First of all, let me understand what migraine means
Migraine is the most common type of primary headache, mainly manifested by episodes of moderate-to-severe, throbbing headache, which is mostly hemiplegic and usually lasts for 4 to 72 hours. Migraine is a common chronic neurovascular disorder that starts in childhood and adolescence, with peak incidence in middle-aged and young adults, and is more common in women.
Causes of morbidity.
The etiology of migraine is unclear and may be related to the following factors.
Genetic factors
Approximately 60% of migraine patients have a family history of migraine, and their relatives are at 3-6 times greater risk of developing migraine than the general population. Consistent Mendelian inheritance patterns have not been found in familial migraine patients, reflecting the interaction of different epistatic rates and polygenic genetic characteristics with environmental factors. Familial hemiplegic migraine is clearly an autosomal dominant inheritance with a high abnormal epistasis and has been localized to three disease loci including 19p13 (associated with mismatched mutations in the brain-expressed voltage-gated P/Q calcium channel gene), 1q21 and 1q31.
Endocrine and metabolic factors
The disease is more frequent in females than in males, with onset in adolescence, easy onset during menstruation, and reduction or cessation of onset during pregnancy or after menopause. This suggests that endocrine and metabolic factors are involved in the development of migraine. In addition, abnormalities in the metabolism of 5-hydroxytryptamine (5-HT), norepinephrine, substance P and arachidonic acid can also affect the occurrence of migraine.
Dietary and psychiatric factors
Migraine attacks can be triggered by certain foods and medications, including tyramine-containing cheese, meat and cured foods containing nitrite preservatives, phenylethylamine-containing chocolate, food additives such as monosodium glutamate (MSG), red wine and wine. Medications include oral contraceptives and vasodilators such as nitroglycerin. Other environmental and psychological factors such as stress, overwork, emotional stress, excessive or insufficient sleep, menstruation, and bright light can also trigger the condition.
Pathogenesis
The pathogenesis of migraine is not well understood, but the following theories are the main ones.
Vascular theory
The traditional vascular theory suggests that migraine is a primary vascular disease. Intracranial vasoconstriction causes migraine aura symptoms, followed by extracranial and intracranial vasodilatation and production of vasoactive peptides in the perivascular tissue leading to sterile inflammation resulting in pulsatile headache. Local compression of carotid and superficial temporal arteries, and vasoconstrictor ergot alkaloids such as ergotamine can relieve episodic headache support this theory. Neuroimaging development of TCD, PET and other clinical applications further developed the vascular origin theory, suggesting that aura and aura-free migraine are the same disease with different degrees of vasospasm. Various neurons have different sensitivities to ischemia, and aura symptoms appear due to vasoconstriction and reduced blood flow after which neurons in the visual cortex are most sensitive to ischemia, so visual aura appears first, and then more and more neuronal functions are affected, and then other neurological symptoms such as numbness of fingers gradually appear.
Neurological theory
The neurological theory suggests that changes in neurological function during a migraine attack are primary and changes in blood flow are secondary. Migraine aura is caused by cortical spreading depressing (CSD), which is a band of inhibitory neuroelectrical activity originating in the posterior cerebral cortex (occipital lobe) caused by various noxious stimuli, extending to the adjacent cortex at a rate of 2-5 mm/min, and accompanied by spreading oligemia. spreading oligemia). Both do not follow the distribution of cerebral arteries, but rather follow the pattern of cortical cellular architecture and generally do not extend beyond the central sulcus, and CSD is a good explanation for migraine aura symptoms. In addition, 5-hydroxytryptamine (5-HT) is involved in headache onset. At the beginning of a headache attack, 5-HT is released from platelets and acts directly on small intracranial blood vessels to constrict them and attach them to the vessel walls. When the plasma 5-HT concentration decreases, it acts on the large arteries and the tensional constricting effect disappears, and the blood vessel wall dilates. 5-HT is both a neurotransmitter and a humoral mediator, affecting both nerves and blood vessels. Tretinoin drugs for migraine are central 5-HT receptor agonists or partial agonists. This confirms the involvement of neurological dysfunction in the process of migraine attacks.
