Search

Objective.—The study explored the hypothesis that spontaneous nystagmus (Ny) in migraine patients can be triggered or modulated by painful trigeminal stimulation, providing evidence of a functional connection between vestibular and trigeminal systems. Background.—Vertigo attacks are reported by subjects with migraine or a familiar history of migraine, also independently of headache episodes. Idiopathic vertigo is three times more frequent in migraine patients than in controls. Vestibular investigations in migraine patients have consistently demonstrated spontaneous Ny both of central and peripheral origin. Design.—In the first phase of the study 10 outpatients experiencing migraine without aura (MO) and 10 healthy volunteers were submitted to the registration of spontaneous primary-position Ny in the dark by Ulmer's video-ocular-nystagmographic equipment. Two electrodes for electrical stimulation were applied on the supraorbital point of one side of the head and the intensity of stimulation corresponding to pain threshold was calculated. Spontaneous ocular movements were recorded for 5 minutes at baseline and after a sequence of five electric pulses (square waves of .5 Hz frequency and 50 μs duration, at pain threshold intensity). Nystagmographic responses were expressed as latency after stimulation, direction of the quick phase, and duration. The second phase of the study explored, with the same procedure, the effects on Ny of supraorbital versus median nerve stimulation in other 10 MO patients. Responses to stimulation were considered the appearance of de novo Ny after stimulation in subjects without baseline Ny, or the change of the frequency (at last a 50% variation) or of the direction of Ny after stimulation in subjects with baseline Ny. The latency and the duration of responses to stimulation were also calculated. Results.—In the first series supraorbital painful electric stimulation was able to modify or to evoke Ny in 8 of 10 migraineurs and in none of 10 volunteers (Fisher's exact test, P < .01). Both the baseline and the induced Ny were second degree, stationary persistent, with a linear slow phase and were suppressed by visual fixation. In the second series, supraorbital nerve stimulation was able to induce or modify Ny in all of 10 patients but only in 1 patient Ny was induced by median nerve stimulation. Characters of Ny were the same as previously described. Statistical comparison of the responses at the two sites of stimulation was significant (Fisher's exact test, P < .01). In those 7 patients who presented de novo Ny after stimulation it was possible to calculate Ny latency and duration. The mean latency was 25 s (SD: 16, range: 14 to 60). The mean duration was 120 s (SD: 94, range: 20 to 290). Conclusion.—The main result of our study is that in migraine patients painful trigeminal stimulation elicits de novo, or modifies pre-existing spontaneous Ny, generally increasing it. The finding was obtained after trigeminal stimulation, but not after median nerve stimulation. We suggest that painful trigeminal stimulation can induce an imbalance of the vestibular system in migraine patients and possibly explain their predisposition to vertigo. Our data require confirmation by other studies.

We have compared the migraine-inducing effect of nitroglycerin ointment applied to the frontotemporal region of the head, which is innervated by the ophthalmic and maxillary divisions of the trigeminal nerve, with that of nitroglycerin applied to the chin (innervated by the mandibular division), the posterolateral region of the neck (innervated by the second and third cervical roots), the lateral surface of the proximal third of the forearm (innervated by the sixth cervical root), and the medial surface of the upper-arm region (second dorsal root). One hundred patients suffering from migraine without aura were randomly divided into five equal groups. Each group received an application of 5 mg nitroglycerin in 2% ointment on a preselected body area for 2 hours. Frontotemporal nitroglycerin induced a significantly greater number of early onset migraine attacks with respect to the arm and forearm regions. In all cases, nitroglycerin applied to the frontotemporal region resulted in subsequent migraine, whereas there was a significant number of negative trials with nitroglycerin applied to the neck, arm, and forearm vs the frontotemporal area. It, therefore, appears that the trigeminal nerve endings in the affected frontotemporal region are particularly sensitive to the migraine-inducing effect of the nitrate. This suggests a peripheral neurogenic hypothesis of migraine genesis.

The hypothesis that alpha-adrenergic receptor blockade accounts for the ability of ergotamine to stop migraine attacks was tested, in migraine patients, in an experimental migraine model based on nitroderivative- induced attacks. In a preliminary single blind, placebo controlled study, thymoxamine, a prevalently post-synaptic alpha adrenergic receptor antagonist, was able to abort migraine attack in 9 out of 10 patients, as opposed to 2 out of 10 by placebo (p0.005 Fisher's exact test). In a subsequent randomized, crossover, placebo controlled double blind study, the ability of a selective alpha-1 adrenergic receptor agonist, methoxamine, to block ergotamine antimigraine effect was studied. In 26 patients migraine was induced in two separate tests and then ergotamine was administered once after methoxamine pretreatment and once after placebo; methoxamine was significantly more effective than placebo in blocking antimigraine effect of ergotamine (p = 0.0055 Fisher's exact test). These results support the hypothesis that ergotamine alpha-1 adrenolytic properties may account for its antimigraine effect suggesting that this action takes place outside the blood-brain barrier, since methoxamine can cross it very poorly. Ergotamine target structure could be the trigeminal innervation of the extracranial and/or dural vessels.

A pharmacological trial has been carried out on 41 out-patients suffering from mixed headache. The prophylactic effect of a timed-release dihydroergotamine formulation was tested versus amitriptyline. Patients reported daily, on appropriate cards, the hours of headache and the degree of pain during the month before therapy and on the following two months of treatment. Whereas amitriptyline was found to be more effective than dihydroergotamine in reducing headache intensity, timed-release dihydroergotamine was found significantly more effective than amitriptyline in reducing attacks of “migraine” type. Les auteurs ont conduit une étude pharmacologique sur 41 patients souffrant de céphalée mixte. L'effet préventif de la dihydroergotamine à libération programmée a été comparé à celui de l'amitriptiline. Les patients ont quotidiennement enregistré, sur des fiches spéciales, les heures de céphalée et le degré d'intensité de la douleur au cours du mois précédant la thérapie et durant les deux mois de traitement. La dihydroergotamine à libération programmée s'est avérée de façon significative plus efficace que l'amitriptiline dans la réduction de la fréquence des attaques de type hémialgique. Gli autori hanno condotto uno studio farmacologico su 41 pazienti sofferenti di cefalea mista. L'effetto preventivo della diidroergotamina a liberazione programmata è stato paragonato a quello della amitriptilina. I pazienti hanno riportato, quotidianamente, su apposite schede, le ore di cefalea ed il grado di intensità del dolore nel mese precedente la terapia e durante i due mesi di trattamento. La diidroergotamina a liberazione programmata è risultata significativamente più efficace dell'amitriptilina nel ridurre la frequenza degli attacchi ti tipo emicranico.

Until the early 1990s, cluster headache (CH) was considered a sporadic disorder, with a prevalence of 69 per 100,000.1 The presence of CH in monozygotic twins2 and in first- and second-degree relatives3 suggested that genetic factors might be involved. Based on a mailed questionnaire, the prevalence of familial CH was 7%, and based on personal examination of alleged familial cases, it was 30%.3 A large epidemiologic study suggested autosomal dominant inheritance can be involved in some families.4 The current study describes a large kindred in which an autosomal recessive model could be involved. The pedigree (figure) includes four related families from the Naples area (southern Italy). The proband (IV-1), diagnosed in March 2000, referred other relatives possibly affected. All living members were interviewed by telephone, and all possibly affected members were evaluated by a neurologist experienced in CH. Clinical information about deceased individuals, obtained from their descendants, allowed us to exclude CH. Figure. Pedigree of a large kindred of four related families in which eight members …