Watch Video About Migraine Pathophysiology



Use the lowest effective dosage for the shortest duration consistent with individual patient treatment goals. The safety and effectiveness of a second dose have not been established.

Non-Interchangeability with Other Formulations of Diclofenac
Different formulations of oral diclofenac are not bioequivalent even if the milligram strength is the same. Therefore, it is not possible to convert dosing from any other formulation of diclofenac to CAMBIA.

The Role of NSAIDs in Treating Acute Migraine Attacks

Migraine pathophysiology allows for medication intervention at multiple stages.2

  1. Environmental stimuli may trigger neurochemical changes in the migraine-sensitive brain3
    NSAIDs may have the potential to prevent the generation of prostaglandins from arachidonic acid, which may help reduce the hyperexcitability of the perivascular trigeminal nerves that innervate the meninges2
  2. Neuroactive substances activate the trigeminovascular system, causing vasodilation and neurogenic inflammation4
    NSAIDs may have the potential to suppress the neurogenic inflammatory response2
  3. Peripheral sensitization occurs2
    NSAIDs may have the potential to interrupt the process of peripheral sensitization5
  4. Central sensitization perpetuates the headache4
    NSAIDs may have the potential to treat migraine pain even after central sensitization has been established, as demonstrated with IV ketorolac2,5*

*IV ketorolac is not indicated for the treatment of acute migraine.


CAMBIA is contraindicated in the following patients:

  • Known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac or any components of the drug product.
  • History of asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs. Severe, sometimes fatal, anaphylactic reactions to NSAIDs have been reported in such patients.
  • In the setting of coronary artery bypass graft (CABG) surgery.


1. Waeber C, Moskowitz MA. Migraine as an inflammatory disorder. Neurology. 2005;64(10 suppl 2):S9-S15. 2. Cady R, Biondi DM. An update on migraine pathophysiology and mechanism-based pharmacotherapeutics for migraine. Postgrad Med. 2006;(special report):5-13. 3. Friedman DI, De Ver Dye T. Migraine and the environment. Headache. 2009;49(6):941-952. 4. Kalra AA, Elliott D. Acute migraine: current treatment and emerging therapies. Ther Clin Risk Manag. 2007;3(3):449-459. 5. Burstein R, Jakubowski M. Managing migraine associated with sensitization. In: Nappi G, Moskowitz MA, eds. Handbook of Clinical Neurology. Vol 97. 3rd series. Philadelphia, PA: Elsevier B.V.; 2011:chap 16.