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The critical flicker frequencies (CFF) of individuals with migraine with and without aura were determined and compared to those of normal controls. Twenty-six migraine patients, 12 with aura and 14 without aura and 30 healthy controls were included. Migraineurs were tested during a migraine-free period, through both the continuous flicker method (CFM) and the forced choice method (FCM). Migraineurs presented a mean flickering fusion threshold lower than healthy controls with the CFM (40.45 vs. 44.33, respectively; P = 0.019) and with the FCM (34.16 Hz vs. 38.5 Hz, respectively, P = 0.019). Both groups of migraineurs had significantly lower thresholds as compared to controls, migraineurs with aura presenting the lowest thresholds for the fusion of flickering ( P = 0.008 and P = 0.0001 with the CFM and the FCM, respectively). Results confirmed and extended previous observations of abnormal flicker fusion thresholds in migraineurs. We hypothesize that this finding might be related to a shorter cortical stimulation silent period.

The idiopathic stabbing headache (ISH) is characterized by a stabbing pain of short duration, variable localization and an errant evolution pattern. As its biological mechanisms are unknown and the treatment options are little effective, this disorder shows a strong impact on the patient's life. Two females and one male, aged 76, 66 and 72 years, respectively, started presenting ISH within 20 days after the onset of a stroke. All the patients were treated for the ISH with celecoxib, a COX-2 specific inhibitor, with full recovery from ISH up to 6 days after it was first administered. The interruption of the drug 60 days after the treatment with celecoxib induced again the appearance of algic symptoms in two patients. We concluded that cerebrovascular diseases (CD) can lead to ISH and that the COX-2 inhibitor can be an effective prophylactic drug for ISH after CD.

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.

The case of a 25-year-old white male, who had migrainous headaches each time he sat in front of his personal computer screen, is described. Changing the screen frequency from 60 to 75 Hz through a Windows command could abolish the headaches. In several surveys, computer screens have been reported to be a migraine trigger. We hypothesize that this environmental trigger may be related to the abnormal flicker fusion thresholds that have been described in migraineurs. It may be that modifying the frequencies of light sources, such as computer screens, could become a non-pharmacological approach to prevent migraine attacks.

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.