top of that he had cocaine and ecstasy in his system. The coroner who investigated the death announced in the news that he recognized both the fact that the man was dangerously overweight and had drugs in his system but the coroner still said that the cause of the man's death at this particular time was the police beating.

Now what the chiropractors are asking you to do in this case is the equivalent of having the police take the position in that case, that since the man was obese and had drugs in his system well it couldn't have been the police beating that did it because he was dangerously overweight and he had all these drugs, that could have killed him anyway.

Commonsense should tell you that you can still beat to death someone who is obese and you can still beat to death someone who has drugs in their system. A person may be in very poor shape, say someone who's homeless and doesn't have enough to eat and sleep out in the cold and still be beaten to death and a good pathologist should be able to see the effect of obesity, the effect of the drugs and the trauma and be able to figure out the cause of death and to screen out the background noise which is in all our bodies all the time and it's going on as we live and breath.

In the case of Lana Dale Lewis what I need you to do is sift through the evidence to determine if the presence of atherosclerosis answers the question of what killed her or if it's simply background noise like this other man's obesity and drugs in his system.

And Ms Vance, I remember a question of yours to Dr. Ramsay. In particular you asked whether he thought that Ms Lewis' arteries were so diseased that it had to be natural causes and of course he answered yes. But Ms Vance, I want to take all five of you jurors through what the experts told us about how to assess the severity of atherosclerosis in order to determine if Ms Lewis' arteries really were so diseased.

One of the things that we were told is that severe atherosclerosis is characterized following a lot of calcium. Specifically here's what we heard on the topic. Dr. Pollanen, again he referred to Robins and as I indicated previously he says that the plaque becomes complicated and then he says it's calcific, which means calcium is being deposited into the wall of the arteries and he also talks about the atherosclerotic process appearing over a period of time and years and the end stage includes mineralization where the deposition of calcium was in the wall of the artery. And it's a degenerative feature of late disease process.

To Ms Rothsteen, who was here for the College, he answered that he felt what his ­ what he was observing, she asked was it calcific. He says, "Correct." Question, she says to him,

QUESTION: And calcific is one of the indicators you told us of the severity of atherosclerosis, is that fair?

ANSWER: That's fair.

Dr. Rhodes, now Dr. Rhodes and Mr. Danson answering questions. Here is the question,

QUESTION: All right and I just want you for the sake of clarity that you agree then with Dr. Deck and Dr. Pollanen's description of what you have just described?

ANSWER: I think I used the same words. As I pointed out this to the jury I didn't mention the area of calcification. You see a little bit here, but remember the tissue has to be decalcified in order to prepare the slides. Calcium in sections like this stay blue and so part of the things, one of the things that happens when the atherosclerotic plaque degenerates is calcium is deposited."

And to me, my question:

"QUESTION: Presence of calcium is there, what's the explanation of the presence of calcium along that vertebral artery," I asked Dr. Rhodes.

He says,

"ANSWER: Definition of calcium in any tissue is a common degenerative change. It's not specific to atherosclerosis. Many, many diseases when tissue becomes damaged, one of the things that happens is calcium precipitates in the tissue.

QUESTION: When you say it's not particular to atherosclerosis, is it something you would have seen in advanced atherosclerosis?

ANSWER: It's a common finding in advanced atherosclerosis. So common that in fact it's used almost in the way we describe it. We would say advanced calcific atherosclerosis and grossly you recognize it because when you handle the artery it's crunchy. I mean you can't put a knife through it sometimes there's so much calcium in it and this is ­ this is the normal course. This is what you see in advanced atherosclerosis."

Dr. Cheung, I asked him about calcium and he told us in his presentation and answers to questions from me that he didn't see any calcium on the CT scan and he would have expected to see calcium on the CT scan because what a CT scan does is it will show bone and calcium is the thing in bone that makes things show up white on things like x-rays and CT scans. So Dr. Cheung specifically looked for that calcium because I said to him, well the theory on the other side is very severe stage six atherosclerosis, heavy calcification. And he said well if you slice the CT scan slices basically through the brain as it takes its pictures you basically see a bunch of rings if it was that calcified and it he said "I didn't see it" and he testified to that here.

Dr. Whitwell I asked her and she answers,

"ANSWER: When calcification is extensive it's best identified macroscopically. There's almost a crunchy crunchiness to the blood vessel.

QUESTION: Would you agree with me that if you found blood vessels that were crunchy upon close examination that would be an abnormal finding and would be identified in the grossŠ" and she said yes.

QUESTION: So if it's not in the gross, one of two things, either an error has occurred or it's not there because there's no crunchiness that was found in the artery.

ANSWER: Correct," she says.

Dr. Richardson answered a question of mine and I put to him that quote from Dr. Rhodes where he says calcification is so characteristic of ­ and Dr. Richardson agreed, he said "Yes, of course. In fact sometimes you could even see bone formation in vessel walls."

"QUESTION: So are you in agreement that if this is severe atherosclerosis you would expect to see heavy calcification?

ANSWER: Yes.

QUESTION: And you don't see any with Ms Lewis?

ANSWER: I don't see any.

QUESTION: Okay, and Dr. Rhodes talked about the fact that the artery was crunchy in severe atherosclerosis on gross. Is that something that you agree with?

ANSWER: Yes."

So groundwork, one of the characteristics we've been told by all these experts to look for is presence of calcification. Now question, was calcification present in Ms Lewis' artery? So in terms of a list of questions you need to ask yourself when you sift through whether or not the evidence supports the severe atherosclerosis, that's one. And I am certain and it's rightly so, your attitude is going to be, well she's going to tell us what her expert said and not surprisingly her experts are going to agree with her. So what you're going to see that I do repeatedly for you ladies and gentlemen is I'm going to show you what the other side said because I want you to understand that this is not just from my side and not just from my experts.

So, and the other thing I'm going to do is I'm going to reference back to hard evidence again, and one of the things that's hard evidence in calcification again is it wasn't seen on CT scan. That's something that you don't need to rely on someone else's interpretation. It's white and Dr. Cheung said it would show up white and he showed you the CT scan and he said it's not there. So with your own eyes you could see that it's not there. There wasn't any white.

And Dr. Rhodes what did he say about calcification? If you'll recall I caught Dr. Rhodes saying some things that aren't at all correct. You might recall this exchange between Dr. Rhodes and I.

"QUESTION: Well actually, what I wanted to ask you was about your testimony with respect to calcium. You've indicated that despite the fact that you didn't see a lot of calcium, you're concluding that it must have been there because you saw some bits of blue remaining and your testimony was, if I'm not mistaken, that a sample of the tissue was decalcified.

ANSWER: I have a great deal of experience with decalcified tissue. I work with it all the time so I know from my experience where I handled the gross tissue and then looked at the slides that once you decalcified it, most of the calcium disappears. That's what you're doing when you decalcify. So I have a great deal of experience saying that after decalcification I see just a little bit of calcium left and extrapolating from that to what must have been there, before you decalcified it."

And so I ask him,

"QUESTION: So you're extrapolating from what you're seeing? I want to be clear on this.

And he says,

"ANSWER: You asked me whether there was calcification, or someone asked me, and my answer to that was, the answer is yes. You asked me how I knew and I said because even the decalcified artery, there was still some calcium remaining.

And then he says,

"ANSWER: I'm just telling you that once you decalcified it, it won't be as blue as it would be if you didn't decalcify it. So I've got a bit of blue, blue" is what he says, "I know there would have been much more blue had we - they not decalcified the tissue."

"So you're extrapolatingŠ" this is what I say to him, "Šand you say there would have been much more blue if it hadn't decalcified is that right?" And he says, "That's correct."

"QUESTION: Okay, so that's your position is that you're extrapolating from what you've seen and your submission on that was it would have been much more blue.

And he says again,

"ANSWER: You see right now a little bit of calcium in the decalcified tissue. You know there would have been more before you decalcified it."

He also answered one of Mr. Danson's questions and he says the same thing. He says, "You see a little bit here but remember the tissue had to be decalcified in order to make slides. Calcium in sections like this stays blue. And so one of the things that happens with atherosclerotic plaque as it degenerates, the calcium is deposited in to it." Dr. Rhodes seemed to forget what other experts clearly told you: no one decalcifies the brain. We heard that from Dr. Richardson and we heard it from Dr. Whitwell and you'll notice when Dr. Ramsay came to testify, he didn't tell you that we were wrong on that.

Use your commonsense. They all told you what decalcification was for. It's to remove calcium from bone. They also explained what happens in an autopsy. The brain gets taken out of the skull. There's no bone. They also told you the brain is very soft tissue. Putting it in a tough solution, acidic solution like what happens in decalcification would mush the brain entirely. It's never done.

And so I ask this of Dr. Whitwell.

"QUESTION: Dr. Whitwell I just want to confirm with you in terms of the brain, the brain was separated out from the body and it is not decalcified, is that correct?

ANSWER: Correct.

QUESTION: You never decalcify the brain. Is that correct?

