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• W2278917888 abstract "The aim of this thesis was to investigate visual responses of people with migraine in between attacks, in order to infer possible mechanism/s underlying migraine pathophysiology. The proposed neural abnormality in migraine is cortical hyperexcitability. To measure neural activity in the visual cortex, previous studies have measured the cortical evoked response to patterned visual stimulation; however, these have yielded inconsistent results. This raises the possibility that mechanisms other than cortical hyperexcitability might contribute to vision anomalies in migraine. In this thesis, people with migraine (with and without aura) were compared to non-headache control participants. By measuring the cortical and retinal evoked responses simultaneously, Experiment 1 aimed to determine whether abnormalities in the cortical evoked response could be explained by dysfunction occurring earlier in the visual pathway. People with migraine showed reduced cortical responses but normal retinal function, indicating that the cortical deficits were unlikely to be a result of retinal dysfunction. The purpose of Experiment 2 was to consider whether loss of visual field sensitivity in people with migraine was related to abnormal cortical and/or retinal function. Performance was compared between two visits: less than and more than seven days after a migraine. Migraine sufferers showed repeatable deficits in the cortical evoked response that were not worse in the days immediately after migraine, implying stability of the cortical deficit. In contrast, Experiment 2 found further reductions in sensitivity in the days immediately after a migraine attack, confirming previous reports. Some individuals showed monocular and/or localised visual field defects that were worse after an attack, suggesting that these might be retinal effects of migraine. The final experiment explored the balance between inhibition and excitation, one of the competing theories underlying cortical hyperexcitability in migraine. Using a perceptual centre-surround task to assess inhibition and excitation simultaneously, Experiment 3 found increased suppression in people with migraine, indicating increased inhibition, for stimuli of lower centre contrast. The contrast-dependent changes in perception were associated with abnormal contrast gain, as demonstrated by increased cortical evoked responses at low contrast and decreased responses at high contrast. Thus, Experiment 3 provided further evidence for cortical hyperexcitability leading to abnormal visual perception in between migraine attacks. However, cortical hyperexcitability cannot account for all vision anomalies in migraine. Rather, there is also the potential for adverse sequelae of migraine, possibly outside of the brain, in otherwise healthy and asymptomatic individuals (Experiments 1 and 2). This thesis has implications for the use of non-invasive, clinical tests of visual function in clinical and research settings. People with migraine, on average, showed abnormal visual responses, even when asymptomatic and tested more than a few days after a migraine. This result reinforces previous suggestions that regular migraine sufferers should be excluded from normative databases. Additionally, there was considerable inter-individual variability in the visual responses, demonstrating that only a subset of individuals with migraine fall outside the range of normal visual performance. Further investigation of these particular individuals is potentially more informative regarding the pathophysiological processes of this debilitating condition." @default.
• W2278917888 created "2016-06-24" @default.
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• W2278917888 date "2013-01-01" @default.
• W2278917888 modified "2023-09-27" @default.
• W2278917888 title "Vision anomalies in migraine" @default.
• W2278917888 hasPublicationYear "2013" @default.
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