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Migraine symptoms
Last reviewed: 04.07.2025

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Migraine symptoms are characterized by typical migraine pain, which is often pulsating and pressing in nature, usually affects half of the head and is localized in the forehead and temple area, around the eye. Sometimes the headache can begin in the occipital region and spread forward to the forehead area. In most patients, the side of the pain can change from attack to attack.
Migraine is not characterized by a strictly one-sided nature of pain; it is considered an indication for additional examination, the purpose of which is to exclude organic damage to the brain!
The duration of an attack in adults usually ranges from 3-4 hours to 3 days and averages 20 hours. With episodic migraine, the frequency of attacks varies from one attack every 2-3 months to 15 per month, the most typical frequency of attacks is 2-4 per month.
Some patients may experience a prodrome (precursor of headache) several hours or even days before the onset of migraine symptoms, including various combinations of symptoms such as weakness, mood deterioration, difficulty concentrating, and sometimes, on the contrary, increased activity and appetite, tension in the neck muscles, and increased sensitivity to light, sound, and olfactory stimuli. After the attack, some patients experience drowsiness, general weakness, and pale skin for some time, and yawning often occurs (postdrome).
Associated symptoms of migraine
A migraine attack is usually accompanied by nausea, increased sensitivity to bright light (photophobia), sounds (phonophobia) and smells, and loss of appetite. Vomiting,dizziness, and fainting may occur somewhat less frequently. Due to severe photo- and phonophobia, most patients prefer to be in a darkened room during an attack, in a calm, quiet environment. Migraine pain is aggravated by normal physical activity, such as walking or climbing stairs. Children and young patients typically experience drowsiness, and after sleep, the headache often disappears without a trace.
The main symptoms of migraine are:
- severe pain on one side of the head (temple, forehead, eye area, back of the head), alternating sides of the headache;
- typical accompanying symptoms of migraine: nausea, vomiting, photophobia and phonophobia;
- increased pain with normal physical activity;
- pulsating nature of pain;
- typical provoking factors;
- significant limitation of daily activities;
- migraine aura (15% of cases);
- headache attacks are poorly relieved by conventional analgesics;
- hereditary nature of migraine (60% of cases).
In 10-15% of cases, the attack is preceded by a migraine aura - a complex of neurological symptoms that occur immediately before a migraine headache or at its onset. Based on this feature, a distinction is made between migraine without aura (previously "simple migraine") and migraine with aura (previously "associated migraine"). Aura and prodromal symptoms of migraine should not be confused. Aura develops within 5-20 minutes, lasts no more than 60 minutes and completely disappears with the onset of the pain phase. Most patients are characterized by migraine attacks without aura, migraine aura never develops or occurs very rarely. At the same time, patients with migraine with aura may often have attacks without aura. In rare cases, a migraine attack does not occur after aura (the so-called aura without headache).
The most common is the visual, or "classical", aura, which manifests itself in various visual phenomena: photopsia, floaters, one-sided loss of the visual field, flickering scotoma or a zigzag luminous line ("fortification spectrum"). Less common are one-sided weakness or paresthesia in the limbs (hemiparesthetic aura), transient speech disorders, distortion of the perception of the size and shape of objects ("Alice in Wonderland" syndrome).
Migraine is closely related to female sex hormones. Thus, menstruation becomes a trigger for an attack in more than 35% of women, and menstrual migraine, in which attacks occur within 48 hours after the onset of menstruation, occurs in 5-10% of patients. In two thirds of women, after some increase in attacks in the first trimester of pregnancy, significant relief of headaches is observed in the second and third trimesters, up to the complete disappearance of migraine attacks. Against the background of taking hormonal contraceptives and hormone replacement therapy, 60-80% of patients note a more severe course of migraine.
Frequency and course of migraine attacks
All the described forms of migraine (except cluster migraines) occur, as a rule, with different frequencies - from 1-2 times a week or month to 1-2 times a year. The course of a migraine attack consists of three phases.
The first phase is prodromal (expressed in 70% of patients) - clinically manifests itself depending on the form of migraine: with a simple one - in a few minutes, less often hours, mood and performance decrease, lethargy, apathy, drowsiness appear, and then increasing headache; with a migraine with aura, the onset is - depending on the type of aura, which can precede an attack of pain or develop at its height.
The second phase is characterized by intense, predominantly pulsating, less often bursting, aching headache in the frontal, periorbital, temporal, less often parietal regions, as a rule, it is one-sided, but sometimes affects both halves of the head or can alternate - left or right.
