NSAIDs in the Acute Treatment of Migraine: A Review of Clinical and Experimental Data

Abstract

Migraine is a common disabling neurological disorder with a serious socio-economical burden. By blocking cyclooxygenase nonsteroidal anti-inflammatory drugs (NSAIDs) decrease the synthesis of prostaglandins, which are involved in the pathophysiology of migraine headaches. Despite the introduction more than a decade ago of a new class of migraine-specific drugs with superior efficacy, the triptans, NSAIDs remain the most commonly used therapies for the migraine attack. This is in part due to their wide availability as over-the-counter drugs and their pharmaco-economic advantages, but also to a favorable efficacy/side effect profile at least in attacks of mild and moderate intensity. We summarize here both the experimental data showing that NSAIDs are able to influence several pathophysiological facets of the migraine headache and the clinical studies providing evidence for the therapeutic efficacy of various subclasses of NSAIDs in migraine therapy. Taken together these data indicate that there are several targets for NSAIDs in migraine pathophysiology and that on the spectrum of clinical potency acetaminophen is at the lower end while ibuprofen is among the most effective drugs. Acetaminophen and aspirin excluded, comparative trials between the other NSAIDs are missing. Since evidence-based criteria are scarce, the selection of an NSAID should take into account proof and degree of efficacy, rapid GI absorption, gastric ulcer risk and previous experience of each individual patient. If selected and prescribed wisely, NSAIDs are precious, safe and cost-efficient drugs for the treatment of migraine attacks.

Effects of NSAIDs on the Release of Calcitonin Gene-Related Peptide and Prostaglandin E2from Rat Trigeminal Ganglia

“…Although NSAIDs have been used clinically for many years, and it is well known that their effects involve inhibition of the two cyclooxygenases (COX-1/-2) expressed throughout the body, it is not clear which mechanism, apart from the established inhibition of prostaglandin synthesis, defines their different clinical profiles, which are highly relevant for the treatment of migraine in patients. Comparative studies between NSAID effects in headache or migraine models are only few [ 12 , 13 ]. In particular, very little is known about the effect of NSAIDs on CGRP in the trigeminal vascular system, but some recent evidence indicate that both nonselective and COX-2-selective inhibitors in vitro are able to block CGRP release from cultured TG cells [ 13 ].…”

Novel Intranasal Delivery of Sumatriptan as a Route to Rapid and Sustained Relief in the Acute Treatment of Migraine

“…24 This is largely due to their availability without a prescription, familiarity, effectiveness in mild attacks, and mostly favorable side effect profiles. 31,32 These treatments include acetylsalicylic acid, ibuprofen, diclofenac, metamizole, naproxen sodium, indomethacin, and ketoprofen. NSAIDs are mainly given orally but some can be administered rectally or parenterally in cases that are resistant to treatment or in emergencies.…”

Systems pharmacology to decipher the combinational anti-migraine effects of Tianshu formula

“…(cyclooxygenase 2, PTGS2) inhibitors are by far the most frequently-used drugs for the acute treatment of migraine headaches (Farinelli et al, 2009;Pardutz and Schoenen, 2010), which inhibit the COXs (PTGS1 and/or PTGS2) activities and then decrease the prostaglandin synthesis to relieve the migraine-related inflammation and pain (Farinelli et al, 2009). Fortunately, 5 compounds of R. chuanxiong, including M005, M006, M062, M122 and M233, may have interactions with PTGS2 and/or PTGS1, which are expected to offer the same therapeutic benefits to migraine patients as the NSAIDs or selective COX2 inhibitors.…”