I just got back from an appointment with my neurologist for another Botox treatment. She said that the US has approved a groundbreaking drug, which is the first of its kind to prevent migraines. She said that it will be approved in Sweden during the autumn this year. It is a shot that is taken once a month, and only given for chronic migrainuers and those who are not responding to Botox treatment.
Here is an article I found that talks all about the new drug:
By Emily Underwood, May 18, 2018
"THE FAILURE of the Substance P–blocking drugs opened the door for CGRP, an obscure, 37–amino acid peptide, discovered largely by accident by neuroscientists Susan Amara and Michael Rosenfeld of the University of California, San Diego. While studying a thyroid hormone called calcitonin, which helps regulate the body’s sodium and calcium levels, Amara and Rosenfeld found that the same gene that encodes calcitonin in the thyroid gland produces a slightly different peptide in another part of the brain. As one of the earliest examples of alternative gene splicing, which enables a single gene to produce multiple proteins, the discovery made a splash when it was published in Nature in 1982.
After finding CGRP is plentiful in brain pathways that process pain and in brain regions that regulate blood flow, neurologist Lars Edvinsson, of Lund University in Sweden, wondered whether CGRP is involved in migraines. His group soon found that CGRP can trigger what was then considered a hallmark sign of migraines: When released from the trigeminovascular nerves, it is a powerful vasodilator of cerebral blood vessels. In 1990, he paired up with neurologist Peter Goadsby, now at King’s College London, to further explore CGRP’s role in migraine patients. After getting permission to take blood samples from the jugular veins of people who had come to the emergency room for a severe migraine, the researchers measured the amounts of a range of different peptides, including Substance P, during and after attacks. “The amazing thing was that CGRP was the only peptide that was significantly released,” Edvinsson says.
At first, Edvinsson and others thought CGRP triggered migraines by expanding blood vessels in the brain. Instead, a growing pile of studies suggested that CGRP was not just a vasodilator, but a previously unknown, pain-signaling neurotransmitter. Other groups found that rising levels of CGRP in jugular blood—not patterns of abnormal blood flow—signaled a migraine attack. Then, in a pivotal 2002 study, Oleson and colleagues injected CGRP into the blood of migraineurs and found that they developed migrainelike headaches within hours, whereas nonmigraineurs got at most a mild headache. That suggested migraineurs are unusually sensitive to the peptide’s effects, Oleson says."