At the same time, some features are noted depending on the lateralization of pain: left-sided pain is more intense, often occurs at night or in the early morning, right-sided pain is 2 times more often accompanied by vegetative crises, facial edema and occurs at any time of the day. During this phase, pallor of the skin of the face, hyperemia of the conjunctiva, especially on the side of pain, nausea (in 80%), and sometimes vomiting are noted.
The third phase is characterized by a decrease in pain, general lethargy, fatigue, and drowsiness. Sometimes the course of an attack has the so-called migraine status (1-2% of cases), when attacks of pain can follow one another during the day or several days. When accompanied by repeated vomiting, dehydration of the body and hypoxia of the brain occur. Focal neurological symptoms of migraine and seizures often appear. All this requires urgent therapeutic correction and hospitalization of the patient.
The most significant clinical differences between migraine and tension headache
Symptoms |
Migraine |
Tension headache |
Nature of pain |
Pulsating |
Squeezing, squeezing |
Intensity |
Tall |
Weak or medium |
Localization |
Hemicrania (frontal-temporal zone with the periorbital region), less often bilateral |
Bilateral diffuse pain |
Time of appearance |
At any time, often after waking up; often an attack occurs during relaxation (weekends, vacation, after resolving a stressful situation) |
At the end of the working day, often following emotional stress |
Duration of headache |
From several hours to a day |
Many hours, sometimes days |
Behavior during an attack |
The patient avoids movement, prefers to lie with his eyes closed if possible, activity increases the pain |
The patient continues his normal activities. |
Factors that relieve headaches |
Sleep, vomiting at the height of pain |
Mental relaxation, relaxation of pericranial muscles |
Clinical types of migraine
Some patients may experience vegetative symptoms of migraine during an attack: increased heart rate, facial swelling, chills, hyperventilation symptoms (shortness of breath, suffocation), lacrimation, pre-fainting condition, hyperhidrosis. In 3-5% of patients, vegetative symptoms are so numerous and vivid that they reach the level of a typical panic attack with a feeling of anxiety and fear. This is the so-called vegetative, or panic, migraine.
In most patients (60%), attacks occur exclusively during the daytime, i.e. while awake, 25% of patients are bothered by both attacks during wakefulness and attacks that wake them up at night. No more than 15% of patients suffer exclusively from migraine during sleep, i.e., pain attacks occur during night sleep or upon awakening in the morning. Research has shown that the main prerequisite for the transformation of migraine during wakefulness into migraine during sleep is the presence of severe depression and anxiety.
In 50% of women suffering from migraine, there is a close connection between attacks and the menstrual cycle. Most attacks associated with menstruation are migraine attacks without aura. It is proposed to divide such attacks into true menstrual (catemenial) migraine (when attacks occur only in the "perimenstrual" period) and migraine associated with menstruation (when attacks can be caused not only by menstruation, but also by other migraine triggers: weather changes, stress, alcohol, etc.). True menstrual migraine occurs in no more than 10% of women. The main mechanism for the development of a catamenial migraine attack is considered to be a drop in estrogen levels in the late luteal phase of the normal menstrual cycle (usually during ovulation).
The diagnostic criteria for menstrual migraine are as follows.
- True menstrual migraine.
- Headache attacks in a menstruating woman that meet the criteria for migraine without aura.
- Attacks occur exclusively on days 1-2 (within days -2 to +3) in at least two out of three menstrual cycles and do not occur during other periods of the cycle.
- Menstrual-related migraine.
- Headache attacks in a menstruating woman that meet the criteria for migraine without aura.
- Attacks occur on days 1-2 (within the range of -2 to +3 days) in at least two out of three menstrual cycles, and also during other periods of the cycle.
Chronic migraine. In 15-20% of patients with episodic migraine at the onset of the disease, the frequency of attacks increases over the years until daily headaches appear, the nature of which gradually changes: the pains become less severe, become constant, and may lose some typical migraine symptoms. This type, which meets the criteria for migraine without aura, but occurs more often than 15 days a month for 3 months or longer, is called chronic migraine (previously, the term "transformed migraine" was used). Along with some other disorders (migraine status, migraine infarction, migraine-induced attack, etc.), chronic migraine was first included in the ICGB-2 section "Complications of migraine".
