Stanford’s Sean Mackey, MD, PhD, on Back Pain and the Brain

Stanford’s Sean Mackey, MD, PhD, on Back Pain and the Brain


So now I have the
distinct pleasure of introducing our first
speaker, Dr. Sean Mackey. So you probably already know
something about Dr. Mackey. But I’m going to go ahead and
give you a complete bio on him. So Dr. Sean Mackey is
the Chief of the Division of Pain Medicine. And he’s Redlich Professor of
Anesthesiology, Neurosciences, and Neurology at
Stanford University. He is the immediate
past president of the American Academy
of Pain Medicine. Dr. Mackey received his
bachelor’s and master’s degree in bioengineering from the
University of Pennsylvania and his PhD in electrical
and computer engineering as well as an MD from the
University of Arizona. He is the author of over
200 journal articles, book chapters, abstracts,
and popular press pieces in addition to numerous national
and international lectures. Under his leadership, the
Stanford Pain Management Center has been designated a
center of excellence by the American Pain Society,
one of only two centers to receive this honor twice. In 2011, he was a
member of the Institute of Medicine Committee that
issued the report on relieving pain in America. He is currently co-chair
of the Oversight Committee for the NIH Health and
Human Services National Pain Strategy. This is an effort to
establish a national health strategy for pain care in the
United States and education and research. Under his leadership,
researchers at the Stanford Pain Management
Center and the Stanford Systems Neuroscience and Pain Laboratory
have made major advances in the understanding
of chronic pain as a disease in its own
right, one that fundamentally alters the nervous system. He has overseen efforts
to map the specific brain and spinal cord regions
that perceive and process pain, which has led
to the development of a multidisciplinary
treatment model that translates basic science research
into innovative therapies to provide more effective,
personalized treatments for patients with chronic pain. And with that, please give a
warm welcome to Dr. Mackey. Thank you, Beth. Again, really excited
to have you here today. My job– in fact,
I have to remember. My job is actually to
stay at the podium. Isn’t it, Ian? I have a tendency
to move around. Beth mentioned Oprah. And I have a similar
characteristic of wanting to wander. But I’m told that
we have one podium mic, so I’ll try to stay put. My job is to set the
stage for you folks. It’s to lay the groundwork
for the remaining speakers, for the rest the speakers that
come forward today, and talk with you about mind/body
approaches on pain, physical therapy approaches on
pain, complementary alternative medicine approaches,
pharmacologic approaches. And so we’re going to
start off with this by, again, giving some
background information and talking somewhat
about the science of pain. It’s always good for you to– one moment. There we go. It’s always good that you know
where your speaker’s funding is coming from. So just in full disclosure,
all of my funding, the vast majority is it’s all
coming from either the National Institutes of Health or
from generous philanthropy. We depend on people such
as yourselves and others to help with the novel
research that we’re doing. A large part of this is also
coming from the National Institutes of Health where I’m
currently heavily conflicted by them and working to become
more conflicted each year. It’s a tough time out there
as we’re all writing grants. I receive no industry support
at all for any of the research or any of the information we’re
going to be providing you. Some of the learning
objectives that we’re looking to help impart upon
you today are the following. Allow me one second here. OK. We want to help you
to better understand the burden of back pain,
the burden on both you, your family, our
society as a whole. We want you to understand
some of the basic science of back pain, some
of the understanding of the mechanisms, what
pain is, what it is not, and then how that
can become a disease in and of its own right. And then we want to set
the stage, as I mentioned, for the remainder
of today’s talks. I’m just going to spend a
moment and get the PowerPoints and the technical
aspects of this worked out right
now so that we don’t have to deal with this later. There we go. And now we’re off and running. All right. Here we go. I mentioned before that pain is
a huge issue in this country, affecting about 100
million Americans. But you’re all here because
of interest in back pain. So where does back
pain fit into this? Well, it fits in very strongly. What we learned from the
Institute of Medicine report on pain is
that back pain is the largest proportion of all
the chronic painful conditions. It accounts for about 28%. Almost 30% of all the pain
out there in this country that’s chronic in
nature is low back pain. You’ll see that headaches and
neck pain are, pardon the pun, neck and neck at about 16%. So it’s a big, big
burden on this country. And I probably don’t
need to tell you that it takes a tremendous toll. Patients, as a consequence
of the back pain, get tremendous emotional
