Extract from the book (in french) by Jan Polak, MD :

'Healing of Migraine & other Headaches'

- Chapters 3 & 4 -

[Guérir des Migraines & autres Maux de tête] Quintessence Publishing, France (2010)

(Text & drawings © Dr. J. Polak)

1. What should be known to

understand migraine
Before we discuss our hypothesis regarding the cause of headaches and migraines, and propose a
simple 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.

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 muscles
according 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.

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¤ 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 does
not 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.
 Effect of shock on joint muscles

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.

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¤ 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.

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¤ 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.
 The Omo-Hyoïdeus muscle could also be involved.

In the next chapter we will explain the importance of these muscles and their spasm in the
mechanism of migraine.

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B. Intracranial venous system

¤ Venous sinuses

The intracranial venous sinuses, located in the dura mater, collect blood from the veins of the
brain. All of them join to form the two Internal Jugular veins, which thus drain most of the blood of
the inside of the skull.

It should be noted that except in the lateral sinus venous blood flows from the front towards the
back, inside the skull.

None of these structures, veins or sinuses, have valves. The absence of valves allows a reversal
of the blood flow in case of need.

The venous sinuses are sensitive structures, which can cause pain in case of irritation.
 The intracranial venous sinuses

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¤ Jugular Foramen

It is a space between the Occipital bone and the Temporal bone.

Throuh it passes the Internal Jugular vein, through which flow about 95% of venous blood from
the interior to the exterior of the skull (that is to say almost all the blood that exits), and nerves IX,
X and XI.
 The Jugular Foramen - Inferior view of skull

Considering the orientation of the bone structures, the Jugular Foramen has an almost horizontal
path, the Temporal bone forming the roof and the outer edge, the Occipital bone the floor and the
inner edge.

Cross section of the base of the skull at the Jugular foramen

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¤ Blood flow

Blood is renewed 11 times per minute in the brain, four times faster than the limbs. It runs at a
speed of 1/2 to 1 mm/sec in the capillaries.
 Cerebral blood flow (CBF), the amount of blood passing through the brain per minute, equates
to arterial blood pressure (ABP) minous venous pressure (VBP) divided by the vascular resistance
(VR).
ABP - VBP
CBF = -------------
VR

Vascular resistance is defined by Poiseuille's law: it depends on the length (L) of the blood
vessel (assumed cylindrical shape and constant), multiplied by the viscosity of blood which is about
2.7 centipoise, divided by the 4th power of the radius multiplied by π.

8L x 2,7
VR = -----------
π r4

This means that the flow is inter alia based on the square of the radius, in other words, a small
decrease in diameter will cause a sharp decrease in flow.

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¤ Pressures

For the blood to circulate through the brain, hydrostatic pressure in capillaries must of course
remain between that of the arteries and that of the veins.

Changes of pressure in arteries, capillaries & veinous sinuses

Blood pressure which is of 100 to 120 mm/Hg in the carotid artery, will have dropped by half in
the intracranial cerebral arteries (it is then no more than 60 on average). It falls between 18 and 20
in the capillaries. The intracranial venous pressure in the sinuses is thus necessarily relatively small
(7-10 mm / Hg), and it is zero or negative at the internal jugular vein, the blood being sucked by
heart.

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¤ Regulation of homeostasis

It is known that if an increase in venous pressure, decreasing the flow in the capillaries, leads to
a fall in perfusion pressure in the capillaries of the brain, causing hypoxia endangering it, a carotid
reflex rapidly causes cerebral arterial vasodilation in order to bring more oxygen.

The regulation of cerebral blood flow actually depends on the sensitivity of the cerebral cortex
to hemodynamic and metabolic changes. Changes in cerebral blood flow may be relatively
localized, but each internal carotid artery seems to provide blood supply to the cerebral hemisphere
located on its side ; the flow is regulated at the level of the carotid sinus before entering the carotid
artery in the skull and its division into three cerebral arteries.