Trigeminal vascular theory
The anatomical and physiological basis of this theory is the trigeminovascular complex. Intracranial pain-sensitive tissues such as cerebral blood vessels, meningeal vessels, and venous sinuses have perivascular nerve fibers that enter the trigeminal ganglion with the ophthalmic branch of the trigeminal nerve or enter the posterior roots of the 1 and 2 cervical nerves (C1 and C2) from the posterior cranial fossa; both of them send nerve fibers to the trigeminocervical complex after the transposition of the trigeminal ganglion and the C1 and C2 spinal ganglia. The trigeminocervical complex is composed of the caudal end of the trigeminal spinal nucleus and the posterior horn of C1 and C2; the trigeminocervical complex emits nerve fibers that cross the brainstem and project to the thalamus. The peripheral pain mechanism of this theory suggests that damage to the trigeminal ganglion may be the neural basis for migraine production. When the trigeminal ganglion and its fibers are stimulated, they cause an increase in the release of substance P (SP), calcitonin gene-related peptide (CGRP), and other neuropeptides. These active substances act on the adjacent cerebral vascular wall, causing vasodilation and pulsatile headache, as well as increased vascular permeability and plasma protein leakage, producing sterile inflammation and stimulating nociceptive fibers to the center, creating a vicious cycle.
Pathophysiology
Intracranial pain-sensitive tissues such as cerebral blood vessels, meningeal vessels, venous sinuses, their perivascular nerve fibers and trigeminal nerve may be the physiological basis of migraine occurrence and nociceptive transmission pathways. Electrical stimulation of the trigeminal ganglion can lead to aseptic inflammation of the dural vessels. The trigeminal vascular reflex theory of migraine suggests that migraine is caused by the release of substance P (SP) and other neurotransmitters from the afferent fiber endings of the trigeminal nerve, and the efferent nerve acts on the intracranial and extracranial vessels, causing headache and vasodilation. The most prominent neuropeptide associated with the trigeminal system is 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 vasodilating effect and causes headache by dilating blood vessels.
Clinical manifestations
Frequent migraine attacks will affect the patient’s life and work, and most directly affect sleep, because lack of sleep will make the patient unrefreshed during the day, and work will be greatly affected. Moreover, some patients often have attacks as soon as they work, which is very delayed. At the same time, when people suffer from headache disease for a long time, their personality changes and they often become irritable. Because the headache is not cured for a long time, life is greatly affected, psychological vulnerability and loss of confidence, and it will have adverse effects on the cardiovascular and cerebrovascular system in the long run. The following are the clinical manifestations of the main types of migraine.
Migraine without aura
Migraine without aura is the most common type of migraine, accounting for about 80%. There may be no obvious aura symptoms before the onset of migraine, but some patients have mental disorder, fatigue, yawning, loss of appetite and general discomfort before the onset of migraine, and the pain may be triggered by menstrual flow, alcohol consumption and hunger on an empty stomach. The headache is slowly aggravated, with recurrent episodes of frontotemporal pain on one or both sides, which is pulsatile. It is often accompanied by nausea, vomiting, photophobia, phonophobia, sweating, general discomfort, and scalp tenderness. Compared with migraine with aura, migraine without aura has a higher frequency of attacks, which can seriously affect the patient’s work and life, and often requires frequent treatment with painkillers.
Migraine with aura
Migraine with aura accounts for about 10% of migraineurs. It may be preceded by symptoms such as tiredness, lack of concentration and yawning for hours to days before the onset of the attack. The most common aura is visual aura, such as blurred vision, dark spots, flashes of light, bright spots and bright lines, or distortion of vision; followed by sensory aura, with sensory symptoms mostly distributed in the face-hand region; speech and motor aura are rare. Aura symptoms usually develop gradually within 5-20 minutes and last no more than 60 minutes; different aura can appear one after another. Headache occurs at the same time as or within 60 minutes after the aura and is manifested as a one-sided or bilateral frontotemporal or retro-orbital pulsating headache, often accompanied by nausea, vomiting, photophobia or phonophobia, pallor or sweating, polyuria, irritability, odor terror and fatigue, etc. Head and facial edema and temporal artery prominence are seen. The headache can be aggravated by activity and relieved by sleep. The pain usually peaks in 1~2 hours and lasts for 4~6 hours or more than 10 hours, and can last for several days in severe cases. After the headache subsides, there are often fatigue, lethargy, irritability, weakness and poor appetite.
(1) Migraine headache with typical aura: It is the most common type of migraine with aura, and the aura is completely reversible visual, sensory or verbal symptoms, but no physical weakness. Migrainous headache with typical aura is defined as a headache that occurs simultaneously with or within 60 minutes after the aura and is consistent with the characteristics of migraine. If the headache that occurs simultaneously with or within 60 minutes after the aura is not consistent with migraine, it is called non-migraine headache with typical aura; when the headache does not occur within 60 minutes after the aura, it is called typical aura without headache. The latter two should be distinguished from transient ischemic attacks.
(2) Hemiplegic migraine hemiplegic migraine: It is rare in clinical practice. In addition to motor weakness, the aura should include one of the three types of aura: visual, sensory and verbal. The aura lasts from 5 minutes to 24 hours, and the symptoms are completely reversible. If at least one of the first- or second-degree relatives of a person with hemiplegic migraine has a migraine aura that includes motor weakness, the migraine is familial hemiplegic migraine; if not, it is called sporadic hemiplegic migraine.