distress, get depressed. They get anxious. They get angry. They also get poor sleep. And sleep, we’re, learning
has a huge impact on not only your pain but also
your quality of life and how you function
the following day. And as I close
out on that slide, it’s clear that back pain
also takes a huge hit on your quality of life. So let’s dive in in
setting the stage here for some of the science of pain. Much of our
understanding of pain– [AUDIO OUT] –philosopher. And he was a brilliant,
brilliant philosopher, one of the grandfathers
of modern philosophy. He came up with the
Cartesian geometry, so he’s an incredible
mathematician. He also came up
with a view of pain. And let me tell you that where
he got many other things right, particularly in the area of
math, when it came to pain, he screwed it up in a big way. He really screwed
it up in a big way. And he put forward
this model that’s illustrated by the small
child with his foot in a fire. And the idea is that this small
child with a foot in the fire– [AUDIO OUT] –bell and causing
the boy to withdraw his foot. What it put forward was a
direct link between stimulus and the response, stimulus
and the perception, suggesting that there is
a one-to-one relationship. And what that model did was it
profoundly and fundamentally altered our view of pain
and set that forward for the next hundreds of years. And it’s only been more
recently that we’ve learned that that model
is entirely wrong. And so I’m going to
show you, hopefully over the next several
minutes, why it’s wrong and how we need to
rethink your pain. It’s helpful when we’re
talking about something new to have a common language, a
common taxonomy, if you will. And so I put forward a commonly
used definition of pain, which is an unpleasant sensory
and emotional experience associated with actual or
potential tissue damage, or described in
terms of such damage. That’s a mouthful, isn’t it? So let’s just distill it
down to a few key words. Pain is an unpleasant sensory
and emotional experience. Think about it. We define it in terms
of an experience. That means it is
whatever you say it is. It is something subjective. It is not something that
we’re able to yet objectively measure, although our
lab and a few other labs are actually out
there trying to make objective measures of pain. So we rely on you to
tell us what it’s like. And as we’re going to show
you, your pain experience is unique to you. I’m going to start off
with a little background. And so we do know that much of
pain starts with a stimulus. So wait a minute
here, Mr. Crumbly. Maybe it isn’t kidney
stones after all that’s causing his low back pain. So I use this slide for our
residents and our fellows. And we start them
off with this slide to help teach him a little bit
about some of the neuroanatomy, the circuits that we
describe in pain processing. So let me just walk you
through this very briefly, because this will set the
stage for much of what we’re going to talk about the
remainder of the day. We all have within us
these little elements in our skin, our soft tissues,
our deep tissues, and our bones that we call nociceptors. Now, it’s a fancy Greek term. But, in essence, a nociceptor is
something that is a transducer. A transducer is
just something that converts one form of
energy into another. So this microphone here,
that’s a transducer. It converts sound energy
into electrical energy. The speakers that you
hear from the ceiling convert electrical
energy into sound energy. In our bodies, we’ve
got a kajillion of these transducers that allow
us to perceive temperature, touch, pH changes, light. We have retinal transducers. And we have them that
are specific ultimately to the experience of pain. And so what happens
is that if you hit your thumb with a hammer
or you step on a tack, you activate these nociceptors
and they’re transmitted up to different nerve fiber types. One of them is called a C
fiber, and the other one is called in A delta. The A delta fiber is
very fastly-conducting. It travels really,
really quickly. The C fiber is slow. It’s pokey, about
one meter a second. Let me give you an analogy. Think back to the last time you
hit your thumb with a hammer. What happened? Or you stepped on a
tack on the floor, or you twisted your ankle. You got that sharp jolt of pain
that went right to your brain, right? Those were your A delta
fibers firing off at 10 meters a second. It gets from your thumb
to your brain like that. And then what happens? You have just enough time to
think to yourself, oh, damn. This is really going
to hurt, right? And then you feel that hot,
burning sensation come over your thumb where you
whacked it with a hammer. Those are your C fibers. They’re slow. They take about a second
to a second and a half to get from here, my
thumb, up to my brain. And don’t you note
that they convey entirely different experiences? Those A delta fibers, which
are fast or prickly, sharp, well-localized, you
know exactly where you hit your thumb with the
hammer, the C fibers, hot, burning, flooding, taking over
a larger part of your thumb. And for the first
time, it’s unpleasant. It’s unpleasant. It’s because those C
fibers are conveying that unpleasantness that’s going
