Cranial sensory innervation is supplied mainly by the trigeminal nerves and by the first cervical nerves. Excitatory and inhibitory interactions among those nerve roots may occur in a mechanism called nociceptive convergence, leading to loss of somato-sensory spatial specificity. Three volunteers in an experimental trial had sterile water injected over their greater occipital nerve on one side of the neck. Pain intensity was evaluated 10, 30 and 120 s after the injection. Two of the patients reported intense pain. Trigeminal autonomic features, suggestive of parasympathetic activation, were seen associated with trigeminally distributed pain. These data add to and reinforce previous evidence of convergence of cervical afferents on the trigeminal sensory circuit.

Thirty-three migraineurs and 23 healthy controls were submitted to pressure algometry before and after light-induced discomfort was elicited by progressive light stimulation in a monoblind fashion. Pressure algometries were performed on the emergence of the supraorbital, infraorbital, mental and greater occipital nerves, and over the temporal muscles, always throughout the same sequence and from right to left. Measurements were carried out before and immediately after light stimulation and after 10 min of the second algometry. The final result for each site measured at each time-point was the mean of the three measurements. Light stimulation was carried out progressively until light-induced discomfort was reported, to a maximum of 20,000 lux. A heat-blocking glass protected patients' eyes. Migraineurs presented significant and persistent drops in pain perception thresholds after light stimulation, at all sites tested (P = 0.002 to < 0.0001). These drops were not seen in controls, in whom, conversely, a less significant increase was seen on right infraorbital and left temporal muscle sites. Our results indicate that in migraineurs, light may have a relevant role in trigeminal and cervical pain perception thresholds.

To investigate the relevance of lacking or diminished visual input on the expression of migraine, we evaluated its prevalence and clinical features in a population of visually impaired subjects. Between September 1999 and April 2000, 203 visually impaired subjects with a headache inventory were surveyed. Those with headache were assessed according to IHS criteria for the presence of migraine. Migraineurs had their symptoms further detailed through an interview and a headache diary. Of the 104 subjects reporting headaches during the last 6 months, 29 had migraine (14.2%). The prevalence of migraine was not influenced by whether the visual impairment was complete or partial. Mean frequency of migraine attacks was 2.7/month. Most subjects (96%) reported severe and/or moderate attacks. Nausea, vomiting, aggravation by activity and phonophobia were reported by 62%, 37.9%, 86.2% and 96.6% of the subjects, respectively. Visual impairment does not seem to influence prevalence of migraine or its clinical features.

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The case of a 42-year-old woman with prolonged migraine visual aura without headache, whose long-lasting episodes of visual aura were successfully controlled by oral sumatriptan, is reported. Effectiveness of sumatriptan was unequivocal, since, after taking sumatriptan, duration of aura would drop from 1.5 h to approximately 20 min. This case suggests that sumatriptan may cross the blood-brain barrier and block spreading depression.