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In the 1940's and 1950's, migraine headache was thought to be vascular in nature and that vasoconstriction (contraction of blood vessels) was responsible for the aura and that subsequent vasodilation (swelling of blood vessels) caused the pain. However, the latest thinking regarding the cause or mechanism of migraine headaches is a neurovascular theory - i.e. a complex series of neurological and vascular events occur and result in migraine headache. It is known that migraine headache is related to a change in the levels of a neurotransmitter in the brain called serotonin which is responsible for transmitting pain messages. While increased serotonin levels causes constriction of the blood vessel walls, decreased levels of serotonin result in dilation of the blood vessel walls which results in the pain of migraine headache.

It appears that there are functional changes in the trigeminal nerve which is a cranial nerve that has many branches that innervate the face, temples, and head. It is also a major pain pathway. Researchers believe that for unknown reasons, the level of serotonin drops and this may cause the trigeminal nerve to release chemicals that cause the blood vessels to dilate (expand). The swollen blood vessels send pain signals to the area of the brain that processes pain (brainstem) which results in pain being felt along the trigeminal pathways, i.e., eyes, temple, face, jaw, sinus, and sometimes the neck. This is why some people are sensitive to anything touching their head during an attack, such as combing or brushing hair.

It is believed that there are numerous triggers that can stimulate the chain of events leading to migraine headache.