to be processed in your brain. We know that these fibers
then come up and synapse. They form a junction, a
connection in the spinal cord. They cross over
to the other side and they head up
to the other side. And once they get up
to the other side, they land in this area called
the thalamus of the brain. It’s like Grand Central
Station in the brain. And the thalamus sends
out these signals to other parts of your
brain where pain is then experienced and processed. The point of this is that what’s
going on out here in your hand or what’s going on in
your back is not pain. It’s not pain. It’s what we call nociception. It’s electrochemical events. It’s electrical signals that are
being generated in one’s back or in one’s thumb. It’s not pain until
it hits the brain and becomes that perception. Now, if we were just bombarded
by all this information on a regular basis that’s
coming into our body, our brains would simply explode. And so we’ve learned
ways to control it. And the ways we’ve learned
to control it are we’ve developed what’s called
inhibitory systems, filters in our brain that come
down from the brain and synapse again
in the spinal cord. And the whole purpose of this
is to turn the signals down that are heading up. And you have a nice balance here
between the signals heading up and the signals heading down. And we’re going to now build on
that over the next few slides. And so the point of
this slide, again, is to drive home the point
that nociception is not pain. Nociception is not pain
and that they’re not necessarily directly linked. But instead, what
goes on with pain is that we take
the signals coming in from our body, the pressure
signals, the temperature signals, the pH changes,
those head to our brain and then they are changed. They are altered by all sorts
of other factors, factors such as cognitive factors,
whether we’re attending to or distracted from pain. You may note that when you’re
not thinking about pain or thinking about something
else that you’re pain goes down. Contextual things such as
expectations and beliefs and placebo play a
huge role on this. Our mood. You’re going to hear this a
lot today, depression, anxiety. And then one of the big
players that Dr. Darnell is going to talk about
is catastrophizing. Catastrophizing,
file that one away. I’m not going to
steal her thunder. She’s going to tell you
about catastrophizing, which is probably one of the
most important ones up here for you to
pay attention to. And then genetics, which
you can’t control the genes that your parents handed
down to you, which give you different susceptibility
to chronic pain and different perception
of chronic pain. And so let’s say that this
slide is going to illustrate where we’re going next. Pain is a thing of the mind. The mind can be controlled. You’re only half Vulcan. What about the
human half of you? It is proving to be
an inconvenience. All right. Spock is talking about
how the human half is causing to be an inconvenience. Let’s talk about that
inconvenient human half here, shall we? So we’ve taken this
information about how things such as mood and
anxiety and beliefs and placebo and other factors play a role. Those aren’t just warm and
fuzzy psychological concepts. Those all exist in our brain. And they all exist in
circuits in our brain. And what we’ve learned
is that, in fact, we can map out areas of the brain
involved with each of these. And that’s what we
spend, in our lab, a large amount of time
doing, is mapping out these circuits in the brain. And so– one moment. What we’ve learned is that
there are areas in the brain, such as the prefrontal
cortex that’s involved with some of
the cognitive aspects, the evaluative aspects, how
we think about pain, what do we want to do about pain. We know that there are
areas such as the insular cortex, a big player
in pain, that’s involved with some of
the emotional aspects and the unpleasantness of
pain, the somatosensory cortex involved with the
location of pain and some of the
intensity aspects of it, the insular cortex involved
with how were we feeling at that moment in time or
a fundamental understanding of our bodily state. All of these play a role,
and many more brain regions, into our understanding of pain. I mentioned to you
that pain involves this balance between
excitation and inhibition. And what we’ve focused
on historically is just the excitatory aspect. That’s where most of the
research was in pain. We always assume
there was some injury, that there was lots of signals
heading up to the brain. And we needed to try to
stamp those signals out. But what we’re now gaining
an appreciation for is it’s not just the signals
heading up to the brain. It’s actually the
inhibitory role of the brain on the
signals coming down that can become dysfunctional. We’re learning that a large
number of chronic pain conditions involve a
dysfunction or abnormalities in those blue
inhibitory pathways coming down from the
brain, such that even with a normal
amount of excitation and normal amount of stimulus,
you could be sitting in a chair and experiencing pain
because you don’t have enough of that filtering ongoing. And that’s where we’re
targeting a lot of our research and a lot of our clinical care. There’s something else
