faq

FAQ


A migraine is a pain which appears progressively, generally on the side of the skull or face and which progressively extends towards the other side.

 It is sometimes preceded by a number of warning symptoms:

  • Irritability, difficulty concentrating
  • Fatigue and a desire to sleep
  • Digestive discomfort

It generally lasts between 4 and 72 hours and can generally recur several times a month, but also sometimes several times a week or even every day.

It is often accompanied by:

  • Digestive troubles (discomfort, gastric pain, nausea, vomiting)
  • Sleepiness, yawning, falling asleep 

It is aggravated by light (photophobia), noise (phonophobia) and sometimes by odours.

It often occurs in particular circumstances:

  • When waking up in the morning, often at about 5 o'clock
  • Several hours after overcoming a stressful situation
  • At the start of the weekend, when setting off on holiday, during activity changes

It is sometimes preceded or accompanied by neurological disturbances (visual, auditory, sensory, motor) called "auras", which regress spontaneously.

It often starts on the same side, but always appears at least once on the opposite side.

You should experience the symptoms described in the IHS criteria, but there is a great deal of individual variation.

The IHS criteria for migraine diagnosis are as follows : 

  • Criterion 1: Your headaches occur in episodes lasting several hours to several days. Between these attacks, you experience no headaches.
  • Criterion 2: You have experienced at least five attacks in your life.
  • Criterion 3: Your headache has at least two of the following characteristics: it affects one side of the head; you experience pulsations; it is aggravated by exertion (climbing stairs, running); moderate to severe pain.
  • Criterion 4: Your headache is accompanied by at least one of the following symptoms: nausea or vomiting; sensitivity to light or noise.

If you answered Yes to the four criteria, you are suffering from migraines.

If you answered Yes to 3 or 4 of the criteria, you are probably suffering from migraines.

If you answered No to at least 2 of the 4 criteria, you are probably not suffering from migraines.

Important note: some pains can resemble migraines without actually being them.

The pain varies from one patient to the next and even from one moment to the next in a single patient.

 

Pain duration:

 

The pain lasts between 4 and 72 hours without treatment. It usually occurs in frequent attacks, ranging from three times a week to once a month.

 

 

Pain location:

 

  • The pain is often unilateral at the start, but can generalise rapidly.
  • It most often begins on one side, but has appeared at least once on the other side.
  • It generally affects the temple, the back of the eye, sometimes the forehead, sometimes the crown of the head, but it can also affect the back of the head, the base of the skull and can extend from the neck to the top of the head and the forehead.

 

 

Pain sensations:

 

  • Grinding
  • Crushing
  • Compression
  • Tightening
  • Clenching
  • Pounding
  • Beating
  • Pulsating

 

 

Pain intensity:

 

Sometimes severe, disrupting daily activities, sometimes preventing any activity at all and forcing the sufferer to lie down in dark, silent isolation.

 

On a pain scale from 1 to 10,

1 = no pain

10 = the most severe pain known

Pain during an attack generally ranges from 6 to 10.

 

Symptoms preceding and accompanying the pain:

 

The pain is preceded by warning symptoms, and sometimes accompanied by auras – spontaneously regressing neurological symptoms occurring within less than one hour.

Yes, it is a question of topography.  The migraine pain is distributed to the forehead by the sensory fibres of the trigeminal nerve. This is where the Trigeminovascular Theory originates from. But many other conditions affect all or part of the same area with more or less identical clinical symptoms.

Here is a non-exhaustive list of the various pathologies resembling migraines, but of widely differing severity and prognoses:

 

Common headaches

  • known to everyone and simply called "headaches",
  • very frequent and not particularly severe.

 

Tension headaches

  • often related to neck arthrosis,
  • contraction of the neck muscles,
  • prolonged periods in the same neck position (generally under working conditions).

 

Neurogenic hyperstimulation headaches

  • often provoked by a noisy atmosphere,
  • sensory overstimulation of all types (visual, auditory, psychological).

 

Arthralgic neck pain

  • always accompanied by osteoarthritic deterioration
  • or post-traumatic neck deterioration (cervical spine).

 

Occipital neuralgia

  • due to mechanical autonomic compression of the occipital nerve in the foramen magnum
  • manifests itself in the form pain in the neck and the back of the head, extending towards the top of the skull.

 

Cluster headaches

  • very brief and severe attacks
  • recurring several times a day,
  • always unilateral
  • accompanied by autonomic symptoms in the form of lacrimation, nasal discharge and hemifacial redness.

 

Trigeminal neuralgia

  • similar to the conditions described above,
  • predominantly affects men,
  • but with few autonomic symptoms,
  • variable location, but always somewhere on one of the three branches of the trigeminal nerve (eye, nostril and ala, or upper or lower jaw).

 

Facial neuralgia "from the cold"

  • accompanied by characteristic hemifacial paralysis
  • can last for several months before regressing more or less completely.

Post-traumatic neuralgia from nervous deafferentation:

  • pain appearing in the area where the nerve has been destroyed,
  • in the form of a permanent, painful tingling sensation.

 

Horton's disease

  • often affects women over 60 years of age,
  • manifests itself as unilateral pain in the temple,
  • accompanied by fever,
  • with palpable induration of the temporal artery, which stops beating,
  • and a risk of rapid blindness if left undiagnosed.

 

Post-herpetic neuralgia headaches

  • generally caused by destruction of the ophthalmic nerve by shingles,
  • manifests itself as the same nervous deafferentation pains.

 

Headaches caused by intracranial hypertension, tumoral or metastatic compression, intracranial haemorrhage, ruptured aneurysm

  • often begin very severely, or as a severe aggravation of previously experienced headaches,
  • rapidly accompanied by progressive, but never spontaneously regressing, neurological disorders
  • significant autonomic disturbances (discomfort, loss of consciousness, projectile vomiting)
  • and rapid deterioration of the patient's general condition.

Migraines tend to take the form of painful attacks which occur repeatedly and quite frequently in each patient. Even in the same patient, the frequency of the attacks can change over the course of the illness.

When speaking of migraine treatment, it is necessary to differentiate between the treatment of the painful attack itself when it occurs, which is simply called attack treatment, and treatment of the recurrence of the attacks, called background treatment.

 

Treatment of the attack relies on medications, which can be:

 

  • Classic analgesics

They act only against the pain, are not specifically for migraines, and are often not sufficient. They carry risk of abusive consumption, from lack of efficiency and, above all, because prolonged consumption of them can itself lead to... migraines!

  • Anti-inflammatory medication

They act against certain pains related to inflammation or an allergic reaction, but are also insufficient and, sometimes when used with analgesics, they carry the same risks. They act indirectly against the pain by reducing the resulting inflammation.

 

  • Anti-migraine medication

These are more specific to migraines. They are several types of them, acting in different ways:

Some may have an analgesic effect on the autonomic symptoms that often accompany pain (nausea, fatigue, irritability, vomiting). They often contain either caffeine or ergot derivatives. They act specifically against migraine pain by decreasing the blood vessel dilation at the base of the skull and in the meninges which causes this particular pain. These treatments have been in use for a long time without losing their effectiveness.