2. Cause & mecanism

of migraine

We now have all the elements to develop our hypothesis about a muscular and venous origin of
migraine (hemicrania), as well as of so-called ordinary headache or tension headache.

We can start putting the puzzle in place.

A. The cause of migraine

We have seen that muscles which maintain posture, consisting mainly of tonic (type I) fibers,
can remain in a permanent spasm after a shock. They are in a state callled contracture.

Thus the Longissimus Capitis muscle, for example (of which we explained in the previous
chapter that it maintains lateral stability of the head on the neck), can become permanently
hypertonic following a shock comming sideways, all the more pathogenic as it is often totally
unexpected, because not seen and therefore not avoided.
This shock may be caused by a missile, a bad fall, or a 'whiplash' while looking through the
window of the vehicle or a fall on his head, or banging one's head, etc.
The initial trauma can also be obstetrical, by pulling too hard on the head of the baby against the
resistance of the body not yet freed.

It's the same for the other muscle that we have cited, the cleidomastoid, which has a similar
function, the actions of these two muscles being complementary.

The muscle spasm will constantly pull the skull downwards. The cranial insertion of the
concerned muscles being the Mastoid process of the Temporal bone, the result will therefore be to
take this bone down regarding the Occipital bone.

Effects of muscle spasm of Longissimus Capitis or Cleido-Mastoideus

Bones are connected by connective tissue. Which, in the living, is elastic. Thus deformable.

The contraction therefore moves the upper part of the Jugular Foramen, formed by Temporal
bone, closer to its base formed by the Occipital bone.

The diameter of the jugular foramen will thus be slightly reduced.

Effects of contraction of the SC or CM on the diameter of the FJ

(Cross section, anterior view)

According to the laws of fluid dynamics, quoted in the preceding chapter, a small decrease in the
radius of a pipe causes a relatively sharp decrease in the flow of liquid in it.

In our case, a slight decrease in the diameter of the jugular foramen have sizeable impact on the
flow of the venous drainage of the skull.
 The muscle contraction that compresses the Jugular Foramen will thus cause increased venous
pressure upstream, inside the skull. Which will cause a slight slowing the evacuation of intracranial
venous blood, resulting in a slowdown of cerebral blood flow, resulting in a decreased supply of
oxygen to the brain.

All this takes place with varying intensity at different times, depending on the occurrence of
factors that increase a usually latent muscle spasm :
• temperature (cold causes muscle contraction),
• stress or fatigue (which also increases muscle tone),
• hormonal changes (which cause an increase in muscle tone during menses, but muscle
relaxation during pregnancy),
• positions stretching the concerned muscles (prolonged during sleep or sudden during sports)
which accentuate the stretch reflex,
• etc.

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Development of the disease process

A migraine crisis occurs therefore in four steps :

q Traumatism and latency.

As an effect of a physical shock, the contraction of the Longissimus Capitis and/or

Cleidomastoid muscles decreases the diameter of the jugular foramen (FJ). This phenomenon,
minimal, may well remain dormant without symptoms for years.

r Cortical Hypoxia (or latency)

If factors aggravating the muscle spasm occur (stress, overwork, sudden stretch of the muscle,
menses, etc..) narrowing of the Jugular Foramen increases. The venous flow out of the skull
becomes smaller and smaller proportionally.

The flow of the cerebral capillary circulation (blood that passes through the brain) is reduced
accordingly, and first in the posterior occipital region (especially n°17 area), because in this region
the venous blood can not easily escape through other channels for lack of close anastomosises.

This may lead to cerebral hypoxia in the areas most affected, and therefore cerebral suffering.
Indeed, a steady supply of oxygen is vital. If oxygen supply failure does occur, there will be signs of
what is called aura, mostly visual troubles like flashes of lightning (which happen before 1/4 of
migraines).

If other areas of the brain are affected first, other neurological signs can occur, including - rarely
- a transient hemiplegia.

It should be noted that the circulatory slowdown spreads gradually into the skull from behind
forewards, from the jugular foramen behind, in the opposite direction of the venous blood
circulation thus, just like a traffic jam stretches.

