Migraine is the most common type of primary headache in clinical practice. The main clinical manifestations are episodic moderate to severe and throbbing headaches. The headaches are mostly hemilateral, usually lasting 4 to 72 hours, and may be accompanied by nausea, vomiting, light and sound. Stimulation or daily activities can aggravate headaches, and a quiet environment and rest can relieve headaches.
The cause of migraine is not clear, and may be related to the following factors:
About 60% of migraine patients have a family history, and the risk of migraine in their relatives is 3 to 6 times that of the general population. Patients with familial migraine have not yet found consistent Mendelian inheritance, reflecting different penetrance and polygenes The interaction of genetic characteristics and environmental factors. Familial hemiplegic migraine is a clear autosomal dominant inheritance with a high degree of abnormal penetrance, which has been located at 19p13 (related to the mistranslation mutation of the voltage gate P/Q calcium channel gene expressed in the brain), 1q21 and 1q31, etc. Three disease gene loci.
Endocrine and metabolic factors
The disease is more common in women than in men, and it usually occurs during adolescence. It is easy to occur during menstruation, and it is reduced or stopped during pregnancy or after menopause. This suggests that endocrine and metabolic factors are involved in the pathogenesis of migraines. In addition, metabolic abnormalities such as serotonin (5-HT), norepinephrine, substance P, and arachidonic acid can also affect the occurrence of migraines.
Diet and mental factors
Migraine attacks can be induced by certain foods and drugs. Foods include cheese containing tyramine, meat and preserved foods containing nitrite preservatives, chocolate containing phenethylamine, food additives such as sodium glutamate (MSG) , Red wine and wine, etc. Medications include oral contraceptives and vasodilators such as nitroglycerin. Other environmental and mental factors such as tension, overwork, emotional agitation, excessive or insufficient sleep, menstruation, and bright light can also be induced.
The pathogenesis of migraine is not yet fully understood. At present, the main theories are as follows:
The traditional vascular theory believes that migraine is a primary vascular disease. Intracranial vasoconstriction causes migraine aura symptoms, and then extracranial and intracranial blood vessels dilate, and vasoactive peptides are produced in the surrounding tissues of the blood vessels, leading to aseptic inflammation and pulsating headaches. Local compression of the carotid and superficial temporal arteries, and the vasoconstrictor ergot alkaloids such as ergotamine can relieve headaches during attacks supports this theory. Neuroimaging has developed clinical applications such as TCD and PET, and further developed the theory of vascular origin, suggesting that migraine with aura and migraine without aura is the same disease with different degrees of vasospasm. Various neurons have different sensitivity to ischemia. The appearance of aura symptoms is due to vasoconstriction and decreased blood flow. Neurons in the visual cortex are most sensitive to ischemia. Therefore, visual auras appear first, and then more and more. Neuronal function is affected, and other neurological symptoms such as finger numbness gradually appear.
Neurology believes that changes in nerve function during migraine attacks are the primary, and changes in blood flow are secondary. Migraine aura is caused by cortical spreading depressing (CSD). CSD refers to the inhibitory zone of nerve electrical activity originating from the posterior cortex of the brain (occipital lobe) caused by various harmful stimuli. This inhibitory zone expands to the adjacent cortex at a speed of 2 to 5 mm/min and is accompanied by expansive blood volume reduction. (Spreading oligemia).
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