Other, more recent treatments are triptans. They are derived from sumatriptan. They produce a particular effect on certain receptors of serotonin, a natural cerebral neurotransmitter. Their complex action will be explained in a different chapter. They are currently the most used and probably the most effective medication, but do not resolve all cases. However, they have sometimes poorly tolerated side effects and are not free from the risk of excessive tolerance and the rebound effect.

 

  • Electrotherapy migraine treatment

It is little known as there was no specific device employing it until CARE-ME® became commercially available. It relieves migraine pain by blocking the pain signals transmitted to the brain by the fibres of the trigeminal nerve. It also relieves a migraine attack and can put a stop to it in a matter of minutes. One of the currents it produces has been known for many years for its analgesic effect. Its complex action will be explained in a different chapter. This treatment has the advantage of rapid action, as it is faster than the most recent medicines. It is also safe from any side effects, tolerance and the rebound effect.

 

Background treatment 

Background treatment is intended to reduce the frequency of migraine attacks. It is employed whenever the number of attacks exceeds two per month.

 

The most frequently used medical treatments are anti-serotonin drugs. They are few in number and not especially effective (no recent progress has been made in this field).

Electrotherapy treatment did not exist before CARE-ME® became commercially available. This device is equipped with a mechanism that produces an intracerebral circuit stimulation effect, simultaneously playing an analgesic role (endorphin secretion) and a regulatory role over the use of one of the neurotransmitters most implicated in the blood vessel dilation which causes migraine pain: serotonin. Serotonin regulation sustainably reduces the frequency of migraines by acting specifically against the cause of the condition.

Migraines are a condition affecting the central nervous system and especially its neurological and vascular components.

As such, it is a neurological condition and the doctor most qualified to make a precise diagnosis is your neurologist.

However, as it is a current condition, you can consult your general practitioner, who will refer you to a specialist if necessary.

If the diagnosis is made easily due to the presence of classic symptoms, it is necessary to be especially careful when a severe symptom appears, in case a neurological disorder is concealing a more severe diagnosis.

It has been found that over 50% of migraine patients do not seek treatment, either due to unawareness of their diagnosis or because they believe that it is useless to talk to their doctor, even though they know that they are suffering from migraines, and think that they must "live with it".

If you are already aware of your diagnosis, remain vigilant to any changes in your symptoms, even if you have experienced migraines for many years. This is also the case if your migraine condition appears very severely or deteriorates rapidly. Consult your doctor immediately.

On a final note, don't be a fatalist! You now have a means of treatment, even if you think you've exhausted the entire pharmaceutical arsenal!

Pain signals are conveyed to the brain region that allows them to be felt by various types of nerve fibres which form part of nerves containing sensory fibres.

Some currents are capable of blocking pain transmission in sensory nerves. There are multiple possibilities:

  • Preventing nerve impulses from appearing in a nerve by modifying the nerve’s excitability. If the nerve is less excitable, then the cause of the pain will need to be stronger for that pain to be transmitted through the nerve to the brain. But the pain is not felt as the nerve impulses occurring from excitation of the nerve do not reach the brain.

  • Blocking the passage of these impulses in the spinal cord or in the brain before they reach the brain centre where they become pain which is felt.

  • Stimulating brain structures (median raphe, periaqueductal grey matter, ventricular tectum) whose role is to implement the "painkiller" circuits that release endorphins (natural morphine) or themselves block pain transmission between the first relays of the sensory nerves and central nervous structures which integrate painful sensation.

  • Reducing the concentration of neurotransmitters such as serotonin in certain circuits, or the release algogenic irritant substances by the nerve endings.

 In the particular case of migraines, electrotherapy can work as a treatment in three different ways:

IT CAN PREVENT THE CREATION OF NERVE IMPULSES IN THE PERIPHERAL NERVOUS SYSTEM:

Pain begins simply as excitation of a nervous fibre. This excitation is in fact a variation in the electronic conditions at the ending of the fibre. This electronic change excites the fibre locally, and this local excitation is transmitted along the fibre to the next nerve relay (the next neuron), like the waves which appear when a stone is thrown into water.

But it is possible to prevent this electronic variation from exciting the nerve fibre by making the fibre "less excitable":

  • The excitability of this resting fibre is a constant which depends on the distribution of electrical charges (electrons and ions) on both sides of the membrane of this fibre, which is only partially permeable to ions. This means that they are distributed unequally as an electric charge on both sides of this membrane as if the membrane were totally permeable. In addition to this, active phenomena (ion pumps) permanently maintain this "difference in electrical potential" between the exterior and interior of the fibre. This could be compared to a mini battery as it involves permanent "electrical potential" which can be used at any moment to create a nervous impulse along the fibre. When a local electronic variation occurs, it depolarises this fibre and a nerve impulse is created and transmitted to the next relay.
  • By delivering a sufficient quantity of electricity to the extremity of this fibre, one can alter this potential. When the difference in potential between the interior and exterior of the fibre becomes negative, that means the fibre is more polarised and it becomes more difficult to depolarise. A much more powerful excitation would therefore be needed for impulses to be transmitted.

It is this property which is exploited in electrotherapy to block the transmission of nervous impulses. When they can no longer reach the nerve centres, pain is no longer felt.

This property can be used locally, at the ending of the nerve, but also in some of the more central relays, using somewhat more complex methods.

This type of treatment is purely palliative, in the sense that it only prevents the transmission of pain without removing the cause. But it is not the only method used in electrotherapy.

  

IT CAN BLOCK THE TRANSMISSION OF NERVE IMPULSES TOWARDS THE INTEGRATING CENTRES:

We have seen that electrotherapy allows the excitability of certain nerve fibres to be reduced. Electrotherapy also makes it possible to increase the excitability of other fibres. Each category of fibre is excited or inhibited by specific currents. In this way, it is possible to excite some and inhibit others.

This is of interest:

  • Starting from the second relay (second neuron), certain fibres use common final pathways even though they convey different information, as is the case for heat and pain signals. By exciting a fibre that transmits heat signals, one can prevent it from transmitting pain signals.
  • In addition to this, starting from the second relay, the signals carried by some fibres have priority over others. This is the case for fibres which transfer certain tactile signals compared to fibres which carry heat or pain signals. By exciting these tactile fibres, one can block the transfer of pain signals. (Gate Control Theory in the dorsal horn of the spinal cord). Electrotherapy allows the stimulation or inhibition of certain fibres as well as the regulation of various activities, like with switches.

 

IT CAN ALTER THE CONCENTRATION OF NEUROTRANSMITTERS IN CERTAIN CEREBRAL CIRCUITS WHICH CAUSE THE DISORDER:

The preferential stimulation of some fibres leads to increased activity in some neuron circuits and some specialised nerve centres. These centres use some neurotransmitters preferentially and release neuromodulators whose effects depend on their concentration. Some centres are relays which act on others by activating or inhibiting more complex nervous structures.

Through these specific stimulations, electrotherapy enables modification of the delicate balance which exists between the various neurotransmitters and neuromodulators, with effects on the way the nerve structures function.

In this way, electrotherapy helps regulate the concentration of neurotransmitters such as serotonin in the central analgesic circuits (endorphin circuits, descending inhibitory circuits).