ANSWER: Yes, that is correct."

QUESTION: So whatever calcium you see on the slides is all there is. It's not a matter that some of the calcium has been removed from the process of decalcification. Is that correct?

ANSWER: That is correct.

And then nobody raised it, so now you know what Dr. Rhodes told you he saw. He saw a little bit. He described in fact to Ms Jones as a hint of blue. That's the amount of calcium that was in Ms Lewis' artery. A hint of blue. And contrast that with what they all told you they need to see if it's severe atherosclerosis, serious, severe, lots of calcification. Dr. Rhodes saying to you if in fact you call it ­ you call it in the name, you mention calcification because it's so much a characteristic of this disease.

So here's where he says to Ms Jones,

"ANSWER: That means the atherosclerosis itself didn't block off the artery. It's calcific. You remember it was hard to see because the calcium's been removed, but there was, there was a hint of calcium.

QUESTION: And that's the blue you pointed out?

ANSWER: That was the blue that I pointed out, exactly right.

ANSWER: Most of the calcium is removed, as you decalcify the block you stop after you get to the point where you can cut the knife through it and that leaves a little bit of calcium. As I showed you in the slide there was a faint hint of blue on the top there so I can't see most of the calcium because most of it's gone but there was ­ there was a faint hint left where there had been some."

Now I don't want to confuse you. The decalcified portion, and you'll see this in an original autopsy report, is the neck. So what happens is after they go in and they get that brain and they snip the arteries, the vertebral arteries and the carotid coming into the brain so they can lift the brain out. What's left, the arteries as they work their way through the bone in the neck, that's the part that's got to go in solution because they can't slice through that with the bone in there mixing up with the arteries. But the brain part, no. And of course nobody saw atherosclerosis extra cranially so what we're talking about was all inter-cranial and that was never decalcified.

And Dr. Whitwell, I asked her a question about whether she saw severe atherosclerosis and she again mentioned that the best place to see severe atherosclerosis would have been in the gross and she says yes, it's crunchy. Yes, I would expect that it gets reported if it's crunchy and she confirms what you heard from Dr. Richardson and Dr. Ramsay that you can see these nodules in the tissue, there's chunks of them and she confirms that's an abnormal finding and yes she'd expect to see it on gross and no you don't see it on the gross here.

And then I ask her specifically, you know I went through the whole list of Dr. Pollanen's observations that he says he makes in support of a finding that she has severe atherosclerosis. I went one by one by one with those points with her and the second point was that Dr. Pollanen says he sees micro-calcification. Actually he's very clever because of course what Dr. Whitwell said to me was, well, micro-calcification implies there are very small amounts. Remember the big words Mr. Paliare said to you today? These experts used too many big words, too many scientific words. Dr. Pollanen was very good at using those very big words. So instead of telling me there was very little calcium he called it micro-calcification. Same thing. Virtually nothing there.

And Dr. Richardson, I asked him what he saw and he said he saw two little specks of blue that I think were calcium that that's all. Otherwise he said no calcification. So what I think you can take from this evidence ladies and gentlemen is that: one, serious calcification is a characteristic of stage six or end stage, or vulnerable plague, whatever you want to call it. What ever we have heard from different experts. Atherosclerosis, in other words atherosclerosis that might kill you. You find serious calcification in that. Dr. Rhodes in fact told us one of the things that happened is that when plaque degenerates and calcium is deposited and he also told us that it's such a finding of severe calcification is so common that it is part of the name of the disease. Number two point you can take from this, Lana Lewis arteries contained a faint hint of calcium. Number three, that is not consistent with stage six or end stage atherosclerosis and is not consistent with level of the disease that could kill a person.

Now, I see that it is five to one and what I plan to do after lunch, just so you know is I'm going to take a look at the other characteristics that we've heard also form a basis of a finding that atherosclerosis is severe. So that's the first one that I've done with you which is calcification and it is five to one so I think it is an appropriate time to stop.

THE CORONER: Very well, Constable Drummond we will recess an hour and 15 minutes.

R E C E S S

U P O N P R O C E E D I N G:

THE CORONER: Ms Oakley?

MS OAKLEY: We ended before lunch on one of the points of Dr. Pollanen and all the pathologists in fact told you to look for if in fact a person has severe atherosclerosis and that's calcification. I took the opportunity to put Dr. Pollanen's exhibit up, Exhibit 36, because I think again it's very important again for you as you are going through the testimony that was heard here whether or not in the end you believe that the evidence supports the findings that Dr. Pollanen has drawn into that diagram and which many, many of the experts came in and said "I agree with that diagram." So just so that you understand: If those findings that underlay Dr. Pollanen's diagram are incorrect, and if the other experts then come in and say "I agree with that," they're wrong too.

The next point I want to bring up in terms of what you find in serious atherosclerosis, and we heard about this, is ectasia. Dr. Pollanen testified he saw ectasia and he drew it into his diagram, that's the wavy line on the left side. He indicated that a finding of ectasia means atherosclerosis was advanced. Here's what he said to Mr. Schneider on this issue on May the 7th.

"QUESTION: Now, what I wanted to ask you was, I assumed that if we're seeing ectasia then the ­ this atherosclerosis is fairly advanced. Am I correct?

ANSWER: Yes."

And once again on the issue of whether ectasia is present or not, Dr. Rhodes is particularly helpful although probably not in a way that he wanted to be. As you may recall I asked him about his observation about ectasia. I asked,

"QUESTION: And you said that you'd be looking for a similar calibre. You rememberŠ" this is me speaking, not Dr. Rhodes "Šthat ectasia is of the calibre of the artery has now turned into sort of like a wavy line, there's areas out and in. It's the calibre, it's not evenŠ" so I asked him, "You said you'd be looking for a similar calibre. Can you show me where in your records where you've measured the calibre along the length of intracranial vertebral artery?

ANSWER: Now this is best judged as you're looking at it and would have been best observed by Doctors Pollanen and Deck as you just look at the artery and you can look at it grossly, not under a microscope when you've got this piece of tissue, this tube."

So he says if you see ectasia you'll see it on gross. He then admits that there's no observation of ectasia on the gross and you guys can see that with your own eyes. There's that hard evidence for you, back in Exhibit 16. I then take Dr. Rhodes' own words where he says ectasia is best observed grossly and this is want happened next,

"QUESTION: Well, what I'm asking you is what you just said about the gross examination of the vertebral artery and that Dr. Deck and Dr. Pollanen would be in the best position in order to see whether or not there might be a ballooning out in some portions of the vertebral artery, and now correct me if I'm wrong, but the only place you could assess the gross observations made by Doctors Deck and Pollanen would have been in the autopsy report" and he says "Well I will correct, because you are wrong. The easiest and best way to look for some sort of dilation like that is when you've got the gross specimen but you can certainly recognize the ectasia looking at a microscope slide because once again you'll have an opportunity to judge the size of the vessel as in comparison to the thickness of the walls and so you can look for damage to the wall where it's abnormally thin and dilated. So you certainly can recognize it at a microscopic level. It's easier if you start with a gross examine."

So basically Dr. Rhodes ends up saying the best place to look for ectasia is grossly but you can also see on the microscope slides.

Okay, so we know that there's no mention in the gross description made by Doctor Deck and Pollanen and yet I do want to remind you that early on Dr. Pollanen told us that in his differential, in other words the list of things that he was looking for when he examined Ms Lewis' specimen both grossly and under a microscope, his list included atherosclerosis. So it's not as if that wasn't in the head of Dr. Pollanen and Dr. Deck from the start. So they're thinking atherosclerosis, they've got the gross, they'd be looking for these things.

And remember one thing here about the microscopic examination. You heard from many of the pathology witnesses that the vertebral artery was not embedded properly in the blocks. The artery was embedded at an angle and this would certainly interfere with looking at the slides microscopically in order to determine the width of the artery lumen and the artery wall. Here's what Dr. Richardson said about this, "Well to evaluate the lumen size of the tube such as this or a vessel you must have sections that are absolutely true at right angles to the wall. If you cut them on an oblique angle and you just look at one section and everything is distorted, this is what's referred to as looking at it en fas (ph), en fas meaning you're looking at it all spread out and it exaggerates the thickness of certain layers. So to do it, you have to have absolutely pure cuts that are at right angles to the access of the vessel. If you don't have that, then it becomes very difficult to evaluate the lesions in the wall."

So I'm going to charitably suggest to you that the reason Dr. Pollanen who was a trainee at the time that he examined these slides and he did not have as much experience as Dr. Deck and Dr. Whitwell and Dr. Richardson and Dr. Ramsay, the reason he sees what he believes to be ectasia is because he does not have enough experience to compensate for the poor placement of the arteries and the blocks. You'll notice that I included Dr. Ramsay in that group. He doesn't see any ectasia, either, ladies and gentlemen. You go back to Dr. Ramsay's exhibit which is 255. He went slide by slide. That was his big claim to fame. He gave us an individual description of 507 slides he looked at. You look at that list. No mention of ectasia.

