Despite an estimated one in 10 people suffering from migraine, no one really knows what causes it, or how to cure or prevent it. This adds up to a catalogue of heavy duty drugs being administered in a hit and miss fashion to treat a condition no one knows much about, despite the fact that there is evidence of a much simpler, safer and, it seems, more effective form of treatment.

Analgesics, including aspirin, paracetamol and codeine, are sometimes combined with a drug called metoclopramide to speed the absorption and enhance the effectiveness of the analgesics. But metoclopramide can cause dystonia, a condition characterized by muscle rigidity, spasms, unusually fixed postures or strange movements. If nausea and vomiting are part of the migraine pattern, analgesics may be combined with anti-nausea drugs, such as perphenazine, prochlorperazine and chlorpromazine. These drugs occasionally cause tardrive dyskinesia, characterized by irreversible twitching, jerking or writhing.

Ergotamine and dihydroergota mine, both 5-HT agonists which reduce swollen blood vessels around the brain, are now favoured migraine drugs. Amongst migraine sufferers taking dihydroergotamine, there have been 18 reported cases of heart attack, three resulting in death. Only two of the patients had a history of heart disease, and 78 per cent had no risk factors for ischemic (reduced blood flow) heart disease. Other possible side effects include nausea, vomiting, abdominal pain, diarrhea, muscle cramps and partial paralysis or muscle weakness.

Sumatriptan is perhaps the best known of the 5-HT agonists. When it was launched in the early 1990s, it was hailed as the most successful migraine medical treatment to date. In two placebo controlled trials which included 1600 migraine sufferers, between 81 and 86 per cent had their headaches reduced from moderate or severe to mild, or none, within two hours. (N Engl J Med, 1991; 325:316-21 and JAMA, 1991; 265:2831-5). However, in another trial, up to 40 per cent of patients whose headaches were reduced by a single dose of sumatriptan experienced recurrent headaches, which were not prevented by repeated doses of the drug (Eur Neurol 1991; 31:306-13).

More recent studies have shown that at least 5 per cent of sumatriptan users experience chest pains similar to those associated with angina. These are probably due to the drug's vasoconstrictive effect; it narrows blood vessels and restricts blood flow. One 47 year old woman with no previous history of cardiovascular disease suffered a fatal heart attack after injecting herself with sumatriptan (The Lancet, 1993; 341: 861-2), and two patients developed serious irregular heartbeats (BMJ, September 19, 1992). The drug may also cause a rise in blood pressure, and researchers have found that some patients taking sumatriptan suffer from increasing recurrences of migraine. In addition, there is evidence of possible dependence on the drug. (For more information on sumatriptan, see WDDTY, vol.5, no.10, p 8-10.)

There have been several comparisons made between sumatriptan and other anti-migraine therapies. When compared with a combination of ergotamine and caffeine (Cafergot), sumatriptan was significantly more effective at reducing the intensity of headache (66 vs 48 per cent). However, migraine recurrence was more common amongst those patients taking sumatriptan than those taking ergotamine/caffeine (Eur Neurol, 1991; 31:314-22).