Abstract
AbstractThe aim of this study is to identify the pathophysiology of “prolonged” migraine aura not clearly understood. We studied cortical cerebral microcirculation by Near Infrared Spectroscopy system (NIRS) and cerebral macrocirculation by transcranial Doppler (TCD) in 8 subjects (3 M and 5 F, age range 21–41 years) during spontaneous “prolonged” migraine aura in according to ICHD-II criteria 2004 (code 1.6.2.) up to 24 hours after the end of aura and compared the results with the headache-free periods. During aura NIRS showed a significant decrease of the Arterial Pulse Wave of Cerebral Microcirculation (APWCM) amplitude (−33 % ± 5.7), p<0.001, and a significant increase of Cerebral Tissue Oxygen Saturation (SctO2) (+15.5 % ± 5.1), p<0.001 contralateral to the symptoms of aura compared with the headache-free periods; TCD showed a significant increase of Pulsatility Index (+36.5 % ± 6.5), p<0.001 and a significant decrease of the diastolic velocity in the posterior and middle cerebral artery contralateral to the symptoms of aura compared with the headache-free periods. In conclusion during “prolonged” migraine aura we find areas of cortical hypoperfusion corresponding to the topography of aura symptoms that are the result of a decreased metabolic demand rather than an ischemic mechanism.
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