Migraine is a recurrent throbbing headache, which is one of the most common types of headaches. It is often preceded by flashes of light, blurred vision, numbness of the limbs, etc., and is followed by a throbbing pain on one side of the head for about a few minutes to an hour, which gradually increases until nausea and vomiting occur and the headache is relieved in a quiet, dark environment or after sleep. It may be accompanied by neurological and mental dysfunction before or during the onset of headache. At the same time, it is a progressively worsening disorder that usually develops with increasing frequency. According to studies, migraine sufferers are more likely than usual to have localized brain damage, which can lead to stroke. The more frequent their migraines are, the larger the area of the brain that will be damaged.
The diagnosis is not difficult with a long history of recurrent headaches, with all normal interstitial periods, a normal physical examination and a family history of migraine. Oculomotor palsy can be caused by aneurysms, and arteriovenous malformations can also be associated with migraine, and a cranial CT scan or cerebral angiogram should be performed to clarify the diagnosis. Complex migraine is often caused by organic diseases, and neuroimaging should be performed. Occipital or temporal lobe tumors may also present with visual field defects or other visual symptoms at the beginning, but as the disease progresses, symptoms of increased intracranial pressure may eventually appear. Temporo-occipital headache in the elderly should be excluded from temporal arteritis, where the superficial temporal artery or occipital artery is thickened like a rope, and the pulsation is significantly weakened or absent, and the artery biopsy shows characteristic multinucleated giant cell infiltration.
Migraine headache – clinical manifestations
According to the international classification and diagnostic criteria of headache formulated by the International Headache Society in 1988, and combined with our clinical practice, they are outlined below.
(a) Migraine without aura (generalized migraine) is the most common.
Episodic moderate to severe throbbing headache with nausea, vomiting or photophobia. The headache is exacerbated by physical activity. The attack begins as a mild to moderate dull ache or discomfort and reaches a severe throbbing or throbbing pain after a few minutes to a few hours. About 2/3 of the headaches are unilateral, but they can also be bilateral, sometimes radiating to the upper neck and shoulders. The headache lasts 4 to 72 hours and is commonly relieved after sleep. There is a clear normal interval between attacks. If 90% of the attacks are closely related to the menstrual cycle, it is called menstrual migraine. The diagnosis can be made only after at least 5 episodes of the above mentioned episodes, excluding various intracranial and extracranial organic diseases.
(2) Migraine with aura (typical migraine) can be divided into two phases: aura and headache.
1.Aura phase
Visual symptoms are most common, such as photophobia, flashes of light in front of the eyes, sparks, or complex visual hallucinations, followed by visual field defects, dark spots, hemianopia or transient blindness. A few patients may develop hemianesthesia, mild hemiparesis or speech impairment. The aura mostly lasts for 5 to 20 minutes.
2. Headache period
It often appears when the aura starts to subside. The pain mostly starts in the supraorbital, postorbital or frontotemporal area on one side, and gradually worsens and extends to half of the head, or even the whole head and neck. The headache is pulsating, throbbing or chisel-like, and gradually increases in severity to a constant pain. It is often accompanied by nausea, vomiting, photophobia and phonophobia. Some patients have flushed face, profuse sweating and conjunctival congestion; some patients are pale, depressed and anorexic. One attack can last for 1 to 3 days, usually the headache is obviously relieved after sleeping, but after the attack for several days in a row, tiredness and weakness. In between attacks, everything is normal. The above typical migraine can be divided into several subtypes.
(1) Migraine with typical aura: including ophthalmic migraine, hemiplegic migraine, aphasic migraine, etc. (1) Migraine with typical aura: including ophthalmic migraine, migraine with hemiplegia, migraine with aphasia, etc. The diagnosis can be made only after at least two of these typical attacks have occurred and organic disorders are excluded.
(2) Migraine with prolonged aura (complex migraine): The symptoms are the same as (1). The aura persists during the headache attack and lasts for more than 1 hour but less than 1 week. Neuroimaging does not reveal the presence of intracranial structural lesions.
