Migraine - Diagnosis

As with other primary cephalgias, the diagnosis of " migraine " is based entirely on complaints and anamnesis data, and in most cases there is no need for additional research methods. A thorough questioning is the basis for the correct diagnosis of migraine. When making a diagnosis, one should rely on the diagnostic criteria of ICHD-2 (below are the diagnostic criteria for the two most common forms: migraine without aura and migraine with aura).

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Diagnostic criteria for migraine

Nature of pain: severe headache; pain intensity increases over minutes to hours; pulsating (vibrating) nature of pain; unilateral localization (hemicrania) more often than bilateral; possible movement of pain localization (migration); increased pain with physical activity; duration of headache from 4 to 72 hours; periodicity of attacks.

Associated symptoms and signs: noise intolerance (phonophobia); light intolerance (photophobia); nausea, vomiting; pale, often pasty skin of the face; arterial hypotension; constipation; aura symptoms occurring in 20% of patients: photopsies (flashing lights, shimmering zigzag lines, lightning); visual field loss (hemianopsia, scotoma); numbness, paresthesia (of the face, hand or other parts of the body); dysarthria; unsteadiness when walking; dysphoria.

The following factors provoke a migraine attack: emotional experiences, stress (usually in the discharge stage), excessive sleep or lack of sleep, noise, bright light, flickering TV screens, unpleasant odors, strong irritants of the vestibular apparatus (swinging, riding a train, car, sea voyages, flying in an airplane, etc.), the period of ovulation and menstruation, physical activity, weather changes, alcohol, long breaks between meals, constipation, some foods (chocolate, cocoa, milk, cheese, nuts, eggs, tomatoes, citrus fruits, fatty foods, celery, etc.), some medications (oral contraceptives), etc.

Among all types of migraine, the most common (in two thirds of cases) is migraine without aura (simple migraine), which begins without any warning signs, immediately with a headache. Often, a migraine attack consists of two phases.

The first is the phase of prodromal phenomena in the form of a decrease in mood (depression, fear, less often - euphoria), irritability and anxiety, tearfulness, indifference to everything around, decreased performance, drowsiness, yawning, changes in appetite, nausea, thirst, tissue pastosity, local edema. This phase lasts for several hours.

The second phase - headache occurs at any time of the day (often during sleep or upon awakening), the pain increases over 2-5 hours. An attack of headache is accompanied by a decrease in the threshold of excitability of the sense organs (hearing, vision). A slight knock, speech of normal volume, and familiar electric light become completely unbearable. Touching the body may also become unbearable.

During an attack, patients try to retire, tightly bandage their head, drink warm tea, coffee, darken the room, go to bed, cover their ears with a pillow and wrap themselves in a blanket. Sometimes a swollen temporal artery is determined, its pulsation is visible to the eye. With strong compression of this artery, the pulsating pain decreases. The conjunctival vessels on the side of the pain are dilated, the eyes are watery, the pupils and eye slits are narrowed (Bernard-Horner symptom), swelling of the tissues around the orbit and temple, the face is pale.

During one attack, the headache may spread to the entire half of the head and include the occipital region and neck. The pulsating pain turns into a pain with a sensation of "splitting" of the head, compression. The attack lasts for several hours (8-12 hours). Some patients experience profuse urination (polyuria) by the end of the attack.

The frequency of migraine attacks without aura varies, their periodicity is individual. They typically develop not against the background of stress, physical tension, but against the background of subsequent relaxation (weekend migraine). Migraine attacks decrease or disappear during pregnancy and resume after the cessation of lactation and the restoration of menstruation.

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What are the different types of migraine?

Diagnostic criteria for migraine without aura and migraine with aura (ICHD-2, 2004)

1.1 Migraine without aura.

• A. At least five seizures meeting criteria for BD.
• B. Duration of attacks 4-72 hours (without treatment or with ineffective treatment).
• C. The headache has at least two of the following characteristics:
  • one-sided localization;
  • pulsating character;
  • pain intensity from moderate to severe;
  • headache is aggravated by normal physical activity or requires stopping it (for example, walking, climbing stairs).
• D. The headache is accompanied by at least one of the following symptoms:
  • nausea and/or vomiting;
  • photophobia or phonophobia.
• E. Not associated with other causes (disorders).