It can also alter the concentration of a product synthesised by nerve endings which acts aggressively on itself. This is the case for migraines, where an excess of serotonin (among others) causes vasoconstriction followed by painful vasodilation of the blood vessels at the base of the skull and in the meninges. 

In this case, we see that the effects of electrotherapy are not limited just to painkilling palliative action, but they are also curative as they act directly against the cause of migraines: excess serotonin.

As we have just seen, in the case of migraines, the current delivered by electrotherapy can simultaneously soothe and cure.

  • It soothes by preventing the creation of painful nerve impulses in the peripheral receptors
  • It soothes by blocking the transmission of pain along the peripheral nerve pathways and by inhibiting certain nerve transmission centres
  • It cures by reactivating the analgesic endorphin system blocked by the chronic pain.
  • It cures by lowering the concentration of serotonin in certain circuits.

For migraine-related conditions which are not caused by excess serotonin, it has the same soothing palliative effect, but no direct curative effect.

This is a device which generates specially studied currents enabling

  • The prevention of the creation of painful nerve impulses at the endings of the trigeminal nerve fibres.
  • The prevention of the transmission of painful nerve impulses in the Aδ and C fibres of this nerve, by stimulating the priority fibres Aα and Aβ which transport non-painful, tactile nerve impulses.
  • The unblocking of the nervous structures responsible for the naturally analgesic endorphin system by stimulating them in a specific way after they have been blocked by the presence of chronic pain.
  • A decrease in the intravascular cerebral concentration of serotonin, which is responsible for migraines, by stimulating the endorphin system, which increases the consumption of serotonin in various circuits.

 

These currents are delivered by electrodes placed on the skin at the location of the peripheral branches of the trigeminal nerve

  • To inhibit the peripheral nerve endings directly.
  • To reach the fibres of this nerve which are responsible for the integration (i.e. the sensation) of pain.
  • To reach, through these same fibres, the structures responsible for the implementation of the analgesic endorphin system.

The currents used are specialised for these various actions. They have been developed and validated, both for their safety and their effectiveness, by clinical experience with more than 5000 migraine patients treated over a period of 20 years (1994 to 2014).

Their characteristics have been studied in order to make them more effective on the targeted structures, while keeping them completely free of risk to the brain under the intended conditions of use.

Their intensity is disproportionate to the currents used completely harmlessly in cerebral stimulation techniques involving the intracerebral implantation of electrodes to treat conditions such as Parkinson's, for instance.

A list of contraindications, to a large degree overestimated, is given for information purposes. We recommend that you consult your doctor if you do not know your diagnosis and you are concerned that you could be one of these cases.

The treatment does not hurt.

 

If you use the treatment when you are not experiencing an attack

  • You will feel the equivalent of the start of an attack, which decreases at each level within a matter of seconds.
  • You can reduce the intensity according to your sensitivity.
  • In most cases, this is not even necessary, and the device can be left to function normally.
  • At the end of a treatment, you will no longer feel anything, except perhaps a sense of well-being similar to that which follows a good night's sleep.

 

If you are experiencing an attack

You will feel a tingling sensation replace the pain during the treatment

At the end of the treatment, your pain will have decreased by at least 50%, or even up to 100%, and you will no longer feel anything, except perhaps a sense of well-being similar to that following a good night's sleep.

Sometimes you will feel no current during the first or even second 5-minute phase. This is normal, and it is just a question of individual sensitivity. The device and its electrodes are not the cause of this. It is not necessary for you to feel the current in order for it to be effective against your migraines.

The therapeutic method used by CARE-ME® was practiced over a period of 20 years, from 1994 to 2014, in a medical environment, on over 5500 patients. During this period, the method was found to be very effective, both as a background treatment and an attack treatment.

Here is the clinical evaluation:

1. DIAGNOSIS

The patients treated were suffering from pathologies diagnosed by the IHS (International Headache Society) as consistent with various types of migraine conditions.

The goal of the diagnosis was two-fold:

  • to ensure that the patient was indeed suffering from a condition that could be treated in this manner; that it was a true migraine or migraine-related disorder.
  • to ensure that the patient was not suffering from a condition which we consider to be a potential contraindication to the use of such treatment.

 

2. CLINICAL USE

The patients selected in this way were treated for 30-minute sessions, according to a schedule of 3 sessions per week on average. The total length of treatment varies according to the greater or lesser speed at which an "attack-free" state, which could be considered as a quasi-recovery, is reached. This cannot be determined more precisely due to the large variation between individuals in the frequency of attacks.

Between 1994 and 2014, 5500 to 6000 patients were treatment according to this method.

The recovery rate is estimated to be above 75% of patients treated. There was never any interruption of the treatment due to any side effects. There was never any refusal of treatment for any reason whatsoever.

It can be confirmed that no undesirable effects were found.

The sensation felt in almost all cases is similar to the start of a migraine attack which then ceases after several minutes of treatment. When a patient is treated during an attack, the painful sensation is reduced by at least 50% by the end of the treatment. In about 80% of cases, there is no longer any painful sensation at the end of the session.

The frequency of the attacks is considerably reduced in three to six sessions (2 weeks of treatment), with a significant percentage of cases seeing a total remission of the condition within about 4 weeks of treatment.

When a recovery is reached, its duration varies according to the patients. It can last from 1 to 20 years (20 years constituting the current maximum recovery).

The effectiveness of the treatment during an attack

  • If the device is used while the patient is experiencing an attack, it is noted that the intensity of the pain is reduced by 50% to 100% in the 5 minutes following the treatment, according to the case.
  • When the pain has completely subsided at the end of the treatment, it does not return sooner than the usual frequency of attacks.

 

Background treatment effectiveness

  • It has been noted that, over the following days, there is generally a reduction in the frequency of attacks, a reduction in the intensity of the attacks, and very often attacks occur and then spontaneously end without the use of medication.
  • Sometimes a single session is enough to make the attacks disappear completely for several months, or even definitively.
  • Sometimes maintenance treatment is necessary every two days over the course of several months.

There is no risk posed by undergoing more sessions in case of necessity. The number of session can be as many as two per day if necessary.

Each case is of course particular and these details are given for information purposes only. In particular, it is recommended to reduce the use of medication as much as possible during this treatment, which should be effective without any associated medication. The regular consumption of chronic painkillers, anti-inflammatory medications and triptans can prevent the treatment from being fully effective, which is why complete withdrawal is ideal.

Yes, because CARE-ME® uses T.E.N.S. currents.

These T.E.N.S. currents are known for their analgesic (painkilling) properties which act non-specifically on the nerve fibres which transport all types of pain signals through the direct transmission of nerve impulses along the fibres known as C and Aδ, according to their size.

In addition to this, these currents also act by blocking the transmission of pain signals within these fibres at the first relay in the spinal cord (or its intracerebral equivalent in the head) (GATE CONTROL Theory).

 

Cases of conditions similar to migraines but which have different causes

As we have explained, this device is capable of blocking the transmission of pain regardless of its origin, which explains why it is effective against conditions similar to migraines which have different causes.

