What Are the Most Common Causes of Migraine Headaches?

The classification of migraine developed by IHS in 2004 is divided into:

Wei Cuibai

(Deputy Chief Physician)

Department of Neurology, Xuanwu Hospital, Capital Medical University

Migraine (migraine) is the most common type of primary headache in clinical practice. The clinical manifestations are paroxysmal moderate to severe, pulsatile headaches. The headaches are mostly lateral, which usually lasts 4 to 72 hours, and may be accompanied by nausea and vomiting. Light, sound stimulation or daily activities can aggravate headaches. Quiet environment and rest can relieve headaches. Migraine is a common chronic neurovascular disease. It usually occurs in children and adolescence, peaks in middle and adolescents, and it is more common in women. The ratio of male to female patients is about 1: 2 to 3, and the prevalence in the population is 5 % To 10%, often with genetic background.

Western Medicine Name: Migraine
English name: migraine
Affiliated Department: Internal Medicine-Neurology

Disease site: head
Multiple groups: female
Contagious: Non-contagious

Migraine disease classification

The classification of migraine developed by IHS in 2004 is divided into:

1 migraine without aura

2Migraine with aura

2.1 Typical aura with migraine headache

2.2 Typical aura with non-migraine headache

2.3 Typical aura without headache

2.4 Familial hemiplegic migraine

2.5 Sporadic hemiplegic migraine

2.6 basic-type migraine

3 childhood periodic syndromes that are commonly precursors of migraine

3.1 cyclical vomiting

3.2 Abdominal migraine

3.3 Benign paroxysmal vertigo of childhood

4retinal migraine

5 complications of migraine

5.1 Chronic migraine

5.2 Status of migraine (status migrainosus)

5.3 Persistent aura without infarction

5.4 migrainous infarction

5.5 Migraine-triggered seizure

6 probable migraine

6.1 Probable migraine without aura

6.2 Probable migraine with aura

6.3 Probable chronic migraine ^[1]

Causes of Migraine

The cause of migraine is unclear and may be related to the following factors:

Genetic factors for migraine

About 60% of migraine patients have a family history, and their relatives have a migraine risk that is three to six times that of the general population. Familial migraine patients have not found a consistent Mendelian genetic pattern, reflecting different penetrances and polygenes. Interaction between genetic characteristics and environmental factors. Familial hemiplegia migraine is a well-defined autosomal dominant inheritance with high abnormal penetrance, and has been located at 19p13 (related to mistranslational mutations in the voltage-gated P / Q calcium channel genes expressed in the brain), 1q21, 1q31, etc. Three disease gene loci.

Migraine endocrine and metabolic factors

There are more women than men in this disease, and they usually occur during adolescence. They are prone to attacks during menstruation, and the attacks are reduced or stopped during pregnancy or after menopause. This suggests that endocrine and metabolic factors are involved in the onset of migraine. In addition, metabolic abnormalities such as serotonin (5-HT), norepinephrine, substance P and arachidonic acid can also affect the occurrence of migraine.

Migraine diet and mental factors

Migraine attacks can be triggered by certain foods and medications, including cheeses containing tyramine, meats and preserved foods containing nitrite preservatives, chocolates containing phenethylamine, and food additives such as sodium glutamate (MSG) , Red wine and wine. Medications include oral contraceptives and vasodilators such as nitroglycerin. Other environmental and mental factors such as stress, overwork, emotional excitement, excessive or too little sleep, menstruation, and strong light can also be induced.

Pathogenesis of migraine

The pathogenesis of migraine is not very clear. At present, there are the following theories:

Migraine vascular theory

Traditional vascular theory holds that migraine is a primary vascular disease. Intracranial vasoconstriction causes aura symptoms of migraine, followed by dilatation of extracranial and intracranial blood vessels, vasoactive peptides produced by perivascular tissues cause aseptic inflammation and pulsatile headache. Local compression of the carotid and superficial temporal arteries and the vasoconstrictor ergot alkaloids such as ergotamine can alleviate headaches during the attack. This theory is supported. Neuroimaging has developed clinical applications such as TCD and PET, and further developed the vascular source theory, suggesting that threatened and non- threatened migraines are the same disease with different degrees of vasospasm. Various neurons have different sensitivities to ischemia. The emergence of aura symptoms is due to vasoconstriction and reduced blood flow. Neurons in the visual cortex are most sensitive to ischemia, so visual auras appear first, and then more and more Neuron function is affected, and other neurological symptoms such as numbness of the fingers gradually appear.