(3) Basal migraine: The aura symptoms clearly originate from the brainstem and/or both cerebral hemispheres, and clinical symptoms include dysarthria, vertigo, tinnitus, hearing loss, diplopia, simultaneous visual symptoms in the nasal and temporal visual fields of both eyes, ataxia, impaired consciousness, and simultaneous sensory abnormalities bilaterally, but no motor weakness symptoms. Headache consistent with migraine characteristics, often accompanied by nausea and vomiting, occurs at the same time as or within 60 minutes of the aura.
Retinal migraine
Retinal migraine is a recurrent, fully reversible monocular visual disturbance, including flickering, dark spots, or blindness, with migraine attacks, with normal interictal ophthalmologic examination. Unlike basal migraine, in which visual aura symptoms often involve both eyes, retinal migraine visual symptoms are limited to one eye and lack neurological deficits or irritation originating in the brainstem or cerebral hemispheres.
Childhood periodic syndrome
Childhood periodic syndrome, which is often a precursor to migraine, can be considered a migraine isochronism and is characterized by periodic vomiting, recurrent abdominal pain with nausea and vomiting, i.e., abdominal migraine, and benign childhood-onset vertigo. The attacks are not accompanied by headache, and migraine may occur over time.
Complications of migraine
(1) Chronic migraine: Migraine can be considered as chronic migraine if the headache attacks are more than 15 days per month for 3 months or more, and headache caused by drug overdose is excluded.
(2) Persistent migraine: Migraine attacks lasting ≥ 72 hours and with severe pain, but there may be a brief period of remission obtained by sleep or medication application in between.
(3) Persistent aura without infarction: Patients with migraine with aura have one aura or multiple aura symptoms lasting more than 1 week in one attack, mostly bilateral; other symptoms of this attack are similar to those of previous attacks; neuroimaging must exclude cerebral infarction lesions.
(4) Migrainous infarction: In rare cases, ischemic infarction in the corresponding blood supply area of the skull occurs after migraine aura symptoms; this aura symptom usually lasts for more than 60 minutes and the ischemic infarction lesion is confirmed by neuroimaging, which is called migrainous infarction.
(5) Migraine-induced epileptic seizure: In rare cases, migraine aura symptoms can trigger an epileptic seizure, and the epileptic seizure occurs during or within 1 hour after the aura symptoms.
Oculomotor paralysis migraine
Oculomotor palsy migraine is characterized by recurrent migraine-like headaches, with headache attacks occurring simultaneously with or within 4 days of ocular muscle paralysis on the headache side. In some cases, MRI-enhanced scans may indicate recurrent demyelination of the affected motor nerve. Therefore, there is a tendency not to consider oculomotor palsy migraine as a subtype or variant of migraine.
Diagnosis
The IHS (2004) Migraine Diagnostic Criteria for Migraine provide for the diagnosis of different types of migraine as follows.
Diagnostic criteria for migraine without aura
(1) At least five attacks meeting the characteristics of (2) to (4).
(2) Headache attacks (untreated or unsuccessful in treatment) lasting 4 to 72 hours.
(3) At least two of the following headache characteristics: (1) unilateral; (2) throbbing; (3) moderate or severe headache; (4) headache aggravated by daily activities (such as walking or walking up stairs) or actively avoided when having a headache.
(4) The headache is accompanied by at least one of the following: (1) nausea and/or vomiting; (2) photophobia and phonophobia.
(5) The headache cannot be attributed to other diseases.
Diagnostic criteria for migrainous headache with typical aura
(1) At least 2 attacks that meet the characteristics of (2) to (4).
(2) At least one of the following symptoms is present in the aura, but there is no motor weakness: (1) fully reversible visual symptoms, including positive (e.g., flashes, bright spots, or bright lines) and/or negative (e.g., visual field defects); (2) fully reversible sensory abnormalities, including positive (e.g., pins and needles) and/or negative (e.g., numbness); (3) fully reversible speech dysfunction.
(3) At least 2 of the following are satisfied: (i) isotropic visual symptoms and/or unilateral sensory symptoms; (ii) gradual progression of at least 1 aura symptom for ≥ 5 minutes, and/or different aura symptoms occurring one after another for ≥ 5 minutes; (iii) each aura symptom lasts 5 to 60 minutes.
(4) The headache occurs simultaneously with the aura symptoms or within 60 minutes after the onset of the aura, and the headache meets items (2) to (4) of the diagnostic criteria for migraine without aura.
(5) It cannot be attributed to other diseases.