What did the other experts say about ectasia? Dr. Richardson said to me, I asked a question,

"QUESTION: Now in diagram Exhibit 36, Dr. Pollanen has also drawn the left vertebral arteries having a wavy in and out appearance and he described that as ectasia and I'm wondering, Dr. Richardson, whether you saw ectasia in your examination of the slides?

ANSWER: No I didn't. I believe last time when I demonstrated this was in a serial of block or series of sections of the artery shows there's no ectasia and the calibre of the reference was uniform throughout."

And then I asked him,

"QUESTION: Again we heard from Dr. Rhodes that ectasia can also be seen grossly. Is that correct?

ANSWER: That's correct, yes.

QUESTION: And is ectasia an abnormal finding?

ANSWER: Yes, it means that somewhere along the line the vessel wall has been diseased or something happened to it. So instead of being the same calibre it's now dilated. If this is just uniform it's called ectasia. If it's unilateral, if it's just off to one side for instance, it's called aneurismal, an aneurysm formation and these are very dangerous to have in blood vessels in the brain so of course you'll note it.

QUESTION: So on gross if you saw a vessel that appeared to have these ballooning about you would make a notation in gross that ectasia was present?

ANSWER: Yes, that's part of the gross examination of the brain since the vessels are so vital to the brain.

QUESTION: Now Dr. Rhodes actually indicated in answer to one of my questions, he said 'The question of whether or not there's ectasia present and where it's present is such a minor point that I did not look for it,'" and I asked Dr. Richardson, "Would you agree with him that the presence of ectasia and where it's situated is a minor point? Do you agree with him?

ANSWER: No. Anywhere you see in a person of this age in their 40s and 50s and even 60s indicate it would be abnormal."

Then I asked Dr. Whitwell the same kinds of questions,

"QUESTION: Did you find evidence of ectasia as you went through?

ANSWER: No.

QUESTION: No, and is ectasia something else that can be seen on gross examination as well?

ANSWER: Yes.

QUESTION: Would it be considered an abnormal finding to be reported?

ANSWER: It would, yes.

QUESTION: And you don't see it microscopically either?

ANSWER: No."

And neither Dr. Deck nor Dr. Ramsay make any mention of seeing ectasia either with a microscopic examination of the slide. So with regards to the second point, this is calcification we've done, now ectasia. Regards to ectasia you can take from the second: number one, ectasia is a characteristic of stage six or end stage atherosclerosis. In other words it is a characteristic of the kind of atherosclerosis that might kill someone. Dr. Pollanen said that the presence of ectasia means atherosclerosis is advanced.

Two, the best and easiest place to make an observation that ectasia is present is in the gross or visual examination of the vertebral artery. Three, no such observation was made about the presence of ectasia and Lana Lewis' vertebral arteries. You would expect that such an observation would be recorded in the gross because ectasia in someone in their 40s, 50s, and even 60s would be an abnormal finding and Dr. Rhodes told us that it is obvious that one would expect that a pathologist would record a normal finding.

Four, the majority of experienced pathologists in this case and the ones who you can be sure are aware that the arteries were not properly embedded did not find any evidence of ectasia in Lana Lewis' vertebral arteries on microscopic examination. Five, that is not consistent with stage six or advanced atherosclerosis.

Next what we heard from Dr. Pollanen that another characteristic that severe and advanced atherosclerosis is a lipid core and inflammatory cells. We heard about the presence of a lipid core and inflammatory cells in vulnerable plaque or advanced atherosclerotic lesion first, not first, but from Dr. Richardson as well. He brought with him a series of articles from Nature Medicine which were published in November of 2002. These articles are Exhibit 246 and one of the articles that Dr. Richardson referenced in this paper is entitled Vascular Proliferation and Atherosclerosis.

The article starts out by saying, "Here we will review the current understanding of the patho-physiological mechanisms and the status of molecular and gene therapeutic approaches in vascular proliferative diseases. The understanding of the patho-physiology of atherosclerosis and related vascular diseases has changed over the last decade providing new perspectives for preventative and therapeutic strategy."

On page 1250 of the article there are a series of four diagrams showing what one would expect to see at each stage of atherosclerosis. The first diagram shows the initiation of atherosclerosis; the second is entitled "an early lesion" and it also shows the presence of foam cells; and you may recall what Dr. Pollanen said about that. He indicated that first in atherosclerosis you see what's called a fatty streak and that's consistent with what you see in this Nature Medicine article.

In the third diagram, labelled "vulnerable plaque" it shows the presence of a lipid core which is made up of abundant foam cells along with "intense inflammation" and the diagram shows that this inflammation is made up by the presence of lots of monocytes which are also known as macrophages and also T-lymphocytes.

You may recall when I cross-examined Dr. Ramsay about these characteristics of safe and vulnerable plaque he first admitted that the last time he studied anything about atherosclerosis was back in school and he also said about Dr. Richardson's description of the stages of atherosclerosis, he says "nice theory." I'm sure you remember that. He suggested this was all new stuff, just theoretical and he even suggested that because the article had been written with the backing of drug companies, question mark, perhaps that was supposed to suggest that it was somewhat self-serving and suspicious.

In keeping with what I'm trying to do for you by showing you that it's not just family witnesses that gave you specific information let's go back to what Dr. Pollanen told you about atherosclerosis. He referenced the book again by Robbin, which he called the bible for pathology students, and Dr. Richardson actually addressed Robbins and he said it's pretty much, it's a very elementary textbook and he said the whole science of atherosclerosis has changed an awful lot since Vercow (ph) and the current concepts are those that I believe are distributed in the review article from Nature Medicine. However, even keeping in mind that Dr. Richardson said Robbins is very basic, if you look at Exhibit 37 which are the pages from Robbins that Dr. Pollanen put in, he spoke about a chart and the chart was the one with the six stages of atherosclerosis. If you look at the chart, lo and behold, under type five lesion you'll find that it says that there's a lipid core or multiple lipid cores. As a matter of fact the chart shows the plaque develops from type one to type six lesions and it talks about the fact that there's a core of lipid that's developing and progressing and then it talks about, at stage type six a surface defect.

So there's Robbins, this basic elementary pathology text Dr. Pollanen describes as a bible for pathology students and it's describing some of the same concepts that Dr. Richardson spoke about which you find in the Nature Medicine article and then you have Dr. Ramsay saying "nice theory." Well didn't he read Robbins? It's not new. According to Dr. Pollanen it's something every pathology student reads.

The other thing that that the article and what Dr. Pollanen told us is that without the lipid core what you have is a simple plaque and he said that as a plaque develops and I think I read this to you earlier, it turns into what's called a complicated plaque and he claimed he saw complicated plaques in Lana Lewis' arteries and that was the basis for his finding that it was advanced atherosclerosis. So you've got the simple plaque and the simple plaque doesn't have things like the lipid core, and then you get the complicated one and it's got lipid core and that's what Robbins says.

Now, I put this "nice theory" comment to Dr. Rathbone and I asked him if he'd had an opportunity to read the Nature Medicine article, and whether he was familiar with it and he says it's similar to what's been described in those articles but those reviews, those articles are reviews he says. "This is material that I knew about in 19 ­ in the late 1960s, studies being done. We have perhaps the largest thrombo-embolism group in Canada, certainly maybe even the world, at McMaster led by Fraser Mustard and I was fully aware of the studies on blood vessels, platelets, and removal of surface material. So yes, this material I was aware had been published many years ago. More detail has now been added, we now found new proteins. We're filling in bits, but the actual information that we have discussed thus far as been known for about 30 years." No new theory.

Then I ask him, "Are you familiar with concepts in the article of vulnerable plaque versus stable plaque?" And he says, "Yes. If the plaque forms and this is the fat deposition that changes and I won't go into the cells unless you want me to, that form these, the fatty cells that form this plaque on the wall of the arteries they get gradually covered over and as you can see in that picture of the articleŠ" and he's at this pointing to the Nature article, "Šthere's a fibrous covering and then the endothelia cells line over this. Now if this covering is thin there is a distinct possibility that the plaque will rupture. If that happens platelets are exposed to these ­ to the material inside the plaque, which the platelets see as a wound and platelets are set up to stop bleeding, so they form this plug on the vessel wall. So if the plaque is vulnerable it has a thin layer on it and it can rupture after a while and certainly we now know that since at least 15 years of studies have been done to show that if you lower the cholesterol by diet, by extreme diet or by various drugs such as Statins (ph) or if you lower the blood pressure one can get changes within these ­ within these plaques so that the protective layers over the very reactive material is just thickened and so the plaque becomes quiescent and so they don't pose as much of a risk. That's why we don't recommend taking out all plaque out of the carotoid." In other words, you heard from a lot of the doctors that they don't go in and do surgery unless you get this really severe narrowing of the arteries and both Dr. Cheung and Dr. Rathbone said that even with a severe narrowing, unless it hits about 90 per cent, he also would be looking for symptoms. So the reason you don't go in I mean, you and I might think ­ I certainly would have thought that something like 70, 80 per cent you might get a surgeon saying better get in there, but in fact what Dr. Ramsay says you don't go in there because most of the time that plaque is just sitting quietly and so you'd actually do more damage to go in.