1.2.1. Typical aura with migraine headache.

• A. At least two attacks meeting criteria for BD.
• B. The aura includes at least one of the following symptoms and does not include motor weakness:
  • fully reversible visual symptoms, including positive (flickering spots or stripes) and/or negative (visual impairment);
  • completely reversible sensory symptoms, including positive (tingling sensation) and/or negative (numbness);
  • completely reversible speech disorders.
• C. At least two of the following:
  • homonymous visual disturbances and/or unilateral sensory symptoms;
  • at least one aura symptom develops gradually over 5 minutes or more and/or different aura symptoms occur sequentially over 5 minutes or more;
  • each symptom has a duration of not less than 5 minutes, but not more than 60 minutes.
• D. Headache that meets BD criteria for 1.1 (migraine without aura) begins during the aura or within 60 min of its onset.
• E. Not associated with other causes (disorders).

According to the international classification developed by the International Headache Society, the following clinical forms of migraine are distinguished:

• I - migraine without aura (previously used synonym - simple migraine) and
• II - migraine with aura (synonyms: classic, associated migraine).

The basis for distinguishing the named forms is the presence or absence of an aura, i.e. a complex of focal neurological symptoms preceding an attack of pain or occurring at the height of pain sensations. Depending on the type of aura, the following forms are distinguished in the migraine with aura group:

• migraine with typical aura (previously - classical, ophthalmic form of migraine);
• with prolonged aura;
• familial hemiplegic migraine;
• basilar;
• migraine aura without headache;
• migraine with acute onset aura;
• ophthalmoplegic;
• retinal migraine;
• periodic syndromes of childhood, which may be precursors to migraine or be combined with it;
• benign paroxysmal vertigo in children;
• alternating hemiplegia in children;
• complications of migraine:
  • migraine status;
  • migraine stroke;
• migraine that does not meet the above criteria.

The classification also provides the main diagnostic criteria for migraine.

Migraine without aura

• A. At least 5 migraine attacks in the medical history, meeting the following criteria B-D.
• B. Duration of migraine attacks from 4 to 72 hours (without treatment or with unsuccessful treatment).
• B. The headache has at least two of the following characteristics:
  • unilateral localization of headache;
  • pulsating nature of headache;
  • moderate or significant pain intensity that reduces the patient's activity;
  • aggravation of headaches with monotonous physical work and walking.
• G. The presence of at least one of the following accompanying symptoms: nausea, vomiting, photophobia and/or phonophobia. It is important to keep in mind that the anamnestic data and the objective examination data exclude other forms of headache. It is very important to have indications in the anamnestic data of a change in the side of the headache, since the presence of only one-sided headache for a long time requires a search for another cause of headaches.

Migraine with aura

• at least 2 attacks that meet criteria B-C;
• Migraine attacks have the following characteristics:
  • complete reversibility of one or more aura symptoms;
  • none of the aura symptoms lasts more than 60 minutes;
  • the duration of the “light” interval between the aura and the onset of headache is less than 60 minutes.

Depending on the characteristics of the aura and clinical manifestations of a migraine attack with aura, it is possible to determine the predominant involvement of a certain pool in the pathological process. Aura symptoms indicate a violation of microcirculation in the intracerebral territory of the cerebral arteries.

The most common aura is visual disturbances with visual field defects in the form of flickering scotoma: sparkling balls, dots, zigzags, lightning-like flashes starting in a strictly defined place. The intensity of photopsies increases over several seconds or minutes. Then photopsies are replaced by scotoma or the visual field defect expands to hemianopsia - right-sided, left-sided, upper or lower, sometimes quadrant. With repeated migraine attacks, visual disturbances are usually stereotypical. Provoking factors are bright light, its flickering, moving from darkness to a well-lit room, in other words, a loud sound, a strong smell.

Some patients experience visual illusions before a headache attack: all surrounding objects and people seem elongated ("Alice's syndrome" - a similar phenomenon is described in L. Carroll's book "Apis in Wonderland") or reduced in size, sometimes with a change in the brightness of their color, as well as with difficulties in perceiving their own body (agnosia, apraxia), a feeling of "already seen" or "never seen", disturbances in the perception of time, nightmares, trances, etc.

