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JACKSON V AEG LIVE July 18

th
2013
Emry Brown (Anthologist)
By way of Video deposition
Direct by Mr Koskoff cross by Ms Cahan
Q. Good morning, Doctor Brown.
A. Good morning.
Q. Doctor Brown, can you tell us, first of all, where it is that your deposition is being taken right
now?
A. This is in Boston , Massachusetts.

Q. And do you what field of medicine do you practice in?


A. I'm an anesthesiologist.
Q. And do you have where is your office that where you practice anesthesia?
A. I practice anesthesia at Mass. General Hospital in Boston.
Q. Okay. And do you have any other offices from which you conduct your professional activities?
A. I do. I have two research laboratories One is at Mass. General Hospital in the Charlestown Navy
Yard; and the other is at MIT Massachusetts Institute of Technology in the neuroscience department.
Q. Okay. Now, first, at Mass. General Hospital you said you have an office. And is Mass. General
Hospital a Harvard teaching hospital?
A. It is.
Q. And so that one of your offices is at Mass. General, and the other one is at the
Massachusetts Institute of Technology, MIT. And what is that what professional activities do you
conduct out of the MIT office?
A. So I'm on the faculty at MIT. I do neuroscience research. It has two main focuses One is on
anesthesia, the mechanism of general anesthesia; and the other is on signal processing,
understanding how neurons represent information to the brain. We develop algorithms to do that. I'm a
statistician, as well as an anesthesiologist.
Q. I see. And in the Massachusetts General office, what are the activities that the professional
activities you conducts from Mass. General?
A. So they're the same, actually, because at Mass. General we conduct our human studies of
anesthesia
A. And I have part of my group there that also works on signal processing algorithms as well. So
both activities both activities are taking place at both sites.

Q. So that you work from both Harvard and MIT?


A. Yes, I do.
Q. Okay. Now, where did you receive your college education, Doctor Brown?
A. I was an undergraduate at Harvard College.
Q. Okay. And then following and when was it you graduated from Harvard?
A. .
Q. Following that, did you further your education?
A. Yes. I spent a year studying mathematics at the Fourier Institute, in Grenoble, France.
Q. And that was a year in mathematics. And then, following that, did you come back to the United
States?
A. I did. I came back and did the M.D./Ph.D. program at Harvard, pursuing my Ph.D. in statistics
and my M.D. at Harvard Medical School my Ph.D. at Harvard University and my M.D. at Harvard
Medical School.
Q. So I just do that over again. You got your M.D. at Harvard Medical School; and at the same
time you were getting your M.D. degree, you got a Ph.D. in statistics at Harvard?
A. That's correct.
Q. Okay. Then, following that, did you have an internship in the field of medicine?
A. Yes. I did an internship in medicine at the Brigham and Women's Hospital.
Q. Is that another Harvard teaching hospital?
A. That's a Harvard teaching hospital.

Q. And then did you do a research fellowship in endocrinology and hypertension also at Brigham
and Women's?
A. I did. I was in the endocrine hypertension division of the department of medicine. The research
was actually on circadian rhythms. That was also at the Brigham.
Q. So that the research that you did is on circadian rhythms now, circadian rhythms we've heard
a little bit about them in this case, but are they was your research in the field of the biological effects of
circadian rhythms, so these clock rhythms?
A. Yes. Basically, what I was working on was developing algorithms to analyze circadian data,
because there were a lot of techniques out there that were very simplistic and really didn't go after the
sort of structure that was in the data; and also it didn't really capture the properties that were there.
So it was much more challenging to make what I consider to be accurate inferences. So that's that
was the research I was working on at the time.
Q. Okay. The well, you know, the word "algorithm" has come up quite a lot. Is there a simple way
of describing what an algorithm is?
A. Yes, certainly. So when a very good example is, like, a GPS that you have in your car that is
telling you where your position is. So what the GPS is doing is, it's collecting information using satellites
to collect information about where the car is on the road. So and that information is a very simple
collection of data points. It's position, perhaps velocity, and maybe the acceleration of the car. Then you
want to draw a path about where the car is going to go or make a prediction about how long it's going
to take to get to a certain location. So you generate a mathematical formula that takes that data in and
makes a prediction about, given the car moving in this direction at this speed, with or this velocity at
this acceleration, how long will it take it to go to location Y or Z? And so the mathematical formula
that actually takes the data and provides that information is an algorithm. So and in the same way,
when you have data which come in in a circadian rhythm which look very much like a sign wave they
go up and down a sign wave of about 24 hours, you'd like to determine certain properties of that data
A. So we have a mathematical algorithm that analyzes the data and gives us back those
properties.
Q. And so that were you working on trying to create these mathematical algorithms so that you
could understand the effects of Circadian rhythm in various aspects?
A. Right. Exactly, to make so more precisely, statistical algorithms. And the only reason I say
"statistical" is because we're dealing with experimental data, and I'm a statistician; and it also just to
reflect the fact that not only were we constructing algorithms, we were concerned about the properties

of them making sure that they function well; they actually give you back the information you're
supposed to give you back; and you have a sense of that. So those algorithms were designed to
help us understand more accurately the properties of biological rhythms, particularly in humans.
Q. Now, in addition to then did you also get a residency in anesthesia where you actually as a
practicing anesthesiologist?
A. I did. I did my residency in anesthesia at Mass. General Hospital after the after the research
fellowship.
Q. And that was for three years?
A. That was for I think two and a half years, to be precise.
Q. Okay. And did you become a practicing anesthesiologist?
A. I did.
Q. And are you still a practicing anesthesiologist?
A. I am.
Q. Okay. Now, I just want to go through some of your academic appointments. At the present time
are you a Professor of Computational Neuroscience in the Department of Brain and Cognitive Sciences
At Mass. at MIT?
A. I am.
Q. And are you also a Professor of Health Sciences and Technology at the Harvard MIT Division
of Health Sciences and Technology At MIT?
A. Well, just a small correction So that
Q. Yes.

A. that title is I took over administrative responsibilities a little over a little less than a year ago in
that division. So right now I hold an endowed chair there at MIT. So it is the "Edward Hood Taplin
Professor of Medical Engineering," technically, at the moment.
Q. Okay. What does it mean to have an endowed chair?
A. The endowed chair means that a donor to the institution has set aside funds that are directed to
pay the salary and usually some research expenses for a given professor. It is set up to give you a
certain degree of flexibility in terms of allowing you to either help with administrative work or pursue
your research slightly more unencumbered.
Q. And in addition to that, are you are you to the endowed chair at MIT, are you also do you
also have an endowed chair at Harvard?
A. I do.
Q. And what is that endowed chair in?
A. It's the Warren M. Zapol Professorship of Anesthesia at Harvard Medical School Mass. General
Hospital.
Q. So that in addition to that, are you the Associate Director of the Institute of Medical
Engineering and Sciences at MIT, or is that where you are now director?
A. So I am. I am the associate director. I am the Associate Director
Q. Okay.
A. of the Institute For Medical Engineering and Sciences at MIT.
Q. And is there also a health sciences and technology program at MIT
A. There is. It's a joint program which
Q. and Harvard?

A. There is. I'm sorry. There is. It's a joint program


Q. And go ahead.
A. I'm sorry. There's it's a joint program which has been going on for a little over years now
between Harvard and MIT; and it's called the Health Sciences and Technology Program, joint Ph.D.
program between MIT and Harvard, and M.D. program, MIT and Harvard; and it is now, on the MIT
side, part of this new institute. So, therefore, my responsibilities, as director of that program at MIT,
are also part of my responsibilities as the associate director of this new institute.
Q. Now, Doctor Brown, are you also on the faculty of the division of sleep medicine at Harvard?
A. I am.
Q. And by the way, do you know Doctor Czeisler there at Harvard?
A. I do.
Q. Have you, in fact, studied under Doctor Czeisler in the area of sleep medicine?
A. I did. When I did my I did my undergraduate thesis at Harvard I'm sorry. I'm sorry. I did my
medical school thesis at Harvard Medical School under Doctor Czeisler; and when I did my fellowship
at the Brigham and Women's Hospital after finishing my internship, I also did that with Doctor Czeisler.
Q. And at the present time you do practice anesthesiology at Mass. General Hospital?
A. I do.
Q. I'm going to just go through just just a few of your other many, many, many qualifications,
'cause your CV is quite long. And are you the Director of the Neuroscience Statistics Research
Laboratory at MI At Mass. General; rather?
A. I am.
Q. And are you a visiting assistant professor have you served as a visiting assistant professor at
the University of Chicago, University of Pennsylvania, San Francisco, Johns Hopkins, New Zealand,
Colombia University? Have you visited all of those places as visiting professor?

A. I have.
Q. And more; is that correct?
A. Yes.
Q. And do you work also in the division at Mass. General in the department of anesthesia and
critical care?
A. Yes, that's where I practice anesthesiology.
Q. And I'm just going to ask you about a few more so you're are you a member of various
learned societies in the field of of anesthesia?
A. Yes.
Q. And also in the field of statistics and mathematics?
A. Statistics.
Q. Statistics?
A. Right.
Q. So that the Biometric Society, for example, is that a is that an organization that combines
statistics with biological data
A. Precisely.
Q. to make sense out of them?
A. Precisely. The study of those problems.
Q. And you're a member of the American Society of Anesthesiologists?

A. That's correct.
Q. Is there a board in anesthesia?
A. There is.
Q. And are you board certified?
A. I am.
Q. Are you a member of the Massachusetts Society of Anesthesiologists, the American Association
for the Advancement of Science and the American Association for the Advancement of Science, I
should say?
A. Yes. And I'm a fellow of the American Association for the Advancement of Science.
Q. Okay. And, by the way, what does it mean to be a fellow? Is that an honorary appointment?
A. It is. You're elected to the you're elect to the rank of fellow.
Q. And what is the American Association for the Advancement of Science?
A. The American Association for the Advancement of Science is an organization it's a nonprofit
organization that looks broadly at scientific issues that affect the United States, as well as the world.
And they bring together scientists from broad disciplines to try to find solutions to these problems.
Q. And so they bring you in as one of the scientists that they wanted to help find solutions for these
very world problems?
A. Yes.
Q. Okay. There is a group called the Society For Research in Biological Rhythms. Is that, again, a
society that that focuses on these circadian rhythms?
A. That focuses primarily on biological rhythms.

