Letter to the Editor
Sumatriptan Arrests Migraine Aura
F. Clifford Rose, M.D., F.R.C.P. London Neurological Centre 110 Harley Street London W1N 1AF England
There is still marked controversy regarding the pathogenesis of migraine.1 Subcutaneous sumatriptan, a 5HT1-Iike agonist, given in a dose of 6 mg subcutaneously, aborts the headache, nausea, photophobia and other features of a migraine attack. Its half-life is two hours; it begins to act within half-an-hour and is usually completely effective within one hour. Since the pathogenesis of the aura is considered to be of a different nature from the succeeding symptoms of the migraine attack, it has often been questioned whether the drug arrests the aura. This matter has not been readily settled because the aura lasts usually for about twenty minutes, a period that may not allow time enough for the injection to be given and its effect noted. It is for these reasons that the following case report is given: A 40 year old man worked for a building society in their rent arrears section. In these recessionary times, he had become under increasing stress and his attacks of classical migraine (migraine with aura), which he had had for five years, had become increasingly frequent. The aura was the typical visual one of a spreading scintillating scotoma.1 Recently he gave himself the standard subcutaneous injection of 6 mg of sumatriptan within two minutes of the onset of the aura, i.e. when the homonymous paracentral scotoma began to flicker at its edges. Within 2-3 minutes of the injection, the visual aura, instead of enlarging and spreading, had disappeared. There was no succeeding headache or nausea. Clearly the evidence afforded by this one attack needs to be replicated, but the patient was a good witness and confident of the accuracy of the events recorded. Even if and when confirmed, it is likely that the protagonists of both the vascular and neurogenic theories will use this evidence to promote their own favoured view. On the one hand, sumatriptan is said not to pass the blood-brain barrier and its action is thought to be on the meningeal vessels and their sensory supply. It is difficult to see how the latter action could explain the phenomenon described, since there is little doubt that the visual aura is produced by changes in the visual cortex, putatively the spreading depression of Leão. REFERENCE
1.
Rose FC: The pathogenesis of migraine. J Roy Soc Med 1991; 84:519-521
Sumatriptan Arrests Migraine Aura
F. Clifford Rose, M.D., F.R.C.P. London Neurological Centre 110 Harley Street London W1N 1AF England
There is still marked controversy regarding the pathogenesis of migraine.1 Subcutaneous sumatriptan, a 5HT1-Iike agonist, given in a dose of 6 mg subcutaneously, aborts the headache, nausea, photophobia and other features of a migraine attack. Its half-life is two hours; it begins to act within half-an-hour and is usually completely effective within one hour. Since the pathogenesis of the aura is considered to be of a different nature from the succeeding symptoms of the migraine attack, it has often been questioned whether the drug arrests the aura. This matter has not been readily settled because the aura lasts usually for about twenty minutes, a period that may not allow time enough for the injection to be given and its effect noted. It is for these reasons that the following case report is given: A 40 year old man worked for a building society in their rent arrears section. In these recessionary times, he had become under increasing stress and his attacks of classical migraine (migraine with aura), which he had had for five years, had become increasingly frequent. The aura was the typical visual one of a spreading scintillating scotoma.1 Recently he gave himself the standard subcutaneous injection of 6 mg of sumatriptan within two minutes of the onset of the aura, i.e. when the homonymous paracentral scotoma began to flicker at its edges. Within 2-3 minutes of the injection, the visual aura, instead of enlarging and spreading, had disappeared. There was no succeeding headache or nausea. Clearly the evidence afforded by this one attack needs to be replicated, but the patient was a good witness and confident of the accuracy of the events recorded. Even if and when confirmed, it is likely that the protagonists of both the vascular and neurogenic theories will use this evidence to promote their own favoured view. On the one hand, sumatriptan is said not to pass the blood-brain barrier and its action is thought to be on the meningeal vessels and their sensory supply. It is difficult to see how the latter action could explain the phenomenon described, since there is little doubt that the visual aura is produced by changes in the visual cortex, putatively the spreading depression of Leão. REFERENCE
1.
Rose FC: The pathogenesis of migraine. J Roy Soc Med 1991; 84:519-521
