Migraine is a very old and common disease. It was described as early as 3,000 years ago and was named migraine by the famous ancient Greek physician Hippocrates 2,500 years ago and has been used ever since. It is important to note that migraine is often recognized by its name and thus misunderstood in the sense that only migraine with dramatic relief is a migraine. In fact, although a significant proportion of migraine headaches do occur on one side, this is not always the case. Statistically, migraine is only 60% of migraine, while the rest of the headaches are bilateral. In many patients, the headache does not stop suddenly and dramatically.
Migraine is a common clinical condition characterized by diffuse or unilateral attacks, severe pain, and recurrent attacks. If you use the keyword “migraine” in Baidu, you will find about 1,800,000 related web pages in 0.001 seconds. This shows the extent of concern for migraine.
According to overseas data, the incidence of migraine is 12.9%-17.6% for women and 3.4%-6.1% for men. The prevalence of migraine in China is 985.2/100,000, with an annual incidence of 79.7/100,000. The recurrent attacks of the disease are difficult to be cured and cause great pain to patients.
Clinical manifestations.
Migraine is characterized by throbbing, unilateral episodic headaches, sometimes severe, without aura (formerly called generalized migraine) attacks usually accompanied by nausea, vomiting, or overreaction to sound, light, or movement, and can usually last 4 to 72 hours if left untreated. Migraine is diagnosed in patients with these clinical features, but not all of them are present in every attack or in every patient.
Pathogenesis.
It is currently believed that migraine is a paroxysmal abnormal response of local intracranial and extracranial vessels to neurohumoral regulatory mechanisms based on genetic qualities Tension and fear, agitation sleep deprivation, climate change noise, flash stimulation intake of certain special foods such as cheese and chocolate can trigger migraine attacks. The true etiology and pathogenesis of migraine are not yet clear, and many theories have been proposed, but the impairment of intracranial and extracranial vasodilatation during migraine attacks has been confirmed.
1. Genetic factors
It is now believed that migraine is genetically related, with a positive family history of 50%-80%. If both parents suffer from migraine, their children suffer from migraine about 70% of the time; the chance of children of single parents suffering from migraine is about 50%; the co-occurrence rate of monozygotic twins is more than 50%. These indicate the important role of genetic factors in the development of migraine, which is polygenic with the exception of basilar migraine and familial hemiplegic migraine, which are autosomal dominant. The causative gene of familial hemiplegic migraine may be located at 19p13.1-13.2 Ducros et al. in 1997 identified the causative gene of familial hemiplegic migraine at 1q21-23, suggesting that the disease is genetically heterogeneous.
2.The theory of vascular origin
In the 1990s, Olsen further developed the vascular origin theory, suggesting that migraine with and without aura is the same disease with different degrees of vascular spasm.
3. Neurogenic theory
It is believed that changes in neurological function are primary in migraine when changes in blood flow are secondary.
(1) Neurotransmitter hypothesis: 5-HT has an important role in the development of migraine, which can cause aseptic inflammation in the blood vessel wall or cause a decrease in local cerebral blood flow through receptors that cause cerebral vasoconstriction and headache. β-endorphin, methiodorphin, substance P catecholamines, histamine vasoactive peptide and prostacyclin are also neurotransmitters that are associated with the development of migraine.
(2) Diffuse inhibition hypothesis (CSD): It refers to the inhibition of cortical electrical activity that occurs in waves from the stimulation site to the surrounding tissues after various factors stimulate the cerebral cortex. This inhibition is in the form of waves that pass very slowly through the cortical area. The diffuse inhibition is accompanied by a significant decrease in cerebral blood flow (lasting 2-6 h).
4. Trigeminal vascular reflex theory
It refers to the release of substance P and other neurotransmitters from trigeminal afferent fiber endings, which act on intracranial and extracranial vessels via efferent nerves, causing headache and vasodilatation. Migraine, as an unstable trigeminal-vascular reflex, is accompanied by segmental defects in pain control pathways that allow excessive impulses from the trigeminal spinal nucleus to be released and excessive afferent impulses from the trigeminal thalamic tract or corticomedullary tract to be responded to. The brainstem interacts with the intracranial vasculature.
5. Other theories
There are other theories about the pathogenesis of migraine, such as low magnesium theory, high potassium induced vasospasm theory, autonomic dysfunction theory and brain cell current disorder theory.