Q. And what is Bayesian analysis?


A. Bayesian analysis is a subfield of statistics which uses a concept called Bayes' Rule. And what
Bayes' Rule is a way of making beginning information from data where you have essentially a three
step procedure. You make a statement about what you know before you see the problem; you
formalize all you understand about it there; you put together what you collect for your experiment; and
then, after that, you have what you call your "posterior understanding"; and that process of going from
prior to data or likelihood to posterior is what's known as Bayesian statistics or Bayesian inference.
Q. And is that one of the procedures that statisticians use in analyzing a statistical problem?
A. It is one, yes.
Q. And there's an International Society For Bayesian Analysis, which you've been a member of
since 1994; is that correct?
A. That's right.
Q. And then you're also a member of the Society For Neuroscience?
A. That's right.
Q. Correct?
A. That's right.
Q. And the International Anesthesia Research Society?
A. Yes, I'm on the board
Q. And
A. I'm on the board of trustees there.
Q. The American Statistical Association, are you affiliated with them as well?

A. Yes, I'm a fellow of the ASA.


Q. And in 2007, sir, were you elected to the Institute of Medicine nominated and selected to be a
member of the Institute of Medicine?
A. I was.
Q. The I know that you're on the various editorial boards of many, many journals, but I'd just like to
go through a few of them. Are you on the associate editor of Anesthesia and Analgesia, a learned
journal?
A. I was until, I think, 2009 I stepped down from that position.
Q. Okay. And what about the Journal of Neurophysiology?
A. I'm on the editorial board, yes.
Q. You're on the editorial board of the Journal of Neurophysiology?
A. I am.
Q. And also what about the Annals of Applied Statistics? Do you have any association with them?
A. Yeah, I stepped down from there, I think, three years ago 2010.
Q. And are you with a group called Stastica Sinica?
A. Yes, I was a guest editor there for a special issue on neuroscience statistical statistical
problems in neuroscience.
Q. Okay. And the Journal of Endocrinology and Metabolism, have you been an editor there?
A. No, I haven't.

Q. Okay. Oh. Have you been a reviewer there?


A. Reviewer.
Q. Okay. That was my misreading here. Now and have you also reviewed for various learned
journals; is that correct? The Journal of Endocrinology is one; is that correct?
A. Yes.
Q. The Australian New Zealand Journal of Statistics, you've been a reviewer for them?
A. Yes.
Q. Neurocomputing, the the journal called Anesthesiology, have you reviewed for them?
A. Yes, I have.
Q. Have you reviewed for the journal called Sleep?
A. Yes. A while ago. It's been it's been a while, but I did.
Q. Okay. And, in addition to being appointed to the Institute of Medicine, you've been a recipient of
various awards over the years. You graduated from Harvard Medical School magna cum laude; is that
correct?
A. That's correct.
Q. And you also graduated from Harvard College magna cum laude in applied mathematics; is that
correct?
A. That's right.
Q. And you won a a prize called the Harvard Medical School Hewlett Packard Outstanding
Medical Student Medical School Graduate Prize when you graduated from Harvard Medical School;
correct?

A. Yes, I did.
Q. Are you listed as the most cited African American as most cited African American
mathematicians in the Journal of Blacks in Higher Education?
A. I was No. 3 .
Q. You were No. 3?
A. I was No. 3.
Q. That's too bad. Do you know No. 1?
A. I do. He's a good guy. He's a good mathematician too.
Q. Okay. And you have been a National Institutes of Health Pioneer Award? What is that?
A. So the
Q. Director's Pioneer Award?
A. So the Pioneer Awards were set up when Elias Zerhouni was the director of NIH. Their purpose
was to try to unstick research in biomedicine by investing in people that they thought had
groundbreaking ideas. And so the award was a five year award for $2.5 million to go after a problem of
your choosing.
Q. And what was the problem that you chose to investigate?
A. General anesthesia understanding the neuroscience of general anesthesia
A.
Q. So is that one of the things that form the basis for some of your understanding of neuroscience
and general anesthesia?

A. It does.
Q. Okay. Were you the principal investigator in a statistical analysis of human circadian rhythms, a
is that one of the grants you received?
A. Yes.
Q. And have you had various international contributions? We've mentioned some of the visiting
professorships, but have you also spoken in the United Kingdom, Spain, Italy, Canada, New Zealand,
Ireland, Japan, Brazil, Argentina, Denmark, Peru, and Sweden?
A. Yes.
Q. Have you been invited to lecture in all of those places?
A. I was.
Q. Do you hold some patents?
A. Yes. Maybe one or two. Not many.
Q. And have you have listed on your CV certain clinical innovations that you have. One of them is
listed as the "Clinical Examination of General Anesthesia Induced Loss of Consciousness." Is that an
innovation of yours?
A. Yes.
Q. What is it?
A. It's a very simple idea; and that is, when we're in medical school, we learn how to do a
neurological exam to figure out the state of a patient who might have a neurological disorder maybe
the patient has had a stroke or has a neurodegenerative disease. And you learn to do a neuro exam so
you can figure out where in the body the effect of the disease is occurring. So what's interesting is,
we learn that in medical school, but we don't apply it to anesthesiology when we practice. Yet, in front
of us every day, as patients transition in and out of being conscious, unconscious, and then conscious
again, there are very similar changes that occur to the ones that occur when people are going in and
out of comas. So what I've done is work out a way to use the neurological exam particularly the coma

exam to track the state of patients as they come in and out of anesthesia, as a more refined way
actually, more clinically refined way to understand their state of anesthesia
A.
Q. And does anesthesia the state of anesthesia bear any resemblance to the state of coma?
A. It does.
Q. And did you also have you also studied the use of high density electroencephalogram
recordings in loss of consciousness under general anesthesia?
A. I have.
Q. And do you have an innovation in that area?
A. Well, there what we're working on now is the idea of again, another very simple idea Using the
EEG in real-time, converting it into a spectrum, and being able to read the state of the brain under
anesthesia
A. This is something that is very simple to do. It's actually available on many monitors that are
now commercially available. And it's a way for anesthesiologists to have a much clearer picture of
what's happening to the brain states of their patients when they're under anesthesia
A. So they can have an idea of whether or not someone was aware; perhaps whether or not
they're adequately anesthetized. So that's an innovation that we're working on now.
Q. Okay. And then you by the way, you used you mentioned the term "EEG." Again, would you
remind the jury what an EEG is electroencephalogram is.
A. I'm sorry. The EEG
Q. What?
A. Pardon?

Q. Go ahead, please.
A. So the EEG is a device that we it's a collection of electrodes that we can place on the
patient's head.
A. Okay. It's a device which is it's a set of electrodes which you can place on a patient's head,
and you can measure the brain waves. The brain waves that you record from a patient are just a set
of very small electrical potentials. And the reason you pick up these potentials is that the activity in our
brains is creates electrical currents; and these electrical currents can be detected on the scalp; and
that's what an electrical that's what an electroencephalogram is. We call it an EEG. Or, simply stated,
it's a brain wave monitor. When we talk about the brain waves, you're talking about these very small
potentials that are readily picked up at the scalp because of the activity that's ongoing in the brain.
Q. Does the normal EEG also record eye movements or the potential for eye movements?
A. You can see the effects of eye movements on the EEG, because an eye movement is a very
large muscle movement relative to the potentials that come from the brain. So, as a consequence,
you can actually see it on the EEG, or you can place a special electrode maybe near the eyes to
isolate that effect specifically. And if you want to remove it from your EEG, you can use it to do that.
So you can remove the effect of it. So, yes, do you you can you do see it on the on the EEG.
Q. Okay. Now, I'm just going to just very briefly you've written journal articles. And about how
many articles in peer reviewed journals have you written?
A. Around 140 or so.
Q. Okay. And have you also written chapters in textbooks?
A. I have.
Q. And various educational materials for seminars and for various groups?
A. Yes.
Q. And have you written editorials in in well, I have listed here about 17 different journals where
you've written editorials on medical matters
Q. is that correct? You can answer.

