[9] Especially, the latter has been attributed to the deficits in motion processing, such as motion aftereffect prolongation,[10] and a decreased ability to detect coherent motion.[11, 12] fMRI relies on the measurement of altered metabolic requirements

that are influenced by neuronal activity. The highly complex mechanism underlying this process of neurovascular coupling is not completely understood, buy Quizartinib but is believed to be based on local changes in cerebral blood flow, arterial and venous cerebral blood volume, and cerebral metabolic rate of oxygen utilization, among others. Thereby, fMRI detects neuronal activity indirectly through the blood oxygenation level dependent (BOLD) effect,[13] and offers a detection of brain activation patterns with high spatial Sotrastaurin research buy resolution. While fMRI has been used to characterize the visual system in healthy humans,[14] similar studies in migraine patients are rare and the results are conflictive. To date, only one previous study has performed MRI with emphasis on interictal motion processing and found that compared with healthy controls, migraine patients showed significantly stronger activation

in the left middle-temporal complex.[15] fTCD assesses vasomotor reactivity within the arterial territory of supply: a task-specific neuronal activation causes an increase in local cerebral blood flow. This method has been applied in migraine patients during visual stimulation showing – among other findings – a greater cerebrovascular response in the middle and posterior cerebral arteries in migraineurs with lesser habituation.[3, 16] Even though Prostatic acid phosphatase lateralization

is a typical clinical feature of migraine, this aspect has been analyzed less frequently in electrophysiological visual processing and cerebral blood flow studies, and the few published studies yielded inconclusive results. While several reports with different techniques did report an interattack asymmetry of findings, a consistent relationship between the side of headache or aura and interictal distribution of functional findings has not been demonstrated.3,17-19 One obvious methodological difference between studies of the visual areas involved in motion perception in migraine patients is the use of a variety of visual stimuli, such as moving dots, rings, gratings, or a black/white checkerboard. As in previous studies,[3, 20] we chose to use a complex, moving, colored visual stimulus resulting in maximum activation of the primary and secondary visual cortices and leading to vertical optokinetic stimulation. Optokinetic stimulation can cause motion sickness due to the mismatch of visual and vestibular perception in otherwise healthy individuals.[21] Migraine sufferers, in turn, have a heightened vulnerability to motion sickness even following milder vestibular stimulation.