Turk Beyin Damar Hastaliklar Dergisi, cilt.17, sa.1, ss.21-28, 2011 (Scopus)
AIM: Till now, lots of clinical and experimental studies to understand migraine pathophysiology have been done. According to the results of these studies, it has been believed that the changes of the intracranial vessels have an important role in migraine pathophysiology, although neuronal mechanisms have been disclosed as primary point of interest. We aimed to assess neurovascular reactivity at posterior cerebral arteries to visual stimulus, and vascular reactivity by means of breath holding using transcranial Doppler ultrasonography in patients with migraine with or without aura. MATERIALS AND METHODS: The study included 18 patients with migraine without aura, 9 patients with migraine with aura, and 26 healthy subjects as control. All patients underwent 2 times examination of visual stimulation and breath holding using transcranial Doppler during headache phase and at least 5 days later of headache phase as headache-free period. RESULTS: Neurovascular reactivities to visual stimulation of patients with aura or without aura are not significant between during attack and attack-free period. Similar result was found in patients with miraine without aura in terms of reactivity to breath holding. In contrast, patients with aura have significant (p<0.001) higher vasoreactivity to breath holding in attack-free period (60.6%) comparing with the attack period (36.7%). Patients with migraine with aura have also significant lower reactivity to breath holding (%36.7) comparing with the controls (53.9%) during attack period (p<0.02). Additionally, neurovascular reactivity to visual stimulation in patients with migraine without aura were found significantly lower (p<0.05) than controls (39.4%) in both attack-free period (33.1%) and during attack (33.8%). CONCLUSION: This study is the first study done by means of both reactivity to visual stimulation and reactivity to breath holding in posterior cerebral arteries during attack period and attack-free period in patients with migraine with or without aura. While patients with migraine with aura do not have different visual reactivity comparing with the controls both attack period and attack-free period, patients with migraine without aura have significant lower visual reactivity comparing to controls both attack period and attack-free period. These results may point out that patients with migraine without aura have lower neuronal energy reserve regardless headache attack than those of patients with migraine with aura. On the other hand, spreading depression during aura phase in patients with migraine with aura might have a protective effect on neuronal energy reserve. Additionally patients with migraine with aura have higher neuronal excitability comparing with the patients with migraine without aura. Vascular reactivity to breath holding was lower during headache attack and normalized after attack, even found to be higher. This result may reveal vascular structure was more impaired in patients with migraine with aura than those of patients with migraine without aura.