Stanford Hospital’s Meredith Barad on Migraine Headaches

Stanford Hospital’s Meredith Barad on Migraine Headaches

So we’re going to cover
the basics of migraine. And then we can get
in a little deeper, whatever aspects you guys
would like to talk about. I thought one of the
ways to do it is just to set it up almost like
a journalistic piece. But let’s talk about
the “what” of migraine. What is migraine? Who gets migraine? Where? And when do people
get migraines? Why do people get migraines? And what can we do about it? So what is migraine? Let’s define migraine. There are two basic
big types of migraine. The largest group,
about 2/3 of people, have migraine without aura. And this is defined by
a headache that fulfills the following criteria. They have to have at
least five attacks of this type of headache. A headache that lasts four
to 72 hours untreated. Has at least two of the
following characteristics. Unilateral– it does not have
to remain unilateral throughout the headache– most headaches
don’t– but usually starts on one side or the other. Pulsating in quality. Moderate to severe pain. Aggravation by or
causing avoidance of routine physical activities. And then at least one
of these qualities is present during a headache. Photophobia, that means
light sensitivity. Phonophobia, sound sensitivity. Or nausea and/or vomiting. And then not attributed
to any other disorder. So that is what we call
primary migraine without aura. And then there is
migraine with aura. And about 15% to
30% of migraineurs have migraine with aura. And this is a little
bit more complicated. So they have a fully
reversible neurologic symptom usually prior to the
onset of the head pain. And the reversible symptom
is most commonly visual; that can be sensory,
such as numbness or tingling in a
part of the body; can affect your speech,
your production of speech or your understanding of
speech, as we saw in that video earlier; motor, could
have some weakness. There can be brain
stem– and by brain stem, I mean dizziness and vertigo are
usually the most common ones. And then retinal is a little
bit of a different one. But, basically,
some visual changes. And then this aura
needs to fulfill two of the following criteria. At least one aura symptom
that spreads gradually over five minutes and/or
two or more symptoms that can occur in succession. Each individual aura symptom
lasts 5 to 60 minutes, and at least one
symptom is unilateral. The aura is
accompanied or followed within 60 minutes by a headache. you So it’s usually
aura, then headache. Sometimes they
overlap each other. But the key to
migraine with aura is that it’s a fully
reversible symptom. Again, and then not
better accounted for by any other diagnosis. And in cases of
severe aura, a stroke or transient ischemic
attack should be excluded. As we said, 15% to 30%
of patients have aura. And some of the auras– the
visual changes, numbness and tingling, weakness,
altered perception, cognitive impairment, expressive
aphasia, meaning your ability to produce speech, receptive
aphasia, your ability to understand speech,
dysarthria, just your ability to speak, the motor control of
your mouth, and incoordination are some auras. But this is an example. These are some examples
of visual auras. And these are taken from
some of the patient websites where patients have actually
made computerized drawings or sometimes hand drawings of
their experiences with aura. So what you’ll notice is this
sort of central– most people have a central loss of vision. That’s called a scotoma. And then there’s usually
a peripheral light– we call it scintillation. So moving lights or clear
lights or fluttering lights, we call that a
scintillating scotoma. Sometimes you see a sort
of cross hatch, up and down pattern. That’s called a
fortification spectrum named after fortification walls
of old middle medieval cities. Some people have seen those. I don’t know if any of you have
ever had an aura like that. But people will look– they’ll
try to describe the aura to me. And I’ll say, did
it look like this? And I’ll show them one of
these computer pictures. And they’re very
impressed at me. But it’s nothing I’m doing. It’s that it’s just very common. I mean many, many, many people
have similar experiences. Who gets migraine? Let’s talk about the
epidemiology of this. 36 million Americans
have migraine. So let’s put that in a
little bit of context. You are often told
in the news that we have a crisis of diabetes in
this country, a crisis of heart disease in this country. 29 million Americans
have diabetes. 26 million Americans
have heart disease. 20 million Americans
have cancer. So migraine beats them all. Migraine is by far one of
the biggest health issues that Americans contend with. Now it affects people
to different degrees. The average lifetime
prevalence of migraine is 18%. So 18% of all
Americans will have a migraine in their lifetime. The estimated average prevalence
in the past year is 13%. So in the past year, 13% of
all Americans had a migraine. Prevalence in children in
adolescence annually is 7.7%– no, sorry, in your
entire childhood, 7.7% of all children
and adolescents will have a migraine. And a very small percentage
of those people, 3% to 4%, develop chronic headache, which
is a headache more than 15 days per month. And that’s typically– question? Can we ask questions? Sure. That’s OK. OK. This 29 million
or 36 million, was this diagnosed by
meeting your criteria or anybody in private care– So the way we got to the number
of 36 million is the question. And the way we got there
was by a very large mail out– obviously not
to 36 million people– but a very large
mail out that has gone out over the
past about 15 years at intervals to Americans. And by looking at the
proportion of those people that fill out that survey
and then send it back, they’ve been able
to duplicate it. But it also fits with
international studies. So internationally about
15% of any given population has migraines. And 3% of the general population
have chronic severe headaches. That’s typically what
we see here at Stanford is the severe headaches. This is more common in females. Two to three females
for every one male. And again this is
consistent across countries. And the risk for this change
in female preponderance for headache emerges at puberty,
females having a 1.5-fold greater risk of headaches at
puberty and a 1.7-fold greater risk of migraine than male
children in adolescence. And that extends
until about menopause. I think we’ll talk about
a little bit later. So breaking it down to
how this divides out, the majority of patients have
one to four severe headaches a month. 63% of migraineurs have one to
four severe headache attacks per month. Sometimes it’s not enough
to bring you to the doctor. Sometimes it is. 10% of patients have
more than four severe. And 3% to 4% have chronic. The course of migraine can
vary over your lifetime. So we used to think that it
was more of a curve like this in that headaches
emerge in puberty, continue in women during
their childbearing years, and sort of taper
off in menopause. But what we have
noticed is that there’s a lot of individual variability. So while that is true
on a large scale, the average migraineur
will have years where they have very active
migraines and years where they have very quiescent migraines. And that doesn’t seem to
follow any one pattern, but seems to be very
different depending on the migraineur for reasons
we don’t really understand. Overall, we see it diminishing
after the age of 50 in women– and in men, also. But in women, we specifically
think it’s tied to menopause. And we see this
diminishment unless women are on estrogen replacement
therapy, in which case we don’t see the diminishment
of migraines around menopause as readily as we would if
they were not on estrogen. The age of onset,
so when you first get your first migraine–
psychosocial stressors, psychiatric comorbidities
may be related to a less favorable outcome. So I think the thing that
holds the most scientific rigor in most studies is this
early age of onset. So kids getting headaches five
years old, three years old, those are the people
that are going to go on to usually develop
more severe forms of headache as they go on through life. There is a genetic
component to migraine. And it’s something that we are
still trying to figure out. We sort of noticed this
way back a long time ago. Green in 1977 put
out a paper that said that 60% of migraineurs
had a positive family history. 53% had a mother
who had migraine. 17% had a father
who had migraine. They went on to do
successive studies looking at a particular type
of migraine called familial hemiplegic migraine. So this is a migraine that
runs in families where you have an aura of weakness
on one side of your body prior to the onset
of the headache. And they were able to
find several genes linked to the familial hemiplegic type
one, type two, and type three. And so that got people
very excited in migraine saying, well, if we found
these candidate genes, maybe there are more
genes that we can locate. We’ve also noticed that
in certain diseases– and these are complicated
medical diseases like CADASIL, which stands for
Cerebral Autosomal Dominant Arteriopathy–
looking at my notes to make sure I don’t mess it
up– with Subcortical Infarcts and Leukoencephalopathy. Big word, right? These are very complex
neurological diseases, but we’ve noticed that
with those diseases, there’s a very profound