"Alice's syndrome" most often occurs with migraine in childhood. The cause of visual auras is discirculation in the posterior cerebral artery pool in the occipital lobe and ischemia in the adjacent areas of its blood supply (parietal and temporal lobes). The visual aura lasts 15-30 minutes, after which a pulsating pain in the frontal-temporal-gastric region occurs, increasing in intensity from half an hour to an hour and a half and accompanied by nausea, vomiting, and pale skin. The average duration of an attack of such a "classic" migraine is about 6 hours. Series of repeated attacks are common. Such migraine intensifies in the first and second trimesters of pregnancy. Less often, the aura is manifested by central or paracentral scotoma and transient blindness in one or both eyes. This is caused by a spasm in the central retinal artery system (retinal migraine). Occasionally, before a migraine attack, transient oculomotor disorders on one side (ptosis, pupil dilation, diplopia) are observed, which are associated with a disturbance of microcirculation in the trunk of the oculomotor nerve or with compression of this nerve in the wall of the cavernous sinus in vascular malformation. Such patients require targeted angiographic examination.

Relatively rarely, the aura manifests itself in transient paresis of the arm or hemiparesis in combination with hypoesthesia of the face, arm or the entire half of the body. Such hemiplegic migraine is associated with a disturbance of microcirculation in the basin of the middle cerebral artery (its cortical or deep branches). If the disturbance of microcirculation develops in the cortical branches of this basin in the dominant hemisphere (in the left in right-handers), then the aura manifests itself in partial or complete motor or sensory aphasia (aphasic migraine). Pronounced speech disorders in the form of dysarthria are possible with discirculation in the basilar artery. This can be combined with transient dizziness, nystagmus, unsteadiness when walking (vestibular migraine) or with pronounced cerebellar disorders (cerebellar migraine).

Also, rarely, girls aged 12-15 develop a more complex aura: it begins with visual impairment (bright light in the eyes is replaced by bilateral blindness within a few minutes), then dizziness, ataxia, dysarthria, tinnitus, short-term paresthesia around the mouth, in the arms, legs appear. A few minutes later, an attack of sharp pulsating headache appears, mainly in the occipital region, vomiting, and even loss of consciousness (syncope) is possible. In the clinical picture of such basilar migraine, there may be other signs of dysfunction of the brainstem: diplopia, dysarthria, alternating hemiparesis, etc.

Focal neurological symptoms persist from several minutes to 30 minutes and no more than an hour. With unilateral symptoms of brain function loss, intense headache usually occurs in the opposite half of the skull.

In some cases, the aura manifests itself in pronounced vegetative hypothalamic disorders such as sympathoadrenal, vagoinsular and mixed paroxysms, as well as in emotional-affective disorders with a feeling of fear of death, anxiety, and worry ("panic attacks"). These variants of aura are associated with microcirculation disorders in the hypothalamus and limbic-hypothalamic complex.

All types of migraine occur with different frequencies - from 1-2 times a week, month or year. Rarely, migraine status occurs - a series of severe, successive attacks without a distinct clear interval.

When examining the neurological status of migraine patients, mild signs of asymmetry in the functions of the cerebral hemispheres are often revealed (in two thirds - against the background of signs of latent left-handedness): asymmetry in the innervation of the facial muscles (revealed when smiling), deviation of the uvula, tongue, anisoreflexia of deep and superficial reflexes, predominantly vagotonic type of vegetative status (arterial hypotension, pallor and pastosity of the skin, acrocyanosis, tendency to constipation, etc.). Most patients with migraine have mental features with an accentuation of personality in the form of ambition, irritability, pedantry, aggressiveness with constant internal tension, increased sensitivity and vulnerability to stress, irritability, suspiciousness, touchiness, conscientiousness, pettiness, a tendency to obsessive fears, intolerance of the mistakes of others, signs of depression. Unmotivated dysphorias are characteristic.

During additional studies, signs of hypertensive-hydrocephalic changes in the form of increased vascular pattern and finger-like impressions are often found on craniograms. Kimmerle anomaly is detected in one third. EEG shows desynchronous and dysrhythmic manifestations. Computer and magnetic resonance tomograms often reveal asymmetry in the structure of the ventricular system.

A special express questionnaire has been developed for the rapid diagnosis of migraine.

• Have you had headaches in the last 3 months accompanied by the following symptoms:
  • nausea or vomiting? YES______; NO______;
  • intolerance to light and sounds? YES_____; NO______;
  • Has your headache limited your ability to work, study, or perform daily activities for at least 1 day? YES________; NO______.