Neurological theory of migraine

Neurology believes that changes in neurological function are paramount during migraine attacks, and changes in blood flow are secondary. Migraine precursors are caused by cortical spreading depressing (CSD). CSD refers to the nerve electrical activity inhibition zone originating from the posterior cortex (occipital lobe) caused by various harmful stimuli. This inhibition zone expands to the adjacent cortex at a speed of 2 to 5 mm / min, accompanied by an expansion of reduced blood volume. (Spreading oligemia). Both do not expand according to the distribution of cerebral arteries, but proceed according to the construction pattern of cerebral cortex cells, and the forward expansion generally does not exceed the central sulcus. CSD can well explain the migraine aura symptoms. In addition, serotonin (5-HT) is involved in the development of headaches. At the beginning of a headache attack, 5-HT is released from platelets and directly acts on the small intracranial blood vessels to shrink them and attach to the blood vessel wall. When the concentration of 5-HT in plasma decreases, the tension-contracting effect on the aorta disappears, and the blood vessel wall expands with headache. 5-HT is both a neurotransmitter and a humoral medium, affecting both nerves and blood vessels. The triptans for migraine are central 5-HT receptor agonists or partial agonists. This confirms that neurological dysfunction is involved in the onset of migraine.

Migraine trigeminal neurovascular theory

The anatomical and physiological basis of this theory is the trigeminovascular complex. Intracranial nociceptive tissues such as cerebrovascular, meningeal blood vessels, and venous sinuses, the nerve fibers surrounding the blood vessels enter the trigeminal ganglia with the trigeminal eye branch, or enter the posterior root of the cervical nerves (C1, C2) from the posterior cranial fossa; two After the trigeminal ganglia and C1 and C2 spinal ganglia are replaced, the nerve fibers are sent to the trigeminocervical complex, which is composed of the tail end of the spinal nucleus of the trigeminal nerve and the posterior horn of C1 and C2; The complex emits nerve fibers that are projected into the thalamus after crossing the brain stem. The doctrine of peripheral pain suggests that trigeminal ganglion damage may be the neural basis for migraine. When the trigeminal ganglia and its fibers are stimulated, they can cause increased release of substance P (SP), calcitonin gene-related peptide (CGRP), and other neuropeptides. These active substances act on the adjacent cerebral blood vessel wall, which can cause vasodilation and pulsatile headache. It can also increase the permeability of blood vessels, exudate plasma proteins, produce aseptic inflammation, and stimulate the afferent nerve fibers to enter the center, forming malignancy. cycle.

Migraine Pathophysiology

Intracranial nociceptive tissues such as cerebrovascular, meningeal blood vessels, and sinuses. Perivascular nerve fibers and trigeminal nerves may be the physiological basis and pain pathway for migraine. Electrical stimulation of the trigeminal ganglion can cause aseptic inflammation of the dural vessels. The trigeminal vascular reflex theory of migraine believes that migraine is the release of substance P (SP) and other neurotransmitters from the afferent fiber ends of the trigeminal nerve. The efferent nerve acts on intracranial and extravascular vessels, causing headache and vasodilation. The most important neuropeptides related to the trigeminal nervous system are calcitonin gene-related peptide (CGRP), followed by substance P (SP) and neurokinin A (NKA). Substance P is a neurotransmitter that transmits and lowers the pain threshold, and has a synergistic effect with neurokinin A (NKA), while calcitonin gene-related peptide (CGRP) has a strong vasodilator effect, which causes headache by dilating blood vessels.