Treatment of migraine
There are two types of treatment: pharmacological and non-pharmacological. One is the preventive treatment that is taken every day with or without migraine attacks to reduce the frequency of attacks and the degree of pain. The second is the treatment of migraine attacks. The latter treatment medications can be further divided into migraine-specific and non-specific medications. Nonspecific medications such as aspirin, acetylated amino acids, noncorticosteroid anti-inflammatory drugs, opiates, and combination pain relievers are used to treat a wide range of painful disorders. Atopic medications include ergotamine, dihydroergotamine, and tretinoin, which are effective in treating migraine and cluster headache, but are different from treating other types of pain.
1. General treatment
Resting in a dark room during the attack is recommended. Generally, if the patient can fall asleep, the headache can be relieved on its own after waking up.
2. Drug treatment
Usually analgesic and sedative drugs should be given early for mild to moderate headache, and antipyretic and analgesic drugs should be used for moderate to severe headache. For those with nausea and vomiting, metoclopramide (methotrexate) or chlorpromazine can be used; for those with vertigo or dizziness, diphenhydramine (vertigo stop) or scopolamine can be used.
(1) Antipyretic and analgesic drugs: acetaminophen (paracetamol) 10-15mg/(kg times), aspirin (aspirin) 10-15mg/kg each time, ibuprofen (ibuprofen) 5-10mg/kg each time, naproxen (naproxen) 5-10mg/kg each time, etc. are commonly used in the early stage of headache. (2) Ergotamine preparation
(2) Ergotamine preparation: such as ergotamine and dihydroergotamine have constricting effect on extracranial arteries. The commonly used compound tablet is ergotamine caffeine (each tablet contains 1mg of ergotamine and 100mg of caffeine), and the dosage for school-age children is 1 tablet each time, which is effective in terminating headache attacks but must be taken at the appearance of aura or when headache first appears (early attack), otherwise it is ineffective.
(3) Triptans: Sumatriptan is a selective 5-hydroxytryptamine agonist with highly selective carotid artery constriction, which is an effective and expensive drug for the treatment of acute migraine attacks. However, its experience in pediatric migraine is limited.
3. Drug prevention for those who still have headache attacks
The following medications can be given to those who still have headache
(1) β-blockers: Propranolol (Takeostasis) is commonly used at a dose of 2 mg/kg per day, divided into 3 oral doses. To prevent hypotension and heart rate slowing adverse reactions, should be a small amount (0.5-1mg/kg per day) to slowly increase the amount until tolerated. The course of treatment is generally 6-12 months after the control of the disease slowly tapered off to avoid the rebound phenomenon of symptoms with a history of asthma is prohibited.
(2) Histamine receptor blockers: commonly used cyproheptadine dose of 0.2-0.4mg/kg per day for 6-12 months or longer.
(3) 5-hydroxytryptamine receptor blocker: commonly used benzothiazide (pizotifen), and histamine receptor antagonism. The dose is 0.5-1mg per time 2-3 times / d glaucoma is prohibited
(4) calcium channel blocking drugs: commonly used flunarizine (flunarizine ciprofloxacin), the dose is 2.5-5mg every night at bedtime, the general course of treatment for 2-3 months.
(5) other drugs: valproic acid (valproic acid) carbamazepine (carbamazepine) colistin (clonidine) phenelzine (phenelzine) amitriptyline (amitrptyline), etc.
Ergotamine and dihydroergotamine are a class of ergotoxine derivatives, which were developed and researched earlier, and have long been used as common drugs for migraine in western countries before the introduction of tritone-based therapeutic drugs. Although these drugs can effectively relieve migraine, their side effects are mainly nausea, abdominal pain and cramps, especially oral ergotamine. Recently, a nasal spray containing ergotamine and dihydroergotamine was introduced abroad, which can relieve migraine headache symptoms within a few minutes by spraying into the nasal cavity when migraine attacks occur.
With the increasing understanding of the pathogenesis of migraine, 5-hydroxytryptamine agonists have been developed as effective drugs for acute migraine attacks. Since the introduction of the first triton, sumatriptan, in February 1991, research on tritons has been flourishing and promising. There are three possible mechanisms of action of tritans: constriction of cerebral blood vessels, inhibition of peripheral nerves, and inhibition of transmission through second-level neurons of the trigeminal nerve cervical complex. Drug prophylaxis is needed for those who have more than three attacks per month, each attack lasts more than 12 hours, or have particularly pronounced symptoms.