This second stage may very well remain asymptomatic, especially if the muscle spasm and the
resulting blood slow down are not too strong.

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 brain
tissues : micro-brain damage has been recorded in patients with aura symptoms.
Not to mention the other side effects.
 On the contrary treating the muscle spasm stop the whole process once and for all.
This can be achieved manually by Brachy-Myotherapy.

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Four 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-sidedness
of 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 both
sides 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.

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 A One should thus distinguish :

- 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 have
had 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 intracranial
venous 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 :

¿ Category A :
 Many factors that increase muscle tone can make manifest the spasm which passed previously
unnoticed. This increase in muscle tone will decrease a little more the diameter of the jugular
foramen, starting the above described process.
These factors are:
• stress (if psyche can not, in light of what we have seen, be regarded as a cause of headache, it
may very well be a trigger) ;
• fatigue, overwork ;
• wind, cold ;
• a shock (not to be mistaken for the causal trauma, whatever its intensity may be) ;
• sport using or stretching intensely the involved muscles, increasing their contraction reaction ;
physical activity can trigger or aggravate migraine because it aggravates spasm by sudden
stretching or solicitations.
• hormonal changes before the periods (sudden estrogen decrease). Since there is no difference
in frequency of migraine between boys and girls before puberty, these changes in the cycle certainly
explain the higher incidence of migraines among women (two times higher than for men), probably
simply because fewer muscle problems remain latent.
• abnormal sleep positions stretching the muscles involved, causing an increase of the stretch
reflex contraction;
• etc.

When these factors increasing the muscle tone come to a stop, the venous flow in the Jugular
Foramen becomes almost normal, at least below the threshold of clinical manifestation, and the
symptoms disappear - until the next crisis is triggered, for the cause itself has not disappeared at all.

¿ Category B:
• trigger factors such as alcohol or chocolate do not increase muscle tone, but increase blood
supply by intracranial vasodilation : however this extra blood runs against the 'dam' of the
previously slightly narrowed JF, increasing intracranial pressure, causing the same pain as with
triggers that increase muscle tone.
Here again there is a circulatory slowdown gradually extending forwards, opposite tothe normal
intracranial venous circulation, just as one finds in a normally well drained cave that a small
underground river quickly filles with water when it rains.
 The course of the migraine attack.

JF = jugular foramen
Oligohemia = Decreased blood supply
Hypoxia = Decreased oxygen supply
Ø = Diameter
 Other substances in some foods may mediate the same process.
• tyramine (certain wines and cheeses)
• phenylalanine (chocolate)
• MSG (some Asian dishes)
• Nitrite (pork)

As for fats, it is known that increase of plasma free fatty acids and decrease of serotonin are
linked, resulting in vasodilation.

¿ Coffee is apart: being vasoconstrictor, it can relieve a crisis, but abuse can increase muscle
tone to the point of producing migraine attacks.
(This is also the case with most drugs intended to stop migraine crisis.)
Withdrawal of coffee, causing brutal vasodilation by stopping the vasoconstrictor effect, can
cause headaches for some days too.
A vicious circle is not uncommon : high consumption of coffee, or of anti-migraine drugs, trying
in vain to stop the migraine attacks that this consumption itself continues to provoke.

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In summary, like most diseases, migraine evolves according to the following sequence:
cause (+/- triggers) → disease → reaction → healing (apparent).

● cause = traumatic muscle spasm of neck muscles

● triggers = factors increasing contracture, or intracranial blood volume
● disease = hypoxia or threat of hypoxia
● reaction = arterial vasodilation causing intracranial hypertension, source of pain
● apparent healing = suspension of triggering effects (but not of the primary cause)

Two comments:
1) as is often the case, it is the reaction that troubles the patient most, because it is causing
intracranial hypertension, the source of pain;
2) the true healing, which will prevent other crises do occur, can only be obtained by manual
processing of the muscle spasm by a specific technique called Brachy-Myotherapy.