migraineous component. So these are patients who
have strokes and a migraine. And there’s been genes that
are linked to those diseases. And in the last 5
to 10 years, they’ve started doing studies
called GWAS studies. And this is Genome-Wide
Association Studies where they search the
genome for small variations in single nucleotide
polymorphisms, or SNPs, that occur more
frequently in people with a particular problem as
compared to average population. And looking at all
those thousands of SNPs, hundreds of
thousands of SNPs, studies have been able to find
about 13 susceptible genes. So we’ve been able to narrow
it down to 13 gene candidates. And there are groups
all over the world that are looking at
these genes and trying to understand if we
could design treatments to better focus on these
genes, if we can develop tests for migraineurs to
get a blood test and see if they
have those genes. That’s not ready
for prime time yet, but it is very interesting
finding that genetic link. All right. So let’s move along to try to
understand what is migraine. We’ll go through this a
couple different ways. And then we can go back to it if
it doesn’t exactly make sense. But I think of migraine
as a brain state of altered excitability
capable of activating the trigeminovascular
system in genetically susceptible individuals. So normally, you have excitatory
and inhibitory processes going on in your brain at all times. And they work together to
keep the brain in balance. And what happens in migraine is
that this gets out of balance. We get some disruption
in this homeostasis. And that activates the
trigeminovascular system in genetically
susceptible individuals. And the result of the
activation of that system is pain, pain in the head. How is that system– what is
the trigeminovascular system? How is it activated? We’re going to talk about that. There’s probably two big
ways that this is activated. Number one is aura. Aura– we’re going to talk about
what it is, but basically aura is a depression of
neuronal function. And aura can trigger
this migrainous process. The other thing that probably
can trigger this process is exogenous triggers or
even endogenous triggers. For example,
changes in estrogen, changes in barometric pressure,
changes in your schedule, change– change in general. Disruption to your
homeostasis can trigger this altered
excitability of the brain. And as my migraineurs,
you’ve probably all noticed that you
all have triggers, some sort of disruption. And it’s usually a change. It’s usually something
that was different than the normal routine. So let’s take aura because
aura– let’s go back to this migraine with aura. And let’s look at this a
little bit more closely. So actually, let’s–
we’re going to go here. What happens when
you have an aura is you have a wave of inhibition
that spreads across your brain, usually starts in the
back and spreads forward. And that’s why visual
changes– because the back is the visual cortex
of the brain– that’s why visual aura is most common. So it usually starts in the
back and spreads forward. And when you get that
aura, what happens is it causes the neurons to
change how they’re firing. And those neurons will
then release hydrogen. They’ll release potassium. They’ll release other
agents like nitrous oxide. And that will cause
some– that will bubble up to the blood vessels
around the brain, cause some dilation or
reactivity of the blood vessels in the brain, which will then
stimulate the trigeminal nerve. And once the trigeminal
nerve starts firing, that’s when you start to
feel pain, when it builds up a critical mass. So to the
trigeminovascular system is this relationship
between blood vessels and the nerve that supplies–
that innervates the blood vessels. So if a blood vessel
changes rapidly, expands or rapidly contracts, that
nerve that supplies sensation gets activated. And in cortical-spreading
depression, when that nerve, when
that blood vessel expands, it also releases a
neural inflammatory soup, a bunch of peptides
which are released, CGRP being one of them. And that also causes
those neurons to fire. So we have dilation, release
of neuro inflammation that causes those
neurons to fire. When those neurons build
up a critical mass, it travels up your brain stem,
travels up to your brain, and it explodes into pain. Some people have a gate on
their– we all have a gate. We all have a gate that keeps
out these excitatory signals. But in migraineurs,
you can imagine that maybe the gate
is a little bit easier to open than in others. So in migraineurs, these
signals are building up. And maybe Nora would be able
to keep those signals at bay, but maybe a migraineur
might not be able to keep those
signals at bay. Those signals travel
up the brain stem, travel up to the cortex where
they are perceived as pain. And so aura is one way that
this process can happen. And then there’s also
peripheral triggers are another way that
this process can happen. So here’s just another
illustration of this process. Here you have blood
vessel dilatation. You have release
of neuropeptides. It activates the
trigeminal nerve. The signals travel
to the brain stem, up to the thalamus,
up to the cortex, where your brain
perceives that as pain because the volume of
those signals is so loud. And then this,
the problem– what happens here is that this
becomes sort of a vicious cycle because as this
nerve is firing, it creates more neuroinflammation. And then more
neuropeptides are released. And then they signal to
keep the nerve firing. So this whole process keeps
on going, keeps on going. And it can be very hard for
some people to shut it down. So let’s take a peripheral
trigger, for example. This would be somebody
who has allergies. So if you have a lot
allergies, it’s spring, you have hay fever. You get a lot of allergens
in your nasal mucosa. You start developing
histamines and mast cells. And all of those cells
coming to the nasal mucosa trigger the trigeminal
nerve to be activated. It starts firing. Because it innervates the blood
vessels when it starts firing, the blood vessels
change their diameter. They contract and relax,
dilate and constrict. And they start releasing
the neuroinflammation. And then the whole
cycle gets started. Signals travel up
the brain stem. And if you’re not able to
gate that appropriately, it can travel up the brain
and change into migraine. Does that makes sense? OK. So let’s talk about triggers. You guys, a lot of people
were nodding their head when we were talking about triggers. I think every migraineur has
their own individual triggers. But what I tell people
is that is usually the change in something. So migraineurs need
to have a boring life, the same thing every day. Got to go to bed
at the same time every night, wake up at the
same time every morning, eat regular meals
every day with protein. Protein helps you burn
calories more regularly. If you’re going to have
caffeine, have a small amount and have it every
day, even on Sunday. It’s when you change
things, that’s when you get into problems. And it’s very hard
to tell a teenager that they have to have
a regular boring life. So a lot of times, migraines–
you’re going through puberty, you’re a teenager, your
migraines are just starting, and you do not want to
have a regular boring life. And so things get
out of control. As you get older, it’s easier
to regulate your schedule. But for my migraineurs that
are going into– my younger migraineurs who are going
into college, going off into the working world,
I tell them to think about having a regular life. So working the
night shift is not going to be a good job for you. Working some job
where you frequently have to change time zones may
be a challenging job for you. So just as a diabetic
needs to tailor their life to their disease,
a migraineur needs to recognize that they
need to work to keep their brain in homeostasis. Question? Have they done any personality
typing for migraineurs? Have they done any personality
typing for migraineurs? No, it’s not like a Type
A, like heart attacks are a kind of a Type A personality. Why is only trigeminal is
the only one that is being– Why is the trigeminal nerve? Well, the trigeminal nerve is
the nerve that is responsible for most of the blood’s– the
sensory innervation of the head and the brain. The brain is not innervated. There’s no sensory
nerves on the brain. But it’s the meninges,
the covering of the brain, that is innervated by nerves. And then the head and the
face is all trigeminal wit the exception of the back right
here and a few parts of the ear are innervated by a couple
other different nerves. So it’s primarily
the trigeminal nerve. Now there is a
parasympathetic nerve bundle called the sphenopalatine
ganglion that is linked in to the process. And the parasympathetic
ganglion is what controls your– just
like sympathetic ganglion– your lachrymation, your
mucus, your sweating. And so that is tied in because
many migraineurs have tearing. They find that they get
very congested here. Sometimes their eyes
get red and irritated. And so that nerve bundle
is also playing a role. And we’ll talk a little
bit later about that because that’s sort of a
target of some of the newer treatments for migraine. All right. So again, I like
this volume signal because this is like the volume
gets turned up in migraine. And it is very hard
for the migraineur to turn it back down again. Let me finish this slide. And then we’ll go
to your question. Just to cap off this why. Aura is caused by this
