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Before we discuss our hypothesis regarding the cause of headaches and migraines, and propose asimple and effective treatment, it is necessary to make a few reminders about certain points of
anatomy and physiology.
We will then have the missing pieces of the puzzle, and we will just have to assemble it.
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A. The Post-traumatic Persistent muscle spasm
¤ Muscles
Muscles are not just the means of making movements : they also serve to maintain positions, to
keep the two parts of a joint together, and to protect the joint against the risk of dislocation in case
of shock.
Therefore, among the skeletal muscles, those of the skeleton, there are two types of musclesaccording to their function : a) the muscles of movement, known as dynamic, and b) the postural
muscles, called tonic. The latter are those who maintain positions and protect the joint.
x¤ Stretch Reflex
This reflex makes that any stretched muscle contracts.
It is the stretch reflex that keeps the positions and postures : when a position is gradually
changing (under the action of gravity, etc.) at least one muscle is stretched. It will thus contract
automatically, to resume the original position as soon as the angle of the joint that it governs when it
is barely modified.
The contraction is of course normally reversible: it stops when the shortening is achieved.
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¤ Consequences of traumatism
The stretch reflex also has an important role in protecting the joint against dislocation in the
event of shock.
During an impact, a bone is suddenly moved : the nearest joint is suddenly mobilized and some
muscles will be strongly strtched at high speed.
Here intervenes the stretch reflex, this time in order to protect against the dislocation of the
joint.
The stretched muscle contracts reflexively, to oppose the shock. The intensity of the contraction
that follows depends on the speed and amplitude of the stretch : it is thus proportional to the
intensity of the shock. But if the shock was very violent and took the person completely by surprise,
it will have led to a strong reflex contraction of at least one muscle which, as can be seen easily in
practice, will tend not to stop its contraction even after cessation of shock : it is hypertonic and may
remain so for months, years, even a lifetime, as if the initial stretch persisted. This involuntary
contraction by permanent, self-sustaining reaction is called 'contracture', and once installed it doesnot yield, neither spontaneously, nor at rest, or even massage.
Its effects even tend to worsen with time.
That is what we call the Post-traumatic Persistent Contracture (PPC). It is a localized muscle
hypertonia, of traumatic origin, recent or remote, of a skeletal muscle, causing permanent
involuntary contraction, with no tendency to spontaneous healing, and thus continuing indefinitely.
It must be noticed that the PPC does not affect any muscle: in practice only tonic posture
muscles may have an PPC, which is explained by their innervation which is somewhat different
from that of the dynamic muscles.
x¤ Consequences of muscle spasm
Localized permanent hypertonicity of a muscle will not be without consequences, as one can
suspect. It can remain latent, non-manifest for years, but sooner or later it tends to be painful and to
limit the range of motions by its local shortening, and its resistance to movements that stretch.
Knowledge of this mechanism is fundamental to understanding the causes and mechanisms of almost all joint pain, including those found or osteoarthritis, and of neuralgias.
It is the understanding of the PPC that allows us to understand the mechanism and treatment of
migraine.
The manual method of treatment that we propose, Brachy-Myothérapy, is a simple, gentle, non-
traumatic therapy, without any side effects. It consists in putting the spasmed muscle passively in a
shortening position, following a precise protocol. This can stop the self-sustaining reflex loop, and
restore proper functioning of muscle.
It breaks the vicious circle of misinformation that stretch receptors often send for years,
supporting contracture.
x¤ Muscles involved in migraine
We already mentionned that we observe that only tonic muscles, ie postural muscles with clear
predominance of slow twitch fibers, can show a sustainable contraction.
In the neck two muscles of this type inserted on the Temporal bone will be involved in
migraines and tension headaches. One is Longissimus Capitis. Going from the lower cervical
vertebras to the Mastoid process of the Temporal bone, it serves to maintain the side stability of the
skull. (As a tonic muscle its contraction does not aim at provoking a movement.) The other one is
the Cleido-Mastoideus muscle, which goes of the collarbone to the Mastoid process of the Temporal
bone. Its action is similar to that of the preceding, with a more anterior point of support.
Nevertheless, the body must respond to this hypoxia or its mere threat, which causes the third
time.
s Reaction: hypervascularity and pain.
To compensate for hypoxia requires that the body urgently provides more oxygen to the brain.
The only way to do this is to bring more arterial blood, by the means of massive vasodilation in the
carotid and the three cerebral arteries on the same side as the initial disorder, since the reflex acts on
the carotid sinus before division of the internal carotid artery in three.
This additional supply of arterial blood (which is often perceived by the patient as a sensation of
pulsation, and may also involve the superficial arteries), runs against the 'dam' of the Jugular
Foramen still shrunk by the spasm of the mentioned muscles. Thus, although this reaction provides
sufficient oxygen to be effective on hypoxia (hence cessation of signs of aura), this localized
increase in blood pressure also causes intracranial hypertension, the clinical signs of which are
headaches (onesided if the cause is onesided) and more or less important nausea and vomiting,.
Nausea and vomiting are probably due to compression of the Area Postrema.
t Evolution to spontaneous healing (but of the attack only).