Clinical manifestations of migraine

Frequent migraine attacks will affect patients' life and work, the most direct is to affect sleep, because lack of sleep, no energy during the day, work is also greatly affected. In addition, some patients often have seizures as soon as they work, which is very delaying. At the same time, people suffer from headaches for a long time, their personality changes, and their temperament often becomes irritable. Because of long-term cure, life is greatly affected, psychological fragility, loss of confidence, and a long time will adversely affect people's cardiovascular and cerebrovascular. Clinically, cerebral thrombosis, hypertension, and cerebral hemorrhage after clinical headache are common. The following are the clinical manifestations of the main types of migraine:

Migraine without threat Migraine

Migraine without threat is the most common type of migraine, accounting for about 80%. There may be no obvious aura symptoms before onset, and some patients have mental disorders, fatigue, yawning, loss of appetite, general discomfort and other symptoms before the onset. Women's menstrual cramps, drinking, and fasting can also cause pain. Most headaches are slowly exacerbated, and the recurrent episodes of bilateral or bilateral frontotemporal pain are pulsatile. The symptoms of the pain may be complicated by the contraction of the neck muscles. Often accompanied by nausea, vomiting, photophobia, photophobia, sweating, general malaise, and scalp tenderness. Compared with migraine with aura, migraine without aura has a higher frequency of attacks, which can seriously affect the work and life of patients. Frequent analgesics are often required for treatment, and a new type of headache is easy to be combined-"drug overuse Medication-overuse headache. Medication-overuse headache. "

Migraine with aura

Migraine with aura accounts for about 10% of migraine patients. Hours to days before the onset may have prodromal symptoms such as burnout, inattention, and yawning. Before or during the onset of headaches, reversible focal neurological symptoms are often the precursors, most commonly visual precursors, such as blurred vision, dark spots, flashes, brightly lit lines or deformed vision; followed by sensory precursors, Sensory symptoms are mostly distributed in the face-hand area; speech and motor threats are rare. Aura symptoms usually develop gradually within 5 to 20 minutes and last no more than 60 minutes; different auras can appear one after another. Headaches occur at the same time or within 60 minutes of the onset of aura, and are manifested as one or both frontotemporal or posterior orbital pulsatile headaches, often accompanied by nausea, vomiting, photophobia or phobia, pale or sweating, polyuria, Irritability, horror of smell, and fatigue, see head and facial edema, and prominent temporal arteries. Activities can make headaches worse and relieve them after sleep. Pain usually peaks in 1 to 2 hours and lasts for 4 to 6 hours or ten hours. In severe cases, it can take several days. After the headache resolves, fatigue, burnout, irritability, weakness, and poor appetite are often observed.

(1) Migraine headache with typical threats: It is the most common type of migraine with aura. The aura is manifested as completely reversible visual, sensory or speech symptoms, but without limb weakness. Migraine-like headaches that occur at the same time as the threat or within 60 minutes of the threat are migraine headaches with typical threats. If the headache that occurs at the same time as the threat or within 60 minutes after the threat does not meet the characteristics of migraine, it is called a non-migraine headache with typical threat; if the headache does not appear within 60 minutes after the threat, it is called a typical threat without headache. The latter two should be distinguished from transient ischemic attacks.

(2) Hemiplegia Migraine Hemiplegia Migraine: Rarely clinically. In addition to the symptoms of motor weakness, the aura should also include one of the three auras of vision, sensation, and speech. The aura symptoms last for 5 minutes to 24 hours, and the symptoms are completely reversible. Migraines occur at the same time or within 60 minutes of the aura. Characteristics of headache. For example, in the first- or second-degree relatives of patients with hemiplegia and migraine, at least one person has a precursor of migraine including inability to exercise, which is familial hemiplegia migraine; if not, it is called sporadic hemiplegia migraine.

(3) Basal migraine: The aura symptoms clearly originate from the brainstem and / or the cerebral hemispheres on both sides. Clinically visible dysarthria, dizziness, tinnitus, hearing loss, diplopia, nasal and temporal vision in both eyes. Symptoms, ataxia, disturbance of consciousness, and paresthesia on both sides, but no symptoms of motor weakness. Migraine-like headaches occur at the same time or within 60 minutes of the threat, often accompanied by nausea and vomiting.

Retinal migraine

Retinal migraine is a recurring, completely reversible, monocular visual disorder, including flicker, dark spots, or blindness, accompanied by migraine attacks. Ophthalmic examination is normal during the episode. Unlike basal migraine visual aura symptoms often involving both eyes, retinal migraine visual symptoms are limited to one eye, and lack of neurological or irritating symptoms originating in the brainstem or hemisphere.

