Abstract
Migraine is a common and disabling brain disorder with a broad and heterogeneous phenotype, involving both pain and painless symptoms. Over recent years, more clinical and research attention has been focused toward the premonitory phase of the migraine attack, which can start up to days before the onset of head pain. This early phase can involve symptomatology, such as cognitive and mood change, yawning, thirst and urinary frequency and sensory sensitivities, such as photophobia and phonophobia. In some patients, these symptoms can warn of an impending headache and therefore offer novel neurobiological insights and therapeutic potential. As well as characterization of the phenotype of this phase, recent studies have attempted to image this early phase using functional neuroimaging and tried to understand how the symptoms are mediated, how a migraine attack may be initiated, and how nociception may follow thereafter. This review will summarize the recent and evolving findings in this field and hypothesize a mechanism of subcortical and diencephalic brain activation during the start of the attack, including that of basal ganglia, hypothalamus, and thalamus prior to headache, which causes a top-down effect on brainstem structures involved in trigeminovascular nociception, leading ultimately to headache.
Highlights
Imaging the Premonitory Phase of MigraineReviewed by: Aynur Özge, Mersin University, Turkey Marco Carotenuto, University of Campania Luigi Vanvitelli, Italy
Migraine is a disabling condition that, in addition to headache, involves often disabling non-headache symptoms
We have recently presented our resting-state fMRI results looking at seed-based functional connectivity with the blood oxygen level-dependent (BOLD) contrast, in nitroglycerin-triggered premonitory symptoms relative to placebo, and shown increased thalamocortical connectivity and functional uncoupling between the pons and the limbic lobe in the premonitory phase, with increased functional coupling between the pons and spinal trigeminal nuclei during migraine headache, suggesting changing alterations in subcortical and brainstem networks in the premonitory phase [42]
Summary
Reviewed by: Aynur Özge, Mersin University, Turkey Marco Carotenuto, University of Campania Luigi Vanvitelli, Italy. More clinical and research attention has been focused toward the premonitory phase of the migraine attack, which can start up to days before the onset of head pain. This early phase can involve symptomatology, such as cognitive and mood change, yawning, thirst and urinary frequency and sensory sensitivities, such as photophobia and phonophobia. In some patients, these symptoms can warn of an impending headache and offer novel neurobiological insights and therapeutic potential. This review will summarize the recent and evolving findings in this field and hypothesize a mechanism of subcortical and diencephalic brain activation during the start of the attack, including that of basal ganglia, hypothalamus, and thalamus prior to headache, which causes a top-down effect on brainstem structures involved in trigeminovascular nociception, leading to headache
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