When aggravating factors contracture disappear (often during a night of sleep) symptoms cease
by themselves, and everything will appear in the order, until the next crisis. Because it is inevitable
as long as we have not dealt with the muscle spasms : the same causes will produce the same
effects.
Chemical vasoconstrictors drugs can stop the third phase (the reaction to hypoxia or its threat,
which is the painful part of the process) but have no effect on the first two stages, thus cannot
prevent relapses. They also tend to increase muscle tone, which is why their abuse also causes
migraines. And one can wonder if stopping the necessary supply of oygen is good for the braintissues : micro-brain damage has been recorded in patients with aura symptoms.
On the contrary treating the muscle spasm stop the whole process once and for all.
This can be achieved manually by Brachy-Myotherapy.
xFour variants in the mechanism and manifestation of migraine:
1 If a single Jugular Foramen (JF) is decreased by a onesided muscular spasm (result of an
often old and hitherto latent trauma), disorder suddenly worsened by triggers, this phenomenon
goes beyond the threshold of clinical manifestation. One JF being narrowed, cerebral hypoxia
suffering is unilateral, and so are the carotid reaction and the intracranial hypertension (ICH) which
follows, manifested through unilateral headache, which will be on the same side as the initial
muscle contraction.
This one-sidedness of the contraction acting on the diameter of the JF explains the one-sidednessof migraine.
2 But it is also possible that the spasms be bilateral, important enough to affect the diameter of
both JF.
This time the venous hyperpressure will be bilateral, as are the resulting hypoxia, the
vasodilatation reaction and the ICH that follows, which will cause global headaches : this is the
bilateral migraine with aura signs and / or nausea or vomiting.
More often the disorder is manifested in the form of so-called (muscle) tension headache ,
without signs of aura or photophobia, nor phonophobia, nausea or vomiting, but that can be just as
painful and debilitating as migraine, even if it does not present any specific signs of the latter.
So there seems to be no real difference between migraine and tension headache. It is only a
question of unilateral or bilateral manifestation of exactly the same phenomenon.
It is just likely that if the muscle disorder is unilateral, it must be more intense, causing a greater
narrowing of the Jugular Foramen, than in a bilateral disorder. Because in the first case part of the
venous blood of the side where the exit is limited can rather easily escape through the JF of the
other side, whereas in the case of a bilateral disorder, the only 'emergency exit' is the venous system
of the foramen magnum (which according to some, however, is not negligible).
3 When the trigger takes place only on one side of contracture, although the muscles of bothsides are initially in a latent spasm, migraine may be sometimes on one side, sometimes on the
other, depending on the trigger (eg sleeping position that strecteches the muscle with a latent spam,
which will then become manifest by the increasing its tone).
4 Finally, in the case of a triggering factor occuring in the case of a latent bilateral disorder, if
the carotid reaction is important it may lead secondarily to hypervascularity of the opposite
hemisphere, resulting in a bilateralization of the migraine crisis, which is not uncommon.
- Firstly, the muscular consequences of a physical shock, often ancient and forgotten : this is the
real cause of migraine, the prime mover.
- And on the other hand the effects of factors which only trigger the headache or migraine crisis,
even if they seem much more spectacular than the old forgotten trauma (even if they would havehad absolutely no consequence the absence of a preexisting post-traumatic spasm).
The initial cause, the prime mover, seems to be always traumatic. There is no evidence to the
contrary, migraine without pre-existing post-traumatic spasm of the Longissimus Capitis or
Cleidomastoid muscles, often long-standing, the result of physical shock that may well have been
forgotten, going back as far as birth (if too brutally 'helped') or childhood (fall while learning to
walk), or maybe later (an accident causing cervical or cranial injury, which both are likely to stretch
suddenly the mentioned muscles).
This contracture remains usually latent, or will be manifested by pain in the neck ; anyway it
will have a significant effect on the diameter of the Jugular Foramen and the rate of intracranialvenous blood drainage, eventually resulting in the migraine attack. Only at this stage will triggers
intervene.
But it is already clear that thorough treatment leading to complete disappearance of migraines,
even after stopping this treatment, can only be the cure of the muscle spasms. This can only be done
manually.
The trigger is just the last straw that broke the camel's back, but if noting such had happenned
before (i.e. lack of muscle spasms acting on the jugular foramen) the straw would not have the
slightest consequence.
B Various researchers have shown that compression of the jugular vein Internal aggravated the
migraine crisis. This confirms our hypothesis, since the only effect of this compression can be to
worsen the slowdown in the venous drainage of the skull, and thus the whole mechanism that
follows.
Conversely, as mentioned earlier, inhalation of oxygen can stop Cluster Headache attacks (even
more intense than migraines, while apparently having the same cause). This shows that it is cerebral
oxygen deficiency that causes the pain response by triggering a carotid dilatation reaction.
(It therefore seems much healthier to stop the crises in this way rather than by drugs, since they
act by preventing the reaction which is supposed to bring the lacking oxygen ...)
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B. Triggers
They only reveal a hitherto latent, unmanifested problem. They are not the cause: if there is
nothing to trigger they do not provoke anything.
It seems that they are of two types, to be distinguished :