that happens with pain, and that’s this concept of what
we call central sensitisation, another mouthful word. But it’s really
easy to describe. Let’s go back to your
hand for a moment. Now, let’s imagine
that you cut your hand. Or imagine you
sprained your ankle. Sharp jolt of pain
goes to the brain. Oh, damn. Really going to hurt. Hot, burning
sensation comes over. Then what happens
about an hour later? What happens an hour later? If you look at the hand,
you get some swelling and redness, right, and heat. You get a release of all of
these inflammatory mediators that cause that
swelling and the heat. That’s a normal process. Then what happens? You go to bed. You wake up the next day. And doesn’t your whole hand or
ankle and lower part of your leg feel stiff, aching,
and sore, right? Think back to that. Well, what’s happened overnight
is that your brain is rewired. It’s completely rewired. And it’s rewired to
expand the zone that is perceived as painful. There’s actually nothing
wrong with the tissue outside that
initial injury zone. It’s entirely normal. It’s stone cold normal. But it hurts. Why? Because your brain has learned
over thousands and thousands of years that it needs to send
you a signal to let it heal up, and so it’s amplifying that
experience so that, back in the caveman days,
the cavewoman days, it would be a signal for
us to sit in the cave and let nature take its
course, let things heal up. And what we would
find is the zones would shrink down and
go back to normal so that you’d go out and
fight the woolly mammoth. But if you went out
when you were injured to fight the woolly mammoth,
the saber tooth tiger, what would happen to you? You’d get eaten. And if you got eaten, you
couldn’t pass your genes down. So this is an entirely
healthy, appropriate rewiring of your brain. It occurs in each
and every one of us. The problem with chronic pain,
these switches don’t turn off. They don’t turn off. So the tissue can be normal,
but you’re still getting these expanded zones. And your brain is
telling you it’s painful. Sit tight. Stay in your caves. Sit on your couch. We’ve also learned that there’s
huge individual differences in our experience of pain,
that each and every one of you is different from the next. And this has come about
through some really fascinating research that’s occurred
over the years that’s led to a variety
of these questions. Why for a given
stimulus, a given injury, is there such a difference
in the perception of pain? Why is there, for a given
injury, the same injury in two different people, a different
degree of disease burden that they have? One person can go back to work. The other person can’t
get off the couch. Why is there such
a large variability after injury or after
surgery with who will develop chronic pain? On average, after a major
surgery, about 10% of people will develop chronic pain,
not a commonly known number. We’re just beginning to learn
what makes those 10% of people unique. And what we’re
learning is it actually may not have a lot to do
with the surgery itself. It may be more what you bring
to the operating room table or what you bring to that
injury, that original back pain injury, that original
car accident. It’s what you bring to that
injury that may then set you up with the likelihood of
developing chronic pain. And so how have we
studied this phenomenon of individual
differences in pain? Well, this was an
interesting study that was done some time ago. They took 500 people,
a little bit more than the number of
people in this room, and they did something
called the cold pressor test. Excuse me. Not this one. I’ll get to the
cold pressor test. They applied a 49
degrees Celsius stimulus, which works out to about
121 degrees Fahrenheit. And they gave it to, for
instance, all of you. And they just asked
a simple question. How much pain did it cause you? And what they found
is a wide variability. They had people who were
saying, you know what? No pain at all. Nothing, guys. It’s a little warm. They had people
saying, yeah, well, it’s kind of painful,
a little mild. They had some saying, yeah,
it was moderately painful. And they had others that
were saying, oh, my god. Get that off. It’s the most painful
thing imaginable. What accounts for the
individual differences? Well, we’ve learned that
there’s a number of genes that are involved, what our
parents handed down to us. But we’ve also
learned other things. You remember that brain
slide I showed you with all those things such
as distraction and mood and placebo? All of those play a factor
in our individual perception of pain. And our speakers today
are going to get into some of that in more detail. I do this same
experiment, by the way, to the medical students
here at Stanford. I teach the pain courses here. And there, rather than
heat, I do something called an ice water bath. I have them dip their
arm in an ice water bath and then pull it out
after 15 seconds. And then they whisper in
our research assistant’s ear what the pain score is. And then at the end of the
hour, I plot it on a spreadsheet and I show them. And it looks identical
to that curve. And I think it’s
very empowering. It’s very informative for