Migraine in children with periodic syndrome

Periodic syndrome in children, often a precursor to migraine, can be considered as migraine allergy. Clinically, periodic vomiting, recurrent abdominal pain accompanied by nausea and vomiting are abdominal migraine and benign childhood idiopathic vertigo. It is not accompanied by headaches, and migraines can occur over time.

Migraine Migraine Complications

(1) Chronic migraine: Chronic migraine can be considered as a chronic migraine if the headache attacks occur more than 15 days per month for 3 consecutive months or more, and the headache caused by excessive drug is excluded.

(2) Persistent state of migraine: The duration of migraine attacks is 72 hours, and the pain is more severe, but there may be a short period of remission due to sleep or drug application.

(3) Permanent aura without infarction: Refers to patients who have migraine with aura who have aura or multiple aura symptoms for more than 1 week in one episode, mostly bilateral; other symptoms of this episode are similar to previous episodes; Neuroimaging excluded cerebral infarction.

(4) Migraine infarction: In rare cases, the ischemic infarction of the corresponding intracranial blood supply area occurs after the migraine aura symptoms. This aura symptom usually lasts more than 60 minutes, and the ischemic infarct focus is the Institute of Neuroimaging Confirmed, called migraine infarction.

(5) Migraine-induced seizure-like seizures: In rare cases, migraine precursor symptoms can trigger seizures, and seizures occur within or within 1 hour of the symptom symptoms.

Migraine ophthalmoplegia migraine

Ophthalmoplegic migraine is clinically manifested as recurrent migraine-like headaches, and headaches occur at the same time or within 4 days of the side-eye muscle paralysis. Droopy eyelids, dilated pupils, and some cases may involve both the pulley and the abductor. Patients with ophthalmoplegia migraine often have headaches that last for one week or more. The incubation period from headache to the occurrence of ophthalmoplegia can be as long as 4 days. In some cases, enhanced MRI scans can indicate repeated demyelination of the affected motor nerve. . Therefore, there is a tendency not to consider ophthalmoplegia migraine as a subtype or variant of migraine.

Migraine diagnosis

The diagnosis of migraine should be combined with the type of migraine attack, family history, clinical manifestations and neurological examination. The IHS (2004) diagnostic criteria for migraine makes the following provisions for the diagnosis of different types of migraine:

Migraine without threat migraine diagnostic criteria

(1) At least 5 episodes meeting the characteristics of (2) to (4).

(2) Headache attacks (untreated or ineffective) last 4 to 72 hours.

(3) At least two of the following headache characteristics: unilateral; pulsatile; moderate or severe headache; daily activities (such as walking or going up the stairs) will aggravate the headache, or actively avoid this type of headache activity.

(4) The headache is accompanied by at least one of the following: nausea and / or vomiting; photophobia and phobia.

(5) Cannot be attributed to other diseases.

Diagnostic criteria for migraine headaches with typical threats

(1) At least 2 episodes meeting the characteristics of (2) to (4).

(2) The aura has at least one of the following manifestations, but no symptoms of motor weakness: fully reversible visual symptoms, including positive manifestations (such as flashes, bright spots or bright lines) and / or negative manifestations (such as visual field defects); fully reversible paresthesia, including positive manifestations (such as acupuncture) and / or negative manifestations (such as numbness); fully reversible speech dysfunction.

(3) At least the following two items are satisfied: the same-direction visual symptoms and / or unilateral sensory symptoms; at least one aura symptoms gradually develop 5 minutes, and (or) different aura symptoms occur successively, the process 5 minutes; each aura symptoms last 5 to 60 minutes.

(4) Headaches occur at the same time or within 60 minutes of the onset of aura symptoms, and the headaches meet the (2) to (4) items in the aura-free migraine diagnostic criteria.

(5) Cannot be attributed to other diseases. ^[2]

Differential diagnosis of migraine

Migraine cluster headache

Cluster headache, also known as histamine headache, is rare in clinical practice. Presented as a series of dense, transient, severe unilateral drilling pain. The location of the headache is mostly localized and fixed to one orbit, the posterior bulb, and the frontotemporal area. Onset is sudden and without warning, the onset time is fixed, lasts 15 minutes to 3 hours, and the onset is from once every other day to 8 times a day. Severe pain, often painful, and facial flushing, conjunctival congestion, tearing, runny nose, and nasal congestion, mostly without nausea and vomiting, Horner sign may be present in a few patients with headache. The age of onset is often later than that of migraine, with an average age of 25 years. The ratio of male to female is about 4: 1.