cortical spreading depression. The cortical
spreading depression may cause activation of the
trigeminovascular system. And that leads to a brain
state of altered excitability in genetically
susceptible individuals. And in that pain,
the pain is caused by the activation of the
trigeminovascular system. Question? My husband has migraines. So it started with visual aura. Now it’s olfactory. Is that normal? And is olfactory more uncommon? So the question is, is
olfactory more common? Visual aura is the most
common type of aura. Olfactory aura is
much less common. But there are many
different types of aura. It doesn’t concern
me if aura changes. Aura can certainly change
throughout a life course. But let’s actually–
let’s hold off. Nora’s telling me that she
wants to do the talk first and then we’ll go to
questions afterwards if that’s OK with you guys. So sometimes migraineurs notice
that they get a little warning. And they might not get an aura. But they do have what we
call premonitory symptoms. And these precede the
headache by about 24 hours. These are subtle,
but the reason why they might be important
for the migraineur is to note when you might be
more susceptible to migraines. So if you should notice these
symptoms– irritability, lethargy, yawning, neck
stiffness, food cravings or aversions, changes in
your bowel or bladder– a lot of women sometimes experience
this premenstrually as well, a lot of similar
symptoms– but those might be times when you might be
more susceptible to migraines. So it might be interesting
to check in and note how you feel in the days
before your migraine. Sometimes you have to
do it retrospectively, but sometimes you
can catch yourself. And the thought
is that maybe this is some sort of
abnormal neural activity that may prime the
brain for migraine. And then post-migraine,
most people feel terrible or different
for a little bit of time. That can be a day or two. They feel like they don’t
have the pain quite as much, but there’s an after
affect, an aftershock. And that’s probably the result
of this hyper-excitability of the brain or a bombardment
of the cortical neurons. So the neurons in
your brain are being hit by these signals coming
from the trigeminal nerve again and again and again. And they’re tired. They’re overworked
and exhausted. And you’re experiencing
that as well. Many people during the
migraine, and sometimes after, will have sensory sensitivity. So that’s why we always
ask about light sensitivity and sound sensitivity. But there are other types
of sensory sensitivity that migraineurs experience. Movement sensitivity, so turning
too quickly might feel strange. Neck stiffness, a
lot of neck pain. Blurry vision,
lightheadedness, vertigo, so feeling that the
room is spinning. And allodynia. Allodynia means that if you
just touch something normally, it’s painful. And a lot of times people
feel that around their hair. They’re brushing their
hair, washing their hair, brushing their teeth. It’s normal activities,
but it feels painful. And sometimes– we
talked a little bit about this– this is the
sphenopalatine– the input of the parasympathetic
system and sympathetic system in the head, but
these autonomic signs. So you have tearing,
irritation of your eyes– we call that
conjunctival injection. Ptosis, so sometimes your
eyelids come down a little lower. One will. Itching eyes, nasal
congestion, runny nose– that’s rhinorrhea– ear
fullness, facial flushing. Very rarely agitation, that’s
not a typical characteristic of migraine. Agitation and restlessness,
if you told me that you felt that way
during your headache, I would wonder if migraine
was the right diagnosis because migraineurs really
like to go into a dark room. I mean, it’s like they
need sensory deprivation. They need to go into a
dark room and lie down. And going to sleep seems
to help the brain get a hold– put that
gate back in place, get that gate locked
up again, and combat that incoming signals. So the things that we will
talk about in treatment are lifestyle modifications,
which I already gave you my little one-minute
spiel about that, but we’ll go over that again;
preventive medications; rescue medications; alternative
medications and interventions. And then we can talk
about extreme treatments. And then we can also talk
about novel treatments, things coming down the pipeline. So the primary treatments
are making sure that your lifestyle
is optimized. And of course, nobody can live
in a stress-free environment. Wouldn’t that be nice if
we didn’t have any pressure or any stress ever? But that’s just not possible. So what we do
encourage patients do is to work on stress
management techniques because stress seems to
be such a common trigger. And it’s actually not
the stress itself, but it’s the relief
from the stress. So it’s after the test is over. It’s after I give
this talk tonight. It’s after a big event. The let down is what
usually triggers a migraine. So it’s managing that. And there’s many
different techniques that psychologists use to help
people manage their stress. We call that putting more
tools in the toolbox. Decreased caffeine intake. And so I do not think you
have to stop all caffeine. I appreciate the
beauty of caffeine. But what I do think you need
to do is keep it at a low dose and keep it constant. So I say one to two
caffeinated beverages a day. And I would much prefer
you to have caffeine than to have sugar. Because caffeine will slowly
take you up and then slowly bring you down. Sugar is like– psh! It brings you up, and
then it pops you down. So again, keeping things
in mind about the delta, we want to try to keep
things as even as possible. So if you are
caffeine drinker, I say have your caffeine at
the same time every day. Make it constant. Dietary trigger management. I put this on the list
not to tell you to do it, but to tell you
that you can make yourself crazy by doing it. So to do it with moderation. So the things that we know
cause migraine are sulfites. Sulfites are in
all types of wine, but more specifically in
red wine and champagne. Nitrates and nitrites, which
are in a lot of processed foods. And, sorry, sulfates
and sulfites are also in dried fruit, all
those dried fruit things. Nitrates and nitrites and MSG,
those are the big ones, OK? If you can avoid those, you’re
doing really, really well. Now every now and
then somebody tells me that they heard like ripe
avocado or this kind of cheese or whatever. I just think it’s
very individual. And if you want to go
through every single food and try to figure it
out, you can do it. But I think you can also make
yourself crazy doing that. So I would say to try to
stay away from the big three. And then try to eat
a non-processed diet. When you look on the back of
a food in the grocery store and there are ingredients
that you do not recognize, try not to put
those in your body. I can’t tell you if those
will cause a headache or not. There has not been a
study done on them. But if they’re
chemicals, they might be more likely than, say, baked
chicken or something like that. So a whole, non-processed
diet is probably the best advice I can give you. Exercise is very hard to do
when you have a migraine. But it is important to do it
because it makes you feel good. And because it can be helpful
to help your brain operate, get back into that homeostasis. So I say try for
20 minutes a day. It doesn’t have to be that
you’re running a marathon. But on the days you’re
not feeling good, put on the glasses,
put on that, try to get 20 minutes of walking in. On the days you’re feeling
good, go to the gym. See if you can do a little
bit more vigorous activity. Try to keep yourself
in your schedule even if it’s not the best day. If it’s a really bad day,
that might be an exception. But the exercise should
be a constant in your life and will help you feel better
and will help your brain idle better and run better. And then regular sleep. We all know that
sleep helps migraines. And it helps your mood. And it is a curative
necessary process. So do it regularly. That’s all I have to say. Please sleep. It is another very
common headache that I see here in the
Bay Area is the I’m doing my start-up company right now. And I have to stay up till
4 o’clock in the morning, programming all night long. And then I have to get up at
6 o’clock to have a meeting. And people think that they
can live like that infinitely. But you cannot. We all need to sleep. Even in Silicon Valley,
we all need to sleep. All right. So if you’re
getting to the point where your headaches are
really getting out of control– and that varies from
person to person– the usual indication
for starting a preventive medication
is about four headaches– six headache days,
a four headache days with at least some impairment. That being said,
I would consider, depending on the debilitation
of your headache, starting it earlier if that was
something that the patient was interested in. One hemiplegic migraine a month
is too many, in my opinion. So you have to tailor it to
the patient and the patient’s needs. Prevention should
definitely be considered if you’re having four or
five migraine days per month with normal functioning, two to
three migraine days per month with some impairment,
two migraine days with severe impairment. If you’re having less than
four headache days a month with no impairment, you can
take a Tylenol or a triptan and it will go away
rather quickly, you probably don’t need to
take a preventive medication. Sometimes we would do
