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Subject: [OM] OT: migraine articles
From: "iwert bernakiewicz" <zuikooh@xxxxxxxxx>
Date: Fri, 11 Jan 2008 15:09:24 +0100
Hello everybody,

following the migraine lead I dug up some articles from the New Scientist
archives. Hope it is usefull for some people...

here it comes, it's quite a read:

Migraines are more than bad headaches

24 November 2007

>From New Scientist Print Edition.
Subscribe<http://www.newscientist.com/subscribe.ns?promcode=nsarttop>and
get 4 free issues.



IT IS becoming hard to dismiss migraines as simply very bad headaches.

Earlier this year, Nouchine Hadjikhani of Harvard Medical School found that
the fibres relaying pain signals from the head to the brain were thicker in
migraine sufferers than in volunteers. She has now found that they also have
a thicker somatosensory cortex - the brain area that processes sensation.

Twelve migraine patients with aura, 12 without, and 12 volunteers had their
brains scanned using MRI. This revealed that the part of the somatosensory
cortex that processes sensations from the face and head was up to 21 per
cent thicker in people with migraines than in volunteers (Neurology, DOI:
10.1212/01.wnl.0000291618.32247.2d<http://dx.doi.org/10.1212/01.wnl.0000291618.32247.2d>
).

Hadjikhani says it's becoming increasing clear that migraines are
symptomatic of progressive neurological disease.



Migraine mistaken

05 July 2003

>From New Scientist Print Edition.
Subscribe<http://www.newscientist.com/subscribe.ns?promcode=nsarttop>and
get 4 free issues.

Helen Simmons, Wendling, Norfolk, UK



To say that because migraine is the result of mis-sensing the world, this
makes the pain unreal, is crass (21 June, p 36). As a migraine sufferer
married to a migraine sufferer, I can tell you that whatever the cause of
migraine, the result is pain, which is very real. The pain is, for me, worse
than childbirth and worse than the breaking of a bone.

Migraine sufferers are already often stigmatised. I can see this being used
as another weapon by the medical community to deny the seriousness of the
pain, rather than as a way to understand and find treatments for this
debilitating condition.

Peter Goadsby is misreading migraine when he refers to other symptoms people
experience during an attack, such as too-bright lights. What he is missing
is that for some people the bright lights are what trigger the attack,
rather than the migraine coming first and the lights then appearing to be
too bright.

Incidentally, the only thing that has brought real long-term relief for me
is a daily magnesium supplement, which has significantly reduced the
frequency, duration and pain of the migraine.

Clare Wilson writes:

While the article suggested that the pain of migraine might not be what it
seems, the author repeatedly stated that attacks feel extremely painful. The
word "unreal" was not used to describe them - the words "torture", "agony",
and "worse than childbirth" were.

>From issue 2402 of New Scientist magazine, 05 July 2003, page 24


Is migraine all in the mind?

21 June 2003

NewScientist.com news service

Helen Phillips



Enlarge image<http://www.newscientist.com/data/images/archive/2400/24005201.jpg>





IF YOU have ever absent-mindedly rubbed your eyes or nose after chopping up
chilli peppers, you'll have some idea of the suffering of one group of
scientists in the name of medical research. A team at the Institute of
Neurology in London have been injecting chilli juice into each others'
foreheads. Lab technician Paul Hammond, who got roped into the experiment,
says it felt like acid was burning into his skin. "It was one of the most
excruciating pains you can imagine," he recalls.

The researchers weren't sadomasochists, as far as we know. Their actions
were part of a much larger research effort that has been shedding light on
migraine. For although in the past few decades we have learned a great deal
about the condition, we still have no idea of its root cause. And while we
have drugs that help some patients, some of the time, understanding the
underlying defect is the best way to boost our chances of discovering a
sure-fire cure.

Now a leading headache researcher at the institute, Peter Goadsby, has a
radical theory. Perhaps, he says, the pain is an illusion. That sounds crazy
to anyone who's ever had a migraine. But Goadsby is suggesting that what
feels like agony is really the brain responding abnormally to non-painful
stimuli. He thinks that in most migraine cases, patients' brains allow
overlarge signals to pass through their sensory systems, turning the normal
background activity of pain-sensing neurons into torture. "The concept takes
the disorder away from being a pain problem to being a sensory disturbance,"
he says.

Many researchers disagree with this explanation, and there are other
competing theories. But a few scientists working independently of Goadsby
have come up with intriguing findings that seem to support his views. And
even some critics agree that the brains of migraineurs appear to work a bit
differently to those of non-sufferers - and not just during an attack. It
seems that migraineurs may constantly experience and react to the world in
an unusual way.