A. Yes, I have. I don't know the exact number. I don't have my CV in front of me, but I that
sounds about right.
Q. I just have one more question to you about the credentials. Were you elected to some a group
called the American Academy of Arts and Sciences?
A. Yes, I was.
Q. And what is the American Academy of Arts and Sciences?
A. So the American Academy of Arts and Sciences is one of the oldest one of the oldest honorary
societies in the United States. I think it was set up by John Adams in the s, shortly after the
American Revolution. And every year they pick a set of new members from the sciences, as well as
the arts. And, again, it's kind of like the American Association for the Advancement of Science. It's a
group of people who come together to go after important problems you know, people who are
considered leaders in their fields to come and try to solve important problems that are confronting the
country and the world.
Q. And when was it you were selected to be a member of the National Academy?
A. The American Academy of Arts and Sciences.
Q. American Academy of Sciences.
A. American Academy of Arts and Sciences.
Q. Of Arts and Sciences.
A. April 6
Q. I'm sorry.
A. April of 5 April of . 2012

Q. Okay. Now, at our request Koskoff Koskoff & Bieder did you agree to consult with us
concerning the matters surrounding the death of Michael Jackson?
A. I did.
Q. And have you accepted for yourself any money for the work that you've done on this case?
A. Yes, I've billed your law firm for my time at a rate of $1,000, an hour, but none of the funds
have come to me. They've gone to they've been donated to Mass. General Hospital.
Q. So at your request, did we donate those funds to Mass. General Hospital?
A. You did.
Q. And have we donated at your request $75,000, to the Mass. General Hospital?
A. That's right.
Q. Have you ever testified in court before?
A. I never have. So I've never testified in court. I've given depositions before, but I've never
testified in court.
Q. Okay. And now I'm going to ask you some questions in connection with sort of a very limited
area here today, and it's going to relate to a chart that was introduced into evidence, but we're going
to need some background for it. And the first thing I have to ask you is, are there are there different
types of anesthesia?
A. Yes, there are.
Q. What are the what are the types?
A. So, roughly speaking, we can divide anesthesia into two groups We can talk about general
anesthesia and perhaps general anesthesia and sedation into one group; and then another group is
regional anesthesia

A.
Q. Now, the type of anesthesia that we're relating to in the Jackson case is which of those two
types?
A. It would be general anesthesia and sedation.
Q. Okay. And let's talk about general anesthesia
A. And can you tell me whether or not general anesthesia is considered a is intended to be a
reversible condition?
A. It is. General anesthesia so in this article that we wrote in the New England Journal in , we
made every effort to make this very, very explicit, what the state of general anesthesia is. So general
anesthesia is a condition that consists of four behavioral states and a physiological state. So the
behavioral states are being unconscious, having analgesia meaning you don't feel pain; not moving
because it's nice if you're not moving around when the surgeons are operating; and then, to that,
having amnesia
A. So did I say that amnesia, analgesia, unconsciousness, and immobility. Right. Amnesia, not
remembering what's happening to you. And then the other part
Q. Now, you
A. I'm sorry?
Q. Go ahead. I'm sorry. Continue.
A. The final part of it is physiological stability, meaning that we maintain your heart rate, your blood
pressure, your breathing, your body temperature all stable during this time while we put you in this
condition so that you can undergo surgery or what would otherwise be an extremely painful or
traumatic diagnostic procedure.
Q. Okay. Now, you mentioned an article in the New England Journal of medicine in . Is that an
article that that you wrote concerning anesthesia?
A. It is.

Q. And what is what is the what is the title of that article?


A. The title is "General Anesthesia, Sleep, and Com
Q. Okay. And what was the purpose of writing that article?
A. The purpose of writing it was several fold The main one to begin with was to make a clean
statement of what general anesthesia is. And in that, we we state right off the bat the definition that I
gave you, and then also point out that general anesthesia is a type of com a It's a reversible com
A. Because in order to provide in order to operate on someone to provide surgery to someone or
have them undergo a very painful diagnostic procedure, they have to be insensate. They have to be in
a condition in which they can tolerate such a traumatic insult. And that is, in effect, what a coma is. A
coma is the state where the patient is unable to perceive or respond to any stimulus that comes in
from the outside environment. Now, unlike comas, which occur because you have a brain injury, the
coma of anesthesia is reversible. We give you a certain set of drugs; we maintain the delivery of those
drugs for a period during the surgery; once the surgery is completed, we turn those drugs off; and we
allow the patient to to recover. So the person goes into the coma and comes back. The reason I said
we wanted to try to make the definition clear is that there is a tendency for people to call general
anesthesia sleep; and it's not sleep. You would not be able to tolerate an operation a major surgical
procedure if you were asleep. And anesthesiologists have the habit of saying "sleep" when they talk to
their patients; and this is understandable, because saying to someone, I'm going to put you into a
reversible coma would be quite disquieting. However, at the same time, it turns out, when it's time to
actually speak precisely about what's occurring, they're unable to do that. So we wanted to clarify
these points. That's just on the definition side. Then what I wanted to do was lay the foundation for a
neuroscience framework for studying general anesthesia
A. So the other thing that we do in great detail in that article is map out the neurocircuitry of how
the various anesthetics three of the four of the important classes of anesthetics work; and this was
a novel undertaking.
Q. Now, is one of the anesthetics that that you have been familiar with working with propofol?
A. It is.
Q. And did you review, by the way, the autopsy of Michael Jackson and the toxicology reports?
A. I did.

Q. And was there was propofol found in his system at the time of his death?
A. It was.
Q. Okay. Tell me about your use of do you use propofol on a regular basis?
A. We I can honestly say we administer propofol to almost every patient I take care of. It's the
it's the most widely used anesthetic, either as an agent to induce anesthesia, or to induce and
maintain anesthesia, or as or as a sedative for procedures that don't require full general anesthesia
A. So it's the most common
Q. Is it
A. I'm sorry.
Q. Go ahead. Keep going.
A. It's the most common
Q. No. I'm sorry. I interrupted you.
A. It's the most commonly used anesthetic.
Q. And you said there are essentially three ways in which it's used, I think. What were they?
A. So to induce anesthesia, to bring the person to bring the patient from a state of being awake
into the state of coma; to maintain anesthesia that is, once you're in the state of once your
anesthetized, administering it as an infusion to maintain you there; and then also to sedate you. If you
needed a procedure let's say like a colonoscopy, which shouldn't require full general anesthesia, but
the procedure would be more easily tolerated if you were less conscious or sedated. Then we can
give an infusion of propofol to do that as well.
Q. How potent a drug is propofol, if you can quantify it in some way?

A. I mean, you know, that's a challenging question to give a like, a sort of a quick answer to. It's
a drug that so relative to let's say, some of the some of the other drugs that are used, let's say, like
the Valium like drugs, you know, benzodiazepines
Q. Uh huh. Yes.
A. it is actually quite potent on a ccpercc basis. You know, if you took, you know, a cc of cc's of
propofol, you'd have a much more profound effect on the patient's level of arousal, compared to which
midazolam, which is a benzodiazapine, just the Valium like drug. Just sort of speaking roughly.
Q. And as a researcher, you made as a researcher you made propofol a part of your research.
A. It is. It's been one of the primary focuses of our research during the last several years.
Q. And without being modest, are you considered one of the world's authorities on the anesthetic
effects of propofol on the brain?
A. Yes.
Q. Is there anyone that you know of who's studied this drug and the effects on the brain more
than you have?
A. I don't think there's anyone who's studied it from in as in the detail from the perspective that we
have. In other words, our perspective is that this is a neuroscience phenomenon. We need to study it
at all levels, both in patients, in volunteers, and in animal models doing modeling, as well as
developing algorithms to analyze the data So no other investigator has a program that integrates
information from all those sources.
Q. Now, in in your review of the Michael Jackson autopsy and the the consultation report of Dr.
Selma Calmes did you see her statement? I want you to assume that she said in that that, quote, "The
levels of propofol found on toxicology exam are similar to those found during general anesthesia for
major surgery, intraabdominal, with propofol infusions after a bolus induction." Did you read that in
your report?
A. I did.
Q. And do you agree or disagree with that statement?

A. In terms of the levels that were there on the in the toxicology?


Q. Yes. Yes.
A. I do. The reason I do is that we just published a paper in the Proceedings of the National
Academy of Science in March of this past year where we used guidelines based on the delivery of
propofol in the operating room to target patients going under becoming unconscious with propofol, and
then recovering consciousness. And the targeted blood levels that we sought to do this were in the
range that appear in the toxicology report. So what does that mean? That means that we targeted
getting blood levels for our volunteer subjects that would produce unconsciousness; and those are
the same levels that were that are in the that were found in Mr. Jackson at autopsy. And the infusion
rates that we used are the same infusion rates that we use when we be when we would be
undertaking or giving anesthesia for a major abdominal procedure. So that's why I say it's consistent
with my understanding of my understanding of how we deliver anesthesia or how of what or what I
would expect will be found from our research and what I know clinically.
Q. Okay. So you've actually done that work and looked at that that issue.
A. Yes.
Q. Doctor Brown, now I want to talk a little bit about sleep. You're not a board certified sleep
expert; is that correct?
A. That's correct.
Q. However, have you have you, as an anesthesiologist, studied the neurophysiology of how
propofol acts on the sleep circuits in the brain?
A. We have. We've we've studied how propofol acts on the sleep circuits of the brain. We've also
studied the the basic physiology of sleep. In other words, how does the body induce sleep?
Q. So that so that you in the course of your work and research, you've had experience in actually
studying the neurophysiology of sleep and how sleep operates?
A. Right. And we we've written about that relationship in that New England Journal article, as well
as in an article we published the following year in the Annual Review of Neuroscience.
Q. Okay. So has sleep been one of the focuses of your research in in recent years?

A. Well, to be clear, not sleep per se, but sleep to the extent that understanding it as an altered
state of arousal which intersects with anesthesia, yes.
Q. Okay. And have you studied the effects of propofol on brain wave activity compared to brain
wave activity during natural sleep?
A. I have.
Q. And by the way, do you know Dr. Charles you did mention you know Doctor Czeisler. Is he is
he a world renowned sleep expert?
A. He is. Sleep and sleep
Q. And
A. sleep and circadian physiology.
Q. Okay. In the course of your research on propofol and brain circuits, have you gained an
understanding of how sleep occurs?
A. Yes. So to to be clear, we've taken the ideas that are present in the literature about how the
sleep circuits work; and we've used those to understand how anesthetics may affect those circuits.
Q. And is that the paper one of the papers you published in the New England Journal about
that very subject?
A. Yes, exactly. Also, very and then related ideas in the Annual Review of Neuroscience article
was published the subsequent year.
Q. And is one of those articles is called "General Anesthesia, Sleep, and Coma "
A. That's right.
Q. is that right? And which is that article? Is that the New England Journal article?

