Let's Fit
The Pieces
Of Migraine

Is There a Need
to Reassess
Migraine Management?

Millions of people suffer from migraine in the United States.1 Although multiple medications and devices are approved for treatment, diagnosis and treatment adherence remain challenging, reflecting need for continued advancement in migraine management.1-3

According to the American Migraine Prevalence and Prevention Study


of patients suffering with migraine received a migraine diagnosis.2


of migraine patients were eligible for preventive treatment, but less than half actually received a preventive treatment.1

In a US Claims Database Study


of patients who received a new triptan prescription did not persistently refill their prescription over a 2-year period.4

Migraine Treatment

Why are

Many patients who use a migraine treatment do not achieve desired efficacy or have difficulty tolerating their medicine.5, 6 Estimates also suggest that a majority of patients who start a preventive treatment for migraine discontinue using it.2,7,8

In Migraine

Researchers continue to uncover new details about migraine. Although elusive for a long time, the underlying migraine pathophysiology is becoming clearer. There are a number of neuropeptides that have been investigated in the complex mechanism of migraine, some of which include CGRP, oxytocin, serotonin, Substance P, and vasoactive intestinal peptide (VIP). 9-11

A body of migraine research over the last few decades suggests that the release of CGRP from trigeminal nerves may play a central role in the underlying pathophysiology of migraine.12

The Migraine Story

Linking CGRP
And Migraine

A close look at the trigeminovascular system reveals the potential role of CGRP in migraine. Stimulation of the trigeminal sensory nerves causes the release of several neuropeptides, including CGRP. Although trigeminal sensory nerves store several neuropeptides, CGRP levels have been shown to be elevated during migraine and return to baseline as pain is alleviated.12

A Closer Look At The Correlation Between CGRP And Migraine12:

  • CGRP is released after nerve activation
  • Perivascular release of CGRP contributes to neurogenic inflammation by inducing vasodilation and dural mast cell degranulation
  • CGRP is involved in transmission of pain
  • CGRP levels have been found to be elevated during migraine attacks
  • Infusion of CGRP can induce migraine attacks in those susceptible to migraine headaches

Lilly's commitment to headache

Lilly has been researching headache disorders including migraine for many years, for both acute and preventive treatment. All compounds studied have had non-opiate mechanisms of action without vasoconstrictive effects.

Where to find Lilly
at congresses

Come see us to learn about our ongoing commitment to migraine research.

American Headache Society
59th Annual Scientific Meeting 2017
June 8-11, 2017 Boston, MA

Diamond Headache Clinic
Headache Update 2017
July 13-16, 2017 Lake Buena Vista, FL

The International Headache Society
18th Congress of The International Headache Society
September 7-10, 2017 Vancouver, BC

American Headache Society
2017 Scottsdale Headache Symposium
November 16-19, 2017 Scottsdale, AZ

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  1. Lipton RB, Bigal ME, Diamond M, Freitag F, Reed ML, Stewart WF; for the AMPP Advisory Group. Migraine prevalence, disease burden, and the need for preventive therapy. Neurology. 2007;68(5):343-349.
  2. Diamond S, Bigal ME, Silberstein S, Loder E, Reed M, Lipton RB. Patterns of diagnosis and acute and preventive treatment for migraine in the United States: results from the American Migraine Prevalence and Prevention Study. Headache. 2007;47(3):355-363.
  3. Kalra AA, Elliott D. Acute migraine: current treatment and emerging therapies. Ther Clin Risk Manag. 2007;3(3):440-459.
  4. Katic B, Rajagopalan S, Ho TW, Chen YT, Hu XH. Triptan persistency among newly initiated users in a pharmacy claims database. Cephalalgia. 2011;31(4):488-500.
  5. Holland S, Fanning KM, Serrano D, Buse DC, Reed ML, Lipton RB. Rates and reasons for discontinuation of triptans and opioids in episodic migraine: results from the American Migraine Prevalence and Prevention (AMPP) study. J Neurol Sci. 2013;326(1-2):10-17.
  6. Blumenfeld AM, et al. Patterns of use and reasons for discontinuation of prophylactic medications for episodic migraine and chronic migraine: results from the Second International Burden of Migraine Study (IBMS-II). Headache. 2013;53:644-655.
  7. Loder EW, Rizzoli P. Tolerance and loss of beneficial effect during migraine prophylaxis: clinical considerations. Headache. 2011;51(8):1336-1345.
  8. Berger A, Bloudek LM, Varon SF, Oster G. Adherence with migraine prophylaxis in clinical practice. Pain Pract. 2012;12(7):541-549.
  9. Edvinsson L, Uddman R. Neurobiology in primary headaches. Brain Res Rev. 2005;48(3):438-456.
  10. Tzabazis A, Mechanic J, Miller J, et al. Oxytocin receptor: expression in the trigeminal nociceptive system and potential role in the treatment of headache disorders. Cephalalgia. 2016;36(10):943-950.
  11. Aggarwal M, Puri V, Puri S. Serotonin and CGRP in migraine. Ann Neurosci. 2012;19(2):88-94.
  12. Durham PL. CGRP-receptor antagonists — a fresh approach to migraine therapy? N Engl J Med. 2004;350(11):1073-1075.