those medical students because it teaches them
an important point. And that is that my experience
of pain based on a constant stimulus is not necessarily
the same as everybody else’s. And my hope is that when they
go out on the hospital floors, when they see patients
in the clinic, they’ll take that
information with them so they realize that
we are all individual and individually wired. OK, this study was
repeated by a friend of mine, Bob Coghill, who does
some incredible work in brain imaging. This was a seminal
paper several years ago. He took the same study,
the same experiment, taking those with
low sensitivity and those with high
sensitivity, and he put them into a neuroimaging
environment, a scanner. And what he found
is the following, that those individual
differences, the differences to the same stimulus could be
accounted for by specific brain regions, areas like the
anterior cingulate cortex that I showed you
before involved with some of the
emotional aspects of pain, the somatosensory cortex,
some of the location aspects. And then also, again,
the prefrontal, these frontal regions of the
brain play a big role there. So we’re learning that much
of our experience of pain is being driven by individual
differences in these brain systems. I’ve had a particular interest
in the role of cognitions and emotions in pain. Why? Because I had a real
eye opener when I first started getting into medicine. As Dr. Darnell mentioned,
I am an electrical engineer by original training. I have a doctorate in electrical
and computer engineering. And coming out of
medical school, you could not have found a guy
more linear and mechanistic than me. I was very– if I
could just figure out how to put a patient
into an equation, I was going to have
them all figured out. I don’t know. What’s so hard about this
medicine thing, you know? Engineering, that was hard. Yeah, I was pretty
confident back then. And then I got in and I started
actually talking with people. I started listening to their
stories about their pain. And I was realizing, boy,
this is really complicated. And what I was
finding is that some of the things, many
of the things, that were driving their
experience of pain were things like fear and
anxiety and catastrophizing, that Dr. Darnell
will talk about. And so we do what we
usually do here at Stanford, is we decided to study it. And so we did some
early work on this in the role of fear and
anxiety related to pain. And so I’ve always been
intrigued by the fact that a person’s anxiety
and fear of pain often has a strong prediction
as to their treatment outcomes and how they’re going
to do with chronic pain, that also people coming in
with high degrees of anxiety, depression,
catastrophizing, history of post-traumatic
stress disorder and then experiencing a
significant injury or surgery are much more likely to develop
chronic pain afterwards. People have historically thought
these are just warm and fuzzy psychological constructs. But many of us were
convinced that these are due to circuits in the
brain and that we can better understand them. And so what we did is, in
this particular situation, we put forward a study
to study the effects of the fear of pain. And what we did here
is that we captured how much fear people have
to everything, to a paper cut, to a major injury,
to a surgical procedure. And then we gave them a
stimulus, a painful stimulus. And we correlated that. In other words, we mapped their
fear of pain onto their brain with that stimulus
that they were getting. And what we found is this
incredible relationship in an area called the right
lateral orbital frontal cortex. And this is an area
of the brain that’s involved with your evaluating
and regulating what you’re going to do to a
painful stimulus. Let’s just do the briefest of
demonstrations here on this, shall we? And can I get just really
quick just a volunteer? Would you be willing
to come up for me? All right, come on up here. Yeah, are you able
to come on up? Yeah. Yeah, we’re not going to
put you on the spot here. This will be easy. I want you to think back. And I want you to remember
that you’re three years old. Remember what it was like
to be three years old? And you were over at
your grandmother’s. And pretend that this
is your grandmother’s favorite casserole dish of all
time, and it’s on the stove. Could you come over
here and put your hands on that for a moment? Now, before you put
your hands on it, I’m going to tell everyone
this has been on the stove and it’s burning hot. It’s burning hot. And so you’re three years old. You go to pick up your
grandmother’s casserole dish. And what are you going to do? Go ahead and pick it up. And then what are you going
to do as a three-year-old? You’re going to drop it. That’s going to hit the ground. It’s going to hit the ground. Now, imagine instead
that you’re 30 years old. You’re over at your
grandmother’s house. It’s her favorite
casserole dish. You go to pick it up you
realize it’s burning hot. What are you going
to do with it? –protection? You’re going to get
some protection. And are you going to drop it
to the floor and let it crash? I don’t think so. I don’t think so, because you
know it’s your grandmother’s favorite casserole dish. That’s what’s happened in
