Understanding CGRP and Why Neuromuscular Dentistry Relieves and Eliminates Migraines

Calcitonin gene-related peptide is the new target for the Pharmaceutical industry for treating Migraines!  

At least three companies are currently investigating drugs to block CGRP according to: Bloomberg July 21, 2015 in an article by David Wainer titled "The Pharma Industry Thinks It Finally Has A Fix For Migraines"

According to Bloomberg, "Amgen, Alder, Lilly and Teva are developing drugs aimed at erasing those episodes entirely -- at least in some patients -- by blocking CGRPs, or calcitonin gene-related peptides, which play a role in inflammation and transmission of pain.

The Calcitonin Gene-Related Peptide is probably the same mechanism that allows Neuromuscular Dentistry to alleviate and eliminate migraines and chronic daily headaches.  CGRP is produced by the Trigemino-Vascular System in the cell bodies of trigeminal nerves located with the Trigeminal Ganglion.  This is the primary source of CRGP related to headaches.

The way Neuromuscular Dentistry affects CGRP is by removing nociceptive input to the CNS, particularly into the Trigeminal Nervous System and negating the production of CGRP.

CGRP is a potent vasodilator and works by the Trigeminal Nervous system control of blood flow to the anterior two thirds of the meninges of the brain.  This is a primary proposed mechanism in Migraine and other neurovascular pain conditions.

The drug companies want to block CGRP's that play a significant role in inflammation and transmission of pain.    They also want to partake in the estimated 8 billion dollars or more that the migraine market can generate.

According to Wikipedia:

• "In the spinal cord, the function and expression of CGRP may differ depending on the location of synthesis. CGRP is derived mainly from the cell bodies of motor neurons when synthesized in the ventral horn of the spinal cord and may contribute to the regeneration of nervous tissue after injury. Conversely, CGRP is derived from dorsal root ganglion when synthesized in the dorsal horn of the spinal cord and may be linked to the transmission of pain."

If the drug companies treat with CGRP blocking agents will this adversely interfere with healing or could it contribute to Dementia, Alzheimers or other neurological problems.  

Correcting CGRP by changing neural input into the Trigeminal Nervous System via neuromuscular dentistry is probably the safest, most physiologic and efficient means of reducing or eliminating migraines thru reduction in CGRP Levels.

Unfortunately for Migraine patients the value of treatment with drugs is 8 Billion dollars so all research is directed toward the largest financial returns.  Effective and safe migraine alleviation and elimination with SPG Blocks and Neuromuscular Dentistry receive minimal funding for studies in spite of effectiveness.

Calcitonin gene-related peptide involved in migraine from trigeminovascular system

A recent article points to the use of CRCP (Calcitonin gene-related peptide) antagonists to treat migraines. Levels of CGRP rise during migraine and experimentally injecting IV CRCP can provoke migraine. Two CGRP antagonists are being tested inthe study from Acta Neurol Belg. 2009 Dec;109(4):252-61.

CGRP is produced by the trigeminovascular system. Many patients who undergo treatment with a diagnostic neuromuscular orthotic frequently see migraines decreased and/or eliminated. A future area of study would be does Neuromuscular Dentistry work by decreasing CGRP release from the trigeminal nerve. I consider most problems to be input/output errors of the trigeminal nervous system. Do noxious inputs from the teeth, jaw muscles, jaw joints, and periodontal ligament cause surges in CRGP in susceptible individuals causing migraine.


PubMed abstract
Acta Neurol Belg. 2009 Dec;109(4):252-61.
CGRP antagonists: hope for a new era in acute migraine treatment.
Schelstraete C, Paemeleire K.

Department of Neurology, Ghent University Hospital, Ghent, Belgium.
Calcitonin gene-related peptide (CGRP) has a widespread distribution throughout the trigeminovascular system and other brain areas involved in migraine pathogenesis. Serum levels of CGRP are elevated during the migraine attack and return to normal with alleviation of pain. Intravenous injection of CGRP in migraineurs results in delayed headache similar to migraine. Since CGRP receptor antagonists lack direct vasoconstrictor activity, this therapeutic approach may offer advantages over the current mainstay of specific acute migraine treatment with 5-HT1B/1D receptor agonists (triptans), contra-indicated in patients with underlying cardiovascular disease. Intravenous BIBN4096BS (olcegepant) and oral MK-0974 (telcagepant), two CGRP-receptor antagonists, were safe and effective in the treatment of migraine attacks in Phase I and II trials. In a Phase III clinical trial, the efficacy of telcagepant 300 mg was comparable to that of zolmitriptan 5 mg. We intend to review the rationale for the use of CGRP-receptor antagonists, and to outline current developments and future perspectives.