(3) Basilar migraine (formerly known as basilar artery migraine): Aura symptoms with clear origin in the brainstem or bilateral occipital lobes, such as blindness, visual symptoms in both temporal and nasal visual fields, dysarthria, vertigo, tinnitus, hearing loss, diplopia, ataxia, bilateral sensory abnormalities, bilateral light palsy or mental confusion. Most of them disappear within a few minutes to an hour, followed by a pulsating headache in the occipital region bilaterally. Everything is normal in the interval period.
(4) Migraine aura without headache (migraine isotonic attack): various aura symptoms seen in migraine attacks appear, but there are times when the headache does not follow. When the patient grows older, the headache may disappear completely while still having episodic aura symptoms, but those who completely show aura symptoms without headache are less common. those who have their first attack after 40 years of age need to be examined thoroughly to exclude thromboembolic TIA.
(C) Oculomotor paralysis type migraine
It is very rare. The age of onset is mostly below 30 years. There is a history of headache attacks fixed on one side, and after an episode of more severe headache (orbital or retro-orbital pain), paralysis of the ipsilateral ocular muscles occurs, most often with ptosis of the upper face. The paralysis lasts for several days or weeks and then recovers. The first few episodes of palsy recover completely, but partial ocular muscle palsy may remain without recovery after multiple episodes. Neuroimaging does not Song body exclude intracranial organic lesions.
(iv) Benign episodic vertigo in childhood (migraine equilibrium attack)
There is a family history of migraine but the child himself does not have headache. It presents with multiple, brief episodes of vertigo, but also episodic balance disorder, anxiety, with nystagmus or vomiting. Neurological and electroencephalographic examinations are normal. Everything is normal in the interval. Some children may turn to migraine in adulthood.
(V) Migraine persistent state
Migraine attacks lasting more than 72 hours (with a remission period of less than 4 hours) are called migraine persistent state.
Migraine headache–Causes
The cause of migraine is not known, but may be related to the following factors.
(1) Genetic factors, as about 60% of patients can ask for a family history and some patients have epileptic patients in their families, so experts believe that the disease is genetically related, but there is no consistent form of inheritance.
(2) Endocrine factors, vascular migraine is mostly seen in adolescent females, with frequent seizures during menstruation, stopping during pregnancy and reoccurring after delivery, while gradually reducing or disappearing after menopause.
(3) Dietary factors, frequent consumption of cheese, chocolate, irritating food or smoking and drinking are all prone to vascular migraine.
(4) Other factors, emotional stress, trauma, worry, anxiety, hunger, insomnia, poor external environment and climate change can also trigger migraine.
Specific explanation.
The etiology is unclear, and about 50% of patients have a family history. The tendency of migraine in female patients to have attacks before menstruation and fewer attacks after pregnancy suggests that the onset may be related to endocrine or water retention. Migraine attacks can be triggered by mental stress, overexertion, sudden climatic changes, bright light stimulation, sun exposure, hypoglycemia, application of vasodilator drugs or reserpine, and consumption of high tyramine food and alcoholic beverages.
Wolff et al. explained the clinical manifestations of migraine by the vascular origin theory. The typical migraine starts with constriction of intracranial arteries, which reduces local cerebral blood flow and causes aura symptoms such as visual changes, sensory abnormalities or mild hemiparesis, followed by dilation of intracranial and external arteries and headache.
Goltman saw intracranial vasodilatation during a migraine attack in a craniotomy patient, but Thie et al. found relatively small caliber of all arteries in a cerebral angiogram during a typical migraine attack, while Olson et al. found relatively small caliber of all arteries in a cerebral angiogram during a typical migraine attack in 11 patients. The cerebral angiograms of Olson et al. in 11 typical migraine episodes were unchanged.
Lauritzen et al. observed by 133Xe-SPECT that rCBF was not abnormal in 12 cases of common migraine attacks, and in 8 of 11 cases of typical migraine attacks, rCBF was reduced by an average of 17% in the hemisphere corresponding to the side of the aura compared to the corresponding area on the opposite side, lasting from 4 to 6 hours during the headache. None of the brain areas with increased rCBF were seen. On examination during the interictal period, no abnormalities were found in either type of migraine, and only one case showed a small hypoperfused area in the insula. Olsen et al. applied intracarotid injection of 133Xe to induce typical migraine, and found that the posterior CBF could be reduced by up to 20 ml/(100 g/min) with a γ-camera 254 probe, and that local hypoperfusion could persist until several hours after the disappearance of aura symptoms. several hours after the disappearance of the aura.