Migraine

Tension headache: also known as muscle contraction headache. Headaches are more diffuse and can be located on the forehead, double temporal, parietal, pillow, and neck. Headaches are often dull, with a sense of pressure and tightness in the head. Headaches are often persistent, and some cases can be expressed as paroxysmal and pulsatile headaches. It is rarely accompanied by nausea and vomiting. Most patients have tenderness points on the scalp and neck. Massaging the head and neck can relieve headaches. More common in young and middle-aged women, emotional disorders or psychological factors can aggravate headache symptoms.

Migraine painful ophthalmoplegia

Painful ophthalmoplegia: It is an inflammatory disease characterized by headache and ophthalmoplegia involving idiopathic orbital and cavernous sinus. It is intractable soreness, tingling, or laceration-like pain after paroxysmal eyeballs and around the orbits, accompanied by eye movements, tackles, and / or abductive nerve palsy. Ophthalmoplegia can occur simultaneously with pain or two weeks after the onset of pain Appeared within, MRI or biopsy can find cavernous sinus, supraorbital fissure or granulomatous lesions in the orbit. The disease can resolve itself after several weeks, but it is easy to relapse. Appropriate glucocorticoid treatment can relieve pain and ophthalmoplegia.

Migraine symptomatic migraine

Symptomatic migraine headaches due to vascular lesions of the head and neck such as ischemic cerebrovascular disease, cerebral hemorrhage, unruptured saccular aneurysm and arteriovenous malformations; those due to non-vascular intracranial disease Headaches such as intracranial tumors; headaches due to intracranial infections such as brain abscesses and meningitis. These secondary headaches can also be clinically manifested as migraine-like headaches with nausea and vomiting, but there is no typical migraine attack. Most cases have focal neurological deficits or irritation, and the brain Imaging examination can show the lesion. Headaches due to internal environmental disorders, such as hypertension crisis, hypertensive encephalopathy, eclampsia, or preeclampsia, can manifest as bilateral pulsating headaches. Headaches are closely related to elevated blood pressure in the time of occurrence, and neuroimaging in some cases Reexamination of white matter damage may occur during the study.

Migraine drug overuse headache

Overdose headaches are secondary headaches. Overdose mainly refers to excessive and regular use, such as a fixed number of days per month or week. It is common in clinical practice to take ergotamine, triptan, opiates 10 days or simple painkillers 15 days for more than 3 consecutive months. Headaches occur or worsen during the above-mentioned overdose. Headaches are related to drugs. They can be migraine-like or mixed headaches with migraine and tension-type headaches. Headaches are relieved or returned to the original headache mode within 2 months after the drug is stopped. Overdose headaches are ineffective for preventive treatment, so it is extremely important to make a correct diagnosis.

Migraine disease treatment

The purpose of migraine treatment is to reduce or stop the onset of headaches, relieve the associated symptoms, and prevent headaches from recurring. Treatment includes both drug treatment and non-drug treatment. Non-drug therapy is mainly physical therapy. Magnetic therapy, oxygen therapy, and psychological counseling can be used to relieve stress, maintain a healthy lifestyle, and avoid various migraine triggers. Drug treatment is divided into seizure treatment and preventive treatment. For best results during seizure treatment, medication should usually be taken immediately after the onset of symptoms. Therapeutic drugs include non-specific analgesics such as non-steroidal anti-inflammatory drugs (NSAIDs) and opioids, and specific drugs such as ergot preparations and triptans. Drug selection should be based on comprehensive consideration of headache severity, concomitant symptoms, and previous medication, etc., for individualized treatment.

1. Mild-to-moderate headache: NSAIDs such as acetaminophen, naproxen, ibuprofen, etc. alone can be effective, if not effective, then use migraine specific treatment drugs. Opioids such as pethidine are also effective in the diagnosis of acute migraine attacks, because of their addictive nature, and are not recommended for routine treatment of migraine, but for cases where ergot preparations or triptan are contraindicated, such as Complicated with heart disease, peripheral vascular disease or migraine during pregnancy, pethidine can be given to stop the acute attack of migraine.

