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We Need Better Preventative Medications

Our previous retrospective study of 540 patientswith chronic daily headache indicated that only 46%achieved long-term (more than 9 months) relief withpreventative medications.1 Each patient in the studyhad been on at least three preventative medications;lack of efficacy was the primary reason for discontin-uation, but side effects resulted in 20% of patients

612 June 2001

discontinuing medication. The percentages of patientswho had relief and continued long-term on preventa-tive medication included: sodium valproate, 35%; se-lective serotonin reuptake inhibitors, 35%; tricyclicantidepressants, 31%; and �-blockers, 22%.

Most controlled studies do not extend beyond 6months; dropout rates are high between months 6and 12. While they may be difficult and cost-prohibi-tive, we need longer preventative studies.

We tell patients not to overuse (or even use) an-algesics or abortives, then we present them with dailypreventatives that often are not effective and have in-tolerable side effects. Patients feel guilty and frus-trated when five or six preventative medications areineffective, and physicians share in their frustration.

We must urge the pharmaceutical companies todevelop novel preventative medications for chronicdaily headache. In addition, it will help patients if wepresent a realistic picture as to the possibilities forsuccess with preventatives.

Lawrence Robbins, MDNorthbrook Court Professional Center

1535 Lake Cook Road, Suite 506Northbrook, IL 60062

REFERENCE

1. Robbins L, Maides J. Efficacy of preventive medica-tions for chronic daily headache. Am J Pain Manage.1999;9:139-142.

Induction of a Migraine Aura in a Patient Suffering From Migraine Without Aura

In patients suffering from migraine with aura(MWA) or migraine without aura (MWOA), a mi-graine attack can be triggered by nitroglycerin(NTG).1-3 The number and the latency of successfulinductions by NTG vary according to its route of ad-ministration: sublingual,4 intravenous,2 and transder-mal.5 Our study group demonstrated that topicalNTG administration at the typical site of pain is ahighly successful, rapid, and tolerated method of mi-

graine induction.5,6 Moreover, topical NTG adminis-tration does not induce the hypotensive effects of sys-temic NTG.5 During induced attacks, the site of painis reported by patients to be typical, as well as itsquality, intensity, and accompanying autonomic symp-toms, except for aura: in fact, patients suffering fromMWA have not reported aura symptoms during theNTG induction test.

We describe a successful induction test withtransdermal NTG administration at the typical site ofpain in a woman suffering from MWOA, who devel-oped a migraine attack preceded by visual aura symp-toms she had never experienced before.

The subject of our report is a 30-year-old teacherwho has suffered from MWOA since she was aged 10years. Her father also has migraine. Her migraine ep-isodes occur six times a month on average, of high in-tensity; they are predominantly right-sided and usuallysubside 2 hours after intramuscular noramidopyrine.Accompanying features are nausea, vomiting, phono-phobia, and photophobia. Pain is increased by briskhead movements. The patient has no other illness.Computer-assisted tomography scan and a cerebralMRI with MR angiography are both normal.

The patient received a 5-mg NTG plaster on herright frontotemporal region, according to the proce-dure described in a previous study.5 Forty-five min-utes later, she began to see “black spots, ball-shaped,weaving across the central region of the visual field,superimposed on normal images.” This phenomenonstarted abruptly, persisted for 1 hour, and then van-ished gradually, while a subtle pain started at the siteof the plaster. In a few minutes, a typical migraine at-tack developed, with vomiting, which lasted 12 hoursin spite of noramidopyrine administration. The pa-tient stated that the attack was very similar to someof her most violent spontaneous migraine episodes,except for the visual symptoms, which she had neverexperienced before. No abnormality was noted onneurological examination or of the arterial bloodpressure which was recorded during the test.

It has been suggested that NTG-induced mi-graine attacks are mediated by the release of nitricoxide (NO),7 which is a potent vasodilator of extra-cranial carotid vessels and of meningeal vessels. Ni-tric oxide seems also to be released during spreading