preventive medication if we have a known trigger. So every time you have
a period, or every time you try to do an intensive
aerobic activity, sexual activity, those can
frequently trigger migraine. So sometimes we will do
preventive medication or even a rescue medication prior. We use a rescue medication
as a preventive. Take it prior to
the known trigger to prevent the headache. We do that a lot for flying,
for people who know they get a headache on the airplane. We can try that. So when we start
preventive medication– and we’ll go over some of
the preventive medications– it can be quite
frustrating for the patient because they just want to
find the right medication and just be done
with the headaches. And there’s a lot
of dissatisfaction on the patient’s part about
having to wait so long and go so slow as we’re
going up on the medications. The reason why we go slow is
because sometimes medications can have side effects. And these are all neural
modulating medications, meaning they all cross
the blood brain barrier. They all interact with the
central nervous system. And sometimes that can
cause some side effects. It can cause dizziness. It can cause fatigue. It can cause cognitive issues. And if we go slower, your
body can get adjusted to that more readily. So that’s why we go slow. They also take time. These are modulating the
way that neurons are firing. These are modulating channels. And we can’t determine
its efficacy in a week. So we sometimes have to wait
six weeks or two months. And that can be
quite frustrating. What we really try to
encourage you to do is to avoid medications
that may aggravate migraine. And so a lot of times
people say getting into the cycle where I’m
using an Excedrin every day. And that actually is something
called medication overuse headache, where you are using
a rescue medication daily and it is actually triggering
a rebound in your headaches. And so what we need to
do is try to get you off of those inappropriate
use of rescue medications and get you on a preventive. And that’s really
hard to do, right? Because you really want to take
your medication that you know that works. And you don’t want to take this
medication the doctor gave you that doesn’t seem to be
doing anything right yet. It’s important to come
back and not to give up. So a lot of times,
people get frustrated, and they don’t want to
go back to the doctor. It’s hard to go
back for follow-up. But there are many
medications to try. And so it’s important to
follow up with your doctor. It’s important for
doctors and for women of childbearing age
and their partners to make sure to discuss
the risk of pregnancy on these medications. Most of these medications
are teratogenic, meaning that they
can affect the fetus. And so if you are
considering a pregnancy, if you are not
using contraception, it’s important to know the risks
before you take the medication. And the doctor should
explain that to you. But if they don’t,
then you should ask. It should involve the
patients in their care to improve patient adherence. This is a paper from
some headache doctors to other headache doctors. It seems obvious,
but is important. And you should choose a
drug based on efficacy. So obviously efficacy, patient’s
preferences, headache profile, the drug’s side effect,
and the presence or absence of coexisting
comorbid conditions. So what we try to do is
give you a medication that will also be helpful maybe
for something else going on in your life. If you are depressed,
we try to choose a medication that
might come from one of the antidepressant families. If you have obesity,
we may try to choose a medication that helps with
weight loss and migraine. If you have high
blood pressure, we might try to choose
a medication that comes from the
anti-hypertensive family. We try to give you a
two-fer to get more use out of the medication. So the American
Academy of Neurology came out with a practice
parameter where they reviewed all of the literature,
all the studies on preventive
medications in 2012, and came out with their
best recommendations as to the most efficacious,
most well-studied medications. So level A is the best evidence. There’s three. And the first one is a
topiramate, which is Topamax. Topamax has 11 studies. It has two large multi-center,
double-blind placebo-controlled trials. The dose recommended
in these studies varied from 50 to 200 milligrams. The typical dose that we
use is 100 milligrams. And there are side effects
to this medication, which can make it challenging for some
people, mainly cognitive side effects. Again, that’s another
reason why we go slow. And we stay as low as possible
to try to minimize those side effects. Valproic acid is another one. And that’s an older
medication called Depakote. It has six randomized
controlled trials. This is a very good
medication for migraine. It has some problems in
that if you get pregnant, it is sort of the most
teratogenic of all the medications that we use
as migraine specialists. So we don’t recommend
it for young women. It can also cause
nausea and vomiting, but many people who are older
and have migraines have been on it for their whole lives, . And it has worked quite well. Beta blockers are probably
the most studied preventive medication. In the United States,
we most commonly use propanalol at a dose
of 80 to 240 milligrams, or metoprolol at a pretty
high dose of 200 milligrams. The side effects are sleep
disturbance, weight gain, and fatigue. So like I was
saying, these drugs all have possible side effects. Not necessarily that you
will have those side effects, but that they do have side
effects that we’ve noticed. And that is, again,
why we go slow. The Level B
preventive medications are SSRIs like Prozac, Paxil. SNRIs, Serotonin and
Norepinephrine Reuptake Inhibitors, Cymbalta and
Effexor are in that category. And then tricyclics,
amitripyline, nortriptyline, desipramine, and imiprimine–
those are all in that family. Those are also all
very good medications that I use very frequently,
but there’s just not quite as much evidence for their
efficacy as the first three. Where do these drugs
work depends on the drug. But in general, some of them
work at the brain level. They work on cortical
spreading depression. They work to modulate
serotonin and norepinephrine. They work at the brain stem
in beta-adrenergic channels in the brain stem. And then they also
work peripherally to mitigate neurogenic
inflammation and quiet down that neuron
inflammatory soup that we were talking about. A few more preventives. There’s also herbs. And these are actually studied. Germany does a lot of work
on herbal medications. And they have double blind,
randomized controlled trials. Butterbur is one of the
most effective ones, 75 milligrams twice daily,
the Petasites extract. There’s been a little bit of
controversy over butterbur because there are lots
of different companies that make it. And it has been taken off
of the market in Europe due to some concern that it was
not being processed correctly. So I think the long
and short of it is to maybe use a little bit
of caution with butterbur and talk to your provider
before buying just any over-the-counter brand. Riboflavin, 400 milligrams, is
found in a randomized control trial to be superior to placebo
in reducing headache frequency and severity. And feverfew was not found to
be efficacious in a randomized controlled trial, but
the extract of feverfew has been shown to be effective. That is available in Germany. And you could go online in
Germany and get that extract. And NSAIDS are not– and NSAIDS
are ibuprofen, Advil, naproxen, those types of medications. They’re not indicated
as a preventive, so not as indicated
as a prophylactic. But a lot of people use
them, were using them. Overall, we try to use them
as a rescue medication, not as a daily medication. So now we can move on
to acute medications. And those are the triptans. Those are the biggest
class of acute medications. These are serotonin agonists. And they act at a
couple different places. They act on the
trigeminal nerve. They act at the brain stem. And they also act probably in
this neuroinflammatory soup we were talking about a little
bit earlier at the blood vessel. They are effective
for acute migraine. And they’re better when
they’re taken earlier. So patients treated within
the first 90 minutes are less likely to experience
a recurrence than patients treated after two hours. A couple contraindications. If you have heart
disease, that’s the main contraindication. So in patients as they
age, you might start off with a triptan in
your 20s or 30s. When you’re getting
into your 60s and 70s, you might need to rethink that
with your primary care doctor if you have any signs
of heart disease because it does cause a
little bit of constriction of the blood vessels– not
a lot, but a little bit. There are many different
kinds of triptans. And the ones that we know most
commonly in the United States are the ones that are generic. So sumatriptan is generic. Rizatriptan is generic. And naratriptan is generic. Just to touch on some of
their differences briefly, the two at the bottom
are the longest-acting. So this lasts about 24 hours. This is about six hours. And the rest of these
medications are shorter acting. Their onset is about 30 minutes. And they last about two hours. So if you are a person who has
a three-day cycle of a migraine or a longer migrate, then one
of the longer-acting triptans would be a better fit for you. They come in many