A. The New England Journal article, yes.


Q. And does it compare those various states?
A. It does.
Q. Okay. Before that work was published, had this work ever been done before?
A. No
A. No one had taken time to that that was one of the that was precisely the reason I I wrote the
paper was that no one had taken time to put general anesthesia next to sleep next to coma and say,
What's the relationship? And that's something which is important not only for us to understand as
anesthesiologists, it's important for us to understand so we can speak to the public in an informed
way. But it's also important for our colleagues in other areas of clinical neuroscience like neurology,
psychiatry, psychology, neurosurgery, sleep medicine to appreciate these relationships, because there
there is a lot of misunderstanding, yet the links are very compelling and very important, because they
give us ideas on how the brain functions and also insights into how we can design new therapies. And
so I thought it was crucial to put these things in one place where everybody would be able to sort of
see and understand them.
Q. Now, can you tell us, based on your research, whether or not the state of the brain during
propofol induced anesthesia is sleep; isn't sleep?
A. It's not it's not sleep.
Q. And do anesthesiologists, though, call it sleep?
A. Yes. And to be fair, it's not that anesthesiologists do not appreciate that it's not sleep. What
they haven't taken time to do is to develop the vocabulary that allows them to speak in a nuanced
way, both when they're talking with their colleagues, and when they're talking with their patients. It's
just very convenient to say "sleep" when they're talking with their patients. However, a very simple
way to say it to a patient which would accomplish the same goal is that, you know, Mr. Jones, you're
going to have general anesthesia for your operation. I'm going to what that means is, you're going to
be unconscious; you're not going to be aware of what's going on; you're not going to remember a thing
that happens to you. You're going to feel you know, no pain. You won't be moving around while the
operation occurs; and we're going to make sure you're breathing well, your heart rate is fine; that you're
you know, you're kept warm and comfortable. And so that's going to be our responsibility during the
case. Now, I've told them exactly just the lay definition of general anesthesia; I didn't have to mention
sleep; and I think most patients can understand that. So that was, again, one of the goals of this
particular paper is to make those terms and that concept clear, because we have need to be able to

talk to our patients, and we need to be able to do science in an informed way and not and not sort of
mislead patients. It would be quite unfortunate if someone came to you and said, Now, I can clearly
see I can't be asleep while I'm having my surgery, because I because I would wake up. And if
someone ever comes back to you with a rejoinder like that, you know, we it suggests we don't know
what we're saying. So cleaning up the vocabulary so we can speak to people and also do our science
is one of the reasons I wanted to make these points very precise.
Q. Okay. And to the extent that anyone uses propofol, any medical practitioner uses propofol as an
agent to produce sleep, would they be mistaken?
A. They would they would be tremendously mistaken.
Q. Now, in order to discover the differences between sleep and anesthesia, would it be of
assistance to you to demonstrate the various brain waves that that you have studied by EEGs?
A. Sure. That would be that would be helpful. It's one way of
Q. And do you have do you have with you a chart that would help explain that?
A. Yes, I do.
Q. Okay. Would you please show us the chart and and demonstrate for us what it demonstrates.
A. Sure. MS. REILLY Michael, can we mark it as an exhibit first?
MR. KOSKOFF Certainly. Let's mark this
MS. CAHAN .
MR. KOSKOFF . That sounds like a good idea.
Q. Okay. Why don't you focus it on the area that you feel we need to focus it on to understand it.
A. Okay. So I'm going to do this in three stages I'm going to talk about awake first; I'll talk about
sleep; then I'll talk about general anesthesia

Q. Okay.
A. So let's start with this diagram up here, which is the awake state. So there's a left-hand side;
there's a right-hand side; and these are two different awake states. This awake state over here is with
EEG that are EEG electrodes that are placed here on the front of the head. And you see this activity
here, which is often called "desynchronized" or "irregular"; and it's usually of a very low amplitude. This
is a very typical EEG pattern that you would see in someone who is just sitting there with his or her
eyes open, and you record from the front of the head. If you now place the electrodes in the back
of the head, have the person close his or her eyes, you get an entirely different pattern. You get this
pattern here, which is these set of oscillations which are going up or down at about cycles per
second. This is called an "alpha oscillation." Most people have it. Perhaps about percent of people
don't. And we tend to lose it as we get older. So this is from the back of the head. And, again, what
the EEG is measuring are these very small electrical potentials that reflect the activity of the brain
coming from multiple sources inside. Now, let's just talk about sleep. So Column this left this right
well, looking at it, the right-hand column here is "sleep." And what I've put down here are the various
stages of sleep. So there are roughly two main stages of sleep There's REM, and nonREM. "REM"
meaning rapid eye movement sleep; "nonREM" meaning nonrapid eye movement sleep. And they have
very different EEG signatures; and they have different physiologic characteristics. So just to remind
you, when you're in rapid eye movement sleep, the eyes are moving; they're darting back and forth;
the brain is actually in somewhat of an awake state. The brain is actually active. The body is actually
somewhat paralyzed. The breathing is and heart rate are actually irregular. When you're in nonREM
sleep, the EEG has a much more has a much slower pattern. The heart rate is slower. The muscle
tone is a little bit higher. The breathing is a little bit more regular. Now, so the the key thing to
understand so so that's the first thing. Sleep is two states REM, nonREM. Now, how do you fall off to
sleep? When you fall off to sleep, the first thing you do is you go into nonREM Stage 1 . And you see
this sort of kind of low frequency oscillation here; and it's a and it has these sort of fine pieces on top.
So it looks like a transition from being away into this particular state. Then, following that, as the brain
shuts down more, you go into Stage 2 nonREM sleep. And Stage 2 nonREM sleep is made up of these
little characteristic bursts right here. Right there; right there; right there; right there. They're called
spindles. They're called sleep spindles; and these things here which are called K complexes. Those
actually demarcate. They actually define Stage nonREM 1sleep. Then Stage 3 sleep, or what's called
slow wave sleep or now Stage 3/4 sleep, because Stages 3 and 4 are put together, is really just slow
waves. And you can see that. You see these waves which are large in amplitude; they're moving very
slowly. Now, here's how sleep works You go into nonREM sleep ; you transition down to nonREM3 ;
then you jump up to REM. You stay there for a period; and you go back and forth with this cycle,
between the REM the nonREM states, and the REM states. You do that roughly every minutes
through the course of the night for seven to eight hours. The deepest stages of Stage 3 sleep are
usually reached in the first two of two cycles, you know, during the night; and then after that, you don't
cycle as deeply. It's not surprising that the REM pattern looks like the awake pattern; because this is
very close to the awake pattern. Because very often when people go into REM, they actually may
wake up for a brief pattern, as opposed to going into the REM pattern, then they'll drop into REM, and
then they'll fall back into the nonREM state. So that is basically sleep. Over here what we've what
we've done is diagram out the stages of general anesthesia that one would go through if the main
hypnotic agent the main drug that's keeping you unconscious were propofol. So this is actually from
propofol. If I give you a small dose of an anesthetic in this case propofol as opposed to becoming
unconscious or the EEG slowing down, it actually speeds up. This is a state called "paradoxical
excitation." It's paradoxical because you give a drug which is supposed to slow the brain down, but it
actually speeds it up. And that might seem a bit counterintuitive at first, but actually this is what

happens when you drink alcohol when you go to a cocktail party. This is like the buzz. This is like the
high. And alcohol itself is a very potent anesthetic. In sufficient doses it could, you know, render you
into a very profound coma also. So so this is not unexpected. Then, as you give more and more of
the anesthetic in this case propofol the EEG now does start to slow; and it goes through a series of
patterns; and the the oscillations get to be deeper, and the frequencies tend to become lower, so
much so you can go to a period here which is called "burst suppression," or we can give enough
propofol in order to have an entirely flat or isoelectric EEG. So two very quick points
A. As I was saying, two quick points During sleep you have a natural oscillation between these two
states roughly every minutes throughout the course of the night for seven to eight hours. When we
place you under general anesthesia, we bring you to one of these states let's say like this one
here; and we hold you there for the hour, two hours, three hours, whatever the time period is that
you're going to have the surgery. So being held in this state here simply is not the same as the brain
moving naturally between REM and nonREM sleep. So, therefore, if you're in this state here under
general anesthesia, there's no way in the world that you could have this going on at the same time
(indicating). By the same token, if you are placed in this state here, let's say for sedation, you're
having a procedure that doesn't require full general anesthesia, you need to be sedated, then you're
held in this state. While you're in this state, again, you're not oscillating. So this is not this state this
anesthetic state is not this state here (indicating). And then the final state here, which is one we
actually use, this is called "burst suppression"; this is a very profound state of brain shutdown.
A. This state here is burst suppression; and we actually use it therapeutically. You may remember
about two and a half years ago when Congresswoman Gabrielle Giffords received her gunshot wound
injury to the head, there was a lot of discussion about the therapy she got. And when the press heard
that she was going to be placed in a medical coma, there's a whole series of articles written around
January th January th, January th of the reason I know is because the Scientific American reporter
called me up to ask me, What's medical coma? Well, what all medical coma is is giving enough drug
and in this case propofol to bring you down to this state, hold you there so that the brain can repair so
that the swelling can go down; so that the energy levels can be reduced, and the brain can be allowed
to heal. So you do this the patient this is profoundly unconscious; okay. And then, when and you
may stay the patient may be maintained in this state for several days, maybe even a week. Once
you're done, you bring them out. So the whole time on the EEG you see this pattern. While this is
there, again, you can't have these sleep oscillatory patterns going on. So that's why that's kind of a
rough overview just speaking in terms of the EEG patterns why general anesthesia, induced with
propofol whether it's for sedation, whether it's for excuse me propofol, whether it's used for sedation,
whether it's used for general anesthesia, whether it's used for medical coma is not sleep.
Q. Okay. Thank you, Doctor. You may resume your seat at this point. So let me just ask you this
quite clearly and directly In a patient who's undergoing Propofol induced sedation or general
anesthesia, is there any REM sleep?
A. No.