However, this painkilling effect is only palliative in this case, i.e. the pain will no longer be felt, but the cause of the condition will persist. Treatment should be recommenced each time a new attack occurs.

 

Cases of true migraines

CARE-ME® is optimised for the treatment of migraines. The current used is a T.E.N.S. current which has been specially studied for migraines. It has the special feature of also acting at intracerebral level on serotonin, the neurotransmitter responsible for the appearance of migraine pain, and does so sustainably.

Therefore, in the specific case of migraines, this device has both a palliative (it prevents pain from being felt) and curative effect (it sustainably cures the cause of the migraines).

For pain during an attack

  • The result is reached in the seconds following the end of a treatment session lasting 30 minutes.
  • The result is a reduction of at least 50%, sometimes 100%.

 

For the frequency of attacks 

  • Sometimes a single session is sufficient to put a stop to the attacks definitively.
  • What happens most frequently is an absence of any attacks for several months (6 months to several years), after a maintenance treatment of 2 months involving 1 session every alternate day.
  • Sometimes a greater number of sessions are needed (up to two per day), over varying periods (from two weeks to one month), before the normal rate of once every two days can be resumed.

It can be definitive. The current remission period is over 20 years. 

Sometimes the attacks recur due to significant stress or a psychological shock which raises serotonin levels. In these cases, it is necessary to resume treatment.

It is very easy and does not require any special knowledge.

The device is completely automatic.

There is no need for you to do anything.

However, if you would like to, you can change the sensation according to your sensitivity level as the device gives you the option of doing this.

In any case, the device will inform you at all times of what you can do. Therefore, follow the instructions carefully if you would like to do anything yourself.

The device will stop on its own at the end of the treatment.

The device and the instruction manual will inform you where to place your electrodes. All you need is an electrode support such as a pair of glasses. You cannot go wrong.

The device has been designed to make any error impossible, and there is no risk of incorrect use.

The device is completely automatic.

 

There is no need for you to do anything. However, if you would like to, you can change the sensation according to your sensitivity level as the device gives you the option of doing this.

In any case, the device will inform you at all times of what you can do. Therefore, follow the instructions carefully if you would like to do anything yourself.

The device will stop on its own at the end of the treatment.

Never remove your electrodes while the device is running (you risk nothing more than an unpleasant charge without any consequences)

If the electrodes move out of position, you will feel a tingling sensation, and you can move the electrodes back into place with your hand and without stopping the device.

To obtain the desired result, follow the recommendations below:

  • Do not hesitate to use your device every time you experience an attack. You can use it up to twice a day if necessary.
  • If one session is sufficient for you, do not hesitate to continue with one session every alternate day for one week in order to consolidate the result obtained if you are experiencing attacks.
  • If one session is not sufficient for you, the right pattern to follow is one session every alternate day for the necessary period of time, which could be several months.
  • Avoid any medications during your treatment. Try to withdraw from them progressively without worrying.
  • If the electrodes move out of position too easily, consider using them only on clean and dry skin. If they still move out of position, wet them slightly and then dry them with a compress before applying them. If this does not work, they will need to be changed.

During the first uses, do not hesitate to use the ORANGE button to limit increases in the intensity of the current. The device has been calibrated according to an average of patients; a more sensitive individual should use the ORANGE button.

For treatment during an attack

  • One session lasts 30 minutes.
  • One session is sufficient to calm an attack.

For background treatment to prevent the attacks from recurring

  • If one session is sufficient for you, do not hesitate to continue with one session every alternate day for one week in order to consolidate the result obtained if you are experiencing attacks.
  • If one session is not sufficient, the correct frequency of treatment is one session every alternate day for the duration necessary, which could be several months.
  • If this is still not sufficient, you can undergo up to two sessions a day without any risk.

For the electrodes to stay in place, the skin needs to be clean. If the electrodes are too dry, dampen them with a little water. To increase the service span of the electrodes, you can clean them with alcohol, and then dry them with a piece of gauze. If it is well taken care of, a set of electrodes can last for 20 treatments. 

If, in spite of these measures, the electrodes still fall out of place, the electrode support will need to be changed. You can order one on the website.

Sometimes, for individuals with very curved foreheads, or men who are not clean shaven, or individuals who transpire more in higher temperatures, the electrodes fall out of position more easily.  In these cases, use the elastic bands provided by placing them on the electrodes to maintain them in proper contact with the skin.

Some individuals do not feel the current during the first two 5-minute phases. This is normal, and it is just a question of individual sensitivity. It does not indicate that the electrode or the device is defective. You can change the intensity to a certain predetermined level for each phase. It is not necessary for you to feel the current in order for it to act effectively against your migraines.

In order to make migraine studies more reliable, and in light of the wide variation in the most common symptoms and the existence of conditions which closely resemble migraines but are not true migraines, the IHS (International Headache Society) has formulated diagnostic criteria for migraines.

The IHS Criteria enable distinction to be made between:

  • Migraines without aura (M-A)
  • Migraines with aura (M+A)
  • Conditions similar to migraines but which have a different cause

You can find these criteria on the IHS website: www.i-h-s.org

Auras are temporary neurological symptoms which appear during migraines with aura (M+A in the IHS classification). These are specific symptoms which are of great diagnostic value. They last between several minutes and one hour. They sometimes precede the onset of pain, but can also occur at the same time as the pain. They are specific in that they always disappear without leaving any neurological trace.

Several types of them are recognized :

Visual auras

The most frequent type, sometimes occurring in isolation, but sometimes associated with other types of auras. They are almost always present when auras of another type occur. They can take numerous forms:

  • The scintillating scotoma is the most common form. This is a blind spot which appears in the field of vision, whether the eye is open or closed. This spot is bordered by shining, scintillating edges, which is what gives it the name "scintillating scotoma."
  • Zig-zags or lightning bolts, also called "fortification illusions" because they appear in the field of vision as broken lines resembling the fortifications built by Vauban.
  • Many other shapes, ranging from vision blurring to partial blindness to more or less elaborate visual hallucinations.

Auditory aura

More or less complex noises or sounds causing auditory hallucinations (they sometimes take a very elaborate form, sounding like Polynesian chants or polyphonic fragments). They are much rarer than visual auras.

Sensory auras

Abnormal sensations (paraesthesia) or tingling occurring at the extremity of a limb (generally a hand) and extending progressively up to the shoulder, and sometimes even the side of the tongue (cheiro-oral aura). They are always unilateral and are sometimes accompanied by other types of aura.

Aphasic auras

Speaking problems which manifest themselves as difficulty finding or articulating a word, or even difficulty speaking, sometimes in the form of mistakes which render the speech incomprehensible (jargon aphasia), sometimes as difficulty reading (alexia), writing (agraphia) or performing calculations (acalculia).

Motor auras

These are motor disturbances which manifest themselves as difficulty in performing a gesture (paresis), and sometimes as total inability to do this (paralysis). They are always unilateral (hemiparesis or hemiplegia).

These auras are of great diagnostic value, which is why it is important to recognise them.

They are also of great neurophysiological significance as there is currently a consensus that they indicate that neurons are suffering from a lack of oxygen due to the vessel constriction phase which precedes the vessel dilation is responsible for migraine pain.