Chronic tension headache and chronic migraine are the main clinical types of chronic daily headache. It has been shown that two main factors play a role in the transformation of episodic migraine into a chronic form: abuse of painkillers (the so-called drug abuse) and depression, which usually occurs against the background of a chronic psychotraumatic situation.
The most important criteria for establishing a diagnosis of chronic migraine are the following:
- daily or almost daily headache (more than 15 days a month) for more than 3 months lasting more than 4 hours/day (without treatment);
- history of typical migraine attacks that began before age 20;
- an increase in the frequency of headaches at a certain stage of the disease (transformation period);
- reduction in the intensity and severity of migraine symptoms (nausea, photo- and phonophobia) as headaches become more frequent;
- the likelihood of the persistence of typical migraine provoking factors and the one-sided nature of the pain.
It has been shown that migraine is often combined with other disorders that have a close pathogenetic (comorbid) relationship with it. Such comorbid disorders significantly aggravate the course of an attack, worsen the condition of patients in the interictal period and, in general, lead to a significant deterioration in the quality of life. Such disorders include depression and anxiety, autonomic disorders (hyperventilation manifestations, panic attacks), sleep disturbances, tension and soreness of the pericranial muscles, gastrointestinal disorders (biliary dyskinesia in women and gastric ulcer in men). Comorbid migraine disorders also include concomitant tension headaches, which often bother patients between migraine attacks. Treatment of comorbid disorders that disrupt the condition of patients in the interictal period is one of the goals of preventive therapy for migraine. In addition, there is a suspected comorbid relationship between migraine and neurological disorders such as epilepsy, stroke, Raynaud's syndrome and essential tremor.
With a separate "basilar artery migraine" there are pulsating pains in the back of the head, visual impairment, dysarthria, balance disorders, nausea, and disturbances of consciousness.
In the ophthalmological form, migraine occurs with lateral pain, diplopia, nausea and vomiting.
A condition called migraine equivalent has been described, in which painful neurological or symptomatic attacks occur without the headache itself.
The symptoms of migraine with aura depend on the vascular basin in which the pathological process occurs:
- ophthalmic (i.e. what was previously called classical migraine), beginning with bright photopsies in the left or right visual fields ("flickering scotomas" according to J. Charcot) followed by short-term loss of visual fields or simply a decrease in it - a "veil" before the eyes with the development of acute hemicrania. The cause of visual auras is apparently discirculation in the posterior cerebral artery basin;
- retinal, which manifests itself as central or paracentral scotoma and transient blindness in one or both eyes. It is assumed that visual disturbances are caused by circulatory disorders in the system of branches of the central retinal artery. In an isolated form, retinal migraine is quite rare, it can be combined or alternate with attacks of ophthalmic migraine or migraine without aura;
- ophthalmoplegic, when at the height of the headache or simultaneously with it, various oculomotor disorders occur: unilateral ptosis, diplopia as a result of partial external ophthalmoplegia, which may be due to:
- compression of the oculomotor nerve by dilated and swollen carotid artery and cavernous sinus (it is known that this nerve is most susceptible to such compression due to its topography) or
- spasm and subsequent swelling of the artery that supplies it with blood, which leads to ischemia of the oculomotor nerve and also manifests itself with the symptoms described above;
- paresthetic, which usually begins with the fingers of one hand, then affects the entire upper limb, face and tongue, and it is paresthesia in the tongue that most authors regard as migraine [Olsen, 1997]. In terms of frequency of occurrence, sensory disorders (paresthesia) usually rank second after ophthalmic migraine. In hemiplegic migraine, hemiparesis is part of the aura. Approximately half of families with familial hemiplegic migraine have been found to have a link with chromosome 19 [Joutel et al., 1993]. Combined forms may be observed (hemiparesis, sometimes with hemianesthesia, paresthesia on the side opposite to the headache, or very rarely on the same side);
- aphasic - transient speech disorders of various natures: motor, sensory aphasia, less often dysarthria;
- vestibular (dizziness of varying severity);
- cerebellar (various coordination disorders);
- Quite rare - basilar form of migraine; most often develops in girls aged 10-15 years. It begins with visual impairment: a sensation of bright light in the eyes, bilateral blindness for several minutes, then dizziness, ataxia, dysarthria, tinnitus. In the middle of the attack, paresthesia develops in the arms and legs for several minutes; then - a sharp pulsating headache; in 30% of cases, loss of consciousness is described.