different forms. So there’s pills. There’s nasal spray. There’s oral dissolvable
tablets for people who are very nauseous. There’s an injectable
for migraines that come on really rapidly. There’s a patch
or a sticker patch that heats up and absorbs
into the skin, which is kind of interesting. And there are some
suppositories as well. The typical approach
that we use is to go for the highest
strength first. So sometimes if you feel
like you’ve tried a triptan and it didn’t work, you may want
to make sure that it was indeed the highest dose available. Sometimes doctors, there
used to be more caution. Doctors used to be more cautious
with using these medications. We now know that they’re very
safe and very well tolerated. And so sometimes I’ll
come across a doctor that gave a patient 25 milligrams
of Imitrex, and it didn’t work. And so the patient thinks,
well, I failed Imitrex. It doesn’t work. But they did not try the full
dose, the 100 milligrams. So I always start
at the full dose unless there’s some very
significant reason why, like heart disease, which
we just talked about, or a pediatric patient. Other acute
medications are ergots. So ergots are an older
class of medications that are very good for
migraine but highly nauseating. So we give them in an IV
or an intranasal form. And we give them with
anti-nausea medication so that they’re tolerated. Orally, it’s almost
never tolerated. There was an
inhaled version that was trying to get FDA
approval, but it has not gotten FDA approval. So we usually give
DHE in the hospital or in our infusion center. And Migranal is
given intranasally. Easily NSAIDS can be good
acute medication. So the oral ones– naproxen,
aspirin, diclofenac– and there’s also–
they’ve been shown to be superior– oh, sorry. And acetaminophen,
aspirin, caffeine is also effective as well. Acetaminophen,
aspirin, and caffeine is a combination that’s
basically available anywhere in the world. It comes in many
different names. I have many patients from
all over the world that bring me a bottle that has
a different brand name. But it seems to be an
age-old recipe for migraines. Cambia is a newer
medication on the market. It is powdered diclofenac. You mix it up with
that two CCs of water. And it’s sort of effervescent
like Alka Seltzer. And you drink it. And because it is
not enteric-coated– so it doesn’t have a coating
like a typical NSAIDS– it gets to higher levels in
your blood system more rapidly. And so many migraineurs
it more efficacious than the typical NSAIDS pills. And Sprix is an intranasal
ketorolac or [INAUDIBLE]. So you spray it up your nose. And it’s also really
helpful for patients, again, who can’t
take the oral NSAIDS. Butalbital is a very
common rescue med that is not well
liked by many doctors but very well liked
by many patients. It’s called Fioricet
or Fiorinal. And the only place you can
get it is in the United States because it’s off the market
in every other country of the world because
it is so addictive. And because it causes
rebound headache if you’re using it more
than five days a month. The chances that you’re going
to worsen your headaches, promote your headaches
is very high. So we really try to
encourage your patients to stop using their
butalbital and try to encourage other doctors
to stop writing it. Sometimes it’s unavoidable. There are certain
reasons why they need to be on that medication. But we really try
to discourage it. Anti-emetics, IV dopamine
antagonists, so IV Phenergan, IV Reglan, IV
Compazine– and oral– can be very good for migraine. You might think they’re
just good for the nausea, but there are also studies
showing that they are very good just for the pain as well. And it may be because
they are sleep promoting. So they help you get to sleep,
which can be very challenging when you have a migraine. But it does seem that
just in and of itself, the anti-emetics, the
dopamine antagonists, are helpful for migraine. The other anti-emetics,
the serotonin receptor antagonists– like Zofran is
probably the more popular one you guys may know–
they have not been shown to be as
effective for migraine. And in some patients, they
actually promote migraines. So just something to
think about if you have an anti-emetic at home. Opiates are not too
good for migraine. So again, they should
be used very sparingly for a rescue therapy. Most neurologists do not
prescribe any opiates for migraine. And the reason is because
there’s very good evidence that, again, opiates
promote migraine. So using opiates more than
eight to 10 days per month can cause a rebound
headache, can increase your risk
of transforming from episodic migraine
to chronic migraine. And some of you may have had
this experience where you’re getting opiates for a surgery. You had a knee surgery
or hip surgery. You’re on Vicodin. And all of a sudden, you
have the worst headache in the world. It actually seems to
encourage headaches in a lot of migraineurs. So getting off those opiates
as quickly as possible is really important for the
majority of migraineurs. Alternative therapies. There are many. And I say, more tools
in your toolbox. If they work, great. I think that I have
patients– there’s studies supporting all of them. And all of them
show as effective. I think if you find something
that works for you, that resonates with you, go for it. It’s not going to stop
all your migraines. Migraine is a chronic condition
that we have to manage. But if there’s one or
two of these tricks that are helpful for you,
that’s fantastic. That’s, again, another
tool in your toolbox. OK, so let’s move on to some
more sort of bigger guns. When we get into a situation
where we have migraineurs who have headaches more than 15
days a month, chronic migraine, we offer them something
called– and they’ve tried and failed preventive
medications or some preventive medications– we offer
them Botox for migraine. Botox is given in 31 different
injections all over the head and neck in places where
migraineurs typically feel pain. The protocol was
developed by a group think of a lot of
prominent headache doctors and then has been tried and
tested in multiple trials and shown that in
about 40% to 60% of patients with
chronic migraine, it’s effective in
decreasing the frequency and severity of your headaches. Injections have to be done every
three months or every 12 weeks usually for most people. But again, this can be
an adjunctive treatment they can be very helpful. We talked a little
bit about IVDHE, but DHE is an ergotamine. It’s effective in eliminating
intractable headache in 89% of patients in 48 hours. So it is a very good
tool for a patient that has a headache that just
skyrockets out of control and is not going to slow down. It’s harder when you’ve been–
had a headache for five years, you’ve been having a
severe constant headache. It may not be as effective. But for patients who are in
a situation where they have their– they’re above and
beyond their usual migraines and they’re in a headache
cycle that won’t break, this can be a very
healthy helpful course. And we bring patients
in the hospital. And we do DHE three
times every eight hours for up to five days. This is called a greater
occipital nerve block. And this is another
technique to break a cycle or to help you taper
off a medication, help break a rebound cycle. So the occipital nerve
feeds into that same part of the brain stem as
the trigeminal nerve. But it’s very hard to do
it the trigeminal nerve block in office. It’s a little bit dangerous. The occipital nerve just
sits right back here. If you push on the back
your head right here, it’s right there. I can put a little bit of
numbing medication in there and inhibit that
nerve input and try to quiet down that building
noise in the brain stem and prevent it from escalating
up to go into a migraine. So there have been
studies where they try to do a series
of nerve blocks, a nerve block every week for a
few weeks, and then every month for a few months, in an attempt
to help the migraineur keep that gate locked and prevent
that escalation of input. The other interesting
new treatment is– so this is not
a new treatment, but it’s one that we’re
doing more frequently to help patients in
addition to medications. This is an older treatment
that got a revitalization. So there’s several
companies that have developed
intranasal catheters that can put a little bit of
numbing medication back in the back of the sinuses here. And then that
medication drips down into this
sphenopalatine ganglion, which is that nerve bundle
that we talked about that sits behind the sinuses. And what it offers
is a little bit of a turning the volume
down on your pain, especially if your
pain has a lot of autonomic or facial features. And again, this is one of those
things that we do repetitively. So we would do it every week
for a few weeks, and then every month for a few
months, while we’re doing medications and
improving lifestyle to try to get a hold
on the migraines. There are lots of
neuromodulators coming on the market nowadays. And these are actually exciting. Some of them work through
electrical stimulation like Cefaly, which is
sort of electrical inputs. And some of them work
like this one, eNeura, which is a magnet, transcortical
magnetic stimulation. And the idea with
the nerve modulator– this is vagal nerve
modulator right here called gammaCore the idea with
those is to provide an inhibitory sensation, which
again travels back to the brain stem and helps clamp down
