Migraine - how to distinguish it from a regular headache? And what to do with the painful symptoms?

Migraine is a very common, multifactorial, relapsing hereditary neurovascular headache disorder. More than a billion people on Earth suffer from it.

Migraine attacks often begin with a conventional first phase, the warning signs (prodrome), then progress to a conventional second phase, auras (transient focal neurological symptoms), the origin of which is believed to be associated with the hypothalamus, brain stem and cortex. The third phase is, strictly speaking, the headache phase. Its pulsatile nature increases with increased intracranial pressure, resulting in nausea, vomiting, and abnormal sensitivity to light, noise, and smell.

Migraines may also be accompanied by abnormal skin sensitivity (allodynia) and muscle soreness. Thus, tracing all the symptoms from phase to phase, we can conclude that during a migraine attack, a whole complex of neural systems of the brain function abnormally.

It's safe to say that the brain of a person with migraines is different from the brain of a person without migraines. A 2015 Journal of Neuroscience article by Rami Burshtein and his co-authors is devoted to a detailed analysis of this thesis. It will be discussed in our retelling. We are aware that this article is primarily for doctors, but we also want to educate the medical community to the best of our ability. Therefore, we enter the appropriate tag.

general description

Migraine without aura (G43.0) is a chronic relapsing disease characterized by sudden attacks of intense pain in the head, often pulsating in one part of the head.
Prevalence: 3.4 per 100 thousand people. Migraine often debuts between the ages of 20 and 35.

There are unilateral (up to 99%) and, rarely, bilateral headache localizations. As the disease progresses, the side of the headache may change.

A migraine attack is triggered by stress, weather changes, lack of sleep or excess sleep, eating certain foods (chocolate, nuts, cheese), drinking alcohol, and fasting. In women, headache attacks may be associated with the menstrual cycle. There may be a hereditary history of headaches.

Mechanism of disease

A mechanistic search for a common denominator in the symptoms and characteristics of migraine strongly points to a genetic predisposition to generalized neuronal hyperexcitability. Increasing evidence of changes in brain structure and function following repeated migraine attacks may explain disease progression.

Prodrome

Prodromes are symptoms that precede the aura and headache (in some people, migraine attacks present with a prodrome and headache). Examination of the symptoms most commonly reported by patients indicates potential involvement of the hypothalamus (fatigue, depression, irritability, food cravings, and yawning), the brainstem (muscle soreness and stiff neck), and the cerebral cortex (abnormal sensitivity to light, sound, and smell), as well as the limbic system (depression and anhedonia) in the prodromal phase of a migraine attack. Given that symptoms such as fatigue, yawning, food cravings, and transient mood changes occur naturally in all people, it is important that we understand how their occurrence causes headaches in migraine patients and does not cause them in those without.

The hypothalamus has recently received much attention as it plays a key role in many aspects of human circadian rhythms (wake-sleep cycle, body temperature, food intake and hormonal fluctuations) and homeostasis.

Because the migraine brain is extremely sensitive to deviations from homeostasis, uncovering the mechanisms by which hypothalamic and brainstem neurons can trigger headache pain is central to our ability to develop treatments that can intercept headache pain during the prodromal phase. It has been suggested that hypothalamic neurons that respond to changes in physiological and emotional homeostasis may activate meningeal nociceptors (a nociceptor is a neuron that carries pain sensations), changing the balance between parasympathetic and sympathetic tone in the meninges.

Another proposal implies that hypothalamic and brainstem neurons (regulators of responses to perturbations of homeostasis) may lower the threshold for transmission of incoming signals from the trigeminovascular pathway through the thalamus to the cortex. This proposal is based on an understanding of how the thalamus selects, enhances, and prioritizes the information it ultimately transmits to the cortex, and how hypothalamic and brainstem nuclei regulate relay (direct, non-collateral) thalamocortical neurons.

Major signal pathways to thalamic trigeminal neurons that appear to trigger migraine

Cortical spreading depression

Clinical and preclinical studies indicate that migraine aura is caused by cortical spreading depression (CSD), a slowly propagating wave of depolarization/excitation followed by hyperpolarization/inhibition in cortical neurons and glial cells.

Although the specific processes that initiate CSD in humans are not known, mechanisms that trigger inflammatory molecules as a result of emotional or physiological stress, such as lack of sleep, may play an important role. In the cortex, the initial membrane depolarization is associated with a large outflow of potassium; influx of sodium and calcium; the release of glutamate, ATP and hydrogen ions, as well as the launch of a cascade of pro-inflammatory reactions. The work of pro-inflammatory molecules in the meninges, as well as calcitonin gene-related peptide (CGRP) and nitric oxide, may be the link between aura and headache.