93% of patients who answered “YES” to at least two questions suffer from migraines.

In most cases, no organic neurological symptoms are detected during an objective examination (noted in no more than 3% of patients). At the same time, almost all migraine patients are diagnosed with tension and pain in one or more pericranial muscles (the so-called myofascial syndrome). In the facial area, these are the temporal and masseter muscles, in the occipital area - the muscles attached to the skull, the muscles of the back of the neck and the shoulders (the "coat hanger" syndrome). Tension and painful muscle compaction become a constant source of discomfort and pain in the back of the head and neck, they can create the prerequisites for the development of concomitant tension headache. Often, during an objective examination of a patient with migraine, signs of autonomic dysfunction can be noted: palmar hyperhidrosis, discoloration of the fingers (Raynaud's syndrome), signs of increased neuromuscular excitability (Chvostek's symptom). As already mentioned, additional examinations for migraine are not informative and are indicated only in the case of an atypical course and suspicion of a symptomatic nature of migraine.

Characteristics of the objective status of patients during an attack and in the interictal state

Objective data during a cephalgic crisis in the study of the neurological status, as already indicated, depend on the form of migraine. At the same time, some additional studies during a cephalgic attack are of interest: computed tomography (CT), rheoencephalography (REG), thermography, the state of cerebral blood flow, etc. According to the thermogram, foci of hypothermia on the face are detected, coinciding with the projection of pain (more than 70% of cases); REG during an attack practically reflects all its phases: vasoconstriction - vasodilation, atony of the vessel walls (arteries and veins), more or less pronounced difficulty in arterial and venous blood flow. The changes are usually bilateral, but more severe on the side of pain, although the degree of expression of these changes does not always coincide with the degree of pain.

According to CT data, with frequent severe attacks, areas of low density may appear, indicating the presence of cerebral tissue edema, transient ischemia. In rare cases, M-echo indicates an expansion of the ventricular system and, as a rule, M-echo displacements are not determined. The results of ultrasound examination of blood flow during an attack are contradictory, especially when studying it in different basins. During an attack of pain on the affected side, in 33% of cases, the blood flow velocity increased in the common carotid, internal and external carotid arteries and decreased in the ophthalmic artery, while in 6% of patients, the opposite changes were observed. A number of authors note an increase in the velocity of cerebral blood flow mainly in the basin of the extracranial branches of the external carotid artery during pain.

In the somatic status, the most frequently detected (11-14%) pathology was that of the gastrointestinal tract: gastritis, peptic ulcer, colitis, cholecystitis. The latter served as a reason to identify the "three twins" syndrome: cholecystitis, headache, arterial hypotension.

In the vast majority of patients, a syndrome of vegetative-vascular dystonia of varying intensity was detected in the interictal period: bright red persistent dermographism (more pronounced on the side of pain), hyperhidrosis, vascular "necklace", tachycardia, fluctuations in arterial pressure, often in the direction of its decrease or persistent arterial hypotension; a tendency to allergic reactions, vestibulopathy, increased neuromuscular excitability, manifested by symptoms of Chvostek, Trousseau-Bahnsdorf, paresthesia.

Some patients showed microfocal neurological symptoms in the form of differences in tendon reflexes, hemihypalgesia, and in 10-14% of cases neuroendocrine manifestations of hypothalamic genesis were observed (cerebral obesity combined with menstrual irregularities, hirsutism). When studying the mental sphere, vivid emotional disorders were found, as well as some personality traits: increased anxiety, a tendency to subdepressive and even depressive tendencies, a high level of aspirations, ambition, some aggressiveness, demonstrative behavioral traits, a desire to focus on the recognition of others since childhood, and in some cases hypochondriacal manifestations.

The overwhelming majority of patients had a history of childhood psychogenia (single-parent family, conflictual relationships between parents) and psychotraumatic situations preceding the onset or exacerbation of the disease. Additional research in 11-22% of cases revealed moderately pronounced hypertensive-hydrocephalic changes in the craniogram (increased vascular pattern, sella turcica, etc.). The composition of the cerebrospinal fluid is usually within normal limits.

