Treatments for specific seizures
Specific treatments for migraine attacks mainly target the serotonin receptors. There are ergot derivatives, which are ergotamine tartrate and dihydroergotamine (DHE), and triptans, which represent nearly 10% of the treatments used in the event of seizures (Géraud et al. 2015).
Ergot derivatives against migraine attacks
They are derived from ergot, a parasitic fungus of the ear of rye and come in two forms: ergotamine tartrate and DHE (Evers et al. 2009). It owes its anti-migraine action to its vasoconstrictor effect on the intracranial arteries and therefore opposes the dilation of the vessels responsible for migraine pain (Ngo et al. 2020).
However, the studies are essentially based on old methodologies, which no longer correspond to current requirements. Like triptans, but to a lesser extent, ergotamine is a serotonergic agonist of 5-HT 1 B and D receptors (Ngo et al. 2020). However, this action is not very specific, because ergotamine also acts on dopaminergic and α-adrenergic receptors, giving it emetic side effects that lead patients to abandon treatment (Donnet et al. 2016).
Prolonged use of these treatments can also lead to symptoms related to a pronounced arterial spasm. We can then observe the appearance of intermittent claudication, which can sometimes go as far as ischemic neuropathy and gangrene in extreme cases.
The combination with a background treatment, such as methysergide or beta-blockers can also potentiate the vasoconstrictor effect of ergotamine, and therefore requires great precautions for use (Géraud et al. 2015).
DHE has a weaker vasoconstrictor effect at the arterial level, but greater at the venous level. Due to its low availability, it is not a crisis treatment when administered orally. On the other hand, by the nasal route, its effectiveness has been widely demonstrated (Piechal et al. 2018). It is this latter form which has a Marketing Authorization in the treatment of migraine attacks, marketed under the name Diergospray®.
Triptans for migraine attacks
In the therapeutic management of the patient, triptans appear as second-line after NSAIDs or aspirin.
There are 7 marketed triptans that have obtained an MA, the most marketed being Sumatriptan. The action of triptans on the 5HT 1 - B and D receptors is both peripheral and central; however, the mechanism of action is not fully elucidated and some authors believe that it is in particular an action at the level of the trigeminal ganglion and, to a lesser extent, a peripheral vasomotor action (Macone et al. 2017).
As far as possible, the triptan should be taken as soon as symptoms appear and it can be renewed two hours after the first dose if the headache reappears. In some patients with very intense attacks, it is possible to combine it with NSAIDs (Macone et al. 2017).
The effectiveness of triptans has been demonstrated several times against placebo and as shown by a large meta-analysis involving 24,000 patients, all oral triptans have shown superior efficacy to placebo. The response rate at 2 hours (transition from a moderate or severe headache to a mild headache) varies from 40% to 70% (Ferrari et al. 2001).
Triptans have also demonstrated efficacy on associated symptoms, nausea and vomiting, photophobia and phonophobia (Géraud et al. 2003). They are mainly administered orally, but Sumatriptan also exists in an injectable form subcutaneously, but not reimbursed by Social Security. However, this form has the highest efficiency, being able to reach 80% response in 2 hours, with a very short onset of action, around 10 minutes. Since 5-HT 1 B receptors are highly expressed in the coronary arteries, the vasoconstrictor effect of triptans can induce coronary insufficiency, but cases are rare (Rothrock et al. 2018).
In fact, the vasomotor action of serotonin on the coronaries rests essentially on the 5-HT 2 A receptors, where the triptans have no influence. However, it is important to inform the patient and contraindicate their use if the patient has a history of myocardial infarction, stroke, peripheral vascular disease or uncontrolled hypertension.
Like non-specific seizure treatments, intensive and prolonged use of triptans can cause medication overuse headaches. Often, the patient does not make a distinction and thinks that the effectiveness of his treatment is decreasing or that the frequency of his attacks is increasing. The reflex is then to increase the doses of the treatment, which leads the patient into a vicious circle, where the increase in doses promotes headaches due to drug abuse.
List with advantages and disadvantages of marketed triptans (Davoine 2016) :
| INN | Specialties | Maximum dose | Benefits | Disadvantages |
| Sumatriptan | Imigran, tab 25, 50mg (spray 10-20mg, SC 6mg, suppository 25mg) | 6 tabs/d | Efficacy of the injectable form and rapid onset of action | |
| Almotriptan | Almogran 12.5mg | 2 tabs/d | Few side effects | |
| Eletriptan | Relpax 20-40mg | 2 tabs/d | Balance between efficacy and side effects | |
| Frovatriptan | Menamig 2.5mg | 2 tabs/d | 4 hour action time | |
| Naratriptan | Naramig 2.5mg | 2 tabs/d | 4 hour action time | |
| Rizatriptan | Maxalt cp 5-10 mg orodispersible | 2 tabs/d | Action in 15 min Consistency of effects No cross-allergy to sulfonamides Orodispersible form | |
| Zolmitriptan | Zomig tab 2.5 mg orodispersible and spray 2.5-5 mg | 4 tabs/d | Up to 4 tabs/d No cross-allergy to sulfonamides Several galenic forms possible |
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