Acute Treatment of Migraine: In acute therapy the key concerns to be addressed from the patient’s perspective are:
- The efficacy of the treatment
- The time to onset of action
- The consistency of response form one attack to the next
- The tolerability of the medication
The two main options in the acute treatment of migraine are Analgesics/NSAIDs and Triptans.
Analgesics / NSAIDs
Up to 1/3 of migraineurs effectively manage their attacks without needing to consult their GP. Paracetamol, aspirin or ibuprofen can be effective for some patients with mild-moderate migraine although the data suggests that their efficacy is limited to about 1/3 of patients.
Analgesics are more effective if taken early in the headache phase. Although generally well tolerated, frequent use can lead to the development of Analgesic Rebound Headache.
Simple analgesics can be combined with other medications to improve their efficacy in migraine treatment. If nausea is a symptom, then the concomitant use of the pro-kinetic drugs Domperidone or Metoclopramide will relieve the nausea and also prevent the gastric stasis associated with migraine, which can slow absorption.
Combination analgesics containing caffeine or codeine are also effective for some, but there is an inherent risk of dependency. Codeine is also a major cause of rebound headache.
NSAIDs such as Naproxen or Diclofenac are also effective in acute treatment. These agents are anti-prostaglandins and limit the degree of vasodilation that occurs in the intracranial arteries during an attack.
The triptans are 5-HT 1B/1D receptor agonists and are a refinement of the original non-specific 5-HT, ergot preparations. They have now largely replaced ergotamine because of their greater efficacy, faster onset of action, and their versatility in formulation. Since their introduction in the 1990s they have brought about remarkable advances in the symptomatic treatment of migraine.
Triptans are licensed for use in patients (both those with and without aura) between the ages of 18 and 65 years. In patients with moderate to severe migraine, studies have consistently demonstrated that triptans are the preferred symptomatic drug class particularly where the patient is unable to carry out routine activities or go about their daily routine because of their migraine.
Therefore, these patients should be prescribed a Triptan before trying drugs that are not as migraine-specific.
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Mode of Action
The triptans have potent agonist activity at the 1B/1D receptor sites. The specificity of these drugs to these receptors sites limits their side effect profile and make them well tolerated.
The triptans have three sites of action:
- They cause vasoconstriction of the dilated meningeal, dural, extracerebral, and pial blood vessels by stimulating the 5HT 1B receptors located on these blood vessels.
- They inhibit the release of C.G.R.P., substance P, and neurokinin from the periphereal end of the trigeminal nerve by stimulating the 5-HT 1d receptor sites located on the pre-synaptic nerve terminals.
- They have a high affinity for the 5-HT 1D located centrally in the region of the trigeminal nucleus caudalis in the brainstem. This site of action modulates in-coming nociceptive or painful sensory information from the periphery and inhibits its upward transmission to the thalamus and higher brain centres where pain is perceived.
Triptans are generally well tolerated. The most common side effects with the triptans are paresthesias, flushing, fatigue, nausea, dizziness and feeling warm. Chest and throat tightness occurs occasionally and is thought to be non-cardiac in origin.
- Pregnant or lactating women.
- Because of their vasoconstrictive properties, triptans act on coronary blood vessels as well as meningeal arteries. Therefore, all of the triptans are contra-indicated in patients with coronary disease, cerebrovascular disease, or untreated hypertension.
- They should also be used with extreme caution in patients with risk factors for cardiovascular disease.
- Patients with Hemiplegic Migraine or Basilar Migraine, two rare forms of migraine thought to be associated with excessive cerebral vasoconstriction.