No changes were found in the EEG (although sometimes "flat" EEGs or dysrhythmic manifestations are encountered); echoencephalography is usually within normal limits. In the interictal period, REG shows a decrease or increase in vascular tone, mainly in the carotid arteries, an increase or decrease in their pulse blood filling and dysfunction (usually difficulty) of venous outflow; these changes are more pronounced on the side of the headache, although they may be absent altogether. No clear changes in cerebral blood flow were found in the interictal period, although the data on this account are contradictory (some describe a decrease, others - an increase), which is apparently due to the phase of the study - soon or in the late period after the attack. Most authors believe that angiospasm causes a decrease in regional cerebral blood flow for a fairly long period of time (a day or more).

In addition to the above-mentioned routine studies, the state of the afferent systems, which are known to be the systems that perceive and transmit pain sensations, is studied in migraine patients. For this purpose, evoked potentials (EPs) of various modalities are studied: visual (VEPs), auditory brainstem potentials (ABSPs), somatosensory (SSEPs), EPs of the trigeminal nerve system (due to the important role of the trigeminovascular system in the pathogenesis of migraine). Analyzing the provoking factors, it can be assumed that in cases of the priority role of emotional stress, it is the changes in the brain that cause a migraine attack. The indication of the role of the cold factor (cold, ice cream) gives reason to believe in the primary role of the trigeminal system in the initiation of a migraine attack. Tyramine-dependent forms of migraine are known - where, apparently, biochemical factors play a special role. Menstrual forms of migraine indicate the role of endocrine factors. Naturally, all these and other factors are realized against the background of genetic predisposition.

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Differential diagnosis of migraine

There are a number of medical conditions that can mimic migraine attacks.

I. In cases of severe migraines with unbearable headaches, nausea, vomiting, dizziness, night attacks, it is first necessary to exclude organic pathology of the brain:

1. tumors,
2. abscesses;
3. acute inflammatory diseases, especially those accompanied by cerebral edema, etc.

In all these cases, attention is drawn to the different nature of the headache and its course, as a rule, the absence of the above-mentioned factors characteristic of migraine and the positive results of the corresponding additional studies.

II. Of greatest importance are headaches based on vascular pathology of the brain. Firstly, these are aneurysms of the cerebral vessels, the rupture of which (i.e. the occurrence of subarachnoid hemorrhage) is almost always accompanied by an acute headache. This is especially important to keep in mind in the case of migraine with aura. The most significant in this regard is the ophthalmoplegic form of migraine, which is often caused by an aneurysm of the vessels of the base of the brain. The development of the clinical picture in the future: severe general condition, meningeal symptoms, neurological symptoms, composition of the cerebrospinal fluid and data from additional paraclinical studies help in the correct diagnosis.

III. It is important to conduct differential diagnosis also with the following diseases:

1. Temporal arteritis (Horton's disease). Common features with migraine: local pain in the temple area, sometimes radiating to the entire half of the head, often aching, aching, but constant in nature, but can increase in attacks (especially with tension, coughing, jaw movements). Unlike migraine, palpation reveals compaction and increased pulsation of the temporal artery, its soreness, dilation of the pupil on the side of pain; decreased vision; more common in older age than migraine. Subfebrile temperature, increased ESR, leukocytosis are observed, there are signs of damage to other arteries, especially the arteries of the eye. It is regarded as a local disease of connective tissue, local collagenosis; specific histological signs are giant cell arteritis.
2. Tolosa-Hunt syndrome (or painful ophthalmoplegia), resembling migraine in the nature and localization of pain. Acute pain of a burning, tearing nature, localized in the frontal-orbital region and inside the orbit, lasts for several days or weeks with periodic intensification, accompanied by damage to the oculomotor nerve (which is important to consider when comparing with the ophthalmoplegic associated form of migraine). The process also involves the nerves passing through the superior orbital fissure: abducens, trochlear, orbital branch of the trigeminal nerve. Pupillary disorders are detected, caused by denervation hypersensitivity of the capillary muscle, which is confirmed by the adrenaline-cocaine test. No other pathology is revealed by additional studies. To date, the cause has not been clearly established: there is an opinion that this syndrome occurs due to compression of the siphon area by an aneurysm at the base of the brain. However, most authors believe that the cause is carotid intracavernous periarteritis in the cavernous sinus - superior orbital fissure area or their combination. Subfebrile temperature, moderate leukocytosis and increased ESR, as well as the effectiveness of steroid therapy, indicate regional periarteritis.