I'm sorry, I think I said something other then - I said Ramsay instead of Rathbone, which I expect to do a couple of times today so I apologize. There are a lot of Rs in this case. I don't know how it happened.

And then I say to Dr. Rathbone, "Two days ago we heard from Dr. Ramsay, a neuropathologist and when I asked him about the vulnerable verses stable plaque his response was something like, 'it's a nice theory.' Is that what this is in your understanding? Is this just a theory that there is vulnerable and quiescent or vulnerable and stable plaque?" And he says, "No, it's supported by a huge amount of evidence over the last 30 years and this is something that's born out in clinical trials. It's born out in laboratory situation and it's the basis on which neurologists make their decisions about how they're going to treat patients with cerebral-vascular disease."

So the Nature Medicine article indicates that a problematic or vulnerable plaque will have a lipid core and the presence of certain cells and cells are foam cells, monocytes, microphages.

Now let's see what the experts said about the presence of these things in the plaque of Lana Lewis. I asked Dr. Whitwell, and her answer to me about what she saw in the plaque, she said, "In fairness most of the ­ well I saw atheroma. I probably for oversimplification described it as atheroma but generally pretty simple plaque." Remember the simple plaque, stage one, stage two.

Now you remember what Dr. Pollanen testified, he testified that atherosclerosis advances in stages. It goes from fatty streak, to simple plaque, intermediate and a few more steps and you get into the complicated plaque. Dr. Whitwell didn't see any complicated plaque. She saw generally pretty simple plaque.

I asked her a question about what she had written into her report.

"QUESTION: So all the plaque you described I do not see you describing any of the cells as monocytes or foam cells or fibroblasts inside the plaque. Would you agree with me?

ANSWER: That's correct.

QUESTION: Dr. Richardson we heard from indicated that the plaque was there but by and large was acellular. There were no cells in the plaque. Would you agree with that finding?

ANSWER: I think that is a fair comment generally."

Dr. Richardson told us that the plaque in arteries was pretty much entirely acellular and you remember Dr. McLellan at one point wanted me to be clear on what I was saying because the word is a single word, "acellular" with the a in the front, meaning no cells there. And he explained what it meant, that there are no cells in the plaque and he told us that cells have a nucleus and when they're stained, the nucleus stain is dark purple. So again, ladies and gentlemen I ask you, you have photographs that have been put as an exhibit. We showed them to you at the time but you're free to look in the jury room again and see if you can see the sign that Dr. Richardson said there are no nuclei, no dark purple spots inside the plaque. It is acellular, there are no cells in there.

And again, I'm going to take you to Dr. Ramsay's report, not my witness. Exhibit 255. He mentions he sees focal, and we've heard that means in a spot, sparse mineralization, and that's the calcium, and collections of foamy cells in one slide. One in 507 that he described. And you can find that one slide in page nine of his report.

Dr. Richardson and Dr. Whitwell both say that they do not see any lipid or fat collections in the plaques. Dr. Ramsay's report does not identify any slides that have any lipid or fat collection. So there's the lipid core that everyone's telling you to look for including Robbins, including Dr. Pollanen, including all of the other pathologists. They said they've got lipid cores. Well, you take a look ladies and gentlemen at any one of the pathology reports we have entered in as exhibits and you shall find nobody has reported a lipid core observation anywhere.

And again, the inflammatory cells. You find this little pocket, a slide in A where they found some foamy cells, that's it.

So with regards to what you find inside a vulnerable or advanced or complicated plaque, you can take from this evidence that: one, a lipid core and the presence of inflammatory cells are characteristic of stage six or end stage or complicated plaque or vulnerable. In other words again, the kind of plaque that will kill someone. Two, the evidence from Dr. Whitwell, Dr. Richardson, Dr. Ramsay is that there is no lipid core and only a rare presence of cells in the plaque in Lana Lewis' vertebral arteries. Three, the absence of a lipid core and inflammatory cells means that the plaque in Lana Lewis' vertebral artery was not complicated plaque. Dr. Whitwell called it simple plaque. Dr. Richardson called it safe plaque that was not in danger of rupturing and causing the creation of thrombus. Plaque which is not complicated and is not the kind of plaque that would rupture is not the kind of plaque that would result in someone's death.

Another observation that Dr. Pollanen tells us to look for in serious or severe atherosclerosis is neo-angiogenesis and plaque haemorrhage. Dr. Pollanen says that these are also characteristics of advanced atherosclerotic disease. He answered some questions about them and here's what he said.

"QUESTION: Okay, neo-angiogenesis meansŠ" and this is to Ms RothsteinŠ

"ANSWER: Proliferation of small arteries within the atheromatic elementŠ", in other words inside the plaque.

"QUESTION: So again something you'd expect to see in end stage atheromatous?

ANSWER: Yes."

Now to Mr. Schneider on May 7th on pages 72 and 73 of the transcript, what he says to Mr. Schneider is I did see neo-angiogenesis but not at the site of haemorrhage. Now he says the explanation for the haemorrhage is the neo-angiogenesis. He then admits though that that's not where he saw the neo-angiogenesis and you won't see it there.

Dr. Ramsay's report again comes in quite handy. Again he goes slide by slide, tells us what he sees. No mention of neo-angiogenesis anywhere in the report. Back to Robbins, they also indicate that a complicated plaque has surface defect of the plaque and haemorrhage of the actual plaque and both Dr. Richardson and Dr. Whitwell testified that there was no connection between the haemorrhage that they saw in the vertebral artery wall and any plaque. And by the way just because there are some red cells in the plaque doesn't mean that it's associated with the plaque. And I can just use a simple example. If you cut your finger and the blood runs down your hand you're going to have blood on your palm, but your palm isn't bleeding so it's the same thing. If there's blood in the artery walls it's going to bleed into the artery walls and just because some of the blood makes it into the plaque doesn't mean the plaque ruptured and in fact that's exactly what Dr. Whitwell says.

"ANSWER: In fairness it is haemorrhage although whether or not it represents intra ­ intra plaque haemorrhage which is generally a large amount of haemorrhage, what I did not see was a large amount of haemorrhage.

QUESTION: So the haemorrhage can in fact come from tissue around the plaque and it could have some bleeding into the plaque?

ANSWER: That is correct.

QUESTION: And that doesn't mean the plaque itself is necessarily the source of blood, it's just the surrounding tissue is bleeding and going to bleed into ­ in the vicinity?

ANSWER: Correct."

You'll see in Dr. Whitwell's report she makes the same conclusion. She says "Yeah, I saw some blood in the plaque. I don't believe it's connected to the plaque." So her observation is a couple cells of blood, not connected to the plaque. So again with regards to what you find in advanced atherosclerosis you can take from this evidence that one, neo-angiogenesis and plaque haemorrhage are characteristics of stage six or end stage atherosclerosis. In other words again, atherosclerosis that you might expect could kill someone.

Two, the evidence from Dr. Whitwell, Dr. Richardson, and Dr. Ramsay is that these characteristics are not present in Lana Lewis' vertebral artery. Three, the absence of these characteristics means that the atherosclerosis in Lana Lewis' vertebral arteries is not severe, it's not stage six.

Now another thing that Dr. Pollanen says is roughened surface of plaque, reduction of lumen sign. Dr. Pollanen explained that plaque might cause a reduction in lumen size in an artery and that the plaque can cause the surface to be roughened and this might cause clotting. We heard from Dr. Cheung, Dr. Rathbone, and Dr. Richardson and others that a closing down of the lumen of the artery or the opening in the middle by atherosclerosis is not of any real concern until the opening is down significantly, 70 per cent or more. Well actually Dr. ­ I'm going to get into the numbers I guess. And I asked Dr. Rathbone when he would send a patient to a neurosurgeon for surgery with occluded vessels and this is what he said. He said, "I refer patients to a neurosurgeon who has atherosclerosis particularly of the carotid arteries. But for the stenosis, the narrowing of the arteries, the most important indication is that the person has some transient warning stroke,T-I-A in the territory in which there is narrowing. Now we look again at the narrowing and we take not just the extent of the narrowing unless it's very high and by very high that'sŠ" sorry I'm just going to pull what he was talking about at the time. He was looking at that photograph which is Exhibit 249 in these proceedings and you'll remember that this is a photograph from Greenfield and the top one shows lumen encroachment and he told us that the dark circle is the original artery and that the layers that you can see building up is the atherosclerosis growing into the lumen. So he said, he looked at this and he said, "The photograph that would be just bordering on very high. We would have to ­ usually surgeons don't operate unless it's over 90 per cent stenosis if it's not symptomatic."