Clinical picture

A migraine attack may be preceded by worsening mood, irritability, anxiety, decreased performance, tearfulness, drowsiness, changes in appetite, increased sensitivity to loud sounds, increased lighting. The duration of an attack of unilateral intense headache of a pulsating nature is 4–72 hours. More often, pain appears first in the back of the head and spreads forward to the frontal region (70%).

Pain in the head interferes with the performance of usual activities and intensifies with adequate physical activity (walking). During a migraine attack, patients develop high sensitivity to bright light, noise, and strong odors. Typical pain behavior - patients try to hide, take a motionless position in a darkened, quiet room. Nausea (70%) and vomiting (30%) are observed. Headache attacks are sometimes accompanied by swelling of the face, pale skin, lacrimation, and rapid heartbeat. Taking analgesics does not relieve headaches. Remissions occur after treatment for several weeks or months.

An objective examination of the patient reveals general hyperesthesia, photophobia/phonophobia/osmophobia, cerebral syndrome, tension and soreness of the pericranial muscles, emotional-volitional disorders and autonomic dysfunction.

Why does migraine occur?

The reasons why migraine with aura occurs, as well as the mechanism of development of the pathological condition, are not fully understood. Experts have put forward a number of assumptions, each of which has grounds and right to exist.

The main causes of migraine with aura – theories:

  • decreased vascular functionality - a sudden narrowing or spasm of blood channels in the brain provokes ischemia, against the background of which an aura develops. Subsequent vasodilation causes cephalalgia;
  • change in blood composition - due to the changed properties of platelets, blood cells stick together. This promotes the production of the hormone serotonin and vasospasm, which provokes an aura. As the volume of the substance decreases, the channels expand, causing pain;
  • decreased nervous activity – creeping depression causes ischemic and vascular changes in the brain. The narrowing and further expansion of the blood channels leads to the appearance of an aura and subsequent headaches;
  • disruption of the relationship between blood vessels and nerves - the dominant theory according to which migraine with aura is the result of a failure of connections between the trigeminal nerve and the blood channels of the brain;
  • hereditary predisposition - statistical studies show that the risks of migraine in people whose family already has cases of the disease are very high.

The onset of a migraine can be caused by the impact of external irritants on the body of a diagnosed person. In each specific case they are individual. Experts highlight a number of main points that need to be paid attention to. In 5-10% of cases, provocateurs are specific and even unusual. In another 5% of cases, exacerbation develops for no apparent reason.

Provoking factors – triggers – of a migraine attack:

  • exposure to external causes - weather changes, bright lights, strong odors, loud sounds, cigarette smoke;
  • lifestyle features - stress, overwork, daytime sleep, jet lag, bad habits, lack of physical activity or too intense exercise without preparation, dehydration;
  • drinks and food – any preservatives or food additives, caffeine, marinades and smoked meats, chocolate, citrus fruits, seafood delicacies;
  • taking medications - this can be any medication, but most often attacks are provoked by taking oral contraceptives and other hormones;
  • brain injuries – the statute of limitations does not matter;
  • changes in hormonal levels - pathological and physiological (pregnancy, menopause, menstruation) processes;
  • “Weekend” attack, an exacerbation can begin after a vacation, on the first working day.

The listed points do not necessarily become the cause of an attack, even in cases where they have already provoked it. In the same way, there is no guarantee that the trigger will not work if the body previously reacted normally to the stimulus. Prevention involves minimizing the impact of all of these points.

Read why the disease occurs in men here.

Diagnosis of migraine without aura

  • Computer and magnetic resonance imaging of the brain (optional in vascular mode).
  • Electroencephalography is necessary to exclude organic brain damage.

Differential diagnosis:

  • Tension headache.
  • Cluster headache.
  • Chronic paroxysmal hemicrania.
  • Headache due to vascular lesions of the brain (vascular malformations, ischemic and hemorrhagic strokes), tumors and infectious lesions of the central nervous system.

Pain for no reason

Migraine is a disorder in the areas of the brain that are responsible for the perception of pain. For example, during an inflammatory process in an untreated tooth, irritation of the endings of the trigeminal nerve occurs. Pain impulses enter the nucleus of the trigeminal nerve, which is located in the brain, and from there into the gray matter of the cerebral cortex, where the realization occurs that the source of the problem is a holey tooth. All pain that occurs in the head area goes exactly this way.

With migraine, the nucleus of the trigeminal nerve is activated, which begins to send pain impulses to the cortex, despite the fact that the nerve endings are in perfect order. It turns out that the headache seems to hurt on its own, because there is no source of pain (pinched nerve fibers, vascular spasm, inflammation).

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Why does my face hurt? Which doctor will make the correct diagnosis?

The exact cause of such violations has not yet been established. Although it is known that migraine is hereditary (the disease is usually transmitted through the female line), a specific gene or set of genes responsible for the development of migraine has not yet been discovered.

