Relevance of Prostaglandins in True Menstrual Migraine

Abstract

Eighteen patients suffering from true menstrual migraine and 12 control subjects were studied. We evaluated in different phases of the menstrual cycle and during the migraine crisis the peripheral plasma concentrations of 6-keto-PGF1 alpha (the stable metabolite of PGI2), thromboxane B2 (the stable metabolite of thromboxane A2), PGF2 alpha and PGE2. The mean values of 6-keto-PGF1 alpha in menstrual migraine sufferers are lower than in normal women throughout the whole cycle. The difference between the trends observed in the two groups is statistically significant (p less than 0.05). The plasma levels of TXB2 and of PGF2 alpha are similar in the two groups investigated, both in basal conditions and during the attack. The plasma concentrations of PGE2 are slightly lower in migraineurs in basal conditions than in normals. However, during the crisis they increase significantly (p less than 0.05). In conclusion, among all the parameters considered, PGE2 seems to play the most important role during the pain phase of the attack. The results of the present study suggest that a deficit of PGI2, one of the most important protecting agents against ischemia, might be a typical feature of menstrual migraine and might cause in these patients a vascular hypersensitivity to different ischemic stimuli.

Polycystic Ovary Syndrome and Migraine Headache, Is There Any Correlation?

“…Different types of prostaglandin play a role in the pathogenesis of migraine [7, 8], and increased levels of plasma prostaglandin E 2 have been found during the pain phase in women with menstrual migraine [9]. Interestingly, it has been shown that endometriosis is associated with a significant increase in prostaglandin production [10,11,12]; therefore, it is possible to hypothesize that the systemic spreading of prostaglandins produced by endometriosis lesions may contribute to the increased prevalence of migraine.…”

Menstrual migraine: A review of prophylactic therapies

“…First, prostaglandins sensitize peripheral nociceptors to pain and are potent mediators of hyperalgesia [9]. Second, prostaglandins such as prostaglandin F 2 increase during an acute migraine attack [10]. Third, injections of prostaglandin E 2 can produce migraine-like headaches in non-migraineurs [11].…”

Menstrual migraine: clinical and therapeutical aspects

“…This cyclical drop in hormone concentrations might trigger an abnormal biohumoral reaction [9][10][11][12][13], partially explaining the different clinical features and perhaps also the different responses to abortive and prophylactic therapy that usually, but not always, occur between menstrual and nonmenstrual attacks [14,15]. MM attacks are generally long and may last even more than the 72 h upper limit proposed for migraine without aura in the IHS classification [3].…”