"So symptomatic is very poor evidence and they do better with surgery but once you become symptomatic and surgery may help if the symptoms have been recent. But one thing we look for is evidence on the ultrasound and on angiography of an ulcer forming on the plaque. So the plaque is no longer smooth but there is some roughening of the surface." So according to Dr. Rathbone, a roughening of the surface of the plaque is the result of a formation of an ulcer. And Dr. Whitwell responded, when I asked her what would you expect to see in serious, severe atherosclerosis on gross. She said you would see ulcerated plaque grossly. So you could see the ulcers on gross. And again nothing like ulcerated plaques or lumens or openings of the plaque were seen on the examination of gross and Dr. Whitwell indicated that.

Dr. Ramsay also doesn't note any observations about the serious reduction in the lumen of the vertebral artery nor any evidence of ulceration of the plaque. Dr. Willinsky, in describing what he saw on the right side of the angiogram, said it was smooth not roughened, which Dr. Rathbone then indicates would mean that on the right side where you're hearing evidence that she had serious severe atherosclerosis on the right side as well, on the angiogram what Dr. Rathbone says is, if you've got a roughened surface you see it on the angiogram, and Dr. Willinsky testified he saw it smoothly. So even if there's atherosclerosis on the right side, what Dr. Willinsky said is it's not ulcerated plaque because it's a smooth surface.

Dr. Cheung also told us that even if you get clots clinging to the wall of the artery you would never get a complete occlusion like what we see on the left side here unless first you have serious stenosis with plaque. Think of this like a flowing river and you're not getting a plug in that river unless you first have an awful lot closing down that river. So in other words water's rushing along, you're going to get branches and ­ and all kinds of debris sticking along side of that river but that's not enough to close a river and what Dr. Cheung said is even if the plaque was causing any kind of clotting along the side you also need this serious stenosis of the atherosclerosis closing down the lumen. So in combination, you get the serious stenosis, then on the part that's remaining you start getting clots there and then you can have it close right down and that just makes sense. You've got it wide open. It's not something they're going to occlude, like what we see in her left side, and that's what Dr. Cheung told us. Impossible, he said.

And again, here's the hard evidence I'm going to ask you people to look at. You ­ I invite you look at every photograph that has been entered in as an exhibit. I challenge you to find any impingement of a lumen that even comes close to this. You will find some impingement which is very minor. It just comes out, like, if you have to put a number to it, ten per cent, 15. You're not getting anything that looks like this in Lana Lewis' arteries. So there's your hard evidence again. Don't take my word for it. Don't take what the experts are saying. Go look at the pictures.

This is Exhibit 248, Block A, and it's just an example of the many photographs that are in these materials. And I just want to be clear. This is all clot. You know that because you've been here forever. Here is the atherosclerosis. So, take the clot out and take a look at how much you would describe that as an impingement on the lumen of this artery. It's barely there. It's barely there and then you compare it to that. Okay?

And I'll tell you something else too. You heard some of the experts say, oh, so she brought in pictures, big deal. You can take pictures of anything you want. So could they. So could they. And in fact Dr. Rhodes did. You remember he brought pictures in. So if there is lumen that is being impinged by 50, 60, 80 per cent why didn't he take the picture? Where is it? He not only took pictures but he put slides on a microscope. He could have shown you that. So yeah, we took our pictures and you know, there's no possible way for me to take 50,000 pictures to cover every single thing that you could see on slide and they say well, there's a problem right there because she's probably only taking the pictures she wants to take, but we also brought in slides and showed you the slides. And I would just remind you they didn't show you anything like that.

So again, what can you take from this evidence? You can take a roughened surface from alterations and a serious reduction in the lumen of the artery are other things you see or might see in stage six or end stage atherosclerosis or advanced atherosclerosis. In other words, again, what are you looking for with respect to atherosclerosis that might kill somebody. The evidence from Dr. Whitwell, Dr. Richardson, Dr. Ramsay, Dr. Rhodes is no serious reduction in the lumen of the artery by atherosclerosis anywhere, anywhere. And there is no ulceration of the plaque surface because the absence of the serious ­ and this is in point three, the absence of a serious reduction of the lumen of the artery and the lack of any evidence of ulceration means that the presence of atherosclerosis cannot explain the full occlusion of the left vertebral artery with thrombus in Ms Lewis' case and it wasn't caused by atherosclerosis.

Now, I'm going to switch to the right side because you heard a lot about the right side proving that, oh, you know she had bad disease on the left and the right was well on its way, and we have 70 per cent stenosis and if we just waited long enough the right would completely occlude just like the left did. Okay, so let's take a look really at what the evidence shows on the right side.

You heard from Dr. Pollanen that he believed that the right vertebral artery was also badly atherosclerosed and had a 70 per cent stenosis and was just on its way to that full occlusion. Dr. Whitwell and Dr. Richardson said that because of the very bad embedding of the arteries on the right side it was difficult to draw conclusions but they both also said there is no evidence of any plaque that is sticking out into the lumen on the right side by 70 per cent.

Dr. Whitwell said she would call the plaque on the right side moderate, not severe, because I put to her, Dr. Pollanen says it's severe. She says, "I'd call it moderate." She also said she could not rule out, and you heard differently from Mr. Paliare today, here's what Dr. Whitwell said about the right side. She said, "I cannot rule out an injury on the right side." You look at her report. She couldn't rule it out. She can't rule it in because it was so badly embedded but she said, "I can't, from what I've seen, rule it out."

We also heard from Dr. Willinsky who said that what he saw on the right side told him that it was atherosclerosis that was causing 70 per cent stenosis and he described what he saw, he said the characteristics of it and he said you know because of this characteristic and that I can conclude that it's atherosclerosis on the right side. So he concludes that the stenosis was caused by plaque, yet he also says like virtually everyone else in the neuro-radiology field, that he would defer to the pathologist. In other words, did the pathologist find the plaque that's sticking out of the lumen by 70 per cent? The answer's no. And not only that, Dr. Cheung said when he looked at it, he said no. It's being caused by clots on the right side, not plaque.

Now, let's be clear what this means because I have to tell you, until I was reviewing these notes I didn't really grasp this. Here's what it means. What Dr. Cheung said was the reason he believed it was clot, not plaque is because he said the plaque would still be there, it's not going anywhere. But the clot he said could dislodge and go up and he in fact said that might be what killed her. It might have been a clot from the right side because he said there's no blood flowing on the left. So he says "I think it might have been in fact a clot from the right, because the blood's still flowing on that side".

When you look at the pathology, even Dr. Pollanen's description, what does he see on the right side? He finds thrombus. It is thrombus. Dr. Cheung is right; Dr. Willinsky, Dr. Rosso are wrong because there is no plaque sticking out into the lumen but there is thrombus. And Dr. Whitwell also finds thrombus on the right side.

Now, I think, I assumed that the clot or the thrombus was there because of the plaque. That's kind of what I was thinking. Oh well, it doesn't matter if it's plaque or thrombus. But now I understand what in fact was being said here, because the other thing that you find if you look at Dr. Pollanen's description in Exhibit 39, which is his November 12th, 2001 report, where he describes what he sees in Block B. He describes blood between the elastic lamina and the media of the artery. That could be a dissection and an injury and that's exactly, exactly what Dr. Cheung felt. That's what he said. In fact, since all the neuroradiologists said to you we would defer to the pathologists, then it's Dr. Cheung who's prove right. It's clot there; it's not plaque and there is evidence that there in fact is blood tracking into the wall in the, and this is a quote, "Šblood between the elastic lamina and the media of the arteryŠ" from Dr. Pollanen quote.

So, to summarize the findings on the right side, there is no plaque which is impinging on the lumen and blocking it off. Dr. Whitwell says the plaque is moderate at best. Dr. Pollanen's own report calls the plaque on the right side "mild moderate" that's his words. Again, page 12 of his report, read it for yourself. There is clot there and it's been described by the other pathologists as well, which is more likely caused by an injury to the right side, not atherosclerosis as so many have tried to say to you.

So what I said to you much earlier, when you go to evaluate which of these two beliefs you think is most convincing I want to encourage you to cast your mind back to the start of the atherosclerotic theory being put forward. I think it's critical because if you go back to how this theory was first being sold to you, you will see that this theory has suddenly needed to be seriously revamped in order to allow it to remain a viable alternative for you, the jury. That revamping was Dr. Ramsay coming in here at the very end of all the neuropathologists and suggesting to you something which had not been suggested by anyone else before. He tried to suggest to you that all of the characteristics of the plaque were not important. He tried to suggest to you that you should just see plaque and that should be enough to establish that's what caused Lana Lewis' death. But that would be in direct contradiction to every other expert, no matter where they stand on the atherosclerotic theory. So, I'm not just pointing out my witnesses here. I'm pointing out what everyone said to you. It's serious, it's severe and here's what we're looking for one by one by one ladies and gentlemen follow along and you will find every single one of the findings they say in her arteries weren't there. So when you review all the evidence I'm going to suggest to you that you should conclude that by all this, that atherosclerosis was not advanced. It was not severe. The exception was what Dr. Deck said and what we heard from other neuropathologists and pathologists is there is a penchant, there is an area in most people where you can get severe atherosclerosis right as the artery enters into the brain, the plugs he called them, just where you get past the dura and he said you know, no one really knows why it's there but it's hypothesized it's because the arteries at that those points are held in one spot by the dura. They don't move around and so there may be some connection that that's what Dr. Deck told us way, way back when, and we've heard that confirmed since then. Dr. Richardson said yes, well known, you find these little plugs. So that's would be about where you want it and that is consistent with what you find in all kinds of people. It doesn't mean you're going to keel over and die.