This would also explain why they appear almost always before the pain.

It is also believed that they disappear without leaving a trace because the lack of oxygenation ceases abruptly as soon as the vessels dilate, causing pain to appear. This means that the anoxia does not last long enough to produce irreversible damage to the neurons.

The literature points to numerous contributory factors of migraines. We believe that the list of contributory factors should be limited to those which are essential in the sense that they can be explained in light of currently available neurophysiological data.

This condition affects anxiety patients in particular, as they are inclined to encounter new causes of their anxiety.

 

Dietary factors

There is a strong tendency with this condition for consequences to be taken for causes, which is the case for patients as much as those treating them. This is particularly true for dietary causes, which are made to fit all explanations. Yet, with the exception of clearly excessive consumption of wine, which leads to dilation of the cerebral vessels, and perhaps some cheeses which can increase cerebral serotonin synthesis (which is responsible for migraines), there are no contributory dietary factors.

Chocolate has often been blamed wrongly. It was even banned from the diet of migraine sufferers after it was supposedly found that they were fonder of chocolate than other individuals. It is in fact true that they often crave chocolate before attacks.

The currently available neurophysiological data suggest that these cravings are a beneficial adaptation, as cacao is one of the best natural products for decreasing cerebral serotonin secretion. It is therefore one of the best self-defence mechanisms for migraine sufferers against their excess serotonin.

Environmental factors 

Once again, there are many factors implicated without proof of their actual effect.

These factors are often symptoms of hyperserotonaemia or of a deficiency within the analgesic inhibitory endorphin circuits. This very much points to the question of whether the consequences have been mistaken for causes.

These symptoms are,

Environmental variations of greater or lesser severity:

  • Temperature, light, atmospheric pressure, sound environment.
  • Change of altitude.
  • Change of sleep/waking patterns.
  • Change in cerebral activity (from the working week into the weekend, holiday activities, etc.).
  • Psychological changes due to significant positive or negative stress (death of a family member, moving home, divorce, or a change of profession, but also good surprises, weddings, etc.).

Metabolic changes:

  • Transient hypertension, or inadequately treated hypertension.
  • Onset of diabetes.
  • Undiagnosed hyperthyroidism.
  • Unknown pheochromocytoma.

Although there is no doubt that familial predisposition is a factor for some migraine patients, proof for hereditary transmission has not always been formally established.

A strong predominance of this condition among women has been observed (3/4 cases).

For certain types of migraine, especially ophthalmoplegic migraines (not to be confused with ophthalmic migraines), certain migraines with regressing paralysis and certain temporarily paralytic migraines affecting children, there is almost certain proof of hereditary transmission, as demonstrated by the discovery of abnormal genes which are responsible.

In addition to this, it appears that homozygous twins are more frequently affected than heterozygous twins, which is clearly indicative of chromosomal genetic transmission.

As we stated in the chapter on the physiopathology of migraines, it is likely that excess cerebral serotonin levels are partially responsible for a more frequent appearance of migraines. This excess serotonin manifests itself in fairly stereotypical personality traits, making it possible to speak of a serotonin personality.

Its distinctive characteristics are:

  • Major hypersensitivity: explosions of joy and sorrow for no particular reason
  • High susceptibility to stress
  • A tendency towards introspection
  • A tendency towards melancholy
  • A relatively phlegmatic character 
  • Vagotonic symptoms: discomfort, paleness, inexplicable tiredness.
  • Digestive hyperactivity: nausea, vomiting, diarrhoea.
  • Certain nutritional behaviours: bulimia, cravings, selective cravings (especially for dark chocolate), sometimes anorexia
  • Difficulties falling asleep, being a "night owl"
  • Waking up in the morning with a migraine (5 am)

Migraines have a very strong predominance in women. 70% of cases are female.

Migraines are a very common condition and are very disruptive for society as they affect mainly the working-age population. They affect between 12 and 17% of the general population, varying according to the country examined. 70% of sufferers are female and 30% are male. 

The women affected are generally in the most professionally and reproductively active age group, between 18 and 50 years (from adolescence to post-menopause). However, women can also suffer from migraines later in life. After the age of 70, it is more often a case of Horton's disease, which is migraine-related and must be treated due to the risk of rapid blindness associated with this disorder. 

Male migraine sufferers are often slightly older (between 25 and 75 years of age). Some differential diagnoses, such as cluster headaches and trigeminal neuralgia are more common in men than in women. 

Children can suffer from migraines at a very young age, and diagnosis is often difficult and neglected (complaints, stopping games and problems concentrating at school are of great value, as is intestinal pain, which is probably related to serotonergic dysregulation).

 

Industrialized countries

A higher prevalence of migraines has been observed in both sexes in industrialised countries, compared to developing countries. However, this observation has certain nuances:

  • First of all, the incidence of migraines in the latter countries is probably under-documented.
  • The conclusion cannot be made that industrial pollution is responsible.

Countries where the tertiary sector dominates have the highest prevalence of migraines (e.g. Luxembourg 20%). It is likely that it is an effect of stress related to level of life and worries about maintaining it.

These are conditions which, like migraines, have a double distinctiveness:

  • Chronic pain of varying duration, occurring in relatively numerous successive attacks spaced out over time, with a fairly fixed topography affecting generally all or part of the face or skull at the beginning, and often generalising later on.
  • These pains are the consequence of a physiopathological disorder, which is known only in some cases, and of which the cause may be neurochemical or mechanical.

There are several conditions which resemble each other closely, but differ in their symptomatology, in turn depending on the physiopathological conditions of occurrence.

See the question "Are there pains which resemble migraines but are not migraines?"

A non-exhaustive list of these pathologies can be established:

Common headaches

  • known to everyone and simply called "headaches",
  • very frequent and not particularly severe.

 

Tension headaches

  • often related to neck arthrosis,
  • contraction of the neck muscles,
  • prolonged periods in the same neck position (generally under working conditions).

  

Neurogenic hyperstimulation headaches

  • often provoked by a noisy atmosphere,
  • sensory overstimulation of all types (visual, auditory, psychological).

  

Arthralgic neck pain

  • always accompanied by osteoarthritic deterioration
  • or post-traumatic neck deterioration (cervical spine).

 

Occipital neuralgia

  • due to mechanical autonomic compression of the occipital nerve in the foramen magnum
  • manifests itself in the form pain in the neck and the back of the head, extending towards the top of the skull.

  

Cluster headaches

  • very brief and severe attacks
  • recurring several times a day,
  • always unilateral,
  • accompanied by autonomic symptoms in the form of lacrimation, frequently nasal discharge and hemifacial redness.

 

Trigeminal neuralgia 

  • similar to the conditions described above,
  • predominantly affects men
  • but with few autonomic symptoms,
  • variable location, but always somewhere on one of the three branches of the trigeminal nerve. (eye, nostril and ala, or upper or lower jaw).

  

Facial neuralgia "from the cold"

  • accompanied by characteristic hemifacial paralysis.
  • can last for several months before regressing more or less completely.

Post-traumatic neuralgia from nervous deafferentation:

  • pain appearing in the area where the nerve has been destroyed,
  • in the form of a permanent, painful tingling sensation.