Olesen et al. measured rCBF throughout the course of a typical migraine attack and observed that hypoperfusion existed in the occipital region prior to the attack, with an average decrease in rCBF of 25-30% and a gradual extension to the frontal region, which lasted for 4-6 hours during the entire headache period. In 6 cases of generalized migraine and 6 cases of typical migraine, 30 minutes to 8 hours after the onset of the attack, when the aura had disappeared and the headache was in progress, there was a general increase in 1CBF on both sides, which could be 25% to 35% higher than in the remission period, with the frontal and temporal cortex and thalamus being the most significant, while the increase in the occipital region was not significantly different from the remission period. There was no difference between the two types of migraine. Thie et al. applied transcranial Doppler (TCD) to examine 10 patients with generalized migraine and found that most patients showed abnormally increased flow velocity of the large arteries on both sides or individual skull bases during the remission phase of the headache. three cases showed abnormally increased cerebral blood flow velocity and broad-frequency murmurs during five migraine episodes. . Qin Zhen et al. examined 99mTc-SPECT in 2 cases of generalized migraine and found hypoperfusion in the posterior parietal cortex and temporal lobe, respectively.
Thus, cerebral blood flow may be seen to be either less, more, or first reduced and then increased, cerebral blood flow velocity abnormally increased, and cerebral vessels dilated or of smaller caliber in a significant proportion of patients during migraine attacks. However, there is no constant relationship between these changes and the type of headache, aura or headache onset. Some changes are posterior to the head, while others are anterior to the head. Not all of the abnormal findings reported by the same authors were seen in all of the same patients observed, and some patients also had localized hypoperfusion areas or increased cerebral blood flow velocity during the headache interval. In conclusion, the relationship between migraine and abnormal cerebrovascular function needs to be further elucidated.
A series of biochemical changes occur in the fashion of migraine attacks. During the aura phase, there may be a transient increase in plasma 5-hydroxytryptamine (5-HT) levels; the metabolite of 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), may be significantly increased in the urine during headache attacks. This suggests that plasma 5-HT is quickly degraded and excreted in the urine. 5-HT has a biphasic effect on smooth muscle, with a decrease in plasma 5-HT causing constriction of small arteries and dilation of larger arteries. Constriction of small arteries causes ischemia in brain tissue, producing aura or other symptoms of neurological damage; dilation of large arteries causes headache. Some of the 5-HT leaks into the extracellular fluid surrounding the blood vessels, and together with histamine, bradykinin, vasopressin, and other neuropeptides, it decreases the pain threshold of the vessel wall and causes “sterile inflammation” of the arteries. The combination of vasodilatation and “sterile inflammation” causes the clinical symptoms of migraine. 5-HT is mainly stored in platelets, and when platelet aggregation is increased or 5-HT releasing factors are present, the platelet 5-HT content suddenly decreases and clinical onset occurs. Certain drugs (e.g., reserpine) have a 5-HT releasing and depleting effect and can induce headache attacks in migraine patients; 5-HT blockers (e.g., dimethyl ergometrine, phenothiazine) are used to prevent migraine attacks. The decrease in monoamine oxidase (MAO) activity during headache attacks may be related to the consumption of large amounts of MAO during 5-HT degradation.
Many experiments have confirmed that platelets in migraine patients are more prone to aggregation than in normal subjects. Platelet aggregation releases 5-HT, ADP, histamine, epinephrine, norepinephrine, arachidonic acid (AA), and thromboxane A2 (TXA2), which further contribute to platelet aggregation. This interaction produces large amounts of catecholamines, AA and TXA2, which have a strong vasoconstrictive and cerebral blood flow reducing effect. Prostaglandin E1 can cause headaches in people who have never had migraines. Estrogen increases prostaglandin synthesis, and some women taking high estrogen birth control pills can trigger migraine attacks.