that 20 to 30 years, is that, during that
period of time, she’s developed an
orbital frontal cortex. And it’s matured and
allowed you to make a decision about your pain,
about what to do about it. A three-year-old is not
capable of doing that. A 7-year-old is not really
capable of doing that. Somebody in their
20s can start to be. So what we’ve learned is
that, in chronic pain, though, that that area of the
brain becomes dysfunctional. It takes on
characteristics that we tend to overvalue and
overamplify the pain. And as such, we tend to be
fearful and we tend to guard. And so what we’re doing
is looking for ways to actually turn that
around and turn that into a more healthy
brain region. So thank you. Thank you. Thank you for letting
me put you on the spot and bring you up like that. Let’s give her a quick– [AUDIO OUT] So we did the same
thing around anxiety. And what we did here is we found
that there were differences related to also anxiety,
how much anxiety you have to somatic sensation. Here, when you’re on
your fifth Starbucks latte and you get a
little heart palpitation and you start feeling
anxious, how much does that anxiety
map onto your pain? And we found this area
in the medial prefrontal cortex maps very, very closely. This is an area also involved
with generalized anxiety disorder, PTSD. And it’s one of
those major filtering regions in the brain that’s
involved with inhibition, that turns the signals down
and it becomes dysfunctional. We elected to take some
of this information and ask this question. Can we take this
neuroimaging information and turn it upside down? Can we, in fact,
help people to learn how to control their brain? And so we developed
some technology here called real time fMRI
neurofeedback in which we put you in a scanner, you see
your own brain activity in real time, and we ask you
to control it using feedback from your own brain. It’s really cool. And we asked this question. Can you learn how to control a
specific region of your brain? In this case, this
anterior cingulate cortex I’ve been showing you,
this area this morning, involves some of the
emotional aspects of pain. And it turns out that you can. You can learn how to build
this area up just like you’re going to a gym and
building up a muscle, and that it actually
has a profound impact on your perception of pain. And so this is one
of the studies. We did this in
healthy volunteers. And this is one of the
studies that were doing here at Stanford now with
people with low back pain, is to teach them how to control
their own brain activity and see if it actually has a
durable response on their pain. We’ve also learned that
chronic back pain fundamentally alters your brain. It changes your brain. It changes the gray
matter in your brain. We’ve learned this
through some studies that we’ve done here where we
developed a neural signatures that help us to
predict whether someone has chronic low
back pain or doesn’t have chronic low back pain. And for many years, as I’ve
been telling this story, people would ask me
afterwards, well, Dr. Mackey, I hear that the pain
is changing my brain. Can that be reversed? Or am I stuck with that? Is it something permanent? And my response back then
was, I don’t really know. But I think that it can go back. The good news is that we’re
seeing some exciting research that, in fact, it
can be turned around. This is some exciting work
done by David Simonowitz and colleagues. And it’s a very
complicated slide. It’s the same slide that I use
in a national presentation. So let me just give
you the short version, the brief vision of this. They took people
with low back pain. They did imaging of them first
to look at those gray matter changes. And then they gave
them something called a working memory task. This is keeping pieces
of information in mind. It’s like giving
you a phone number and asking you to recite it
backwards and found that there was impairments
in working memory and in areas of
the brain that are involved with working memory. They then went through treatment
for their low back pain. Their pain got better. Imaged them again. And the good news was that
the gray matter returned more to a normal state and the
working memory performance improved, suggesting that,
with appropriate treatment, those brain changes can
actually get better. Let me close out
on one last study that we did that was a
lot of fun and I think gives us a lot of
hope for the future. And that is on the
best analgesic of all. That is love. And I don’t mean a live
opioid-releasing viral endosome. No. We’ll see if we can get
the audio up any more. But for those of
you can hear, it’s Dionne Warwick’s what the world
needs now is love sweet love. So what we did is
we decided to take on studying this intersection
of passionate love and pain. I often go to the
Society for Neuroscience with a guy, Art Aaron. He and his wife study
passionate love. I study pain. And the wine was flowing. And he was talking about
the neural circuits and passionate love. I was talking about the
neural circuits and pain. We had some more wine. And we did what we usually do. We came back to Stanford and
decided to study it together. And we got Dr.