So what exactly does a migraine feel like? Anyone who's ever had one knows
full well that this is no ordinary headache. It is one of the most awful
experiences you can have. My mother says hers can be worse than childbirth.
Mine feel like a nail driven into my skull, eye or brow. But the pain has a
more disturbing and emotional quality than any broken bone or wound. The
pain is organic - it moves and grows, like an alter ego, yanking at my
stomach, filling every thought. It absorbs every last drop of consciousness.

And migraine is far more than head pain. Sufferers may also get a stiff
neck, sore eyes, throbbing sinuses, violent sickness or stomach ache. They
may find lights become painfully bright, noises excruciatingly loud, or
smells nauseating. You can throw in lethargy, inability to concentrate,
yawning, depression, dizziness, hallucinations, blind spots, pins and
needles, even one-sided temporary paralysis in rare cases.

One in six of us will experience this condition at some point in our lives.
About one in 20 has to write off more than one day a month to the condition,
and a wretched few have one every day.

The field of migraine research is still adjusting to its most recent
revolution in thinking. It is well accepted that the brain itself contains
no pain-sensing neurons. Instead it is the meninges, the membranes covering
the surface of the brain (which are inflamed in meningitis) that seem to be
where the pain is felt. For most of the past 50 years, most doctors were
convinced migraines stemmed from a problem with the blood vessels supplying
the meninges - the so-called vascular theory. According to this, the strange
visual disturbances or "auras" seen by some sufferers before an attack were
due to the blood vessels contracting. Later there would be a rebound
dilation of the vessels, causing the pain. The vascular theory was even the
basis of a new class of anti-migraine drugs called triptans that contract
blood vessels and help many patients.

But over the past decade or so, several research findings have shifted the
blame from blood vessels to neurons - in particular the fine branches of the
trigeminal nerve, which innervate blood vessels around the meninges, among
other things. One reason was that brain scans during migraines have shown
that dilation fails to coincide exactly with the pain. Also, triptans were
found to calm hyperactive nerves as well as constricting blood vessels. And
the merciless chilli experiments carried out a few years ago by Goadsby and
another group showed that blood vessel dilation is a consequence of head
pain, not the cause. "It's a disorder of the nervous system," he says. "The
blood vessels are doing what they're told to."

So the key question to answer has become what causes the neurological
problem in the first place.

An important step came in 1995, when Cornelius Weiller, then based at the
University of Essen in Germany, and his colleagues PET-scanned the brains of
nine people during migraines. They found that several areas were abnormally
active, including parts of the brainstem, through which pass all neurons
from the spinal cord to the brain, including pain signals.

After the migraine had begun, the patients were given triptans, which saw
off their headaches. The activity levels returned to normal in most brain
areas, but not in the brainstem, suggesting that there the abnormality was
intrinsic to the migraine process, not a result of the pain.

Another clue about the cause of migraines has come from genetic research. In
1996 a mutation in a calcium channel gene was found to be responsible in
people with a rare form of the disease called familial hemiplegic migraine.
Calcium channels are proteins that span the cell membranes of neurons. They
allow an influx of calcium ions that helps to regulate neuronal impulses.
And this February a mutation in a channel that pumps sodium and potassium
ions in and out of neurons was also found to cause the condition.

The commoner forms of migraine have not yet been linked to any mutations,
but they do run in families, with complex inheritance patterns that suggest
several genes may be jointly to blame.

Goadsby believes that a big hint about the cause of migraine comes from the
many other strange symptoms that people experience besides head pain. During
an attack, patients may feel that lights are too bright, sounds too loud or
smells unpleasantly strong. Goadsby thinks that this mis-sensing of the
world might be not just a weird side effect, but a fundamental part of the
condition. "Migraine is primarily a disorder of sensory processing," he
says, "not a disorder of pain at all. Migraine is like the world shouting at
you."

His theory is that while the signals in the trigeminal nerve are no stronger
than normal, the reaction to them in the brainstem is huge - effectively
generating pain from almost nothing. The peculiar "premonitory" symptoms
that migraineurs may develop in the hours before an attack - including
yawning, concentration problems, stiff neck and mood changes - could signal
that the brainstem is beginning to misbehave.

So where in the brainstem could everything be going wrong? The trigeminal
nerve enters at a region called the pons (see Diagram), from where some
neurons travel up past an area called the periaqueductal grey (PAG) and into
the rest of the brain. There are neurons that return from the PAG to the
pons, to damp down trigeminal signalling in a negative feedback loop. The
German researchers suspected it was the PAG showing up in their brain scan
study, as it was already known to be involved in pain signalling - but the
scans' resolution wasn't good enough to tell.