 

Horton's disease

  • often affects women over 60 years of age,
  • manifests itself as unilateral pain in the temple,
  • accompanied by fever,
  • with palpable induration of the temporal artery, which stops beating,
  • and a risk of rapid blindness if left undiagnosed.

Post-herpetic neuralgia of the face

  • generally caused by destruction of the ophthalmic nerve by shingles,
  • manifests itself as the same nervous deafferentation pains.

  

Intracranial hypertension headaches caused by tumoral or metastatic compression, intracranial haemorrhage, ruptured aneurysm

 

  • often begin very severely, or as a severe aggravation of previously experienced headaches,
  • rapidly accompanied by progressive, but never spontaneously regressing, neurological disorders,
  • significant autonomic disturbances (discomfort, loss of consciousness, projectile vomiting),
  • and rapid deterioration of the patient's general condition.

Pain intensity can be tested easily and very reliably. Sophisticated tests exist, but are reserved for fundamental research as they are difficult to conduct. This research has shown that its reliability and reproducibility are not greater than for the Visual Analogue Scale (VAS).

This scale is a simple line which on one side shows the 10 cm line without any marked graduations. The user slides a cursor across the line and places it between the start of the line (furthest left) and the end (furthest right), according to the intensity of the pain.

The furthest left signifies no pain. The furthest right represents the worst possible pain. On the other side of the ruler, which is hidden from the patient who is testing his or her pain, graduations in millimetres allow the practitioner to note the value according to the position where the patient has placed the curser.

Studies have shown that for constant pain, the assessment given by the patient is extremely precise and reproducible, without possible bias as the patient has no precise indication of how he or she compares to others.

Migraine pain ranges between 6 and 10 on the VAS during an attack.

This scale can be used in different ways. What matters is the question put to the patient before he or she responds using the scale.

The scale can be used to assess:

  • the intensity of pain felt at that moment,
  • the intensity of a past pain recalled from memory,
  • the intensity of pain felt at that moment compared to a past pain recalled from memory,
  • the residual intensity of pain following or during treatment.

Finally, this assessment can be made using an adapted graduated ruler, but also by asking the patient to rate the pain mentally from 1 to 10.

There are other pain assessment scales besides the VAS. They are based on the same principle but test different aspects of pain. For example:

  • assessment of psychological impact
  • assessment of emotional impact
  • assessment of physical disability
  • assessment of occupational disability
  • assessment of resulting absenteeism
  • assessment of impact on family
  • assessment of social impact

The trigeminal nerve is very widely implicated both in the physiopathology of migraines and in the expression of pain from migraines and related disorders.

DESCRIPTION AND FUNCTIONS:

The trigeminal nerve takes its name from the fact that its fibres innervate half the face with three branches:

  • The ophthalmic branch, which extends from the ear to the forehead area just above the eyebrows,
  • The nasal branch, which extends from the ear to the ala and bridge of the nose,
  • The mandibular branch, which extends from the ear to the corner of the mouth and which gives off one branch for the upper lip and one branch for the lower lip and the chin.

These branches are sensory and provide sensation (and pain) to the face, but they also have an autonomic contingent which regulates, in particular, the size of the surface vessels according to local heat conditions, as well as sweat activity.

In order to gain a good understanding of pain transmitted via the trigeminal nerve, it is necessary first of all to discuss the Aδ and C nerve fibres.

The Aδ and C sensory fibres transport acute and chronic pain, and react to local variations in pressure, temperature and chemistry. They are each distinct:

  • The Aδ fibres: quite large, myelinated, and therefore transport nerve impulses rapidly. These fibres are responsible for precise and immediate transmission of acute pain. The excitatory neurotransmitter which they use is glutamate, which acts rapidly on these receptors, with its effect disappearing in a few thousandths of a second. The distal free endings of these fibres are directly excited essentially by mechanical (pressure, contact) and heat phenomena. These fibres are linked, through a relatively direct chain of three neurons, to the thalamus and the cortical and sub-cortical integration zones. They are responsible for the immediate sensation of pain, with good topographical precision.

  • C fibres: smaller in size, unmyelinated, which means they conduct nerve impulses more slowly. These fibres are responsible for transmitting less immediate, more diffuse pain. The neurotransmitter which they use, among others, is substance P, which acts much more slowly on these receptors and has an effect which can last several minutes. The free distal endings of these fibres are directly excited by mechanical-type polymodal phenomena (pressure, contact), temperature, but most often chemical phenomena. These fibres join the thalamus and the cortical and sub-cortical integration zones via a more complex and slower chain of neurons, and in close connection with the structures of the upper medullary region. Here, they enter into contact with the reticulated substance neurons responsible for cortical arousal, the median raphe neurons of the periaqueductal grey matter, and the ventricular tectum involved in the endorphin regulation of pain. These regions themselves are dominated by the inhibitory neurons of the limbic system. They are responsible for the sensation of prolonged, chronic, imprecise, diffuse and dull pain.

 The trigeminal nerve also has deep sensory Aδ and C branches, but mostly autonomic fibres which innervate the vessels at the base of the skull and in significant part of the meninges, mainly in the anterior and superior areas of the brain.

The trigeminal nerve can also be the site of "referred pain" – this phenomenon generally occurs when an internal organ is innervated by collateral nerve fibres coming from a cutaneous nerve. In the case of the trigeminal nerve, these sensory fibres at the cutaneous facial departing point have collateral fibres which are responsible for the sensory innervation of the base of the skull and the meninges. This means that nociceptive nerve impulses originating from these vessels may be responsible for referred pain in the area of cutaneous trigeminal innervation of the corresponding hemiface. There are some Aδ fibres in contact with these vessels which are excited by pressure caused by the vasodilation of these vessels. This vasodilation is recognised as being the cause of migraine pain.

INVOLVEMENT OF THE TRIGEMINAL NERVE IN MIGRAINE PHYSIOPATHOLOGY:

When serotonin, a neurotransmitter responsible for the vasoconstriction and vasodilation of the vessels at the base of the skull and in the meninges, releases its receptors, it causes severe dilation of these vessels which are innervated by the trigeminal nerve. This causes at least two of the phenomena responsible for the appearance of pain in the side of the head and the skull: 

  • The phenomenon of referred pain: The pressure due to the dilation of the vessels at the base of the skull and in the meninges excites the Aδ fibres of the trigeminal nerve in contact with them. The latter then transmit pain to the brain. But they also excite the collateral fibres coming from the corresponding hemiface and are also carried by the trigeminal nerve. The pain therefore also appears at the end of these fibres, i.e. in the hemiface.

In response to this immediate pain transmitted by fast Aδ fibres, the autonomic fibres of the trigeminal nerve release algogenic substances, which are often vasodilatory, and which aggravate the pain through the same process via the Aδ fibres and by a slower and longer lasting secondary process via the C fibres. These C fibres are excited by the algogenic substances and by the variations in local chemistry that they cause. This causes a veritable "vicious circle" which translates into a migraine attack.