2. Moderate-severe headache: Migraine specific treatment drugs such as ergot preparations and triptan drugs can be directly selected to improve symptoms as soon as possible. Although some patients have severe headaches but have responded well to NSAIDS in the past, they can still be used. NSAIDS. Ergot preparations: non-selective agonists of 5-HT1 receptors. The drugs include ergotamine and dihydroergotamine (DHE), which can stop the acute attack of migraine. Triptan: It is a selective 5-HT1B / 1D receptor agonist, which may exert analgesic effect by constricting cerebral blood vessels, inhibiting neuropathic transmission of peripheral nerves and secondary neurons of the "trigeminal neck complex". Commonly used drugs are sumatriptan, naratriptan, rizatriptan, zomitriptan, and amotriptan. The ergot and triptan drugs adverse reactions include nausea, vomiting, palpitations, irritability, anxiety, and peripheral vasoconstriction. A large number of long-term applications can cause hypertension and ischemic necrosis of the limbs. The above two drugs have a strong vasoconstrictive effect, and patients with severe hypertension, heart disease and pregnant women are contraindicated. In addition, if ergot and triptan drugs are applied too frequently, they may cause overdose headaches. To avoid this, it is recommended that the drugs be used for no more than 2 to 3 days per week.

3. Concomitant symptoms: Nausea and vomiting are concomitant symptoms of prominent migraine and common adverse reactions to drugs. Therefore, combined antiemetics (such as metoclopramide 10mg intramuscular injection) are necessary. For severe vomiting, it can be given Small doses of perphenazine and chlorpromazine. People with irritability can be given benzodiazepines to promote sedation and fall asleep.

Prognosis of migraine disease

The prognosis for most migraine patients is good. Migraine can be relieved gradually with the increase of age, and some patients can stop migraine from 60 to 70 years old.

Migraine disease prevention

1. Avoid headache-causing factors: To prevent the onset of migraine headaches, first eliminate or reduce the causes of migraine headaches. In daily life, avoid direct stimulation of strong light, such as avoiding looking directly at the reflection of automobile glass, and avoiding from darker rooms. Bright outdoor view. Avoid facing neon lights. Avoid emotional stress, avoid taking drugs such as vasodilators, avoid drinking red wine and eating foods containing cheese, coffee, chocolate, smoked fish, etc.

2. Drug treatment: Preventive treatment is suitable for: Frequent attacks, especially those with more than one attack per week that seriously affect daily life and work; The treatment in the acute phase is ineffective, or the acute phase treatment cannot be performed due to side effects and contraindications. ; special variant migraine that may cause permanent neurological deficits, such as hemiplegia migraine, basal migraine or migraine infarction. Prophylactic drugs need to be taken daily, at least 2 weeks after the drug is effective. If there is an effect, continue to take it for 6 months, and then gradually reduce the dose to discontinuation. The clinical drugs for migraine prevention include: beta adrenergic blockers such as propranolol and metoprolol; calcium antagonists such as flunarizine and verapamil; Epilepsy drugs, such as valproic acid, topiramate; antidepressants, such as amitriptyline, fluoxetine; 5-HT receptor antagonists, such as phenothiazine. Among them, propranolol, amitriptyline, and valproic acid are three structurally unrelated drugs, which are the main preventive treatment drugs. If one drug is ineffective, another drug can be used.

Migraine disease adjustment

At present, there is no specific treatment method to eradicate migraine. The most effective treatment method is to prevent the inducing factors during the interval of migraine headache. details as follows:

Migraine away from tyrosine foods

Tyrosine is the main cause of vasospasm and easy to cause headaches. Such foods include: cheese, chocolate, citrus foods, and pickled sardines, chicken liver, tomatoes, milk, lactic acid drinks, etc.

Migraine reduces alcohol intake

All alcoholic beverages cause headaches, especially red wine contains more chemicals that cause headaches. If you must drink, it is best to choose colorless wines such as vodka and white wine.

Migraine learns to decompress

Relax, choose bubble warm water bath, do yoga and other relaxation exercises to avoid headaches.

Regular migraine exercise

For people with migraine, focusing on breathing training and breath-adjusting exercises (such as yoga and qigong) can help patients stabilize the autonomic nervous system, reduce anxiety, and tighten muscles.

Migraine life pattern

Create a quiet environment, maintain a regular schedule, and go to bed and wake up regularly even on holidays.