2022 年 39 巻 3 号 p. 200-203
The trigeminovascular theory is currently widely accepted as a pathological hypothesis for migraine. Cortical spreading depression (CSD) evoked by unidentified cause may stimulate the trigeminal nerves distributed in the dural and cerebral pial arteries. Inflammatory neurotransmitters such as calcitonin gene–related protein (CGRP) and substance P are released from the trigeminal nerve endings, causing local aseptic inflammation. This local condition propagates to the periphery via axons and further spreads aseptic inflammation, and is transmitted from the trigeminal nerve to the cerebral cortical sensory area via the brain stem, causing pain and various symptoms. Furthermore, it has been suggested that the sensitization phenomenon and the descending pain modulatory pathways are involved in the headache attacks, and that the hypothalamus is involved in the prodrome stage of headache.
In addition to triptans and analgesics, empirical medication for the prophylaxis have been used to treat migraine. CGRP has been shown to play a major role in the pathophysiology of migraine in recent years. Studies have suggested that blocking CGRP signaling is an effective preventive and therapeutic strategy in patients with migraine. In Japan, two anti–CGRP antibody drugs and one anti–CGRP receptor antibody drug were launched in 2021, and their usefulness has been shown in clinical practice.