But why do widespread vasoregulatory disorders and many biochemical changes affecting the whole body cause only headache? Why are most headache attacks lateralized? Sometimes they alternate between right and left?
The neurogenic theory suggests that the origin of migraine is in the central nervous system, and that endocrine changes and vasodilatory disorders are a secondary phenomenon, i.e., the vascular findings of migraine are secondary to the “release” of the nerve center. Migraine presents with a variety of complex symptoms as a result of cortical dysfunction, probably due to a decrease in the excitatory threshold of the hypothalamus/mesencephalon, causing headache attacks.
Neurons containing metanephrine 5-HT innervate certain cranial blood vessels, and their cell bodies are located in the blue spot and interstitial nuclei of the brainstem, respectively. Stress, anxiety, fatigue or other factors lead to increased excitation of brainstem neurons and release of transmitters, causing changes in cranial vasomotor activity, cerebral ischemia and “aseptic inflammation” of blood vessels, which stimulate injury receptors of trigeminal nerve endings in blood vessels and produce pain sensation in the brain. In addition, trigeminal nerve endings can release vasoactive substances (vasodilators and pathogenic peptides, substance P) into the large intracranial and extracranial vessels.
Migraine headache – pathogenesis
Headache is produced when nociceptive nerve endings, i.e., nociceptive receptors in intracranial and extracranial tissue structures, are stimulated by physical (e.g., inflammation, injury or swelling compression) or chemical (e.g., norepinephrine, 5-hydroxytryptamine, bradykinin, etc.) pathogenic factors, producing abnormal nerve impulses that travel through nociceptive transmission pathways to the central nervous system and ultimately to the cerebral cortex.
(A) Structural organization of the skull
The human skull is a circular bone cavity composed of many flat bones, called the cranial cavity. The cranial cavity is covered by the scalp, subcutaneous tissue, cap fascia, blood vessels, nerves and periosteum immediately on the surface of the skull from outside to inside, and these structures are collectively called soft tissues; there are meninges, brain tissue, blood vessels and nerves in the cranial cavity. The meninges are divided into dura mater (close to the inner surface of the skull), arachnoid and soft meninges (close to the surface of the brain) from outside to inside, and there is a cavity between the arachnoid and soft meninges called the subarachnoid space, which is filled with cerebral crest fluid that plays a protective role for the brain. The brain tissue is divided into the cerebellum, cerebellum and brainstem, and the cerebellum is separated from the cerebellum by the cerebellar curtain (canopy). The brain stem is a small, slender “gourd”, which is connected to the cerebellum and cerebellum through the fissure of the cerebellum and continues downward to the bone marrow, where the nerve fibers and some nerve centers are concentrated, and is the most important part of the brain tissue, and there are several bone holes of different sizes and shapes at the bottom of the cranial cavity, through which nerves and blood vessels pass, connecting the whole body to the brain.
(B) Structures sensitive to pain inside and outside the skull
Various intracranial and extracranial tissues can be divided into pain-sensitive tissues and insensitive tissues because of the number and nature of nerve endings. Headache is mainly caused by the stimulation of pain-sensitive tissues.
If we take the skull as the boundary and divide the head into intracranial and extracranial parts, we can refer to the following structures as pain-sensitive structures.
1. Intracranial structures sensitive to pain
(1) The venous sinus and the proximal end of the large vein that drains into the venous sinus.
(2) The dura mater at the base of the skull.
(3) The arteries that innervate the dura mater.
(4) The large arteries that make up the arterial ring at the base of the skull.
(5) The trigeminal, glossopharyngeal and vagus nerves.
(6) Cervical segment 1 to 3 crural medullary nerves.
2.Extracranial structures that are sensitive to pain
(1)Scalp, subcutaneous tissue, capillary tendon membrane, and periosteum at the base of the skull.
(2) Extracranial arteries, with the superficial temporal artery, occipital artery and posterior auricular artery being the most sensitive.
(3) Head, face and neck muscles: mainly the bilateral temporalis and posterior cervical muscles.
(4) Extracranial peripheral nerves: such as supraorbital nerve, auriculotemporal nerve, greater occipital nerve, lesser occipital nerve and greater auricular nerve.