on those ascending signals so that your brain’s not sending
that signal up to the brain. This magnet, this
is a handheld magnet that you click if
you have a migraine. And we think it is helping
at a cortical level modulate those neurons in the brain. So that is also a really
exciting treatment that is– and these are all
things that you are able to do in your own home. Cefaly is on the market. You can buy Cefaly. The vagal nerve stimulator,
I do not believe is out on the market yet. And this one, the eNeura
transcortical magnetic stimulator, is in
trials right now. But it is available with
a doctor’s prescription. And you can rent it. And the nice thing about these
is that they are not harmful. Other than a tap or a pulse,
it’s not going to hurt you. It’s a very safe, very
well tolerated treatment. So there’s one new medication
that everybody is really excited about in migraine. And that is called
CGRP modulators. So CGRP, remember, is
the predominant peptide in this neuroinflammatory soup. And the thought is that
if you can stop CGRP, maybe you can stop this
neuroinflammatory process and break up this vicious cycle. There was a CGRP
antagonist, a class of medications that
were being brought to market a couple years ago. They failed to make it through
their phase two or phase three studies. And now there are three
monoclonal antibodies. I believe three
companies are doing this. These are going to be delivered
either IV or sub q monthly. So the idea is this is
like a monthly maintenance to try to minimize, quiet down
this neuronal inflammation, this neuroinflammation,
and prevent migraines. And so far, everything is
looking really good in terms of these companies’ studies. So we’re all keeping our fingers
crossed because this would be a very novel treatment. It seems like it’s very safe
in all the studies so far, and very simple
for the patient’s. Just like you have your monthly
infusion for bisphosphonates, for some of the
bone medications, this would also be a monthly
infusion for migraine, which would be really neat. So I think we talked about
some of the resources. American Migraine Foundation,
American Headache Society, the National
Headache Foundation, 36 Million Migraine Campaign. We have a great video. If you Google Stanford
Headache College, my colleague Rob Callan
has a cartoon video where he talks about migraine. And it’s very clever
and well done. And this, I took from the
American Headache Society patient site. It’s called “The
Migraineur’s Bill of Rights.” So I think that as migraine
patients, many of you may have felt that your
complaints have been minimized or you’ve been pushed away
by doctors who weren’t interested in your migraines. And I think it’s
important that you all know that we take migraines
very seriously here at Stanford. And many places, many
academic centers do. I would encourage you, if you
haven’t seen a headache doctor, to see a headache doctor,
somebody who’s had a fellowship training specifically
in headache and who is interested in
trying their best to help work with you to manage
your headaches. I’ll leave that up for
another minute in case anything else wants to read it. It’s a lot of rights. But the point is that
you have the rights. I like this one. I have the right to be treated
courteously and responsibly in the emergency room. That’s a big one that a lot
of migraineurs struggle with. All right. And then finally, I think I
talked about this already. But this is the 36 Million
Migraine Campaign again. We’re trying hard to change
the course of this disorder. And if you happen to have any
donations just lying around and want to give
to this campaign, I think it’s a
really good resource. OK, I’m happy to take questions. Thank you. [APPLAUSE] Yes? [INTERPOSING VOICES] Oh, sorry. We’ll do you next. I know you mentioned
the hormone with women. In men, is a hormone
issue considered or no? Yes, it is. It’s just not as
well– oh, sorry. I’ll repeat the question. The question is,
in women, we know that estrogen and the changes
in estrogen, fluctuations in estrogen seem very
closely tied to migraines. In men, is there a
hormone issue as well? There probably is. It is not as well studied
or parsed out as in women. So I do not regularly
check testosterone levels with the exception
of my patients who are on chronic opiates. And we know in chronic
opiates, that that really alters testosterone
levels, which makes you feel lousy in general,
the lower testosterone levels. So oftentimes, as I’m weaning
my male patients off of opiates, I’ll also be supplementing
with testosterone until they can get their
testosterone levels back to normal. What about aura symptoms
without any headache? Right. What about aura symptoms
without any headache? So I do think it happens a lot. And a lot of
migraineurs describe that, where they don’t
fully go into migraine. So when you think
about it, you’re probably having the cortical
spreading depression, like we talked about. And the trigeminovascular
system is activated. But for some reason,
you’re able to gate that. You’re able to stop that
system from mounting an assault on your brain. And what factors allow you
to gate it sometimes and not gate it other times, I
don’t know the answer. I had the headache problem
in my 20s and got rid of it by just a very mild
lifestyle change. Had no further symptoms at all
until my late 50s when I was diagnosed with Meniere’s. But I have since
learned it’s Meniere’s. It’s migraine. And I’ve had
olfactory experiences. So I hear that a lot,
actually, that women– and I think, as
people age, sometimes they can have different
neurological symptoms. They’ll go to the doctor. They’ll be worked
up for a stroke. They’re told they’re
not having a stroke. And it’s attributed to migraine. And so we think, like we talked
about earlier, migraine changes throughout life. And the typical experience
is that the attacks are very severe and
profound when you’re young. When you get older,
they may become either less severe, but more
chronic, or just less severe. And then when you reach
another point in life, a little bit older, you may have
different neurological symptoms without the headache at all. And that can sometimes
be mistaken for stroke. And why those three phases
occur I’m not exactly sure. Another question in the back. So you may have
mentioned this another– is there any association between
motion sickness and migraine, especially– Well, is there any
association between motion sickness and migraine? I think that there
is a paper saying that patients who
have motion sickness are at an increased
risk for migraine. I think that many
migraineurs have motion sensitivity in general. It’s one of the top
sort of sensory features that migraineurs have. So I would suspect yes. [INAUDIBLE] children
that come in. And they have a lot
of motion sickness. You can tell them that they’re
more at risk of developing migraine at older age. You could. [INTERPOSING VOICES] So the question is,
if a child comes in, and they’re having a
lot of motion sickness, do you tell their
mother that they’re going to at risk for
developing migraine? Well, you ask about the
history. [INAUDIBLE] Right. So I sort of think
there’s a couple risk factors in childhood. There’s abdominal
migraines, which are severe stomachaches that
are not really attributed to any mechanical issue. There is motion sickness. There’s brain
freeze, that feeling that you’ve had if you get
a Slurpee really quick. And then there’s– [INAUDIBLE] aura. Would that go under
aura, the brain freeze? Maybe. Maybe. I’m not sure what the
actual mechanism is of that. It’s post-stress,
post-event migraine. That’s how I started
with mine at five. At five? After the circus,
after the Ice Capades. Yeah. Oh, really? So there’s a couple markers. I think there’s a phenomenon
called alternating hemiplegia of childhood, where
they have alternating weakness that’s really not
attributed to any other cause. So there’s a couple
things that physicians see that makes them say, well,
they might be a little bit more vulnerable to migraines. Whether you go on and decide
to tell the parents that they might get migraines, I’m going
to leave that to your judgment. I probably would not worry the
parent at that point in time. Yes? I’m in the software world. So I’m curious what
software tools you use in your department
to help your patients either determine their triggers
are manage their treatment to see which drugs work or
not, or what kind of tools you’re using right now
to help that along. So the question is,
what kind of tools are we using to help that along? Mostly software. Mostly software. So I wish I had that
PowerPoint with us. We use something called CHOIR
which is Collaborative Health Outcomes measurement– some
sort of outcomes measurement– that was developed at
Stanford by Sean Mackey. And the idea is to
understand all pain using numerous different measures,
not only your pain score. So we ask about sleep. We ask about depression. We ask about anxiety. We ask about physical
function, ask about anger, social isolation. We really try to assess a
patient from all of the factors that pain reaches into because
pain is not only a number. Pain can really
change your life. And so we assess a
patient using those. They’re called the promise
measures developed by the NIH. And we assess them through that. If the patient
wants to use an app to keep track of
their migraines, there are many, many apps. And I don’t endorse
any one particular app. But some patients