Goadsby and his colleagues investigated by injecting a chemical called
agatoxin, which blocks the guilty calcium channel, into the PAGs of
anaesthetised rats. In response to a small stimulus to the meninges they saw
higher firing rates in the trigeminal neurons compared with control animals.
If the rats hadn't been unconscious they would have been having the mother
of all migraines. Blocking the calcium channels somehow reduced the activity
of the negative feedback neurons, allowing greater activity in the
trigeminal neurons, the researchers proposed in their paper (The Journal of
Neuroscience, vol 22, p RC(1-6)).

But Goadsby no longer thinks the PAG is the only source of trouble. That's
because this year his group performed PET scans of eight patients in the
middle of a migraine attack, using higher-resolution cameras than those of
the German researchers. The new study, presented in April at the American
Academy of Neurology meeting in Honolulu, showed the pons lighting up, not
the PAG. Goadsby thinks it was in fact the pons that was active in Weiller's
earlier scans.

Goadsby says the pons "fits even better" with his theory than the PAG.
Animal studies have shown the pons is an "attention centre", controlling how
much notice the brain pays to sensory information. The region also helps
control our sleeping and waking patterns, which go awry in migraine, and
altered sleep patterns are one common trigger of attacks.

Stephen Silberstein, a prominent migraine researcher at the Thomas Jefferson
University Hospital in Philadelphia, calls Goadsby's latest findings "very
exciting". Not only might Goadsby have explained at least one way to cause a
migraine, but the rat studies suggest new ways to test the effectiveness of
drugs, something which has been especially hard to judge in the early stages
of drug testing, says Silberstein.

If Goadsby is right, you'd expect migraineurs to experience other types of
pain differently, not just that in the head. This does indeed seem to be the
case. In a series of experiments over the past few years, Marina de Tommaso
from the University of Bari in Italy found that during an attack, there is a
general increase in pain sensitivity all over the body.

This year she published a study (Pain, vol 101, p 25) showing that even
between attacks, migraineurs experience pain differently. She used a laser
to heat a patch of their skin to produce mild pain, while giving them
distracting tasks such as word games. Such diversions normally cause the
pain threshold to rise, but in migraineurs it didn't change. "Possibly there
is some problem with their attention to a stimulus," she says - a finding
that would fit with Goadsby's faulty pons idea.

Migraineurs also seem to differ in the way they pay attention to non-painful
sensations. If people are exposed to repeated sounds or images, the neuron
responses in the cortex of the brain usually decline over time. Jean
Schoenen from the University of Liège in Belgium showed in 1998 that in
migraineurs, such cortical activity fails to decline. In some, the
electrical activity even increased.

And Frances Abbott of McGill University in Toronto found that migraineurs
seem to suffer more aches and pains and have lower thresholds to cold pain,
even between attacks (New Scientist, 16 November 2002, p 22). She also found
that her migraine group were more likely to be very mildly depressed. But
Abbott is unconvinced that her findings back Goadsby's theory. She thinks
that migraine may be a subtype of depression, with the headache and other
symptoms being side effects. After all, chronic pain conditions and
depression have long been associated, she says. And rather than the pain
being generated in the head, she suggests that what makes the body more
sensitive could be an increased number of sensory nerve endings in the
peripheral nervous system.

Too touchy

Rami Burstein of the Beth Israel Deaconess Medical Center in Boston also
thinks the problem could lie outside the brain. He says Goadsby's theory is
"very attractive, but it lacks evidence". Burstein thinks that peripheral
sensitisation, as seen in migraineurs' oversensitive skin sensations, means
the process starts with sensory neurons releasing chemicals that make the
brain's neurons more responsive. It sounds similar to Goadsby's idea, but
the key question is whether the pain is real, triggered from bona fide
sensory signals, or an artefact of oversensitive brain neurons. It's an
important distinction, because it could affect where treatments should be
targeted.

But Stephen Silberstein thinks both could be right. It could be either
peripheral or brain sensitisation that sets the process off, he suggests, or
even something else. It may well vary from person to person. "They are
probably both right," he says. After all, he points out: "Migraine is not a
single disorder, it's a group of disorders."

And there are competing ideas about the root cause of migraine. One of the
leading theories concerns the strange visual disturbance known as an aura
that is experienced before migraine in a minority of patients (estimates
range from one-fifth to one-third). The aura seems to coincide with a wave
of abnormal brain activity known as "cortical spreading depression", which
travels from the back of the head to the front.