(5) Other tissues: the mucosa of the nasal cavity, paranasal sinuses, external ear, middle ear, and dental pulp are rich in nerve endings and sensitive to painful stimuli. In contrast, the skull, most of the soft meninges, all of the brain parenchyma, the ventricles, the ventricular canal, and the choroidal filaments do not produce pain.
(C) Innervation and pain sites of intracranial and extracranial structures
The nerve impulses generated by pain-sensitive structures inside and outside the skull must be transmitted through the corresponding nerve fibers to the central nervous system and finally to the cerebral cortex for analysis and integration in order to produce pain sensation.
1.The pain of various extracranial structures is mainly conducted by the trigeminal nerve and upper cervical nerve, and partly by the glossopharyngeal nerve and vagus nerve.
2.The intracranial innervation consists of the trigeminal nerve, the linguopharyngeal nerve, the vagus nerve, the cervical 1-3 nerve roots and the sympathetic plexus around the cerebral artery.
(1) The anterior cranial fossa, middle cranial fossa and tissues on the cerebellar curtain are innervated by the trigeminal nerve, so the pain is often manifested in the forehead, orbit and temporal region. The tissues under the cerebellar curtain in the posterior cranial fossa are innervated by the glossopharyngeal nerve, vagus nerve, and 1-3 cervical nerve roots, and the pain is often in the occipital and cervical regions.
(2) The superior dural branch from the 2nd and 3rd cervical nerves enters the skull and distributes to the dura, vertebral artery and posterior dural artery near the foramen magnum. In the initial stage of the pontocerebellar angle auditory neuroma, the pain produced by the stimulation of the tumor projects to the 2nd and 3rd cervical nerve innervation area, which may produce a limited headache in the lower occipital region of the affected side.
(3) Most of the pain sensation at the start of large vessels in the intracranial internal carotid artery, middle cerebral artery, anterior cerebral artery and posterior cerebral artery is felt by the trigeminal nerve, and part of it comes from the sympathetic plexus on the arterial wall. For this reason, pain sensation in the intracranial artery often radiates to the periorbital, prefrontal and temporal areas.
In conclusion, usually when the pain-sensitive structures on the cerebellar curtain are stimulated, the pain sensation is reflected in the frontal, temporal or parietal regions, and this nociceptive sensation is conducted by the trigeminal nerve; the headache caused by the structures in the posterior cranial fossa under the curtain is mainly reflected in the occipital, inferior occipital and upper cervical regions, and is conducted by the glossopharyngeal, vagus and upper three pairs of cervical nerves.
The pain sensation in the face, eyes, nasal cavity, paranasal sinuses and oral cavity is conducted by the ophthalmic, maxillary and mandibular branches of the trigeminal nerve respectively; the pain sensation in the soft palate, tonsils, pharynx, posterior tongue and nasopharyngeal canal is conducted by the linguopharyngeal nerve, and the pain sensation in the external auditory canal and part of the auricle is conducted by the middle branch of the facial nerve and vagus nerve.
(D) Causes of headache
The causes of headache are many, and they are mainly physical factors, biochemical factors, endocrine factors and psychogenic factors.
1.Physical factors
(1) Headache is caused by inflammation, injury or pressure of swelling on pain-causing structures inside and outside the skull.
(2) Vessels are pulled, stretched or displaced: Headache caused by the pulling or displacement of the intracranial cerebral basilar artery ring and its main branches, venous sinus and the proximal end of the large cerebral vein that drains to the venous sinus is called traction headache. It is commonly seen in the following 3 conditions.
① intracranial occupying lesions: such as brain tumor, cerebral hematoma, brain abscess, etc.
(ii) Increased intracranial pressure: cerebral edema, hydrocephalus, venous sinus thrombosis, brain tumor or compression blockage by brain cysts affecting cerebral crest fluid circulation, etc.
(3) Decrease in intracranial pressure: It is common after lumbar puncture and lumbar anesthesia, due to more loss of cerebral crest fluid and decrease in intracranial pressure, which causes headache due to dilatation or traction of intracranial venous sinuses and veins.