Q. In the patient who is undergoing Propofol induced sedation or general anesthesia, is there any
nonREM sleep?
A. No.
Q. Do such patients undergo the normal sleep cycles?
A. Okay. While they're under the anesthesia
Q. Yes.
A. no.
Q. Okay. And so even if the levels of propofol given to a patient are not enough to put him all the
way into general anesthesia but are only enough to put him into a state of sedation, does that person
have REM sleep?
A. If that state of sedation is being created by placing them there and maintaining it with a with an
infusion, no, they will not have the states of they will not have REM and nonREM sleep.
Q. And is there and there's no nonREM sleep in that state either; is that correct?
A. No nonREM or REM.
Q. Okay. Once the drugs take over, are you going to get any normal sleep? By "the drugs" I'm
referring to propofol here.
A. Okay. So once the drug is initiated and maintained; right
Q. Yes.
A. you don't have REM or nonREM sleep
Q. Okay. Now

A. initiated and maintained. I'm sorry.


Q. Yes. Okay. And now, Doctor Brown, you mentioned that the brain has certain sleep circuits;
is that correct?
A. Yes.
Q. And would you just very briefly tell us what those sleep circuits are and how they work; and if
you'd like to use a pad or markers or anything to do so, please feel free to do that.
A. Sure. So I'll just draw I'll just draw it very schematically here. So the brainstem. So the part the
lower part of the brain (witness draws diagram). So this is the this is the midbrain up here (indicating).
This is what we call the pons. And here's the medulla. So this is the lower part of the brain. It's the
area that is responsible for maintaining sort of the you know, heart rate, respiratory control; and also
the arousal centers are sitting here (indicating). So the sleep circuits kind of start right here. This is
sort of kind of a brief little schematic. About here is where the hypothalamus is (indicating). So the
hypothalamus is a very important kind of regulatory center. It controls the circadian rhythms,
controls appetite. It controls actually the sleep circuits. There's a series of nuclei in here. We won't go
into the details of those. But let's just talk about the hypothalamus. Then so that's the control center,
kind of like command and control. And then sitting here, in the various parts of the midbrain again,
this midbrain and pons, this area of the brain, which is sort of right down here at the base you have a
whole set of arousal centers. There's one here I'm just going to use a different color. There's one
here, which is the ventral periaqueductal grey. There's another one here; two together here; there's one
down here; there's one here, one here (indicating). So what are these? These are groups of nuclei,
groups of nerve cells that send very long nerve endings up to the brain, and they keep us awake. They
keep us aroused. So to be conscious, you have to have two things You have to be awake; and you
have to be able to process. So this part of the brain sends axons up to the cortex, which would be up
here; and it keeps us awake; and it allows the cortex to process. You have to integrate those two
features in order to have consciousness. Now, here's how the sleep circuits work. I'm going to draw
this in red, because this comes over; they have connections to all of the centers. All these major
arousal centers here in the brainstem and I'm going to put little labels on them for what they stand for
Locus coeruleus; this is dorsal raphe; and this one is going to be very important later on LDT/PPT.
And just one other little detail These nuclei each or these centers give off different neurotransmitters.
So this one gives off norepinephrine kind of like adrenalin from the brain. This one gives or serotonin.
That's the one you think about with depression. This one here gives off dopamine, the reward sort of
neurotransmitter. This one here gives or acetylcholine; all right? So how does this work? In order to fall
off to sleep, you have to shut the brain down. So if these guys are the major arousal centers that are
keeping the brain awake, the way this works is, the hypothalamus this area called the ventral lateral
preoptic area or the median preoptive area the name isn't important it comes on. It comes on; and it
shuts these areas down. Shuts them all down. When that occurs, if you're looking at your EEG,
what you see is this (indicating).
A. Okay. What you see is this; and this is this first this is the first stage nonREM . Okay. Now, as
this inhibition increases, you now go into this pattern where you see the spindles. 2 a bit; and that's

nonREM (witness marks diagram). All right. Now, the inhibition increases more; and you get the third
pattern, which I'm just going to draw very simply here like this. And this is nonREM , or what we call the
"slow waves." And it's the most obvious, because you can see you have slow waves (indicating). Now,
here's the key thing; all right. This is the thing that really separates physiology which the body is
doing from something that we do with drugs. For you to go into REM sleep, you have to be in this
state where these things are shut down, and one center one center has to become active. And the
center that becomes active is this one right here, this LDT/PPT. This guy says, Wait. Hey, I'm done,
guys. I'm going to come active. You know, I'm going to go tell the cortex to turn on. And that's exactly
what it does. It projects from the thalamus and turns the cortex on. That's why I'm just going to draw
this in a different color when that happens, what you get over here is your REM pattern. Okay. So this
is how the circuits this is how these circuits, sitting here in the hypothalamus and the midbrain and
pons, actually induce sleep. And so the cycling that occurs because you have this command and
control center here, which tells everybody to shut down; one center gets released, when everybody
shuts down, you go through the stages of nonREM. When this center here gets liberated, it generates
REM. And that cycling occurs throughout the night for, again, every minutes, roughly seven to eight
hours. Now, it's very simple to see why propofol won't produce sleep. Propofol will not produce
sleep. Here's the reason All these little inhibitory connections here that are used to shut this down,
they have a neurotransmitter called "GABA. " Now, what propofol does is, anywhere in the brain that
there's a GABA A receptor, when you administer propofol, because it's so soluble, it goes there. So
this is a very refined, very delicate, very balanced sort of physiologic circuit. So what propofol so it
allows this system to sort of come on and oscillate between these two states. When you give propofol,
it's very indiscriminate. It comes in, and it knocks out all of these circuits here (indicating). In addition,
you have your respiratory centers down here in the medulla, and also in the pons. Propofol also knocks
those out. And, in addition, up here in the cortex I'm just going to write "cortex" here and put it
down here propofol knocks out all the all the neurons or excuse me it enhances inhibition of all the
inhibitory neurons in the cortex as well. So simply stated, cortex the propofol overwhelms the sleep
circuit, overwhelms the respiratory circuit, overwhelms the cortex; and generates dynamics that are
completely different from what you see with sleep. So once you've administer propofol, this sort of
refined dynamic that you see with sleep simply can't occur.
Q. Thank you, Doctor, that's a very, very enlightening explanation. MS. REILLY And, Michael,
before we go on, we're just going to put an Exhibit sticker on this drawing.
Q. So, Doctor, when we broke off, you had just described how the sleep mechanism works; and I
want to just ask you, if a person is under Propofol induced sedation or general anesthesia, is it possible
for the brain to go through REM and nonREM sleep cycles?
A. No. It's not possible.
Q. Okay. Now, Doctor, did you review slide , Plaintiffs' Exhibit that was introduced as a as a
demonstrative exhibit during Doctor Czeisler's testimony?
A. Yes, I did.

Q. Okay. I just want to ask you about some of the items on the right hand side of the chart. Can
you tell me whether general or not whether or not general anesthesia is a drug induced coma?
A. It is. It is.
Q. Does this coma fulfill the biological need for sleep?
A. It doesn't.
Q. Does it provide for consciousness at all?
A. So if you're under general anesthesia, then one of the first criteria for being one of the one of
the first the first criterion is being unconscious. So, therefore, you cannot be conscious under general
anesthesia.
Q. Can you tell me whether or not there's profound unresponsiveness?
A. When you're under general anesthesia, you achieve unresponsiveness.
Q. And when in the Propofol induced general anesthesia, can they can the patient be awakened
until the propofol is is withdrawn?
A. So let me just clarify something here.
Q. Okay.
A. With propofol, it cannot produce general anesthesia by itself. What propofol can do
Q. Okay.
A. is produce unconsciousness. If someone is unconscious, you will get amnesia, because if
you're truly unconscious, you can't remember. Someone in a coma can't remember; all right. Now, to
get the other conditions the other behavioral conditions, let's say, like analgesia you have to give
other drugs; okay?
Q. I get it.

A. All right?
Q. Okay.
A. Now, for surgery for light procedures, the level of being insensate because you've altered
arousal the level of propofol is sufficient. And then the final thing is, the muscle relaxation; you get a
mild bit of muscle relaxation with propofol, but what we typically do for surgery is that we add a muscle
relaxant in addition. So propofol, to be clear, is predominantly providing the unconsciousness state of
general anesthesia.
Q. Actually, don't look at the chart, but one of the the chart says on the righthand side, "No REM
sleep." Is REM sleep possible with propofol sedation?
A. No.
Q. Is REM sleep is nonREM sleep proper possible with propofol sedation or anesthesia?
A. Or general anesthesia?
Q. Yes.
A. No.
Q. And what is isoelectric EEG? What does that mean?
A. So the isoelectric EEG actually, it's on the panel here. We can just actually show you. It's on the
figure.
A. The isoelectric EEG basically means flat line.
Q. Uh huh. Okay.
A. So this bottom line here so after burst suppression, if you give more propofol, the burst will get
smaller and smaller, and all you'll have is just the flat the flat line here, which is this (indicating).

Q. Uhhuh.
A. So this is the flat line or isoelectric; and this is the deepest state of brain shutdown that we can
produce with propofol; and it's actually done when there's surgery that takes place when you do total
circulatory arrest you actually stop the heart, and you operate on a person that has a heart not beating,
because of a very tricky maybe valve repair, or they may be operating in the brain. So you would
actually induce this state in someone. So this is the most profound state of coma that can be induced
with propofol. It's usually done with the drugs, as well as hypothermia as well, not just propofol alone.
Q. Okay. Does general anesthesia in general anesthesia, is there general is there an
insensitivity to pain?
A. Yes, there is. That's one of the criteria meaning, what we call "analgesia" or "antinociception";
that to have general anesthesia, you have to you have to make it so that the procedure the patient is
undergoing does not hurt.
Q. Okay. And is that insensitivity to pain that's caused by that is not caused by the propofol
A. Okay. To be clear
Q. is that correct?
A. Well, to be clear
Q. Yeah.
A. propofol can produce a small part of it, right, and the reason it can
Q. Okay.
A. produce a small part of it is, because it's not because it's treating the pain circuit; it's making
you unaware. If you're unaware so to to be very concrete, when someone goes for a colonoscopy
which is a procedure that's not that painful, but it's uncomfortable they often don't give you have a
pain medication to go through the procedure; they give you propofol.
Q. Uhhuh.

