Migraines & Headaches

8/8/2019 Migraines & Headaches

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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 tounderstand migraine

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.

x

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.

x

¤ 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.



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.

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.



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.

xB. 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

x¤ 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 theinner edge.

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

x¤ 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 r 4

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.

x¤ 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.

x¤ 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.

xDevelopment 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 braintissues : 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.

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.

x



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 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 ...)

x

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 withtriggers 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 supplyØ = 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 arelinked, 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.

xIn 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.

Migraines & Headaches

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