IV. The next group is diseases caused by damage to organs located in the head and face area.

1. Headaches associated with eye pathology, mainly glaucoma: sharp, acute pain in the eyeball, periorbitally, sometimes in the temple area, photophobia, photopsies (i.e. the same nature and localization of pain). However, other signs of migraine pain are absent, and most importantly, intraocular pressure is increased.
2. The following forms are also significant:
   1. bilateral pulsating headache may accompany vasomotor rhinitis, but without typical attacks: there is a clear connection with the occurrence of rhinitis, nasal congestion, caused by certain allergic factors;
   2. in sinusitis (frontal sinusitis, maxillary sinusitis) the pain is usually local, although it can spread to the "whole head", does not have an attack-like course, occurs daily, increases from day to day, intensifies, especially during the daytime, and lasts for about an hour, does not have a pulsating character. Typical rhinological and radiological signs are revealed;
   3. with otitis, there may also be hemicrania, but of a dull or shooting nature, accompanied by symptoms characteristic of this pathology;
   4. Costen's syndrome may cause sharp, intense pain in the temporomandibular joint, sometimes affecting the entire half of the face; the pain is not pulsating or paroxysmal, and is provoked by chewing or talking. There is clear pain upon palpation in the joint area, the cause of which is a joint disease, malocclusion, or poor prosthesis.

A number of authors distinguish a syndrome of vascular facial pain, or, as it is more often called, carotidynia. It is caused by damage to the periarterial plexuses of the external carotid artery, the carotid node and can manifest itself in two forms:

1. Acute onset in young or middle age; pulsating burning pain appears in the cheek, submandibular or temporomandibular region, tenderness is noted when palpating the carotid artery, especially near its bifurcation, which can increase facial pain. The pain lasts 2-3 weeks and, as a rule, does not recur (this is a very important feature that distinguishes it from the facial form of migraine).
2. Another form of carotidynia is described, more often in elderly women: attacks of pulsating, burning pain in the lower half of the face, lower jaw, lasting from several hours to 2-3 days, recurring with a certain periodicity - 1-2 times a week, month, six months. In this case, the external carotid artery is sharply tense, painful on palpation, its increased pulsation is observed. Age, the nature of pain, the absence of heredity, the presence of objective vascular changes during external examination and palpation allow us to distinguish this form from true migraine. There is an opinion that the nature of this suffering is infectious-allergic, although there is no fever and blood changes, and no significant effect of hormonal therapy is noted (it is relieved by analgesics). The genesis of this syndrome is not entirely clear. It is possible that any harmfulness - chronic irritation, local inflammatory processes, intoxication - can underlie carotidynia. We must not forget about the group of craniofacial neuralgias, which primarily include trigeminal neuralgia, as well as a number of other, less common neuralgias: occipital neuralgia (neuralgia of the greater occipital nerve, suboccipital neuralgia, neuralgia of the Arnold nerve), lesser occipital, glossopharyngeal nerves (Weisenburg-Sicard syndrome), etc. It is necessary to remember that, unlike migraines, all these pains are characterized by severity, "lightning-fast", the presence of trigger points or "trigger" zones, certain provoking factors and the absence of typical signs of migraine pains (mentioned above).

It is also necessary to differentiate migraine without aura from tension headache, which is one of the most common forms of headache (more than 60% according to world statistics), especially from its episodic form, lasting from several hours to 7 days (while in the chronic form headaches are daily) from 15 or more days, in a year - up to 180 days). When conducting a differential diagnosis, the following diagnostic criteria for tension headache are taken into account:

1. localization of pain - bilateral, diffuse with a predominance in the occipital-parietal or parietal-frontal regions;
2. nature of pain: monotonous, squeezing, like a “helmet”, “helmet”, “hoop”, almost never pulsating;
3. intensity - moderate, sharply intense, usually not increasing with physical exertion;
4. accompanying symptoms: rarely nausea, but more often loss of appetite up to anorexia, rarely photo- or phonophobia;
5. a combination of tension headache with other algic syndromes (cardialgia, abdominalgia, dorsalgia, etc.) and psychovegetative syndrome, with emotional disorders of a depressive or anxious-depressive nature predominating; pain in the pericranial muscles and muscles of the collar zone, neck, and shoulders.

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