The symptoms indicated are based on narrowing of the basilar artery and/or its branches (posterior or posterior cerebellar, internal auditory, etc.); disturbance of consciousness is caused by the spread of the ischemic process to the reticular formation of the brainstem. Diagnosis is usually aided by a family history, the paroxysmal nature of typical headaches, complete regression of the described symptoms, and the absence of any pathology in additional studies. Subsequently, upon reaching puberty, these attacks are usually replaced by migraine without aura. Patients often describe an aura that is not followed by a headache. This type of "migraine without headache" is more common in men.
In recent decades, another special form of unilateral vascular headaches has been described - cluster headache, or cluster syndrome (synonyms: Harris migraine neuralgia, Horton's histamine headache). Unlike ordinary migraine, this form is more common in men (the ratio of men to women is 4:1), and young or middle-aged people (30-40 years) are affected. An attack is manifested by severe pain in the eye area, spreading to the periorbital and temporal regions, accompanied by lacrimation and rhinorrhea (or nasal congestion) on the side of the headache, more often on the left; the pain can radiate to the neck, ear, arm, and is sometimes accompanied by Horner's syndrome (ptosis, miosis). If with ordinary migraine patients try to lie down and prefer peace, quiet, and a darkened room, then with cluster headache they are in a state of psychomotor anxiety. Attacks last from several minutes (10-15) to 3 hours (the average duration of a pain attack is 45 minutes). Attacks occur in series - from 1 to 4, but not more than 5 per day. Often occur at night, usually at the same time. Last 2-4-6 weeks, then disappear for several months or even years. Hence the name "cluster" headache. Nausea and vomiting occur only in 20-30% of cases. Exacerbation occurs more often in autumn or winter. The appearance of patients is noteworthy: tall, athletic build, transverse folds on the forehead, "lion" face. By nature, they are often ambitious, prone to arguments, outwardly aggressive, but internally helpless, timid, indecisive ("the appearance of a lion, and the heart of a mouse"). Hereditary factors in this form of migraine are noted only in a small number of cases.
There are two forms of cluster headache: episodic (the period of remission is several months or even years, occurs in 80% of cases) and chronic (the duration of the “light” interval between pain attacks is less than 2 weeks).
The so-called "chronic paroxysmal hemicrania" (CPH) is quite close to the described form in clinical manifestations [Sjaastad, 1974]: daily attacks of intense burning, boring, less often - pulsating pain, always one-sided, localized in the orbital-frontal-temporal region. The duration of one paroxysm is 10-40 minutes, but their frequency can reach 10-20 per day. The attacks are accompanied by lacrimation, redness of the eye and rhinorrhea or nasal congestion on the side of pain. Unlike cluster syndrome, women predominate (8:1), there are no long "light" intervals, no "bundles". A "dramatic" effect is observed with the use of indomethacin: attacks that have lasted for many years pass within a few days after treatment.
Complications of migraine
Early clinical observations and especially recent advances in the development of modern research methods (computer tomography, evoked potentials, nuclear magnetic resonance) suggest that in some cases frequent, prolonged attacks of migraine attacks may serve as a prerequisite for severe vascular lesions of the brain, most often of the ischemic stroke type. According to the data of the computed tomography (CT) performed in this case, foci of low density were detected in the corresponding zones. It should be noted that vascular accidents most often occur in the posterior cerebral artery basin. The authors consider the presence in the anamnesis of such patients of frequent migraine attacks with acutely developing headache and subsequent ischemic process as a "catastrophic" form of migraine. The basis for the assumption of a common pathogenesis of these conditions (migraine, transient ischemic attacks) is the similarity of discirculation in various vascular basins of the brain (according to angiography and CT) in the above processes.
In addition, the follow-up study of 260 patients who had migraine attacks in the past revealed that 30% of them subsequently developed hypertension. There are indications of a combination of migraine with Raynaud's phenomenon (up to 25-30%), which reflects disturbances in diffuse neuroregulatory vascular mechanisms.
The literature also describes patients with migraine attacks who then developed rare epileptic seizures. Subsequently, the above-mentioned paroxysmal states alternated. EEG showed epileptic activity. Certain significance is given to brain hypoxia caused by frequent severe migraine attacks, although the genesis of these states is not entirely clear. There are indications when mitral valve prolapse and migraine symptoms are combined (20-25%). The issue of the possible risk of cerebrovascular disorders with a combination of the above processes is discussed. Observations are given on the combination of migraine with Tourette's disease (in 26% of the latter), which is explained by the presence of a serotonin metabolism disorder in both diseases.