A. And what propofol is doing is it's making you sort of lightly unconscious. It's mildly sedating you.
So when you're mildly sedated, you're also unaware, and you can be unaware to pain. So that's how
propofol is actually providing some component of analgesia, if you would, all right. So, in general,
you're right. For general anesthesia, we would add in another drug, which is typically one of the opioids
or a narcotic or ketamine, for example.
Q. All right. And then the last thing I wanted to ask you is that, assuming that Doctor Czeisler
testified that it dissipates the sleep drive without fulfilling the sleep need, you've already talked about
the fact that it doesn't fulfill the sleep need, but can you tell me, is there any neurophysiological
reason why it would dissipate the sleep drive?
A. Well, I think the reason for the reason for dissipating the sleep drive probably relates to
something that's seen very commonly with propofol particularly when patients have propofol for
procedures that don't require general anesthesia like sedation they commonly report feeling good,
feeling refreshed. All right. So why does that how is that occurring? Well, one of the things that we
know is that propofol actually causes release of dopamine. I said earlier that dopamine is one of the
neurotransmitters. It's released at a number of places in the brain; and it serves multiple roles. So one
of the roles that dopamine serves is in motor function. I think most of us are aware that people that
have Parkinson's disease, they have very difficult sort of rigid motion rigid movements; and this is
because they have a deficiency in dopamine. Dopamine is also important for cognition. It's also
important in reward. There are a lot of studies that show when rewards are given, there's increased
activity in the parts of the brain that produce dopamine. One of them is the nucleus accumbens. So
dopamine is kind of like the endorphins that we all hear about. When you're running, they the levels
go up. When you're the levels go up when you're the levels go up when you are running, and you're
enjoying the run. Dopamine does something very, very similar. It gives you this good feeling. And
what's most likely occurring is that propofol is inducing this release of dopamine; that's being
interpreted as the refreshing sensation of that can be interpreted as the refreshing sensation of natural
sleep, when, in point of fact, based on what I explained earlier, propofol cannot produce natural sleep.
So if you asked me what would be a possible mechanism for dissipating a sleep drive, that's what I
that's what I that is what it would most likely be.
Q. So, Doctor Brown, you were just talking about this idea of the dopamine release that propofol
causes.
A. Yes.
Q. And you said that it gives a patient a good feeling, similar to running?
A. Similar to endorphins released during running.
Q. Right. And is that something that you've described as a sense of euphoria previously?

A. What I described as a sense of euphoria yes, I I did use the term "euphoria. "
Q. Okay. And you're saying now that that sense of euphoria is the same thing as feeling well
rested, or is that two different sensations?
A. So what I'm trying to do is again, this is a this is a question of vocabulary mapping on to actual
science. So what I'm trying to do is give you a sense of kind of a lay explanation of what these
sensations are like. So I'm not talking about anything different. I'm trying to give you a sense in lay
terms of what these states are like.
Q. Okay. So there's a good a good feeling that's associated with propofol; and that good feeling
some people could interpret as feeling refreshed and other people could interpret as euphoria; is that
are we on the same ?
A. So some people could interpret it as as feeling refreshed, feeling, you know, invigorated.
Some people may interpret it as euphori
A. And, actually, what happens is, it's it's really, really interesting. When you watch people after
they've had it, they they a very common type of statement is, you know, Wow, that that felt good. That
felt great.
Q. Okay. But there's there's dopamine just to make sure we're clear, there's a dopamine release,
and people interpret that different ways. But that's what you're ascribing to that's what you're saying
would cause some people to say, I feel refreshed; I feel rested when they awaken after propofol
sedation?
A. I think that's the most probable reason there is.
Q. Okay. And is that speculation on your part, or is there some research that confirms that?
A. There is robust research to the extent that we make extrapolations all the time from animal
models to understanding things in humans. So to to understand this in humans it's only now that we
are in a position to actually simultaneously measure possibly in humans release of dopamine from
an area like that. So the study that I described with release of the dopamine is actually a rat study; and
the correlation between what's known in the body of neuroscience between this reward sensation
there are tons of studies which have looked at reward when you put that together with what's known
about what propofol does, when you put that together with the clinical picture, I think there's an
extremely tight linkage and correlation between that.
Q. Okay. Are there human studies at this point or or no, that address that issue?

A. Are there human studies of what?


Q. The that show the dopamine release as a result of propofol sedation?
A. As I said, we've only only now are imaging techniques making it possible to actually label and
track dopamine on this level. So looking specifically at this question, no. But, again, the correlation,
putting together the entire body of information is extremely compelling.
Q. And you said that sense of the dopamine release tends to happen where people are sedated
with propofol, as opposed to under general anesthesia from propofol; is that right?
A. So no, it's not that I said that that doesn't happen then. It may happen in both cases; and
there's no reason to think that it doesn't. The behavioral response is something you can you can
observe when people have had the sedation. And the reason is, it's because, when you have a
colonoscopy, the procedure itself is not that it's not that uncomfortable, such that the anesthetic you
only really have one drug. So you're it's almost doing a study almost like a volunteer, where you give
them propofol, and you look to see what happens. So it's where you can actually easily perceive it.
What confounds the situation is general anesthesia or when someone is placed in a medical coma is
that you've given propofol, but a whole slew of other drugs. So being able to observe the behavioral
state is much more difficult.
Q. Okay. What percentage of patients who wake up after propofol anesthesia or sedation report
this sensation of a good a good feeling that you associate with the dopamine release?
A. It's an amazingly high fraction. It's an amazingly high fraction. In fact, I the you know, I don't
know that there are actual data on it, but it's very easy to verify with anesthesiologists who do a lot of
cases of sedation like this, or just by asking gastroenterologists. This is one of the reasons that
gastroenterologists want to use propofol as a sedating drug, because of this good feeling one of the
reasons is because of this good feeling that patients have afterwards. So this is well known. So it's a
high fraction. I can't give you a precise number.
Q. In your practice, what percentage of the patients would you estimate to observe this happy
feeling or reporting this happy feeling after propofol anesthesia?
A. I don't do a large fraction of sedation cases. I do mostly general anesthesia cases.
Q. It's not a hundred percent of people, though, that wake unfeeling a sense of euphoria or
feeling refreshed after propofol anesthesia; correct?

A. I can't say, 'cause I haven't asked every person that's had it.
Q. And you haven't you haven't reviewed any research results or studies that have been
published discussing that; correct?
A. I'm sorry. What? Is what correct?
Q. That you haven't had reviewed any research reports or studies that have discussed a
percentage
A. Well, again
Q. of what percentage of people
A. So on the percentage
Q. just for the record?
A. So on the percentages, what I've looked at is reports from the gastroenterology literature and
actually talked with gastroenterologists; and they actually report this very reliably. So and just just to
make the point, in the United States in the United States, total intravenous anesthesia is not used as
widely as it is in Europe and South America. So two years ago, I was in Chile giving a lecture on
anesthesia; and I talked about the mechanism of propofol and how it worked; and literally seven or
eight people in a row came up, and the first question they ask is, How do you explain this good feeling
that I see when patients wake up from propofol? And that's because they're doing total intravenous
anesthesia, which means that propofol, along with maybe one other drug, is the only anesthetic. So
the likelihood of seeing this in that case is actually very high. So you formed opinions about you've
reviewed the records for Michael Jackson that were provided to you in connection with this case;
right?
A. Yes.
Q. And at your deposition you expressed an opinion that you think what might have been
happening with Mr. Jackson is that he had this euphoric feeling after propofol, which he interpreted as
being well rested?
A. Right; that he had this good feeling with propofol that he interpreted as that he could have
interpreted as being well rested, because he was not having restful sleep if he were receiving propofol
as a as a sedative for sleeping.

Q. And you haven't looked at medical records of Mr. Jackson's experience with propofol from
before ; correct?
A. No, I haven't.
Q. And what's the basis for your understanding that from the records that Mr. Jackson believed
that propofol was giving him the restorative benefits of sleep?
A. So my understanding is Mr. Jackson was using propofol over many days. How many, I don't
know. And, you know, for someone to continue to use it, they must have had some perceived benefit.
Q. Okay. And what's your basis for thinking that Mr. Jackson was using propofol over many days?
A. So there are I mean, there have been a number of sources of that information. It's been in the
press. It's been he had high levels of propofol in his you know, in his in his bloodstream. I you know, I
knew that, you know, even though I didn't review the medical records, there were, you know, mentions
by a number of people that he was that he was using it. So I I my impression was, looking at the my
impression was, looking at the I'm sorry. I was under the understanding that this was the night that
he died was not the first night he used propofol.
Q. Right. And I'm trying to understand what the basis for that understanding that you have is.
A. So there were
Q. And I'm talking here about propofol for sleep, not, you know, if he's had propofol in connection
with various medical procedures historically.
A. So the so as you're aware, one of the things that I reviewed in the you know, and I discussed
with you at my deposition was the you know, Doctor Murray's police report.
Q. His interview with LAPD?
A. Right.
Q. And I believe you said at your deposition that a number of the statements that he made in that
to the police you found to be not credible; correct?

A. That's correct.
Q. Including that he said he administered only a small amount of propofol in a single bolus on the
night of the 24th, leading into the morning of the 25th?
A. Yes.
Q. Which you believe to be false, because that was inconsistent with the autopsy and toxicology
information that you reviewed?
A. That's correct.
A. And actually, Ms. Cahan, can I just site one other source?
Q. Uh huh. Sure.
A. So I also I also read Doctor Czeisler's testimony.
Q. Uh huh. His trial testimony?
A. His trial testimony. And in there, in that trial testimony, the figure of days was mentioned for him
using days or two months was mentioned for Mr. Jackson using propofol.
Q. Right. And do you know what the source of that day stat was?
A. I don't know. I'm just
Q. Okay.
A. I'm just saying, that was another source for me.
Q. And did you read the complete testimony that Doctor Czeisler gave at trial, both transcripts,
both days?