Treatment of migraine without aura

  • Drugs whose action is aimed at stopping an attack (analgesics, antiemetics, triptans, ergotamine-containing drugs) and preventing attacks (b-blockers, anticonvulsants, antidepressants, Ca2 channel blockers).
  • Non-drug methods: psychotherapy, biofeedback, acupuncture; post-isometric relaxation, massage, manual therapy.
  • Preventing exposure to provoking factors.

Treatment is prescribed only after confirmation of the diagnosis by a medical specialist.

Essential drugs

There are contraindications. Specialist consultation is required.

  • Sumatriptan (a drug with antimigraine activity). Dosage regimen: orally for the relief of acute migraine attacks, adults are prescribed a dose of 50 mg, in some cases - 100 mg. The tablets should be swallowed whole with water.
  • Naratriptan (a drug with antimigraine activity). Dosage regimen: orally, during an attack, once 2.5 mg. If migraine symptoms resume, do it again no earlier than 4 hours later. The maximum daily dose is 5 mg.
  • Paracetamol (analgesic, antipyretic). Dosage regimen: for adults to relieve pain orally at a dose of 500 mg - 1000 mg up to 4 times a day.
  • Voltaren (non-steroidal anti-inflammatory drug). Dosage regimen: for migraine attacks, IM at a dose of 75 mg, as early as possible after the onset of the attack, followed by the use of suppositories at a dose of up to 100 mg on the same day, if required. The total daily dose should not exceed 175 mg on the first day.
  • Motilium (central acting antiemetic). Dosage regimen: orally before meals, adults and adolescents over 12 years of age, 10-20 mg 3 or 4 times a day. The maximum daily dose is 80 mg.

General information

Migraine with aura is one of the forms of primary cephalgia (headache), i.e. it occurs completely independently, and not as one of the symptoms of any disease. According to experts in the field of clinical neurology, migraine occurs in 18% of women and 6% of men. About a quarter of migraine cases are migraine with aura. The aura is one that appears within 10-60 minutes. before an attack of migraine cephalgia, temporary visual, sensory, speech disturbances, changes in taste, smell or auditory perception. As a rule, a migraine aura lasts no more than 60 minutes. Sometimes it does not lead to headaches.

Among the classic cases of migraine with aura, migraine attacks with so-called prolonged aura can be observed. An extended aura is said to occur when at least one of its symptoms lasts more than 60 minutes, but the data from a neurological examination and neuroimaging methods do not reveal any pathology. If a migraine aura lasts more than 7 days, then it is highly likely that a complication such as a migraine infarction will develop, the presence of which is confirmed using neuroimaging methods.

Recommendations

A consultation with a neurologist and magnetic resonance imaging of the brain are recommended.

Leading specialists and institutions for the treatment of this disease in Russia:
Doctor of Medical Sciences, Head of the Department of Russian State Medical University, Professor, Academician of the Russian Academy of Medical Sciences Gusev E.I.
Leading specialists and institutions for the treatment of this disease in the world:
G. AVANZINI, Italy.

Features of aura development

The condition is characterized by sudden development. The duration of the aura lasts from several seconds to several minutes. Sometimes others don’t even notice changes in a person’s condition. In most cases, connection with the outside world is maintained, although there may not be a reaction to external stimuli. At the same time, the patient remembers the content of his condition.

Then an attack develops: convulsions are accompanied by loss of consciousness. Or, sometimes, a person returns to a normal state without having an attack.

Thus, the appearance of an aura does not always indicate the development of a seizure. And the onset of an attack in epilepsy, in turn, is not always preceded by an aura. Most often, the condition occurs during generalized convulsive seizures, when the pathology affects areas of the brain in both hemispheres.

A neurologist can diagnose aura in epilepsy using an EEG. The doctor receives additional information by observing the patient’s reflex actions.

Incidence (per 100,000 people)

MenWomen
Age, years0-11-33-1414-2525-4040-6060 +0-11-33-1414-2525-4040-6060 +
Number of sick people0.010.010.011002502502500.030.030.03400100010001000

Types and categories of aura

Depending on the location of the epilepsy focus, the aura has different forms. There are 3 main types:

Each type, in turn, is divided into several subcategories of its own.

Sensory aura

With an epileptic aura of the sensory type, disturbances in vision, hearing, taste, and smell are noted. They are also joined by somatosensory, autonomic, and abdominal disorders.

Depending on the disturbances caused, the aura can be:

  1. Visual. Most common. Blind spots, lights, and multi-colored spots appear before the eyes.
  2. Auditory. The patient hears ringing, voices, music, and grinding sounds.
  3. Olfactory. Involves increased sensitivity to aromas, a sensation of unpleasant odors that appears suddenly.
  4. Tasty. Constant feeling of bitter, sour, salty taste in the mouth.
  5. Somatosensory. A feeling of burning, numbness, and itching occurs in a certain part of the body.
  6. Abdominal. It manifests itself as a feeling of tightness between the throat and stomach.
  7. Vegetative. Its symptoms are rapid heartbeat, a feeling of suffocation, and intense thirst. It is important to distinguish autonomic symptoms before the onset of a seizure in epilepsy from ordinary manifestations of stress.

