[4] However, this pattern of results was not observed with other oral triptans. Systematic elucidation of treatment-emergent nausea is warranted given its impact on the patient and the course of treatment of migraine. Should treatment-emergent nausea prove to be caused by use of oral triptans, then use

of non-oral formulations with less or no nausea-triggering or -exacerbating capability should be considered. In designing studies to investigate treatment-emergent nausea, the possibility that oral triptans could induce nausea in some patients and relieve it in others should be borne in mind. In the event that oral triptans induce nausea in some patients learn more and relieve it in others, the impact of oral triptans on nausea could be obscured in a study employing a between-subjects design. A within-subjects design would be the most appropriate means of assessing the impact of oral triptan therapy on treatment-emergent nausea. The data reviewed in this paper may have important clinical implications. If pretreatment nausea predicts poor response to oral triptans, and oral triptans are associated with iatrogenic nausea, then the use of selleck compound oral triptans in migraine attacks with nausea or in patients prone to nausea should be reevaluated, and alternative routes

of triptan administration should be considered. Because these observations are derived from a small evidence base, additional research is needed to explain the relationship between nausea and oral triptans and to refine the treatment approach to migraineurs whose attacks include nausea as a prominent feature. The author acknowledges Jane Saiers, PhD (The WriteMedicine, Inc.), for assistance with writing the manuscript. Dr. Saiers’ work was funded by NuPathe Inc. “
“The pathogenesis of medication overuse headache is unclear. Clinical and preclinical studies have Osimertinib consistently demonstrated increased excitability of neurons in the cerebral cortex

and trigeminal system after medication overuse. Cortical hyperexcitability may facilitate the development of cortical spreading depression, while increased excitability of trigeminal neurons may facilitate the process of peripheral and central sensitization. These changes may be secondary to the derangement of central, probably serotonin (5-HT)-, and perhaps endocannabinoid-dependent or other, modulating systems. Increased expression of excitatory cortical 5-HT2A receptors may increase the susceptibility to developing cortical spreading depression, an analog of migraine aura. A reduction of diffuse noxious inhibitory controls may facilitate the process of central sensitization, activate the nociceptive facilitating system, or promote similar molecular mechanisms to those involved in kindling.