Last year, Michael Moskowitz of Harvard Medical School showed that in rats
at least, this wave seems to activate the trigeminal nerve (Nature Medicine,
vol 8, p 136). He found that trigeminal nerve activity seems to cause the
leakage of proteins from the blood into the meninges, which could cause
irritation and pain, not to mention blood vessel dilation.

Few researchers doubt Moskowitz's findings. Silberstein calls the work
"clear and definitive", but the fact remains that it doesn't seem to explain
the majority of patients who don't get an aura before their migraine.
Silberstein thinks that this is where Goadsby's theory could come into its
own, explaining the non-aura group. Other researchers argue that a subtle
aura could well be present, just unnoticed, even in supposedly non-aura
migraine sufferers. Goadsby himself believes the brainstem problems could
start well before any aura.

Whoever is right, understanding the basic biological process that causes
migraines is likely to point the way to better treatments. Goadsby has ideas
for drugs that would damp down the oversensitivity in the brainstem,
although he won't give details yet. Ideally they would be able to stop a
migraine in its tracks if taken during the premonitory stage, when patients
first experience those strange sensations. Other new classes of drug are
also coming through clinical trials, and may well help, despite the
uncertainties surrounding migraine's origins.

But Goadsby, at least, is convinced we won't get far without considering his
radical theory, however strange it sounds. "To say the pain is not really
happening is quite a leap of faith," he acknowledges. But when light feels
painfully bright, we know it hasn't really become brighter, or a painful
sound any louder. "So maybe it's not so hard to believe that there's not
really any worse pain, but that the brain is somehow misreading the
signals."

Common triggers

Many migraines appear to occur spontaneously. But some people find there are
triggers that make their attacks more likely. These can be as mysterious and
variable as the condition itself. Some are easier to avoid than others.

FOOD

Red wine and cheese cause attacks for many, while for others it may be
matured, smoked or fermented foods. The chemicals tyramine and
phenylethylamine, known as biogenic amines, may be to blame. Bacteria known
as lactobacilli are used in manufacturing to decompose bitter-tasting
compounds, making wine and fruit juices taste better. These bacteria produce
biogenic amines, which are also found in fermented or matured products such
as soya foods, mature cheese, smoked and tinned fish.

HORMONES

For nearly two-thirds of female sufferers, attacks seem to be set off by
variations in oestrogen levels during the menstrual cycle. The trouble zone
may be menstruation itself or ovulation. Conversely, migraines may reduce in
frequency during pregnancy. Some women may also be sensitive to the
synthetic forms of hormones in the contraceptive pill or hormone replacement
therapies.

STRESS

Both the presence of stress or its sudden removal - such as the start of a
weekend or holiday - can trigger a migraine attack. Too little or too much
sleep, or jet lag, can have the same effect. Escaping the stress of work,
perhaps coupled with a lie-in, can make weekends the prime attack time for
many migraine sufferers.

OTHER FACTORS

Missed meals can also be to blame. Low blood sugar, or a sudden sugar rush
can be bad. Caffeine, which is in some painkillers, may be a trigger. Even a
change in the weather or atmospheric pressure can bring on a migraine. Other
possible triggers include toothache, a hot bath or extreme emotions, such as
anger or grief.

FURTHER INFORMATION

Migraine Action Association: www.migraine.org.uk

The Migraine Trust: www.migrainetrust.org

American Council for Headache Education: www.achenet.org

US national migraine association, MAGNUM: www.migraines.org

World headache alliance: www.w-h-a.org





Head-to-toe migraine

16 November 2002

>From New Scientist Print Edition.
Subscribe<http://www.newscientist.com/subscribe.ns?promcode=nsarttop>and
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IT SEEMS migraine is not just a pain in the head, but reflects a more
general sensory problem.

Frances Abbott of McGill University in Montreal compared migraine sufferers
with people who don't get the headaches, and found that even between
attacks, people with migraine are less sensitive to a light touch on any
part of their skin. But they are much more sensitive to potentially painful
signals such as pressure on the skin or extreme cold, as well as suffering
more aches, pains and itchiness. Migraine may reflect a general problem with
regulating the strength of sensory signals, she suggested at the Society for
Neuroscience meeting in Orlando, Florida, last week.

Migraine sufferers also showed more sub-clinical signs of depression.
Perhaps depression and migraine have some common cause, Abbott speculates.

>From issue 2369 of New Scientist magazine, 16 November 2002, page 22

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