A. I think I did, yeah.


Q. Okay. And did you review any of the portions of the transcript that were not actually Doctor
Czeisler's testimony? Like, there were some sidebars and arguments to the Court?
A. I did.
Q. Okay. And did you look at the PowerPoint I know you were just shown slide from Exhibit .
Did you look at any of the rest of that PowerPoint presentation
A. You know, I don't
Q. that was used for Doctor Czeisler's testimony?
A. Oh. I'm sorry. I only looked at
Q. Go ahead.
A. I'm sorry. I didn't mean to interrupt you. I only looked at slide .
Q. Do you understand that Doctor Czeisler offered the opinion at trial that propofol dissipates the
sleep drive without fulfilling the biological sleep need?
A. Yes, I did I do understand that.
Q. Okay. And do you agree with that?
A. I think that's a very plausible I I agree with that.
Q. And is that your opinion, to a reasonable degree of medical certainty, that propofol dissipates a
person's drive for sleep?
A. So what Doctor what Doctor Czeisler said seems to be very reasonable, very plausible to me.
Since I'm not a sleep expert, and I don't study sleep drive, I can't give an expert opinion on that point.

Q. And based on your the experience that you do have studying the physiology of sleep and its
intersection with anesthesia, understanding that you're coming at a from a somewhat different
perspective than Doctor Czeisler, do you hold an opinion, to a reasonable degree of medical certainty,
that propofol dissipates a person's drive for sleep?
A. I I don't have a so, again, the what I laid out for you was a way through which someone could
have the perception that he or she may have received restful sleep after having received propofol.
The idea of dissipating the sleep drive is something that Doctor Czeisler articulated. I'm saying it seems
very reasonable. It's not something that I'm not a sleep expert.
Q. Right. And I think we can I think we can agree with that. I'm just trying to understand the
from your perspective, the implications of Doctor Czeisler's testimony that, in this case, he believes
there was propofol was substituted for sleep for a number of days; and I'm trying to understand
whether you agree or have a basis a knowledge base sufficient to agree or disagree with the idea that
you wouldn't then just fall asleep during the day at some point because your brain needs to get that
REM and nonREM activity
A. So let me respond this way So one of the reasons that I agreed to assist with this case is that I
wanted to make clear statements about what the anesthetics are doing to the brain. I've done that.
I've told you precisely how they affect the sleep circuits. We can go into more detail about that, if you
would like. The inference from there about how you then subsequent what the implications of the use
of this and how it affects sleep is falls now into the domain of someone who is a sleep expert who
says, Oh, among the various things which could alter your sleep, oh, here is propofol. Now let me
investigate that. That's outside my purview.
Q. Okay. In your experience, if you've anesthetized a patient with propofol for several hours and
this can be propofol with other anesthetic agents for a procedure, is that patient typically unable to fall
asleep later that night because they've had anesthesia?
A. So let me give you an idea of what happens if patients remain in the hospital. So we go back
and see them. We may see them that afternoon or see them perhaps the next morning. And their
sleeping habits are usually something which we don't discuss in detail. You know, sort of more
immediate in our minds are any things which might be complications from the anesthesia do they
have their pain well controlled? Are there other physiological problems that need to be addressed?
So I can honestly say we haven't or I haven't systematically queried my patients about their sleep
habits following the anesthesia. And remember, there's a very, very strong confound there. A typical
anesthetic for a patient has at least drugs.
Q. Right.
A. So to try to ascribe the effect to propofol would be exceedingly naive.

Q. Okay. So in your in your experience, as a practicing anesthesiologist, you have not assessed
whether a patient's nighttime sleep is affected by having had propofol, perhaps in combination with
other anesthetic agents, for a series of during the day?
A. So, again, my research is on studying how propofol acts in the brain to create the various
states of altered arousal which are commonly associated with anesthesia. There's an intersection of
that with sleep the sleep circuits, because propofol, as I demonstrated, acts on those same circuits.
The questions you're asking now fall into the realm of someone who's a sleep expert; and sleep, the
so the implications of anesthetics as a mechanism for impairing sleep is not something that falls into
the purview of my research.
Q. Are you aware of any studies where a human was given propofol every night for weeks or
months at a time as a substitute for sleep?
A. No, but then, again, I haven't looked for one.
Q. Okay. Are you aware of any research studies in humans about the effects of giving propofol
every night for a lengthy period of time instead of sleep?
A. None come no, none comes to mind right off the bat, no.
Q. Let's talk a little bit about the factual basis for the idea that Dr. Czeisler testified about that Mr.
Jackson went two months without any sleep and instead received only propofol. Okay?
A. Okay.
Q. You said you reviewed the police interview of Dr. Conrad Murray?
A. Yes.
Q. And you believe that, at least in some instances, Doctor Murray was not being truthful in that
interview?
A. So what I what I was suggesting was that he I noticed in speaking specifically about
propofol, I noticed some inconsistencies with the way we administer the drug that suggested that what
he said wasn't correct.

Q. Right. And we talked a little bit earlier about the dosage that he stated he provided was
inconsistent, you believe, with the autopsy and toxicology results?
A. Yes. Do you believe, based on the police interview that Doctor Murray gave the LAPD, that
Doctor Murray gave Mr. Jackson propofol every night for approximately days before Mr. Jackson
passed away?
A. So I have no way of knowing exactly what Doctor Murray did every night when he took care of
Mr. Jackson.
Q. And do you do you have any understanding of whether Mr. Jackson actually got any real sleep
during that day period?
A. I because I don't know what I have no
A. I have no idea what transpired in Mr. Jackson's boudoir during the time he was under the care
of Doctor Murray.
Q. Right. So you don't know whether Mr. Jackson took naps?
A. I have no way of knowing.
Q. Or whether Doctor Murray took some nights off?
A. I have no way of knowing.
Q. Or whether the infusion of propofol was continuous for each and every night?
A. I have no way of knowing.
Q. Don't know the levels of sedation that were achieved or not achieved using propofol during that
time period?
A. Except for the last night.
A. That's pretty clear.

Q. Okay. So remember for the purposes of the following questions we're setting aside the police
interview; okay? So having done that, have you seen evidence in this case that allows you to
determine the number of days that Michael Jackson used propofol in the spring and summer of ?
A. That's not something that I've looked into.
Q. Have you seen evidence in this case to allow you to form an opinion about whether Mr. Jackson
used propofol for sleep on a nightly basis in the spring and summer of ?
A. I mean, I was asked to look at to help understand the mechanisms through which propofol
works. I wasn't asked to look at Mr. Jackson's behaviors.
Q. Have you seen evidence in this case sufficient for you to develop an opinion about whether Mr.
Jackson used propofol for sleep on a nightly basis in the spring and summer of ?
A. So the reason I have not done so was not was that was not something I was looking into,
based on my expertise.
Q. Fair to say that you have not looked into what evidence may or may not exist about how much
propofol Mr. Jackson may have been getting on a nightly basis in the spring and summer of ?
A. So, again, that was not something that I was looking into.
Q. You spoke a little bit earlier when Mr. Koskoff was questioning you about your work in applying
the is it the Glasgow Coma Scale
A. I don't
Q. to analyze anesthetic states?
A. I don't think I used the word "Glasgow Coma Scale."
Q. Right. I think you said "coma scale." And I'm trying to understand what scale you used there.
A. I think I said the "neuro exam."

Q. Okay. The neuro exam you use generally for people in comas, you've developed the technique
of applying that to analyze an anesthetic state?
A. Yes.
Q. Okay. And how long
A. So again , it's a neuro exam. It's just a neuro exam.
Q. Right. Okay. How long can someone be in a profound coma and live?
A. Many years. There are tons of cases of that.
Q. Okay. And when people are in a profound coma you showed us on those brain waves that's
not the same as REM or nonREM sleep; right?
A. That's right.
Q. And those people don't die from lack of sleep. They can remain in a coma for years; correct?
A. They can. But, you know, it's very interesting. You know, Niko Schiff has written about this, like,
there's actually I'm not up to date on this, but there's information about whether or not these people are
getting, you know, various states of sleep for people in com
A. Now, again, coma so you have to be very careful here, because when you anesthetize
someone and place them in a coma, that's quite different from someone ending up in a coma because
there's been damage to their brain tissue. When the brain has been damaged, you have to try to
discern the level of coma, what areas of damage, what anatomy is still in intact, what physiology is still
intact? So making a link between a patient in coma and someone who's in a coma because of
anesthesia on this basis doesn't make sense.
Q. And I think you said people can remain in medically induced comas under anesthesia for a
fairly long time?
A. So you can be there for several days.

Q. Okay. And were you speaking also earlier about the small a small dose of propofol giving that
paradoxical excitation?
A. Yes.
Q. And is that consistent with a dosage for most people of or cc's?
A. I beg your pardon? How much?
Q. What amount of propofol would create the paradoxical excitation that you see in sedation?
A. It it varies based on person. And that's really the that's really the challenge that the
anesthesiologist has. You know, he or she starts with a low dose, which might be a cc, and then
works up to try to find the sedative state just beyond that state of paradoxical excitation. So I couldn't
begin to give you, like, a figure, because it varies quite a bit, depending on patients.
Q. So if you've given someone something
A. And the other thing too is it's not a given can I just finish?
Q. Please.
A. It's also not a given it's not a given that everybody will go into it. It's not a hard-and-fast rules,
but it is appropriate it's important to realize that that state is there.
Q. Okay. And that state if you want to give someone propofol sufficient to sedate them but not to
induce general anesthesia, can you just show us on the chart what brain wave states you're going to
be hitting?
A. If you want to just sedate them?
Q. Yes.
THE WITNESS Can you see it?
MS. CAHAN Yes.

