A typical migraine attack is thought to have five phases: prodromal, aura, headache (attack) ,remission, and recovery. There are various triggering factors of migraine such as stress, menstruation, hunger, lower atmospheric pressure, lack of sleep, excessive sleep, smells, neck tension, strong light, alcohol, tobacco, diet, exercise, and sexual activity. Most of the migraine prodromal symptoms are related to the hypothalamus, which is the center of autonomic nervous system regulating hormones, feeding, and sleep, and can trigger headache attacks. Migraine patients notice increased appetite, light/sound sensitivity, fatigue, and swelling during the premonitory period, and PET scans have demonstrated activation of the hypothalamus, periaqueductal gray matter, and dorsal pons during the premonitory period in patients with migraine, and fMRI showed increased functional connectivity of hypothalamus, dorsal pons, and spinal trigeminal nucleus during the premonitory phase. Cortical spreading depression (CSD) is considered to be a phenomenon related to aura, but migraine without aura (MO) cannot be explained by the onset mechanism of CSD. In MO, the hypothalamus is thought to be directly affected by external and internal triggers and it activate migraine generators in the periaqueductal gray matter and the other areas. This article provides an overview of the relationship between migraine-inducing factors and the hypothalamus, triggers of CSD development, and recently identified migraine-inducing substances.
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