Rizat

Rizamig tablet is indicated for the acute treatment of migraine attacks with or without aura in adults.

Cardiac events are rare and most have been reported in patients with risk factors predictive of CAD. Cardiac events reported have included coronary artery vasospasm, transient myocardial ischemia, myocardial infarction, ventricular tachycardia, and ventricular fibrillation. In general, chills, heat sensitivity, facial edema, hangover effect, and abdominal distention were reported infrequently. Rarely fever, orthostatic effects, syncope and edema/swelling were reported.

Rizamig should only be used where a clear diagnosis of migraine has been established. Rizamig should not be given to patients with documented ischemic or vasospastic coronary artery disease.
Drugs in this class may cause coronary artery vasospasm, patients who experience signs or symptoms suggestive of angina following dosing should be evaluated for the presence of CAD or a predisposition to Prinzmetal’s variant angina before receiving additional doses of medication, and should be monitored electrocardiographically. Rizamig should be used with caution in patients with moderate hepatic insufficiency.
For a given attack, if a patient has no response to the first dose of rizatriptan, the diagnosis of migraine should be reconsidered before administration of a second dose.

There are several physiological and molecular processes implicated in the pathophysiology of migraine. Vasodilation of intracranial extracerebral blood vessels, particularly those supplying the dura mater, has been associated with migraine pain. Activation of the trigeminovascular system leads to the release of vasoactive neuropeptides from the trigeminal nerve innervating the intracranial vessels and dura mater. Vasoactive neuropeptides cause perivascular inflammation and vasodilation in the periphery. Migraine-associated nausea and vomiting are thought to arise from the activation of central and nociceptive sensory neurons that project to autonomic brain-stem nuclei and higher subcortical and cortical pain processing centres. An imbalance in serotonin (5-HT) levels has also been documented: 5-HT binds to 5-HT1B and 5-HT1D receptors to promote trigeminal neuronal firing and vasoconstriction.
Rizatriptan is a selective agonist at the 5-HT1B and 5-HT1D receptors on intracranial blood vessels and sensory nerves of the trigeminal system. It binds to these receptors with high affinity.9 The exact mechanism of action of rizatriptan has not been fully elucidated; however, several documented pharmacological actions of rizatriptan may contribute to its antimigraine effects. Rizatriptan causes vasoconstriction of intracranial extracerebral blood vessels, which is thought to occur primarily via 5-HT1B receptors. Rizatriptan also inhibits nociceptive neurotransmission in trigeminal pain pathways. It attenuates the release of vasoactive neuropeptides by the trigeminal nerve, which is thought to occur via neurogenic and central 5-HT1D receptors. Rizatriptan inhibited neurogenic dural vasodilation and plasma protein extravasation in animal studies.