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Current theories on the aetiology of migraine headache suggest that the symptoms are due to local cranial vasodilatation and/or to the release of vasoactive and pro-inflammatory peptides from sensory nerve endings in an activated trigeminal systemThe therapeutic activity of rizatriptan in migraine can most likely be attributed to agonist effects at 5-HT 1B/1D receptors on the extracerebralintracranial blood vesselswhich become dilated during a migraine attackand on nerve terminals in the trigeminal systemActivation of these receptors results in cranial vessel constrictioninhibition of neuropeptide release and reduced transmission in trigeminal pain pathways.
Factors that trigger this headache type are a muscle strainstress or anxiety.
Cases of life-threatening serotonin syndrome have been reported during combined use of selective serotonin reuptake inhibitorsSSRIsor serotonin norepinephrine reuptake inhibitorsSNRIsand triptansThere have been reports describing patients with symptoms compatible with serotonin syndromeincluding altered mental statusautonomic instability and neuromuscular abnormalitiesfollowing the use of SSRIs or serotonin norepinephrine reuptake inhibitorsSNRIsand triptans.
There are no adequate and well-controlled studies in pregnant womenthereforerizatriptan should be used during pregnancy only if the potential benefit justifies the potential risk to the foetus.
Serious cardiac eventsincluding some that have been fatalhave occurred following use of 5-HT 1 agonistsThese events are extremely rare and most have been reported in patients with risk factors predictive of CADEvents reported have included coronary artery vasospasmtransient myocardial ischaemiamyocardial infarctionventricular tachycardia and ventricular fibrillation.
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