- Inflammation involves prostaglandins (hormone-like substances) and neuropeptides (molecules formed by the linking of amino acids) that result in vasodilation.
- Vasodilation, or widening of the blood vessels, activates pain receptors surrounding the brain called nociceptors.
- Nociceptors, or pain receptors, transmit pain signals to the higher centers of the brain, including the thalamus and cerebral cortex, creating the first sensation of pain
- Peripheral sensitization, resulting from activation of the nociceptors, leads to increased stimulation of the nerve cells in the trigeminal nerve. This prolonged stimulation of the main sensory nerve (trigeminal nerve) results in central sensitization.
This new understanding of the multi-mechanisms of migraines also explains why migraine sufferers may experience a variety of non-traditional migraine symptoms in addition to head pain and nausea or vomiting and sensitivity to light and sound. For example, stimulation of the trigeminal nerve may cause referral of pain to any of the nerve’s three branches, resulting in sinus or facial pain. It can also cause a referral of pain to the sensory nerves of the posterior head and neck, resulting in neck pain
Implications for Migraine Therapy
Current migraine-specific therapies do not fully address the multiple components of migraine pain – the inflammation, vasodilation, nociception, and peripheral and central sensitization.
Triptans treat migraines by preventing the release of inflammatory substances and pain transmitting signals. However, they do not address the inflammation, which has occurred long before a person feels pain and takes their medication, nor do they reverse central sensitization.
General pain relievers, like non-steroidal anti-inflammatory drugs (NSAIDs), do not target all of the known pain processes that occur during migraine.
There is a medical need for treatment that addresses multiple mechanisms of migraine.
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"Multi-Mechanism of Migraine: Implications for Migraine Therapy
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"Before the Pain: Understanding the
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