Giffin, Nicola J.; (2003) Studies on the early phases of migraine. Doctoral thesis (M.D), UCL (University College London).

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Abstract

Migraine is characterised by recurrent, episodic attacks of headache, often heralded by non-headache features in the premonitory and aura phases. Recent advances in genetics and electrophysiology have suggested factors in the aura and premonitory phases that may contribute to the episodicity of the disorder. My aim was to study these non-headache features using a variety of methods to gain understanding of attack initiation. An electronic diary study showed that patients who claim they can predict an attack from premonitory symptoms can do so with reasonable accuracy. A subset of these patients was further investigated using functional imaging, electrophysiological and biochemical methods. Functional imaging did not demonstrate significant change of brain activation in the premonitory phase compared to the headache and interictal phases. I have helped to develop a novel electrophysiological technique, the nociceptive specific blink reflex, to study in vivo changes in trigeminal nociception in migraineurs and as a model of trigeminal nociception in healthy volunteers. A longitudinal study using the nociceptive blink reflex did not demonstrate a significant change in trigeminal nociceptive transmission interictally. A longitudinal study of NO urinary excretion highlighted a population difference in NO metabolism between migraineurs and controls but did not show any relationship with migraine attacks. Clinical study of kindreds with hemiplegic migraine, linked to CACNA1 A mutations, revealed subjects with ataxic migraine, benign paroxysmal torticollis of infancy and progressive intellectual decline and coma. Voxel base morphometry of a kindred with ataxic migraine showed cerebellar atrophy in subjects with the genotype but not in phenocopies. Diffusion weighted imaging of patients with persistent visual aura did not show any significant change. There is clinical evidence for changes in the premonitory period, but I have not been able to correlate these with changes in functional imaging or trigeminal nociceptive transmission. The premonitory phase is most likely to be generated by discrete areas of the hypothalamus. Mutations in the CACNA1 A gene may lead to structural and functional cortical and cerebellar changes that lead to a phenotypic spectrum of neurological disability.

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