(3) Vasodilation: Various causes of intracranial and extracranial vasodilation can produce headache. For example, acute intracranial and extracranial infections, hypoglycemia, hypercapnia, plateau hypoxia, gas or alcohol poisoning, seizures, acute intracranial pressure drop caused by lumbar puncture, sudden hypertension, etc., can cause the dilation of intracranial and extracranial blood vessels and produce painful symptoms.
(4) Stimulation of meninges: inflammatory exudate in meningitis, blood stimulation of meninges in subarachnoid hemorrhage, or pulling on meninges in cerebral edema can produce headache.
(5) Contraction of head and neck muscles: When the head and neck muscles are continuously contracted due to inflammation, injury or psychogenic factors, local blood flow is blocked, which can lead to the accumulation of various metabolites and the release of lactic acid, bradykinin and other pain-causing factors to produce headache, called tension headache.
(6) Nerve stimulation or lesion: Headache can be produced by self-inflammation of cranial nerve and cervical nerve or stimulation by tumor and inflammation of surrounding tissues, such as trigeminal neuralgia caused by occipital neuritis, trigeminal neuritis, pontocerebellar horn tumor or cerebral arachnoiditis.
(7) Involvement pain of head: also known as radioactive headache, lesions in the eyes, ears, nose, paranasal sinuses, teeth and neck can not only cause local pain, but also spread or reflect through nerves to the head and face, and the headache is mostly on the side of the lesion.
2.Biochemical factors
In recent years, some biochemical factors related to headache have received increasing attention. For example, 5-hydroxytryptamine (5-HT), catecholamines, bradykinin, prostaglandin E and β-endorphin, substance P, etc. have obvious changes in the blood of patients with headache (especially migraine).
3.Endocrine factors
Many clinical cases can prove that the attack and relief of headache are related to endocrine. For example, migraine is mostly seen in young women and often starts in adolescence. About 60% of female migraine attacks are related to the menstrual cycle; 80% of female patients experience significant relief or even complete disappearance during pregnancy. Tension headaches tend to worsen during menstruation and menopause. Hyperthyroidism also tends to cause headache attacks.
4.Psychogenic factors
It is the headache caused by mental factors. For example, the mental burden caused by long-term work and life pressure, the injury to self-esteem, and the worry and boredom caused by the conflicts and entanglements of family and colleagues can trigger the dysfunction of vegetative nerves for a long time and lead to the headache due to vasodilator disorder. In addition, changes in weather, noise, bright light stimulation and atmospheric pollution can also cause emotional instability and induce headaches in a few people.
Migraine headache – preventive treatment
There is no specific treatment for migraine headaches that will never come back! However, it has been proven that the most effective treatment for patients is preventive treatment during the interval of migraine, in addition to psychological adjustment and dietary regimen.
1.Less exposure to 3C foods
Cheese cheese, chocolate, citrus foods, marinated sardines, chicken liver, tomatoes, milk, lactic acid drinks, etc. are rich in tyramine. And tyramine is the main cause of vascular spasm, so if you have a history of migraine, then it is best to stay away from these foods.
2. Beware of sausages and hot dogs
Sausages, hot dogs, ham, bacon and other cured and smoked meats, processed meats and other foods containing nitrites, as well as foods containing MSG can cause you migraines, so it’s best to eat as little as possible in your daily life.
3, be wary of sugar substitutes food
Studies have found that the sugar substitute “aspartame” (Aspartame) can over-stimulate or interfere with nerve endings, increasing muscle tension and triggering migraines. Low-sugar colas, low-sugar sodas, sugar-free chewing gum, ice cream, multivitamins and many prescription drugs all contain aspartame. So people who are allergic to sugar substitutes can trigger a headache with a small sip of low-sugar soda.
Tip from “Petite”: Pay attention to the food content label on the product packaging. It is found marked with: Amino acids (amino acids), Aspartic
acid (aspartic acid) or Phenylalanine (phenylalanine), you should try to avoid.
In addition, Liu Yanping, a nutritionist at the Union Hospital, suggests that if you want to sweeten your food or drink, it is best to use honey instead of white sugar and sugar substitutes.
