our
understanding of migraine disease has changed while there is much yet to learn
let us review some of the most important principles about this medical condition
migraine is a disease of the nervous system in the past we believe that migraine
headaches were caused by changes in blood vessels in the brain
now it is clear that what happens in the brain is much more complicated the
underlying problem with migraine sufferers is that their nervous system is too
sensitive or too jumpy it reacts to small or normal stimulation with
an exaggerated response those triggers may be the result of something we
consumed excess stress a lack of sleep or a change in the weather and how
hypersensitive the nervous system is and what triggers the nervous system
varies between people in other words migraine disease is not
a single disease but a spectrum with symptoms ranging from mild and occasional
to debilitating and daily why is this genetics play a part in migraine disease
let's remind ourselves about how the nervous system works if we look
at what we think of as a nerve we see how it is made up of a bundle of similar
neurons each individual neuron has a cell body with long extensions when
specialized sensors are stimulated an electrical message starts on its
way to the brain but it is actually the flow of the
charged sodium ions into the cell through ion channels followed by the passing
of potassium through separate ion channels out of the cell that generates the
electrical signal an electrical wave then moves rapidly towards the
brain at some point each neuron reaches its limit and the signal must be
transferred to the next set of neurons here calcium channels open and
secondarily cause the release of chemicals called neurotransmitters into the
synapses where receptors on the adjacent neurons must detect the
neurotransmitters and regenerate the electrical signal it is during this complex
process that mistakes can be made think of a genetic defect as a mixed up
message about how the cell is to make things.
for example one of the
known genetic defects of migraine is one where the cell is instructed to produce
a protein that cannot fold into its normal three-dimensional shape when
positioned in the cell membrane and an electric signal comes along the
defective protein may open up and let calcium ions into the cell
but it might not be able to snap back into a fully closed position allowing too
much of the electrically charged calcium into the neuron in this case the neuron
would keep releasing neurotransmitters and the next cell would
generate an exaggerated response the consequence is that the neuron has
overreacted to a stimulus this is not just theoretical there are known genetic
defects of ion channels in families who suffer from migraine additionally
research has revealed genetic mistakes affecting how
neurotransmitters are made released and inactivated therefore each individual
inherits a mixture of genetic errors this may partly explain the broad spectrum
of migraine symptoms and how between individuals migraine might affect a
lot of different parts of the nervous system not just the pain pathways to
illustrate this let's look at the trigeminal nerve this nerve has branches that
innervate facial muscles temporal mandibular joint paranasal sinuses
and teeth when stimulated branches of the trigeminal nerve
transmit information back to the brain through the trigeminal nucleus in the
brainstem from here this message is sent to other parts of the conscious brain
that acknowledge the pain and the need for action but for a
migraine sufferer the threshold for initiating.
this distress signal is lower
than normal and the amplitude of the warning is abnormally high cortical
spreading depression so what causes the intense headache of migraine the current
theory is that a trigger either in the brainstem or in
periphery sets off an abnormal electrical event called a cortical spreading
depression this is a wave of electrical activity that sweeps slowly across the
surface of the cortex a cortical spreading depression first
initiates flashing lights or abnormal smells followed by an intense headache the
electrical depolarization results in a release of neurotransmitters and other
molecules that cause secondary inflammation a person then experiences light
sensitivity nausea foggy thinking and fatigue for hours by
mechanisms that are still to be defined the chemical reactions of a cortical
spreading depression appear to affect the dura where blood vessels dilate and
contract mast cells release their potent inflammatory chemicals and
trigeminal nerve fibers send signals back to the brain stem while cortical
spreading depressions cannot explain many of the symptoms of migraine disease it
is likely an important event in generating the most familiar brief intense
experiences of migraine sufferers migraine has a chronic form
central sensitization it has been observed that migraine sufferers have scarring
within the brain this may be a complication from the repeated inflammation
associated with cortical spreading depressions or other migraine
events within the brain eventually parts of the damaged nervous system simply
generate low-grade frequent unwelcome symptoms such as increased sensitivity to
touch or light daily headaches tinnitus or diminished cognitive functions
central sensitization partly explains why migraine sufferers
have different symptoms at different stages in their lives also the damage to
blood vessels from inflammation.
may explain the higher rates of stroke in
migraine sufferers and head trauma to the hypersensitive central
nervous system may make migraine sufferers more vulnerable to chronic headache
syndromes the brainstem may be the core of migraine disease another factor in
migraine disease is that abnormal electrical activity of one set of neurons may
affect the behavior of adjacent ones the brain stem is the
crossroads of much of our brain circuitry it is here that information
controlling many body functions congregates in clusters of cell bodies called
nuclei when electrical messages arrive in one nucleus they may be
rerouted to other parts of the brain stem hypothalamus thalamus and cortex these
nerve centres have exotic names such as the trigeminal nucleus pol Viner dorsal
raphe and locus karolius while the trigeminal nucleus is the control center
for headache pain these adjacent nuclei controls stress
balance mood sleep and the autonomic system an example is the generation of
symptoms from the nasal and sinus region many people mistake their chronic
migraine symptoms for a recurring infection in fact one form of chronic
migraine disease is where the trigeminal nucleus generates signals that the
brain interprets as abnormal pressure or pain.
from within the paranasal sinuses
teeth or eyes adjacent to the trigeminal nucleus is the superior
salivatory nucleus this nerve center controls the production of
nasal secretions and the size of the turbinates within the nose a migraine
sufferer not only feels sinus pressure but also experiences nasal congestion and
the runny nose the interplay between these nuclei may be another
explanation for why some migraine sufferers have so many related symptoms many
of which do not involve pain female hormones effect migraine disease sex
hormones as estrogen and progesterone have a profound but poorly understood
effect on our nervous system sex hormones affect the nervous
system of all women but for migraine sufferers their rise and fall throughout a
lifetime helps to explain why the symptoms of migraine change so dramatically
for women estradiol better known as estrogen has a complicated role
in our nervous system for example for any one neuron there are s per dial
receptors on the nucleus as well as the surface of the cell and we know of
genetic defects of both these receptors independent of the hormone receptors
we know that estrogen also sensitizes our body to pain
while we still have a lot to learn about sex hormones we do know that they play
a critical role in the waxing and waning of migraine disorders the several
biological mechanisms that describe how migraine disorders occur explain
why there are different strategies for treating migraine disease and why no one
approach works for everyone you
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