Nat Rev Neurol. 2010 Oct;6(10):573-82. Epub 2010 Sep 7.
CGRP and its receptors provide new insights into migraine pathophysiology.
Ho TW, Edvinsson L, Goadsby PJ.
Clinical Neuroscience, Merck Research Laboratories, North Wales, PA 19454-1099, USA.
Over the past 300 years, the migraine field has been dominated by two main theories-the vascular theory and the central neuronal theory. The success of vasoconstrictors such as ergotamine and the triptans in treating acute migraine bolstered the vascular theory, but evidence is now emerging that vasodilatation is neither necessary nor sufficient to induce a migraine attack. Attention is now turning to the core migraine circuits in the brain, which include the trigeminal ganglia, trigeminal nucleus, medullary modulatory regions, pons, periaqueductal gray matter, hypothalamus and thalamus. Migraine triggers are likely to reflect a disturbance in overall balance of the circuits involved in the modulation of sensory activity, particularly those with relevance to the head. In this Review, we consider the evidence pointing towards a neuronal mechanism in migraine development, highlighting the role of calcitonin gene-related peptide (CGRP), which is found in small to medium-sized neurons in the trigeminal ganglion. CGRP is released during migraine attacks and can trigger migraine in patients, and CGRP receptor antagonists can abort migraine. We also examine whether other drugs, such as triptans, might exert their antimigraine effects via their actions on the neuronal circuit as opposed to the intracranial vasculature.
Ok so check it out, when a patient is treated with FCR the trigeminal nucleus is effected in a big way! The trigemonal nerve innervates the sinus’ and the face. Releasing the “stress” to the pathways to the trigeminal nucleus is exactly why we see such good results with migraine patients. Why not just the problem instead science is looking for a chemical or drug the block the CGRP. You see the CGRP is released by the Trigeminal nucleus and it causes a migraine. You block the receptor sites for CGRP, which block its ability to act on the brain and therefore no migraine. Well in a healthy brain there is a majority of the efforts in inhibition. That means your brain is calming or blocking many signals. This is healthy! Loss of this inhibition i.e. loss of the control of CGRP release from the trigeminal nucleus. FCR resets the resting state of the neuronal pools in the trigeminal nucleus.
Yours in Health,
John Lieurance, DC