A. So you would be probably in this state here (indicating).


Q. Okay. So you won't go down into those three bottom phases? MR. KOSKOFF Can you
identify for the record what that state is?
A. I'm sorry. It says "Phase ."
Q. It says "Phase " in Column B of Exhibit And if someone has someone can be maintained in that
state of sedation if they're given a continuous infusion of propofol at a relatively low level?
A. Possibly, possibly. You may have to change the infusion rate to maintain the state, because the
brain's response is dynamic. So even though you maintain a constant rate, the brain's response could
be such that the person could become deeper or lighter. Case in point The surgeon all of a sudden
applies a more painful stimulus. As a consequence, to maintain the same state, you may have to
increase the infusion. Case in point The surgery induces the stimulus. Now the patient starts to drift
deeper and deeper, so may have to decrease the infusion. So it's not that simple.
Q. Right. But in but in either instance, you have to continuously provide propofol if you want to
maintain someone's level of if you want to maintain someone in a sedated or anesthetized state;
correct?
A. That's typically the way it's done.
Q. Fairly soon after the propofol stops and I understand it depends on the dosage that's been
given and for how long the person will regain consciousness?
A. Usually within some reasonable amount of time, the person will regain consciousness.
Q. Okay.
A. And then what that
Q. So
A. Let me just finish. What that what that means, though, is actually can can vary quite a bit,
because that might mean somebody being mentally conscious meaning they respond to you

intermittently, or someone might just be quite happy with the person just breathing, not really
responding to any questions or so, but being functional so that they could go to the recovery room.
So, again, there's this very broad continuum that is used when people look at recovery after
anesthesia. And that's one of the things that doing this neuro exam has helped us really appreciate.
Q. And when the propofol stops some reasonable period of time after the propofol stops, the
person is awake; correct?
A. So, again, "awake" meaning awake is no longer just like you were before. You may have
different levels of being awake. So the person is not necessarily back at the same state that he or she
was in before the surgery. In fact, you don't want to be exactly in the same state that you were in before
the surgery, because if you've had something which is extremely painful, you actually want to ideally
have year cognitive function come back, but you want to have a level of analgesia that allows to you
tolerate the pain that you would have as a consequence of having had the surgery. So you, therefore,
cannot be awake in the same way you were before the surgery.
Q. But at some point you will want to be fully awake and return to normal consciousness; correct?
You're not changed forever after you've had anesthesia for surgery?
A. Well, again, you have to be very careful, because the effects of anesthesia can persist for a
number of days; and that's something which is being actively investigated. We would like for that not
to be the case, but it is not clear if some of these persistence effects are due to, like, the anesthesia,
the surgery. So it's not that it's not that cut and dry.
Q. Would dopamine release cause a person to stop sleeping for extended periods of time?
A. Would dopamine release cause someone to stop sleeping?
Q. For an extended period of time.
A. So dopamine release from where? Injecting dopamine?
Q. No, from your brain.
A. From which part? There are about four sites that release it. Pick one.
Q. Does it does it cause a different result, depending on which part of the brain the dopamine is
released?

A. Pick one; I'll tell you.


Q. Can you put up your chart that's Exhibit .
A. Sure.
Q. So when propofol is administered, what part of the brain releases dopamine?
A. So meaning for the euphoria?
Q. Yeah.
A. Meaning for this this state of good feeling?
Q. Yeah.
A. That's not that's not up here.
Q. Okay.
A. It's at nucleus accumbens.
Q. What part of the brain releases dopamine for that state of for that feeling of euphoria?
A. So the nucleus accumbens.
Q. Okay. And if dopamine were released there for some other reason, would that cause a person to
stop sleeping for an extended period of time?
A. It's really just so , again, in what context or what have you you know, remember, that's being
released from there all the time. It's not like it's just sitting there, not releasing; and all of a sudden it
just releases. That's being released all the time. So so I'm not quite sure what you're it's not like it's
turned off.

Q. Are there right. Do you know the level of dopamine or the change in the amount of dopamine
released with with propofol?
A. I I don't. But we could easily check it. I don't know the I don't know the figure.
Q. Are there other drugs that cause a similar release of dopamine in that part of the brain similar to
propofol?
A. There are there are a number of agents that that could do this. So you could you can do it
by just actively you can do it by actively administering a number of drugs. So one I can think of
some that would release it and some that would just make the levels higher.
Q. Okay. You sat for a deposition in this case in April; right?
A. That's right.
Q. And have you done work on this case since that time?
A. I have.
Q. Approximately how much in terms of hours?
A. So up until I think the day that I came out to California, which was I think May 16th or 17th, I
and that up to then, I had done about 75hours. And then, when Ms. Reilly and Mr. Koskoff let me
know that I have to testify again, I started working on it subsequently. So since then, you know, maybe
15 hours or so 12,15 hours.
Q. Is that including your travel to Los Angeles and back
A. So the 75-
Q. or separate from that?
A. The 75 was included in all of that.

Q. Okay. And can you break out, after your deposition but between but before May 16th or 17th,
about how much time you put into the case?
A. I'm sorry. I missed that. Which time frame?
Q. After you were deposed on April
A. Uhhuh.
Q. 5 th
A. Uhhuh.
Q. but before you flew out to Los Angeles on May 15th or 16th or 17th
A. Right.
Q. about you approximate about how many hours you
A. You know, I honestly don't remember now. I can't tell you.
Q. And do you know what kind ever work you were doing during that time period? Were you
reviewing additional records or testimony, reviewing research? Something else?
A. It was some combination of all the above. I mean, I can honestly tell you I mean, you know, if
you had asked me this a few days after or, like, on the 16th or 17th, I could probably give a detailed
description. But right now I've written and worked on so many things since then, I could not in any way
give you a reasonable idea of what I did what the actual time breakdown was.
Q. Okay. And you've had communications with Plaintiffs' counsel since your April 5th deposition?
A. Yes.
Q. With Mr. Koskoff?

A. Yes.
Q. With Ms. Reilly?
A. Yes.
Q. With Mr. Panish?
A. I've never met Mr. Panish. I've never spoken with Mr. Panish.
Q. With Mr. Boyle?
A. You know, I think I met Mr. Boyle, but I don't remember. I think I might have met him when I
came to Los Angeles, but I'm not sure. We
Q. Okay. Were there other sorry. Go ahead.
A. I'm not sure.
Q. Are there other lawyers for Plaintiffs in this case that you remember meeting or speaking
with?
A. The only other person that I remember distinctly speaking with was is it Ms. Chang? Is it Deb
Chang?
Q. Uhhuh.
A. Ms. Chang.
Q. Okay. And at some point on May 16th, it was decided that you were not going to testify on
May 17th?
A. That's correct.
Q. Was that after you discussed the opinions that you would offer in this case?

A. That was after I that was after we discussed the opinions, that's right.
Q. And did Plaintiffs' counsel ask you to offer opinions at trial in in this mid May time frame, did
they ask you to offer opinions at trial that you hadn't offered at your deposition?
A. Not at all, no.
Q. Did they ask you to offer opinions that you were not comfortable offering at trial?
A. No, never.
Q. At what point did you learn that you were not going to be testifying at trial on May 17th?
A. About
A. 6.45p m. on May 16th.
Q. That must have been fun. And was that decision a decision by Plaintiffs' counsel or by you?
A. That was a decision by by Plaintiffs' counsel.
Q. Okay. And were you given an explanation as to why you weren't going to be testifying that day?
A. Yes.
Q. And what was that explanation?
A. So the explanation was, is that you remember in my deposition when you asked me for the
opinions I was going to offer, I think I listed down about six other six or seven things that I was going
to testify to.
Q. Uhhuh.

A. And five of the seven or six of the seven really related to Doctor Murray and his and his
substandard care that he had given Michael Jackson. And Ms. Koskoff and I'm sorry Mr. Koskoff and
Ms. Reilly felt that the defense had ceded those points; and so there was really no need for me to
testify on those issues. So they decided not to call me.
Q. Okay. Have you spoken with Doctor Czeisler at any point since you gave your deposition in
this case?
A. No, I haven't talked to him.
Q. Did Plaintiffs' counsel discuss Doctor Czeisler's deposition testimony with you at any point?
A. They recommended that I read it. But we haven't discussed it.
Q. Did Plaintiffs' counsel discuss Doctor Czeisler's trial testimony with you at any point? I know
you
A. Excuse me. I'm sorry. I misunderstood you. I thought you were talking about his trial testimony.
I I didn't they didn't say anything about his deposition. I'm sorry. That was a misstatement. I thought
you were talking about his trial testimony.
Q. Okay. Got it. Have you reviewed Dr. Paul Early's and Torin Finver's story sorry study titled,
"Addiction to Propofol A Study of Treatment Cases"?
A. You know, I read that a while ago, but I I don't remember. I couldn't comment on it now. I
haven't I haven't looked at it recently.
Q. Okay. You don't you don't recall your impressions of that study?
A. Not in detail. I couldn't I couldn't begin to I couldn't begin to discuss that with you right now.
Q. Doctor, Ms. Cahan asked you about Murray's statement; and in her question, she said, Do
you recall Doctor Murray's statement where he said that he had administered propofol nightly to Mr.
Jackson for the for the times repeatedly days before his death? In fact, do you and you have
read Doctor Murray's statement; is that right?
A. Yes, I have.

Q. And, in fact, didn't he say that he administered it every night up until the st for continuous
infusion of propofol up until the 21st of June for 60 nights straight, then, on the nd, he gave he started
to wean him from propofol; and that he gave him no propofol at all on the 23rd of June?
A. So that seems like a more accurate description of what was in the in the report, but I haven't
looked at it in in while, so but that seems more accurate. Total Length

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