These structural abnormalities in the network of motion-processing areas could explain the cortical hyperexcitability observed in migraine sufferers and establish a biological basis for the clinical observation of heightened vulnerability
to motion sickness that migraine sufferers often report.93,94 The finding in patients with or without aura of thickness abnormalities in area V3A (characterized by changes involved in visual aura) raises questions regarding a potential “silent” CSD in non-aura patients. Another study explored the dynamics of the basic interictal state with regard to the extrastriate, motion-responsive MT area (MT complex) using functional MRI and coherent/incoherent moving dot stimuli.95 In MT, control subjects showed stronger bilateral activation compared with migraine patients. Patients, however, displayed Selleck FK228 significantly stronger activation mainly on the left side in response to visual stimulation in the superior-anterior portion of the MT complex, representing the medial-superior temporal area. These findings strengthen the hypothesis that hyperresponsiveness of the visual cortex in migraine goes beyond early visual areas, even in the interictal period. Functional MRI studies
revealed that patients with migraine display enhanced interictal reactivity of the visual cortex.96 A BOLD functional MRI study noted significantly higher number of MRI-activated voxels in migraineurs at low and medium-low medchemexpress luminance levels, but not at medium-high selleck chemical and high light stimuli.97 Light discomfort was higher in patients at all intensities tested, but there was no correlation with the number of activated voxels in the occipital cortex and photophobia. Repetitive light stimuli failed to demonstrate a lack of habituation in migraineurs;
therefore, the authors proposed that interictal hyperexcitability of the visual cortex may arise through a distinct, possibly dual mechanism: constitutional defensive and acquired sensitization. A study investigating changes in brain metabolites after visual cortex activation in migraineurs and normal subjects used MRS,98 which allows measurements of metabolic activity to be made after neuronal activation, found that migraineurs with aura have a more consistent decrease in N-acetylaspartate signal and a slight increase in lactate peak compared with those without aura and non-migraine controls. This could indicate a decreased mitochondrial efficiency in the occipital cortex of migraine patients with aura. Functional MRS investigations of cortical lactate changes during prolonged visual stimulation showed that in patients with aura and additional symptoms, lactate increased only during stimulation, only in visual cortex, while in migraine with visual aura resting lactate was high in visual cortex, without further increase during stimulation.