So to summarize: the plaque only had a faint hit of calcium deposit, a few cells, no lipid core, and impinged very little on the lumen of the artery. No evidence of ulcerated plaque. There you go, those are all the criteria that we've been told to look for in serious and severe atherosclerosis. And of course, if you go one by one by one, and ladies and gentlemen I have to tell you that if this inquest had not gone this long and we hadn't heard from so many experts and you guys were not at the level that I know you are in terms of understanding this, this would not be possible to go through and actually say fine, you guys tell us to look for this, this, this, this and this; let's look.

Remember what Dr. Ramsay said to you at the end? He said "I'm really not comfortable with explaining things on a microscope. I just want to tell you what my opinion is." Thankfully you don't have to take that because you know so much that you now can decide for yourself whether calcification was really there or not. You've got all the evidence. You've got all the tools. You've got all the information. You've got all the reports. Decide for yourselves.

And the experts who have concluded that Lana Lewis died as a result of trauma to her neck. They didn't reach their conclusion just by ruling out atherosclerosis. I mean, they did that because I said to them, "Look, here's a competing theories. Think about it. Tell me yes, no, do you see these things? Don't you see these things?" So we looked at both.

But there were definite signs of information that trauma was the cause to these individuals who concluded it was trauma. There were six: One, the clot was most organized and oldest in the neck and so this pointed to them that the clot started in the neck and not intracranially. Two, there were signs of trauma in the neck, like a removal of the endothelia or inner layer of the vertebral artery in the neck and evidence of reactive changes which is healing process in the neck. Three, no atherosclerosis in the neck area so atherosclerosis could not be responsible for the start of the clot in the neck. Four, the clots found in the visual cortex of the brain are about the same level of organization as those found in the neck so it appears that the clots came from there, and not intracranially, because they don't look anything like the clot found intracranially. Five, the atherosclerosis is not of the level of severity that would explain the most unusual situation of a 45 year old woman dying from atherosclerosis. And six, the start of the clot is much lower than testified to by Dr. Pollanen, putting the end of the thrombus far away from the alleged atherosclerosis intracranially.

So let's start with one, the clot was most organized and oldest in the neck. I'll tell you what's funny about this because we have heard an awful lot about this aging stuff. What's funny is, when I reviewed this stuff, it was Dr. Pollanen who gave some of the most firm answers in terms of age. He said to Dr. ­ Ms. Rothstein for example, he said, "If you're trying to differentiate between trauma on the one hand and disease on the other, one way of starting to weigh those two would be to know where the thrombus starts." So right away he identified why it's important to know where the thrombus begins. "The experts have concluded that the thrombus in her neck was the oldest site of thrombus development."

Dr. Whitwell, question to Dr. Whitwell,

"QUESTION: Well Dr. Whitwell I have a question to you in regards to aging. You indicated that aging is also dependent on, for example, on flow or source of blood, right?

ANSWER: Yes.

QUESTION: Would you agree with me then that the end of A, which is the most intracranial portion segment, also has a source of blood?

ANSWER: Yes.

QUESTION: So if A and W are about the same age and they both have a source of blood they would look approximately the same would you not agree?

ANSWER: They would, yes. I would not disagree with you.

QUESTION: And would you agree with me that it is not what you're seeing in the slides. That in fact W is most significantly more advanced than what you're seeing in clot A?

ANSWER: I said that ­ I said is that in my opinion I thought that W was older than what I saw in A. And I could not say categorically but that was what I thought when I looked at it and I don't know what you mean by significantly either. That had the appearance of being to me probably older than A. I cannot say more than that.

QUESTION: In any event, in the end after taking all these things into consideration is it your opinion that W is older but you just can't tell how much older then from whatever else you see?

ANSWER: Yes, probably, probably."

In her report which is Exhibit 254 on page ten, she says "Block W, in the artery there's organizing thrombus with proliferation of vessels and that's fibroblast indicating organization. No atheroma is seen or dissection is present. The organization appears more advanced than in sections from Block A."

And on page 11 of her summary of neuropathological findings she says, "One, extra-cranially left vertebral artery, which is Block W, thrombus was evidence of organization including new vessels and fibroblasts. No significant atheroma at this level. Two, thrombus of the intracranial portion of the left vertebral artery. Variable atherosclerosis present in the left vertebral artery with full sign of very early organization present. However, this appears less than that identified under one."

It's not as organized intracranially as extra-cranially and she said that, and she equates that to being older. On page 12 of her report she says,"The likely sequence of events would be that she, Ms Lewis, suffered an extra-cranial thrombus at the site identified in Block W, where there was organization of thrombus taking place. No significant atheroma is present. There is no dissection visible at this point, however, Block U1 shows where in my opinion is a genuine, albeit relatively small dissection. In addition it is known that the endothelia cell damage can also occur during vascular injury allowing exposure of damaged intimae and the potential for clot formation."

Interestingly, as I said earlier, a lot of the best evidence about the fact that the clot in W is oldest, is from Dr. Pollanen. Here's what he said to Ms Rothstein.

"ANSWER: I mean essentially if you have a thrombus, it's organization occurs when it's exposed to the intima. So, the ­ the part of the thrombus which is exposed to the intima the longest would show the maximal degree of organization."

And then Mr. Schneider puts to him, he says,

"QUESTION: And Dr. Deck indicated to us, at the tail end of the thrombus, and he found this of great significance, that the tail end of the thrombus is the oldest site of the thrombus. Do you agree with that or do you disagree with that, I just want to be clear?

ANSWER: The degree of organization is consistent with that interpretation.

QUESTION: Okay, and ­ okay so you don't disagree with Dr. Deck on that point, that the thrombus is oldest in the tail and here in the extra-cranial section, is that correct?

ANSWER: Correct.

QUESTION: And is it your opinion that the tail end of the thrombus extra-cranially is not associated with atherosclerosis?

ANSWER: That is true, yes."

Then to Ms Rothstein again,

"QUESTION: But Dr. Deck says, in any event, it's somewhere ­ let's take it at its highest, somewhere where the oldest or most organized, let me say this, the most organized part of a clot is that's the birthplace. That's it, that's the birthplace. You've told us, Dr. Pollanen, that no, no, no the birthplace is intracranially. Somewhere in proximity to the atherosclerotic disease. So we're still struggling to understand if it's true that organization may be a sign of older, and if it's true, therefore, why isn't more organized down here than it is up here? Why isn't this the birth place? Can you help?

ANSWER: As I indicate, it could be the birthplace, however, the major difficulty with that proposal is that number oneŠ" here's the difficulty he was saying that it started extra-cranially, "Šthe birthplace of the thrombus occurs in a non-atherosclerotic segment of the artery which means it has to have occurred by an intimal injury." Is that circular logic or what? He says, I won't say that's the oldest because if I say that's the oldest and it's not in an area of atherosclerosis it means there has to have to been intimal injury. Yeah, it does.

Then he says, "So you must assume that the presence of an intimal injury to be ­ to be there to make the thrombus. And the episode which fulfills that requirement is trauma." But then you have to explain he says, why the next section of the artery immediately above it has a fresh subadvential dissection. Well, frankly one doesn't fit with the other. The question to him was "Do you think it's oldest outside?" And he says "Yes, but if I say it's oldest outside there's no atherosclerosis so I have to say it's trauma."

Then he says, "But let me be very clear about this. The simple presence of an organization, the focus of maximal organization fulfills the requirement of Berkhows (ph) Triad so on that basis cannot be discarded as inconsistent."

By the way, Dr. Pollanen himself indicated that the theory being proposed by the people who decided that it's atherosclerosis and not trauma, is that the clot looks more organized in W but is actually not older because W has a source of fresh blood. Now Dr. Pollanen says that's actually not logical to him. You remember he liked the word logical, and he said it's not logical when that theory was put to him, and it was put to him. It was put to him by Mr. Foster,

"QUESTION: And I'm going to suggest the most obvious thing that's happening is that fresh blood is reaching the partial occlusion, correct?

ANSWER: Fresh blood is reaching that region in a state of turbulence.

QUESTION: Right. Nonetheless it's bringing with it whatever ­ whatever things blood brings with it that are good to the healing process.

ANSWER: All of the components of blood would be present at that site.

QUESTION: Right, and the presence of fresh blood, turbulent or otherwise, was certainly or would it assist in the organization process of the thrombus in that area?

ANSWER: It would promote it.

QUESTION: So logically one would expect to see more organization in the area of the thrombus to which fresh blood is being supplied than one would see anywhere else in the totally occluded portion of the thrombus correct? Well you're looking at me sceptically. Help me understand.