find them useful– trigger trackers,
headache trackers. I try to focus more on the
functionality of the patient because you can
spend a lot of time getting caught up in the
minutiae of your headache. And so the first
question I try to ask my patient is, how many good
days did you have this month? And what did you do with
those good days, right? Because we want to get into
what you do with the headache, but we want to focus
on the positive also. Question in the back. So, yeah, I’ve noticed– just
living with a migraineur– that it doesn’t seem
like that much has really happened as far as progress. And I’m wondering if the
funding is– NIH funding or wherever– is not that
great for migraine, or some of the things like this. Yeah, definitely. I mean, compared to– Cancer, for example. Exactly. For the number of people
that have the disease, the amount of funding we get
is very disproportionate. So yes, there is that. On the flip side, I know
it’s happening slowly, but considering where
we were 20 years ago, we really have developed
a lot of medications for migraine and working into
the neural modulatory and CGRP modulators. I do think it’s an exciting time
to have a migraine because I think there’s more
hope on the front. So hang on. I think it’s going to
keep on getting better. You gave an example of somebody
that was able to prevent– or is able to prevent–
a migraine attack before flying by taking the
acute medication in advance. So are you suggesting that
is there, perhaps, research that indicates that,
if by some means, you can have a migraine
forecast in some way, shape, or form, that if you take acute
medication in advance, then perhaps you can preempt and
bypass the migraine whatsoever. So the question is,
if there was a way that we could predict when
your migraine is going to come, could you then take a
preventive medication? And I know that
there are companies that are very interested
in that forecast, trying to understand
that forecast. I think it varies
from person to person. The premonitory symptoms
that we talked about, that sometimes
occur in patients 24 hours before their headache–
the irritability, yawning, lethargy, changes in bowel
or bladder patterns– can be a warning. So if you pay attention
to your headaches and you try to see what happens
in those premonitory– what’s that premonitory phase
like for me, that could be a warning
for you saying, hey, I think I’m going
to get a headache. But typically the
way I do it now is just if you know a trigger
is coming up, take a triptan. Emotional times,
you’re getting married, you’re doing something that
you know causes a headache, it would be OK to take a
triptan if we weren’t doing it more than 10 days a month
because that’s the magic number that you’re really
supposed to use your rescue medications without getting
into rebound headache. Question back there. Yes, someone that I
care for has recently had a migraine that
led to a stroke. I wasn’t there when it
happened, but what can we look for that might be
something that I can be ready for the 9-1-1 moment? That’s a very rare case. So that is very unusual. [INTERPOSING VOICES] So the question was,
somebody that she cares for has had a migraine
that led to a stroke. And how could we prevent that? How could we be
on guard for that? 99% of the time, it’s
not going to happen. And it makes us think that
maybe the two processes are true-true and not related. It’s hard to know. There are very definite
reports of this happening in the literature. But is it the adrenalin
from the headache? Is it some of the
neuroinflammatory mediators that are
released from the headache? What is triggering the
stroke is very hard to know. Is it the increased heart
rate and blood pressure from being in pain? I would say that if a patient
has a very severe headache and they’ve tried their
rescue medications, most patients will
have a threshold that they know that they need
to go to the emergency room. And that that’s OK to go
if you pass that threshold. What we try very hard to do
is to develop a rescue plan, and then a next-level rescue
plan so that we can hopefully prevent patients from having
to go to the emergency room. But if you’re used to a
certain type of headache and then your
headache exceeds that, I think it’s OK to be
worried about that. And I think it’s OK
to seek out help. Right next to her. I get a lot
barometric headaches. And the first
thing I notice when I’m getting a barometric
headache is the sinus issue. And so I’m wondering if one of
the sprays or the inner sinus, if you know if those
are more effective for the barometric headaches
because those I can’t predict. And then the other question
is I get a migraine every time for PMS. There’s no debate there. And so should I
take a triptan when I start feeling PMS,
just preventatively? So two questions. The question is,
is there anything to do about barometric
pressure headaches, and specifically
intranasal medications? I’ve never seen a
study on that, but I think it’s a very
interesting question. A lot of people feel
barometric pressure changes in their sinuses because
sinuses are closed cavities. The only thing I know to tell
you about parametric pressure is that the place
in the United States where the barometric pressure
changes the least is Hawaii. So there you go, if you’re
looking for a place to move. I think that the
intranasal medications might be worth a try,
certainly, for that. And the other part of the
question was about the PMS. So there are some
treatment strategies for menstrual migraine. And they can involve
estrogen manipulation. And they can involve SSRIs, just
like premenstrual dysphoria. So taking an SSRI in the
week before, the week that you feel PMS
is a possibility. If you notice that your migraine
starts within a day or two of actually getting your period,
then usually what we try to do is consider triptans
if you’re still within your monthly
allotment of triptans. So if you can tell me that I
can use the triptans the five days of my PMS. And then I’ll only use them
another five days a month, then that would be OK. But if you can’t,
then we might need to consider playing around with
estrogen via patch, oral pills, or considering an
SSRI for the PMS week. Yes? Is there any extra significance
to a migraine that wakes you up in the middle of the night? Like, you go to
bed feeling fine, and then you wake up with
this just splitting headache? The only thing I
really think about what that is sleep apnea
and making sure that you are getting
enough oxygen to your brain at nighttime. So for patients that wake up
with headaches or patients that have predominant
morning headaches, we really try to investigate
your sleep patterns. I think you had
a question there. Yeah, you used the
adjective vagal one time. Is the vagus nerve
involved with migraine? I’m blessed right now. At age 75, I don’t
have them any more. But when I was in my 50s, I
was devastated at least once or twice a month, every month. I retired at about 60. That was another blessing. And I haven’t had
any problems since. So the question is,
does the vagal nerve play– how does the vagal
nerve play into migraine? So the vagal nerve
supplies sensation to the infra-temporal part
of the head, the meninges and the skull. So there is some sensory input
into that bundle of sensation, bundle of nerves that’s
traveling up to the brain that the vagal is
contributing to. And this company gammaCore
has been experimenting with this device, this
vagal nerve simulator, for both cluster headache
and for migraine headache. I don’t exactly know
the proposed mechanism. And I don’t think
they know the proposed mechanism because I’ve looked
at their slides, and it’s vague. And there’s some arrows
going up somewhere. So I don’t think
it’s really known. But I think they
know that it works on a certain subset of people. And it is a
non-invasive treatment. So that’s where they’re
going with that. OK, I think we have time
for– Nora says no more. One more. Nora says one more. How about all the
way in the back? You talked about
abdominal migraine. How do you explain that
from your slides earlier explaining the flow of– Yeah, so in the brain stem,
when you get migraine, you have light sensitivity,
sound sensitivity, nausea, and vomiting. That nausea and
vomiting is coming from an area in the brain stem. And that is why we
try to give treatments for nausea and vomiting
that target the brain stem. So Phenergan,
Compazine, Reglan– they cross the blood-brain barrier. They act on the brain stem. So in abdominal
migraine, we speculate that it is coming from
the brain stem itself. The symptoms are coming
from the brain stem and not from the stomach. So the GI doctors will
have a good look-over, say everything seems to be fine. Maybe peristalsis is
a little bit slow, meaning the movement of
food is a little bit slow because that can also be
controlled by the brain. The brain-stomach connection
is a little bit tricky because the stomach has
its own nervous system, but there’s a lot of input from
the brain into the stomach. So there is another subset
of abdominal migraine called cyclic vomiting
syndrome where people will continue to vomit
for hours at a time for no apparent reason. And they’ll go through
a whole GI workup. And the treatment for
it is a tricyclic, which is a medication
that modulates the brain, crosses the blood-brain
barrier and acts on the brain. Thank you, guys. I’m here to answer a few more
questions up here afterwards. [APPLAUSE]