I - Position of the problem

The most commonly accepted theory attempting to explain the physiopathology of migraines is the Trigeminovascular Theory. This theory is based on the combined action of neurogenic inflammation of the endings of the trigeminal nerve innervating the hemiface, and its vascular effects (mainly vasodilation) on the vessels of the meninges innervated by the nerve endings from the same trigeminal nerve.

However, this theory postulates that the "prime mover" of a migraine attack is hyper-excitability of the free trigeminal nerve endings, without a clear explanation being given for the origin of this phenomenon. In addition to this, no explanation offers understanding of whether the neurogenous inflammation is the consequence of vasodilation, or whether, on the contrary, the latter is the cause of the former.

Yet it seems that, while maintaining the main lines of logic of the Trigeminovascular Theory, both at neurogenic and vascular level, a more rational construction of the relevant elements could allow the pathophysiology of migraines to be approached without resorting to current assumptions.

From this new perspective, it becomes possible to understand why the electrotherapy migraine treatment technique is effective, not only given the immediate palliative analgesic action during the attack, but also the curative long-term curative neurochemical action produced by background treatment.

II - Newly proposed physiopathological explanations

The chain of physiopathological events leading to a migraine attack could be as follows: 

  • An increase in cerebral serotonin concentration within certain circuits is the initial cause of the appearance of migraines. This increase could be genetically determined in some individuals (which is why sets of siblings can be affected by migraines). In other individuals, it can be acquired, sometimes also due to genetic predisposition, from repetitive bouts of stress (this appears to occur most frequently in women during adolescence), which are known to have a tendency to raise serotonin levels in the limbic system with all the known psychological consequences.
  • This initial increase in serotonin is responsible for the initial vasoconstriction of the vessels at the base of the skull and in the meninges, the factor of hypoperfusion and neuronal ischemia not causing the "auras" which precede migraine pain.
  • Secondarily, when Serotonin releases its receptors, vasodilation occurs at an even greater level than the level of implicated serotonin, and leads to a mechanical excitation of the nociceptive Aδ fibres of the trigeminal nerve, causing the initial localised migraine pain. This pain is also projected to the facial territory of the trigeminal nerve by the mechanism of referred pain.
  • A little later, but in a more diffuse, imprecise and longer lasting manner, the pain originates from the slower chemical excitation of the nociceptive C fibres, due to the algogenic substances released by the dilated vessels through plasma extravasation.
  • The pain impulses from the C fibres excite the Periaqueductal Grey Matter (PAG) and the Median Raphe (MR), structures which are maintained in a state of inhibition by the limbic system. These first two structures release locally the endorphins responsible for blocking the limbic system's inhibition of themselves. These structures are then believed to be able to activate descending inhibitory endorphin and serotonin circuits which block the passage of the peripheral pain signals from the C and Aδ fibres.
  • However, this is only possible while the impulses are variable, with the neurons neglecting the persisting signals through the phenomenon of neuronal tolerance. Yet the vasodilation persists, as do the mechanical and especially the chemical consequences. The PAG and MR cease their local production of endorphins and return to a state of inhibition by the limbic system. The migraine attack continues until the slow reduction in vasodilation and the disappearance of the chemical algogens.
  • The direct consequence is a "non-consumption of serotonin"; the descending inhibitory serotonergic circuits are no longer activated by the PAG and the RM. This becomes the vicious circle which progressively aggravates the attacks, their frequency and their duration.
  • The increase in serotonin in these circuits leads indirectly to an increase in the number of potential receptors to serotonin, through the phenomenon of receptor externalisation, depending on the concentration of serotonin circulating in the vessels, an additional aggravating factor in attacks.
  • Hyperserotonaemia aggravates the reactivity of the limbic system, making the individual more vulnerable to stress, which itself is responsible for an increase in the general level of serotonin.

Hyperactivity of the limbic system increases the latter's blockage of the PAG and MR, i.e. the naturally analgesic endorphin system, thereby prolonging the pain.

The majority of migraines are caused by excess cerebral serotonin in certain neuronal circuits. Serotonin causes a decrease in the size of the blood vessels at the base of the skull and in the meninges by fixing onto the specific receptors located in the internal wall of these vessels. However, it is not this vasoconstriction of the vessels which is responsible for the migraine pain itself. Visualisation of the size of the vessels during a painful attack in PET scan studies demonstrates that when the pain begins, the vessels are dilated and not constricted.

The pain is in fact caused by the dilation of the vessels which occurs after the serotonin has released its receptors.

Triptans are derived from sumatriptan, a synthetic molecule which has the property of attaching itself relatively sustainably to serotonin receptors. This means that serotonin is unable to cause vasoconstriction of the blood vessels in the first place, or the secondary vasodilation during the release of receptors. Like serotonin, triptans have a vasoconstrictive effect, but they remain attached to receptors for longer and lead to vasodilation being more evenly spread over time than serotonin when they release their receptors. In this way, they have a palliative effect on the migraine pain.

However, one must be wary of abuse of triptans.

The number of free receptors available to attach to serotonin is not immutable. This number is proportionate to the quantity of freely circulating serotonin. Through a phenomenon known as receptor externalisation, new receptors appear in the internal wall of the vessels when the amount of serotonin increases. Furthermore, this phenomenon explains the progressive aggravation of migraines when external conditions cause an increase in serotonin.

Triptans, however, "occupy" the serotonin receptors and progressively cause an increase in the amount of circulating serotonin lacking receptors to bind to. This initially leads to the appearance of new receptors available to serotonin. But, if the process continues, the triptans which were occupying the receptors eventually release them, and after some time, the number of free receptors once again becomes significant, as does the quantity of serotonin spared by the presence of triptans. After this, there is a rebound phenomenon, as a large quantity of serotonin meets with a significant quantity of available receptors.

Furthermore, it must be noted that triptans have a strictly palliative effect on migraine pain, as they simply prevent the painful vasodilation of the blood vessels which follows the release of receptors by the serotonin which was bound to them.

Triptans do not have a truly curative effect as they do not act on the true cause of the disorder, which is an excess of serotonin in certain circuits (among other probably equally implicated neurotransmitters).

Electrotherapy treatment technique for migraines and related disorders:

This new technique is based on three necessities:

  • Blocking the pain signals as quickly and for as long as possible starting from the onset of the attack in order to prevent the vicious circle from becoming established (attack treatment).
  • Preventing new attacks (background treatment).
  • Developing an automatic system which enables the necessary currents to be applied to the trigeminal nerve.

1. Attack Treatment

The pain signals delivered by the Aδ and then the C fibres can be blocked in many ways according to the level and speed of their effect:

  • Hyperpolarisation of the nerve fibres by the current with the aim of making the fibres harder to depolarise, i.e less excitable.
  • A collision of impulses involving blocking the afferent nociceptive impulses with an efferent counter-current applied to the same fibres at a more proximal location.
  • Blocking the first "gate control" neuronal relay using the stimulation of large proprioceptive Aβ fibres at a low intensity and high frequency. These fibres block the flow of nociceptive impulses through presynaptic inhibition of the C fibres.
  • Stimulation of the endorphin circuits of the PAG and the MR by excitation of the C fibres at high intensity and low frequency.