ANSWER: It's perhaps a slight over simplification. The organizational process involves multiple factors, not simply blood in the artery. And it would involve the infiltration of cellular material from the intimal layer of the artery and I agree with the fact that the organization, the degree of organization at that site, extra-cranially, appears to be the oldest across the entire vessel across the entire length of the artery." Then he says, "I don't believe you can make an inference from that to being the site of intimal injury. I don't see a logical connection." So he's back to being concerned that if he says it's oldest there's an intimal injury there. Question from Mr. Foster:

"QUESTION: Is there no difference between more organized and oldest? Are you suggesting that it's solely by age the tail end of the thrombus being exposed to a variety of things including fresh blood and healthy tissue? Are you suggesting that in spite of fresh blood, healthy tissue and whatever else is going on, that it's proper to use the word oldest in this area as simply or as opposed to simply more organized?

ANSWER: I think when you have a cellular infiltration into a thrombus, that is older than when you have a thrombus that lacks cellular infiltration. So I think one would be on reasonable grounds scientifically to call that the oldest site of thrombosis.

Mr. Foster tries it again, "And I guess from a logical perspective all I'm suggesting to you, if that is happening one would reasonably expect to see to see this area better organized, more organized than any other place, and wouldn't it be and it wouldn't be because of age, it would be because of fresh blood, healthy tissue.

ANSWER: I do not agree with the logic of that statement.

QUESTION: And I'm just trying to understand why not? Why then ­ sorry, then we're going to go to your response about the connections, but why ­ why don't you agree? Why don't you agree with fresh blood, healthy tissue, only partial occlusion therefore one would reasonably expect a higher degree of organization in that site than anywhere else?

ANSWER: Because cellular infiltration is one of the basis of timing histological dating or timing in pathology. When you have ­ the best way to describe it is a succession of cellular infiltration amongst the last infiltration into an organizing thrombus would be endothelial cells from the intima. And they form small capillaries and we can talk in great detail about that process but that's what's been happening in the thrombus there which says to me that there has been a certain infiltration of cellular elements, which puts it into an older category than a fresh category."

I'm certain, I'm certain you forgot that because after Dr. Pollanen all we heard about was the theory of the fresh blood and that means that just because it looks older it's not, it's more organized but it's not older. This is exactly what Dr. Fornasier said too. He said there's a specific, logical, expected sequence of cells showing up in a clot and that's how you date it. You look at it and say, "This one, it hasn't got any cells. It's just red cells. They're loose. It's brand new. This one's got some cells, it's a little older. This one's got this kind of cell, that shows up after that kind of cell. This one's got cellular infiltration. It's older than all of them." And that's what Dr. Pollanen said, and the thing that was bugging him, which I don't really understand is what he kept saying is "But yeah, but if it's oldest, you can't explain that with atherosclerosis so I've got to go back to the trauma theory and I don't want to do that." But scientifically he said that's what makes sense, it's the oldest.

Number two, in terms of supporting a trauma theory. There were signs of trauma in the neck area like a removal of endothelia or inner layer of the vertebral artery in the neck and evidence of reactive changes in the neck area. Do you know how many pathologists said that they saw the reactive process going all the way up? Dr. Deck says it, Dr. Richardson says it and Dr. Whitwell. They all see, and "reactive" being that there are white cells accumulating on the outside of that adventitia going all the way up, and they all said that that is evidence of trauma. And remember when I had Dr. Ramsay here, and I put the slide on the microscope and I said to him, "Do you see it right here Dr. Ramsay? Do you see right up here, there's the cells?" He said, "No, I don't see anything." Well, interestingly, Dr. Deck, Dr. Whitwell, Dr. Richardson they saw the cells. You can see the cells yourselves because you can actually look at the photographs. You'll see the cells. You'll see the nuclei outside the adventitia and if you look at them, you'll actually find them all the way up.

And this is really interesting I found. Ms Rothstein said to Dr. Pollanen, "What would you histologically ­ what would you see that would be evidence of the healing process of the dissection?" I wish I could actually put this up for you but I'm not going to take the time to do it because when you put what he says in his testimony next to his observations that he made in his October 9th, 2001 report, they're so close I couldn't believe it. So he says to Ms Rothstein, "If trauma was there what would I expect to see?" He says, "Here's what I expect see. He says you would see evidence first of the dissection itself, blood cells regenerating, red cell regeneration, the formation of fibroplasias which is essentially the early parts of scar tissue formation. Granulation tissue formation is the other word for it."

October 2001 report he says, he looks at W and he says "Here's what I see in W. This segment of the artery contains an occlusive thrombus that has an intimate association with one portion of the intima. In this region of the artery, there was organization of the thrombus characterized by amorphous degeneration of blood elementŠ" which he says he'd expect to see, "Šand focal endothelia cell proliferation with aggression and formation of small endothelia-lined spaces. Routine and special stains reveal that the endothelia cells proliferation is associated with fibroplasias, which he also says he's seen, and collagen deposition which in his testimony he agreed would be consistent with scar tissue.

So, on the one hand, when he's in the stand he says this is what I expect to see. If you look at his October 9th, 2001 report, he does see it and he adopts this.

Number three in terms of why the experts who have said that it's trauma, that they felt it was trauma. We've already gone through which is there was no atherosclerosis in the neck so atherosclerosis could not be responsible for the clot in the neck. Nobody's disagreed with that.

Four, the clots found inside the visual cortex of the brain are about the same level of organization as those in the neck, so it appeared that the clots came from there not intracranially. And again, there is no substantial disagreement on this. Those clots look the same as what you see in W. They don't look the same as what else is going on in A and U and so on.

Five, again the atherosclerosis is not the level of severity you would expect in the most unusual situation of a 45 year old woman dying and of course we just dealt with all of those characteristics of atherosclerosis which aren't there.

Six, this is really important. Six, the start of the clot is much lower than testified to by Dr. Pollanen putting the end of the thrombus far away from the alleged atherosclerosis intracranially. It's very important for a number of reasons. And it's so important I need to take you through some of the history of how we learned of this fact.

In the Exhibit 16, which is the gross examination this is the description. It says "The left vertebral artery in the foramen transversariumŠ" so we know now what that is, which is the C1 bone, "The left vertebral artery in the foramen transversarium is occluded by thrombotic material from the level of the adontoid process to the segment of the artery just distal to the point where it enters the posterior process."

Here's what Dr. Deck and Dr. Pollanen say. They saw clot from C1 all the way up visually. Then Dr. Pollanen does a December 19th, 2000 report and by the way I'm going detour here for about a second here to deal with something Mr. Paliare says which really was wrong. Dr. Pollanen is the one that discovered the missing slides because he went to find them for his December 19th 2000 report and it's in there in the introduction to his report. He had to cut new ones. Let's not put everything on Dr. Deck. The man wasn't even there. He was sick and it was Dr. Pollanen doing it and he testified to that. Dr. Deck wasn't in the building so I know we want to blame everything on Dr. Deck but the man wasn't even here and you know what, I don't remember the evidence of Dr. Deck on the issue of the cut slides but I will tell you that if he didn't say it wasn't me that lost them, it's just because he was a good man that didn't point fingers at others. But it wasn't him that lost them. And he wasn't even here to figure out that they were lost and you can go back to the December 19th report which is Exhibit 42 and read that for yourself.

So Dr. Pollanen cut some more slides December 19th, 2000 and this is his description of the microscopic. He says, for the left vertebral artery extra-cranial segment, he says "There was organizing thrombus present in the lumen of the extra-cranial segment of the left vertebral artery. The most inferior extent of the thrombus in the histological sections is at the point that the artery exits the foramen transversarium in the transverse process of the first cervical vertebrae."

Okay, so he says it twice now. October 9th, 2001 report of Dr. Pollanen on page three, which is Exhibit 44, here's what he says about the Block W.

"Block W, St. Michael's Hospital, recut microscopic slides. Description, section showed two portions of the left extra-cranial vertebral artery. One portion of the artery is cross-sectioned in the foramen transversarium. The other portion of the artery is longitudinally sectioned and has a length of 12 millimetres. The cross-sectioned arterial segment reveals the presence of sub-occlusive organizing thrombus."

So you can see the problem. In all of his reports Dr. Pollanen describes the clot at one to C1. Into the foramen transversarium, and he says it over and over again, but when he draws this diagram, Exhibit 36, he doesn't show the clot going as far as C1 and not only the diagram is different. When Dr. Pollanen's in the stand, it's Mr. Schneider who actually says to him "Well this isn't fitting with your report. Your reportŠ" Mr. Schneider says, "Šsays that the clot goes down to C1. Which is correct?"

So, because, Dr. Pollanen on the stand says, he describes it as the extra-cranial segment thrombus is poking down from the intracranial segment. In other words it's all intracranial, just a little, little piece coming out. That's what he says in testimony.