25 Replies to “Stanford Hospital’s Meredith Barad on Migraine Headaches”

  1. My doctor has prescribed me two opiates for when my triptan fails (tramadol and oxycodone). Tramadol was first and doesn't work on my migraine pain; oxycodone was last week, my doctor told me it would probably make me sleep (which I said was good), but I took one when I had a migraine and all it did was keep me awake all night, doing nothing for my pain. I will ask her for a higher dose sumatriptan after watching this.

  2. So very helpful. Thank you so much. This is the clearest explanation I've heard. I have suffered since puberty and have increased exponentially since going through menopause, sadly.

  3. Thank you so much for this talk. As a life long migraine sufferer, this is an excellent resource… extremely useful.

  4. I had real bad headaches before I went on Effexor. It's all relative, though. I think maybe it wasn't as bad as what some other people describe. After I started Effexor, I had few, and far fewer. I did have the scintillating scotoma. Laying down in a dark, quiet room helped greatly . In the past, I had in the past
    the scintillating scotoma but without headache. Maybe once in the last
    month and once in the last year.

    It's one of many drugs that doctors say works to prevent headaches. There are probably better drugs than Effexor. That drug has a 'discontinuation syndrome', which requires very strict tapering to go off it. I read that taking Benadryl helps with the withdrawal, but that's just a 'wive's tale', not scientific evidence. Lots of people say it helps.

    The trick that worked for me when reaching super low dose, to take that for a long time and taper very, very slowly at the end, even for several months, I find. I'm not a doctor. Your doctor will have a method that works better for you. FInd a specialist, though.

  5. I got headaches when I was about 6 years old maybe 7 and it wasn't like the headaches that normal people get it would feel like my skull was being electrocuted not like a very painful electrocution like kind of like like my head was in a vice staticky I would cry and keep my dad and his girlfriend up all night they did cats scans on my head I stopped getting them around the age of 20 now I don't get them at all they would affect my whole body weird I couldn't be around anybody when I got older I had to go pee by myself

  6. I get visual migraines that aren't nearly as bad as the ones i wake up with. Those I can barely stand or see straight. Slideshow like vision and nausea.A lot of times 2 hours after waking up, pacing around in pain and discomfort i'll puke and get instant relief. My sinuses during this time have so much pressure and drainage too . My pupils also become very constricted too i've noticed.Also a day before a visual migraine i have a hard time focusing and extrremly angry/irritable. I have hit my head hard, needing stitches a few time when i was younger and wondering if i have CTE or something? I'm 29 and it's worse than ever.
    If i drink half a beer i usally end up with the latter pukey headache in the morning. I have some sort of head pain every few days…. Rainy, stormy days = sinus headache for me.

  7. Thank you for this information. Doctor what is the gate called that you are taking about that helps control overload?

  8. Im not a very educated man but being a sufferer of this very painful affliction i honestly don't think there is a trigger,I believe that if you do suffer them you will have them at any time,feeling happy or sad,awake or asleep.If you are a migraine sufferer then you will not stop them by any means.And as for pain relief,well i have never found any thing that will ease them.I can say though that as i have aged they are becoming far less painful.

  9. I am surprised to hear that women on estrogen experience a delay in decrease of migraines because of the chemical delay in menopause. Two years ago I had a hysterectomy and oophorectomy, and have horrible hot flashes, so I am on estrogen. I've tried to go off the estrogen several times due to weight gain and just to see what happens. Every single time I do that, my migraines come much more frequently and are significantly more disabling. As long as I maintain proper use of the estrogen (remember to change the patches on the right days), I don't get migraines. I know everyone is different, but this seems contrary to what you said in your presentation. Any ideas? Not sure if anyone monitors these comments at all.

  10. Does anyone who suffers from migraine also suffer from tooth/ gum/ oral pain of non-dental origin? I suffer from tooth pains with no apparent cause and I think it may be related to the trigeminal nerve- I am a migraine sufferer with aura.

  11. Meredith, God bless you for your work. I am 58. I’ve had migraines as long as I can remember. Until I stumbled on to your videos yesterday 1.28.19 As I was in agonizing pain and in bed for two days from onset w/aura 24 hrs earlier and a friend had to bring me 7Up for nausea, I have been beyond frustrated; especially with dr.s. And 99.9% uneducated people who are clueless about migraines! Most assume ”YOU” must be doing something wrong! I 😍love how you said “focus on the good days.” and ”over stimulus!” That's it! Especially loud abnoxious people! I look forward to your next updates.

  12. Multiple inputs for migraine, and there's many sorts.
    Possible inputs:
    – intracranial pressure changes. hypo- or hypertension…can be due to
    infection, csf flow obstruction, obesity, systemic hypertension,
    dehydration, vitamin A toxicity which causes brain swelling.
    – vascular, as in dilation, most likely autonomic driven.
    – cervicogenic, as in originating from the cervical spine, usually facet
    jt inflammation, but also be other pathologies (syrinx, cysts, etc).
    – toxins

    Conservative therapy:
    – hydrate with 1 liter of water, despite lack of thirst.
    – RICE to suspect facet jts in the neck….not an ice pack, but
    industrial strength ice applied 30mins on/15mins off…repeat until pain
    is <4/10.
    – craniosacral or craniocervical therapy to help ease ICHT.
    – mobilization of cervical and thoracic facet jts by a physiotherapist.
    – manipulation of thoracic facet jts and cervical by a cautious physio,
    osteopath, or chiropractor.
    – anti-inflammatories for inflammatory inputs.

  13. I’m 52 and they are alive and kicking. Still chronic. But I am also not in menopause yet and am estrogen dominant and take extra progesterone to balance things out but it doesn’t work. Still hoping for a cure. 🙏🏼

  14. I’m only 19, but I’ve been having migraines since 12. Not very many, maybe one every 4-5 weeks, but all of them are preempted by giant blurred patches of my vision, and the sudden urge to curl up and die when exposed to sunlight or loud noises. Almost always triggered by sudden weather changes, and if I get the right drug cocktail soon enough, the pain will just be a dull throb when it happens, and the headache will only last about 45 minutes. If I don’t head it off during the aura….I usually need the ER. Morphine does absolutely nothing, toradol works better, but only after several doses, and once, the pain knocked me out for 36 hours and I don’t know what they gave me. I work with heavy machinery all summer, and without that aura….I’d probably end up driving into a wall.

  15. Mostly headache is caused due to many reasons like cold, opposing to light, listening to big sounds, etc. Few symptoms of headache include pain in the face, headache, nasal congestion, etc. Headache treatment through homeopathy is safe and it reduces the chance re occurrence of it

    This fool-proof system can boost the oxygen level in your brain and eliminate your pain with simple, powerful, step by step exercises … permanently curing your Migraine and all types of headaches

  16. I have taken loads of vestibular migraine medication but none of them really work. When I started out this impressive migraine guide “Mοyοkοn Axy” (Google it), I seen a huge difference within just Two weeks. Daily headaches are all subsided. The severity of headaches has been lowered immediately after 3 to 4 weeks of applying this medication. .

  17. I`m a migraine patient who has applied several vestibular migraine remedies. I started off making use of this vestibular migraine procedure “Mοyοkοn Axy” (Google it) so as to get rid of migraine and headache. Migraine in my system (around each and every 8 to TEN hours) and also a full blown migraine takes place several times every week. .

  18. I have tested a number of vestibular migraine therapies and none of them completely satisfied me. My personal search carried on right up until I came across and also tried using this amazing vestibular migraine tutorial “Mοyοkοn Axy” (Google it). My round of migraine would likely last Eight to 10 hours, not including a full blown migraine. This develops several instances in 7 days. .

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