 

2. Background Treatment

  • Background treatment is based on the need to reduce the level of circulating serotonin. This reactivates the endorphin system which had been deactivated by the constant nociceptive impulses, and in so doing, reactivates the descending inhibitory serotonergic circuits.
  • To do this, it is necessary to stimulate the Aδ and C fibres electrically in a variable manner by using currents of variable frequency over time.
  • According to the frequency, the stimulation affects either the Aδ or C fibres. The neurons of the endorphin structures of the PAG and MR are no longer the site of increasing neuronal tolerance. This leads to reactivation of the endorphin system and an increased stabilising consumption of serotonin.

 

3. Automatic application of currents to the trigeminal nerve.

The currents used to obtain these results are well-known. These are T.E.N.S. currents (Transcutaneous Electrical Nerve Stimulation), with special characteristics in order to meet these specific goals for migraines.

The difficulty hinges on:

  • the place of application (the trigeminal nerve of the face)
  • the need to vary the parameters of the currents over time.
  • the only possible solution is to automate the treatment completely so that the patient can treat him- or herself without any special knowledge and without risk, while being aware of the particularities.

 The automation of treatment poses certain problems: 

  • Automation must take into account the variation in individual sensitivity:
    • It is therefore imperative to enable the patient to adjust of the levels of intensity according to his or her sensitivity.
    • However, this adjustment capability must be well regulated at all times to prevent the patient from receiving excessively strong stimulation, and also to prevent the intensity from falling too low and risking a total loss of effectiveness.
  • The automation must take into account the variation in physical parameters according to time.

The intensity of the stimulation must be constantly adapted to:

  • the variation in cutaneous resistance which progressively decreases over time.
  • the adaptation of nerve fibres which increases over time.

The creation and propagation of nerve impulses: 

Pain is transmitted in the form of nerve impulses:

Pain forms in the peripheral tissues by causing a change in the local electric and electronic conditions.

Nerve endings which are influenced by these electric variations are found everywhere in the body. These nerve fibres are distinct due to their size (which defines the speed of signal transmission) and their cerebral destination, which enables them to transmit pain signals to the brain (nociceptive fibres). There are several types of them and they can be differentiated essentially by the speed of their transmission of signals and the purpose of their signal (fine sensory, crude sensory, thermo-algesic, motor, autonomic). These fibres make up nerves which can be sensory, motor or autonomic, or combined, consisting of a variable proportion of several categories. This means that nerves are not comparable to electrical wires which transmit a current, even though nerve impulses are transfers of electrons.

These fibres are in a state of rest comparable to a succession of small electric batteries assembled in a line, extending from the periphery to the nervous centre, like a precarious domino line (all that is needed is a light push for the first impulse to be transmitted to the end of the construction). Each small battery has a potential of -70 mV if we take into account the negative pole (external pole) on the outside of the fibre and the positive pole (internal pole) on the inside of the fibre.

All that is needed is a change in the electric conditions facing these small batteries, along a nerve, for the negative pole (external pole) of this battery to become positive in relation to the positive pole (internal pole), which itself becomes negative. This is called depolarisation.

The depolarisation of this small battery is transmitted to the next small battery, like falling dominos, and this local depolarisation spreads from one to the next until depolarisation of the neurone which the excited fibre issues from, at the nervous centres involved. Pain is therefore transmitted to the brain in the form of a nerve impulse.

The place where the depolarisation (and therefore the pain signal) occurs depends on which fibre has been excited. It is topographically related to the origin of the signals. In this way, the pain is felt at the point where the signal was created.

But not all pain signals are transmitted

For pain to be transmitted, it is necessary for the local electrical changes to be significant enough to invert the potential of a resting battery, i.e. to make its potential change from de -70 mV to a positive value between + 20 and + 70 mV, according to the sensitivity of the nerve. Without this, the depolarisation is insufficient to be transmitted from battery to battery until it reaches the nervous centre.

However, it has been found that each nerve has individual sensitivity on one side, and variable sensitivity on the other.

Furthermore, it is possible to reduce the sensitivity of a nerve. To do this, it is necessary to subject it to a charge current that is sufficient to for each battery to increase its resting polarisation. For example, increase this polarisation to -120 mV instead of -70 mV.

Therefore, in order to excite the nerve, i.e. to depolarise it, it would be necessary for the local electrical variations (the pathological pain phenomenon) to bring 50 mV more to this battery than in the previous instance (i.e. a total of 120 mV to reach transmissible depolarisation). If this value is not attained, i.e. if it is insufficient to depolarise the nerve, the pain will not be transmitted, and therefore will not be felt.

This particularity has been exploited in order to reduce the transmission of pain using electrotherapy. It is therefore a matter of hyper-polarising the nerve endings in the area of pain.

The pain fibres

Pain is initially a nervous impulse which is transmitted to specialised nerve centres by special fibres in certain nerves. These fibres differ in their characteristics (size, chemical composition, etc.), which gives them original properties. 

The sensory fibres are the Aδ and C fibres, which transfer acute and chronic pain, and react to variations in pressure, temperature and local chemistry. They are each distinct:

The Aδ fibres: quite large, myelinated, and therefore transport nerve impulses rapidly. These fibres are responsible for precise and immediate transmission of acute pain. The excitatory neurotransmitter which they use is glutamate, which acts rapidly on these receptors, with its effect disappearing in a few thousandths of a second. The distal free endings of these fibres are directly excited essentially by mechanical (pressure, contact) and heat phenomena. These fibres are joined to a relatively direct chain of three neurons, the thalamus and the cortical and sub-cortical integration zones. They are responsible for the immediate sensation of pain, with good topographical precision.

C fibres: smaller in size, unmyelinated, which means they conduct nerve impulses more slowly. These fibres are responsible for transmitting less immediate, more diffuse pain. The neurotransmitter which they use, among others, is Substance P, which acts much more slowly on these receptors and has an effect which can last several minutes. The free distal endings of these fibres are directly excited by mechanical-type polymodal phenomena (pressure, contact), temperature, but most often chemical phenomena. These fibres join the thalamus and the cortical and sub-cortical integration zones via a more complex and slower chain of neurons, and in close connection with the structures of the upper medullary region. Here, they enter into contact with the reticulated substance neurons responsible for cortical arousal, the median raphe neurons of the periaqueductal grey matter, and the ventricular tectum involved in the endorphin regulation of pain. These regions themselves are dominated by the inhibitory neurons of the limbic system. They are responsible for the sensation of prolonged, chronic, imprecise, diffuse and dull pain.

A distinct feature of pain fibres is that they also transmit variations in local temperature – this is why we refer to a thermo-algesic circuit and fibres. This explains the calming effect of heat and cold.

When the nerve fibres are used to transfer a nerve impulse corresponding to a change in the local temperature (a variation which can be positive or negative, i.e. heating or cooling), they are incapable of transferring nerve impulses corresponding to a pain at the same time.

This means that if the local temperature is not stabilised, then the pain is soothed. (The principle of hot/cold immersion).

However, as soon as the temperature becomes stable, the pain reappears as the thermal receptors only transmit impulses during temperature change and are incapable of transmitting information about an absolutely fixed temperature value, which allows pain impulses to be transmitted once again.


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