Symptoms

Occurrence (how often a symptom occurs in a given disease)
Severe headache spreading over the entire head100%
Sudden intense headache100%
Increased irritability (nervousness, psychosis)100%
Pale skin90%
Apathy (indifference, indifference)80%
Other various forms of sleep disorders70%
Frontal headache (migraine)50%
Flashing "flies" before the eyes50%
Nausea50%
Tearing20%
Vomiting of various types, including indomitable10%

Types of migraine aura

An aura is a list of neurological symptoms that are reversible and occur simultaneously with or before a painful attack. The combination of these factors is called associated migraine.

Separately, experts identify a condition in which an aura appears without a headache. The patient experiences transient visual, motor, sensory or behavioral disturbances that last 20-30 minutes and resolve. A migraine aura without headache is characterized by the absence of cephalgia. It most often affects mature men. The symptoms of the pathology are similar to the clinical picture of cerebral ischemia, and therefore require a doctor’s assessment and diagnostics.

A migraine aura can be:

  • visual – the most common form in which the visual perception of the world suffers. It can manifest itself in the form of dots, lines, “blind” spots, and zigzags. Patients with visual aura may feel as if they are blind in one or both eyes and have trouble reading texts;
  • with impaired sensitivity - one side of the body is affected, mainly its upper part. The aura is characterized by the appearance of “goosebumps”, tingling, and numbness. Symptoms usually start in the hand, travel up the arm, reach the head and even affect the tongue;
  • with movement disorders - the clinical picture is characterized by muscle weakness of one arm or leg, sometimes the entire half of the body is affected. Reversible paresis of the limbs rarely occurs;
  • with a speech disorder – the patient finds it difficult to speak and compose meaningful sentences, he has difficulty finding words. Speech disorders are often complemented by a decrease in the ability to memorize and repeat words, distinguish between numbers and letters;
  • mixed – combines two or more forms of aura.

In some cases, the symptoms of the aura cause the patient even more discomfort than the attacks of pain themselves. If they last only a few minutes, experts recommend waiting them out or taking medications for cephalalgia for migraines in advance. If symptoms are severe, additional therapy may be administered at the discretion of the physician.

Learn more about the symptoms of ocular migraine here.

Causes and provoking factors

In 99% of cases, the appearance of the disease is associated with a person’s lifestyle and physiological characteristics.

These include:

  • genetic predisposition;
  • state of the nervous system;
  • stress, neuroses, depressive disorders;
  • hormonal disorders.

In 90% of cases, the disease can be triggered by vascular diseases: oxygen starvation, narrowing or dilation of blood vessels.

The disease is also influenced by factors such as:

  • bad ecology;
  • mental stress;
  • unfavorable weather conditions;
  • smoking;
  • work in noisy workshops;
  • long stays in the subway, at discos, at public events.

Aura in neurology is

Aura (ancient Greek αὔρα - light breeze, breath) (“partial” (focal, not developed) epileptic attack) - any sensation or experience that regularly precedes an epileptic attack or is an independent attack. It is a symptom of epilepsy.

The manifestations of the aura are very diverse and depend on the location of the part of the brain whose function is impaired (convulsive focus). This may be an increase in body temperature, a feeling of anxiety and restlessness, a sound, a strange taste, smell, a change in visual perception, an unpleasant feeling in the stomach, dizziness, a state of “already seen” (deja vu) or “never seen” (jamais vu). ), a feeling of inner bliss or melancholy, and other sensations or experiences.

Pros and cons of aura

The attack itself is not remembered by the patient. But the arrival of a harbinger of a seizure - an aura - is recorded by his consciousness. Most often, the appearance of an aura causes negative emotions in patients. Physical and emotional discomfort is caused by various unpleasant sensations, hallucinations, and an understanding of the inability to control one’s actions. Many patients experience headaches and depressed mood several hours before the aura appears.

However, no matter how strange it may sound, there are also positive aspects in the aura:

  • knowing about the approaching attack, the patient can take a comfortable position, free his hands from objects, and thus protect himself from injury;
  • There is time to warn loved ones about an impending seizure. This makes it possible to provide first aid as quickly as possible;
  • Many patients, being in a state of aura, manage to turn off the gas and turn off the devices.

Often, epilepsy can manifest itself for a long time only as isolated auras. However, their frequent occurrence indicates a high probability of developing an epileptic attack. Therefore, in case of any such violations, you should immediately consult a specialist.

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