So here's what transpires. First, he says to Mr. Schneider that the reason that he said what he did in his December 2000 report is he says he made the observation without actually looking at the slides. I don't know. It's pretty darn clear. He describes the slide and he describes what he sees there. Then, to Ms Rothstein again he describes to Ms Rothstein, he says, "The most inferior extent or the most extent of the thrombus is in the transverse segment of the extra-cranial segment of the vertebral artery." He claims he doesn't know which side was up of the block. Now, again, you guys have been here so long, you know this. If slide number one showed a cross-sectioned piece of artery with bone surrounding it, guess which end is which? And that's what he describes. He describes, and in fact what he says is, you'll remember what he says is the St. Mike's slides they revealed a piece that they hadn't seen before.

So, just again ladies and gentlemen, to point this out, if slide number one is cut here and there's 30 or so slides and they all show a cross-section, inside bone, when the St. Mike slides were cut they began to reveal this piece up here. That's the piece Dr. Pollanen says was revealed for the first time by Dr. Fornasier when he cut further into the block. So how could Dr. Pollanen claim he doesn't know which end was up? It's real obvious which end was up. The cut, cut, cut, cut; cross-section, cross-section and then all of a sudden you start getting piece of cross-section, piece of longitudinal when you're cutting it this way.

Now why did he fight so hard about the start of this? What's the big deal? I mean, so he comes in and says "I thought it was there but it's actually a lot lower." Here's what he says. "One way of interpreting the maximum extent of organization of a thrombus is that is ­ where it first started."

"QUESTION: Right and for exampleŠ" this is Ms Rothstein again, "Šif Dr. Deck is correct well that the thrombus started down here, in other words lower, because he sees thrombus all the way here, let's just take for the purpose of argument thrombus is all the way down here. In other words down to that bone, the significance of that is there's very little atherosclerosis through here as well as we'll come to. We can see that in the diagram right?

ANSWER: That is true.

QUESTION: And so it would be less likely that the thing that caused the thrombus to form in the first place was atherosclerotic disease. That would follow.

ANSWER: If the thrombus occurred at that section of the artery, obviously that section of the artery did not have atherosclerosis so you would be looking for another cause."

That's Dr. Pollanen telling you if it went as far as that I'd have to look for another explanation.

"QUESTION: Right but conversely it's your contention that if the thrombus starts intracranially in proximity to all the atherosclerosis then it's not the only thing but it's one of the things that leads you to the conclusion that the atherosclerosis causes thrombus to form.

ANSWER: That would be my explanation for how the thrombus formed."

Now there's all kinds of places you can look to confirm where that clot goes to. It's not just the pathology slides but all the pathologists have confirmed it's down that low. Dr. Cheung, when he was asked to draw, where does it show on the angiogram he showed it going all the way to the base of C1. And you remember the missing piece of tissue? We don't have the artery between C1 and C2, and in fact Dr. Cheung puts the source of the injury according to matching it to the angiogram as just below C1. We don't have that artery. The block is bone alone. The artery is missing in X.

Dr. Norris, this is really interesting because I thought Dr. Norris was just wrong - he was wrong. Remember, Mr. Danson said to him, "I bet you can't say where that dissection is?" And Dr. Norris says, "Fine show me the angiogram." And he gets up and looks at it and he goes, and he puts an X and the X was down at C1 and we all went, I went like this ­ oh, and then he said, "Oh well but I'm not a neuroradiologist so you know, don't take my word for it but if I had to mark it it would be down at C1Š" is what he put. That was Dr. Norris.

So a lot of importance on where did that thrombus start. Dr. Pollanen himself tells us that one way to interpret the maximum extent of the organization of a thrombus is that that's where it first started. He also says if the thrombus occurred in that section of the artery, obviously that section of the artery did not have atherosclerosis, so you would have to be looking for another cause.

Then the other thing that's important is that it shows you that this is one of the bases that Dr. Pollanen in fact concluded, that it was atherosclerosis. He said that the clot actually was pretty much where the atherosclerosis was and there's just a little bit of a tail sticking out, but it was really you know, focussed around the atherosclerosis and there's this little bit of a tail. So that was part of what he said. That was one of the reasons that he said it's atherosclerosis, because he said it's only a little bit, and the rest of it is all around where the atherosclerosis is.

Now, what I found shocking, you heard all about the highest scientific principles. Dr. Pollanen said to Mr. Schneider, I am going to go to the lab on my break ­ do you remember this ­ and I am going to check whether it's my diagram that's correct or whether it's my reports. And he came back after looking at slides, and ladies and gentlemen, you ­ you can tell it's in the bone, and he came back and told us no, my diagram is correct.

And I asked Dr. Whitwell, you may remember, I said is there any way that someone who specifically went to determine a question of how far south did the clot go, and they're experienced and they know what they're looking for, is there any way that they could conclude that the clot doesn't go to C1 and she said, "No. I have no idea how that could happen." Neither do I, ladies and gentlemen. Neither do I.

And the other important thing about that clot is now you get to see which of the other experts fell all over themselves to support Dr. Pollanen without looking for themselves. This is an easy point. There's no interpretation here. There's no, "well, you know I see some cells. No it's really that cell. It's that kind of cell." It's "where's the clot?" And when the clot is surrounded by bone it's really basic. So, if you've got experts who are willing to come into this courtroom and say "Hmm, yup, that's what I saw too," they didn't look. They were busy supporting Dr. Pollanen, regardless of the actual facts in this case. That's what that tells you, because it's not an interpretative point.

And, you know, one person who did that and I, again, didn't realize this until I was reviewing the material, was Dr. Rosso. Dr. Rosso can't read an angiogram? He's not looking at the pathology. He can see where a clot goes down. He, in his testimony, he says the clot only comes to ­ according to what he saw in the angiogram. Again, how can we believe his position that he doesn't see a rat's tail, because that's an interpretation question, when he hasn't told us this really simple thing of how far down does a clot go, and he couldn't tell us.

I mean Dr. Norris he wasn't a neuroradiologist. He says, "I'll defer to the neuroradiologist on this but from where I see it" and he points to C1. And so, Dr. Rosso whose job it is to read angiograms, he can't read them as well as Dr. Norris can, apparently?

And again, what you'll find is Dr. Ramsay gave up the ghost on that one and so did Dr. Willinsky. It was late in the day then, the proof was really solid. So you hear from Dr. Willinsky and Dr. Ramsay, 'Yup, clot's in C1." No point anymore, the cat's out of the bag. But everyone before that, I ask them the question, do you agree with what Dr. Pollanen has drawn here and they said yes. And if they can't ­ I mean there's no interpretation so why don't they say well you know, what everything says, "I saw that clot going much lower. Sure, I saw calcification and I saw haemorrhage, but that clot went much lower in my examination of the slides, or in my examination of the angiogram" and they didn't do it.

So that says to me that they were willing to follow Dr. Pollanen anywhere because the theory was: it's not chiropractic manipulation, so we're on his side. Whatever he says, whatever. We agree with him. What's he saying? We got it.

When Mr. Foster asked you on Monday, are you angry? Here's where I think you should be angry. This inquest was improperly and unfairly lengthened as a direct result of Dr. Pollanen's involvement in this case. He cut slides badly. He lost pieces. He didn't identify left and right. He didn't look and label things properly and now we find out that on top of everything else he is prepared to leave this courtroom, go to a lab, look down a microscope, see something that we can all tell is there, and come back and say no, it's not there. The clot started much higher up.

And, of course, I know you know my issue was the fact that he wasn't a pathologist at the time. And the only reason, I have to tell you this keeps coming up and coming up and coming up, is because all the other lawyers in this case, they decided they didn't want to acknowledge this, so throughout the inquest all the lawyers insisted on referring to him as a pathologist and a neuropathologist which would force me to stand up and say excuse me, Dr. Pollanen's not. You know, if they want to pretend it doesn't exist, that's great. But it does exist. And that, as well, was problematic. I mean, I'm not taking away from what Dr. Pollanen has done, but then, come in here and tell us "I'm a trainee, I've written a book, I've got this gold medal, I've written all kinds of papers. I'm still training right now." For you, as jurors, part of what you're going to be doing is balancing, okay this expert said this and this expert has experience here, and his expertise was 30 years, and this expert is the head of this. That's what you'll be doing so, it's only fair to put it out on the table for you, "yeah, I've got a gold medal, not a lot(?) but I'm still training." That's all. I'm not saying he shouldn't have testified. I am saying he shouldn't have spent four days pretending he was something he was not. And what I'm telling you too is, what's this stuff from the other lawyers to pretend that he didn't mislead? Oh, you heard Mr. Foster on Monday. Mr. Foster says to you guys, "who was misled? He said he was a consultant." This is Mr. Foster's question ­ question to Dr. Pollanen.

"QUESTION: Now as a scientist sir, as a neuropathologist, what if anything do you make of that statement?" He asks him. And then he asks him another question where he says,

"QUESTION: As far as you as a scientist sir, a neuropathologist, know, the entity of the so-called sub-endothelial dissection does not exist correct?"

So he told you on Monday that there was nothing that fooled him? He knew a