4, careful use of painkillers, cold syrup
Painkillers can be a tempting trap. Many people take painkillers privately in an attempt to relieve pain, but overdosing on painkillers will not only fail to relieve pain, but will instead cause drug-induced “rebound headaches” and leave you with chronic migraines. If you eat more than 2 or 3 times a week painkillers to relieve pain, please seek medical attention immediately!
5, to some magnesium it!
Magnesium can regulate blood flow, relax muscles. For some people, even just a little magnesium deficiency, can trigger a headache. The United States National Headache Foundation recommends that the best daily supplement 500 to 750 mg of magnesium.
Tip from The Dainty: Magnesium supplements can have the side effect of diarrhea, so it’s best to take them as prescribed after consulting your doctor. Or on a regular basis to eat more food with high magnesium to supplement, such as: whole grain foods, nuts and seeds (such as sunflower seeds, almonds, cashews, hazelnuts, etc.), cauliflower, tofu, etc.
6, supplement vitamin B2
Studies have found that oral high-dose vitamin B2, can reduce the frequency and duration of migraine attacks, but its dose should not exceed 400 mg a day.
7, coffee, let you rejoice let you worry
Caffeine will stimulate the nervous system and interfere with sleep, drink more addictive, while quitting coffee can trigger migraines. Therefore, it is best to consume less than 100 mg of coffee in a day (about a cup of strong coffee).
8, drink less red wine
All alcoholic beverages can trigger headaches, especially red wine contains more headache-inducing chemicals. If you really want to drink a couple of glasses, it is best to choose vodka, white wine such as colorless wine.
9, learn to reduce stress
If you often cause migraines due to work stress, you may want to take a warm bath often, or try some muscle relaxation techniques, such as abdominal whistling skills: slowly inhale, so that the abdomen fully outside the drum, exhale, feel the abdomen gradually flattened.
10, regular exercise
The doctor pointed out: for people with migraines, emphasis on breathing training, breathing exercises (such as yoga, qigong), can help patients stabilize the autonomic nervous system, reduce anxiety, muscle tightness and other symptoms.
11.Sleep regularly, refuse to be reversed in the morning and evening
Maintaining a regular routine, going to bed and getting up regularly even on holidays, is especially important for people with migraines. Because, lack of sleep or too much sleep can easily trigger migraine.
12. Make good use of hot packs and ice packs
When you have a headache, try putting a hot pack on your neck and an ice pack on your forehead. Hot and cold stimulation can help you effectively relieve muscle tension and reduce pain.
13.Do shoulder and neck exercises regularly
Experts have found that pressure on certain parts of the neck and shoulder muscles can exacerbate migraines and even cause chronic migraines in people who have never had them before. So for office workers, if you need to use the computer for a long time, pay attention to the screen and seat height and sitting position, and every 50 minutes of work, it is best to take a 10-minute break, and often around the neck and shoulders.
14. Drink more water during menstruation
Migraines often occur during women’s menstrual periods, so when your period is approaching and between periods, it is best to drink more water than usual to help detoxify your body and effectively reduce the chance of migraines.
15. Be careful with your perfume and many cleaning agents
Strong odors, such as cigarettes and cigars, paint, exhaust fumes, cleaning agents and chemical detergents, printing inks, etc., can trigger migraines. It is best to open windows frequently during the day and try to avoid places with strong irritating odors such as gas stations.
16, careful use of contraceptive pills
Some women start to have migraine attacks after taking birth control pills for the first time. Some expert studies have concluded that women suffering from migraines taking birth control pills can even increase the risk of stroke.
17. Wear your sunglasses
Neurologists warn that strong sunlight and reflective flashes can increase the incidence of migraines by 25-30%. So people with migraines would be wise to wear sunglasses when they go out to avoid strong sunlight.
18. Create a quiet environment
Strong light and a noisy environment can trigger migraines. More than 70 percent of migraine patients are super sensitive to loud noises. When decorating, it is best to have workers strengthen the sound insulation of the room, and it is best to choose a slightly thicker style of curtains.
20. Eat fish to prevent headaches
Eating fish at least 3 times a week and taking some fish oil supplements can effectively reduce the frequency of migraine attacks.