Not all throbbing headaches are migraine, but many are.

 

Migraine is a neurologic condition that causes many sufferers to withdraw to a quiet, dark corner and lie quietly until the attack ends.  The condition, according to the Penn medicine website “impacts over 37 million men women and children in the U.S.”  And (per Danish Professor Messoud Ashina) affects about a billion people, mainly females, worldwide.  That’s one in 8 of us. 

Ashina “describes migraine as a condition where people suffer from recurrent headaches of moderate-to-severe pain that last 4 to 72 hours—and/or in people whose head pain that is unilateral, pulsating, and aggravated by physical activity. 

·         Some of these people will experience “nausea, vomiting, photophobia, and phono-phobia, and some say their severe headaches are “preceded by an aura, which is characterized by reversible focal neurologic symptoms, typically comprising visual or hemi-sensory disturbances.”

There’s much that sufferers and non medical people do to prevent and moderate attacks.  They are not the subject of this blog. 

Recent research and treatments have focused on the role of the fifth cranial nerve-the trigeminal nerve.  There are 12 cranial nerves.  2 start in the brain; The other ten emerge from the brain stem, a stalk-like part of the nervous system that connects the brain and the spinal cord.  Some cranial nerves help regulate the heart and breathing rate.  Others control the motor and sensory functions of the face and neck.  The trigeminal nerve supplies most of the nerve and motor function of the head.  Its activation is believed to often be largely responsible for the headache and neurological phenomenon of migraine.  In these people the trigeminal nerve releases vasoactive peptides—CGRP—calcitonin gene-related peptides.  Peptides (small proteins).  When they participate in a migraine attack the peptides induce an inflammatory reaction and trigger other neurons in the brain stem and the thalamus.

Insights from clinical models of migraine and supportive preclinical data were the basis for the development of therapies that block CGRP.  Some but not all of these treatments are effective for the treatment of migraine. Some provide only modest therapeutic benefits.   Three small CGRP antagonists have proved beneficial for the initial treatment of migraine, and four monoclonal antibodies targeting CGRP or its receptor have often proved effective for the prevention of migraine.  The drugs are expensive and don’t always work.

Before going to these new drugs, Dr. Ashina, the Danish neurologist, suggests that a person who feels a migraine coming on should immediately start taking a medication that alleviates or removes the pain. He recommends a nonsteroidal antiinflammatory drug like ibuprofen, aspirin, or diclofenac.

When that’s not working he tries a triptan—like sumatriptin. There are currently seven oral triptans (almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan, and zolmitriptan) available.  In some people one works and a second doesn’t.  Subcutaneous sumatriptan is the most effective dosing method on the basis of the proportion of patients who report freedom from pain at 2 hours after treatment.  Its use is limited because it costs more and is less widely available than oral triptans. Subcutaneous sumatriptan is therefore first offered when a patient has had inadequate pain relief from oral triptans.

When these approaches fail he tries drugs that target CGRP or its receptor.

==A 6 week study of migraine sufferers who had a migraine 7.5 to 7.9 days a month was published in the New England Journal of Medicine in 2021.  It found that Atogepant, an oral, small-molecule, calcitonin gene–related peptide receptor antagonist, decreased the frequency of migraine attacks.   In the study 214 patients took 10-mg of atogepant daily.  223 took 30-mg, and 222 swallowed a 60-mg pill. An additional 214 migraine sufferers were given a placebo.  At 6 weeks the people who took the placebo had attacks on 2.5 fewer days, those taking 10 mg of Atogepant--3.7 fewer days, people taking 30mg 3.9 fewer days, and those ingesting 60 mg 4.2 fewer days. Adverse events included constipation and nausea.

https://www.nejm.org/doi/full/10.1056/NEJMoa2035908

==A 6 week study of migraine sufferers who had a migraine 7.5 to 7.9 days a month was published in the New England Journal of Medicine in 2021.  It found that Atogepant, an oral, small-molecule, calcitonin gene–related peptide receptor antagonist, decreased the frequency of migraine attacks.   In the study 214 patients took 10-mg of atogepant daily.  223 took 30-mg, and 222 swallowed a 60-mg pill. An additional 214 migraine sufferers were given a placebo.  At 6 weeks the people who took the placebo had attacks on 2.5 fewer days, those taking 10 mg of Atogepant--3.7 fewer days, people taking 30mg 3.9 fewer days, and those ingesting 60 mg 4.2 fewer days. Adverse events included constipation and nausea.

https://www.nejm.org/doi/full/10.1056/NEJMoa2035908

---in another study 500 plus people having a migraine attack were treated with a 75 mg pill of an Oral Calcitonin Gene–Related Peptide Receptor Antagonist named rimegepant.  500 were given a placebo.  19.6% of the people who took rimegepant group and 12.0% who took a placebo were pain free 2 hours after receiving the medicine 

https://www.nejm.org/doi/full/10.1056/nejmoa1811090


https://www.nejm.org/doi/full/10.1056/NEJMra1915327

https://en.wikipedia.org/wiki/Brainstem

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