Jared Younger, who was a post-doc at
the time, who’s now an associate professor
at UAB, involved. And we decided to take
on passionate love, because this is a phase of a
romantic relationship where your deeply focused
on the person that you’re in love with. You feel great when
you’re with them. You feel a craving when
you’re not with them. Doesn’t that, by the way,
just sound like an addiction? Doesn’t it? And it turns out it is. It is an addiction. Because it turns out that
those areas of the brain have been mapped out
for passionate love are the same areas that are
involved with addiction. And so if you’re addicted
to heroin, cocaine, if you like to hit the lattes
real hard, if you’re like me and you like dark chocolate
in the afternoon, what happens is these circuits
all get engaged. And the one in particular
that we were focusing on is one called the
nucleus accumbens. This is an area
rich in dopamine. It’s your feel good
chemical in the brain. It’s the one that gives you
this nice sense of feeling good after a latte, after
dark chocolate, or when you’re in love. And so we looked at
this intersection between passionate
love and pain. And what we did is we put up
flyers on Stanford’s campus and we asked this
simple question. Are you in love? Are you in love? We want to study you. And I’ll tell you. Within two hours,
we had 16 couples banging on our door
saying, we’re in love. We’re in love. Study us. It was the easiest
study we’ve ever recruited for in the entire
history of our division. We should have done
this years ago. Because when people are in love,
they want the world to know. So we asked them to bring
in pictures of their beloved and bring in pictures
of an equally attractive acquaintance. And then we would flash
them pictures of each one and we’d cause them pain. Yes, we do these things here. And we pay these
students really well. We don’t harm them,
but we do cause pain. And what we found is
that love works great. It’s fantastic. It caused about a
40% reduction in pain when you see the one
you’re in love with. Isn’t that amazing? And it turns out
the more in love you were with the person,
the more analgesia, the more pain relief you’ve got. Now, how do we know how
much in love somebody is? Well, because the psychologists
have got scales for everything. And they’ve got something called
the passionate love scale. And it talks about what
percentage of the time do you spend thinking
about your beloved. We had Stanford students
thinking about their beloved 80% of the day. I have no idea when they
found time to study. But they had three
times the analgesia of people who thought about
their beloved less than that. And so then we put them
into an imaging environment. And what do we find? Lo and behold is this
tremendous activity in the periaqueductal gray. This is an area involved with
your endogenous pain relieving medications in your own brain. They’re natural pain relievers
and, yoohoo, this error in the brain called
the nucleus accumbens, which is involved
with dopamine release and this great intersection. That means love works
and it works great. What does that mean for you? Well, I can’t write
you a prescription for a passionate love
affair every six months. That won’t fly, unless
you’re in Vegas. But what we can do
is encourage you to do things that are
novel, that are exciting, that are salient,
that are different. Go for a moonlit
walk on a beach. Go for a walk, if you
can, in the hills. Go read an exciting
and new book. Listen to some beautiful music. It will have an
analgesic benefit. And you’re going to
hear stories today about how to put all
of that together. So in bringing
this to closure, I don’t need to tell
you that back pain has a huge impact on the person,
their family, and society as a whole. But I hope I’ve convinced you
that chronic back pain can cause fundamental changes
in the nervous system. And one of the
key messages here, this distinction between
nociception and pain, it’s not all about
the back, folks. But guess what? It’s also not all
about the brain. It’s all of it. It’s everything. And so our goal here
is to target everything and to help you get
your lives back. So with that, let me close
out on one last bit of hope and excitement here, and that is
the national pain strategy that was alluded to earlier. I was honored to co-chair
this with Dr. Linda Porter from the NIH. This is an effort to develop a
comprehensive population level strategy for pain prevention,
treatment, management, education, reimbursement,
and research. That’s a mouthful. In other words, we’re
trying to transform this country’s care for pain. And that plan that should be
released by Health and Human Services very shortly is going
to be very specific targets with specific stakeholders
that are going to be involved. And why I’m bringing
this up to you is we need all of your help. We need all of you
engaged and involved with this to get the
word out, to lobby your congressmen and
congresswomen, the stakeholders and say, this is important. Let’s make a difference
in this country. Let’s transform it and
make a cultural shift. So I want to give our thanks
out to the Stanford Systems Neuroscience and
Pain Lab, or SNAPL, where we study the best
things on Earth that hurt. And with that, I’m going to
close out, say thank you. Thank you.

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