The journal of headache and pain
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Review
The premonitory phase of migraine is due to hypothalamic dysfunction: revisiting the evidence.
To critically appraise the evidence for and against premonitory symptoms in migraine being due to hypothalamic dysfunction. ⋯ The current trend to accept that premonitory symptoms are due to hypothalamic dysfunction might be premature. More rigorously designed studies are needed to ascertain whether the neurobiologic basis of premonitory symptoms is due to hypothalamic dysfunction or rather reflects modulatory input to the trigeminovascular system from several cortical and subcortical areas. On a final note, the available epidemiologic data raises questions as to whether the existence of premonitory symptoms and even more so a distinct premonitory phase is a true migraine phenomenon. Video recording of the debate held at the 1st International Conference on Advances in Migraine Sciences (ICAMS 2022, Copenhagen, Denmark) is available at: https://www.youtube.com/watch?v=d4Y2x0Hr4Q8 .
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To investigate specific brain regions and neural circuits that are responsible for migraine chronification. ⋯ Our data suggest that CeA PKC-δ positive neurons innervated by PBN CGRP positive neurons might contribute to the chronification of migraine, which may serve as future therapeutic targets for chronic migraine.
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New daily persistent headache (NDPH) and chronic migraine (CM) are two different types of headaches that might involve vascular dysregulation. There is still a lack of clarity about altered brain perfusion in NDPH and CM. This study aimed to investigate the cerebral perfusion variances of NDPH and CM using multi-delay pseudo-continuous arterial spin-labeled magnetic resonance imaging (pCASL-MRI). ⋯ The multi-delay pCASL technique can detect cerebral perfusion variation in patients with NDPH and CM. The cerebral perfusion changes may suggest different variations between NDPH and CM, which might provide hemodynamic evidence of these two types of primary headaches.
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Calcitonin gene-related peptide (CGRP) antagonizing drugs represents the most important advance in migraine therapy for decades. However, these new drugs are only effective in 50-60% of patients. Recent studies have shown that the pituitary adenylate cyclase-activating peptide (PACAP38) pathway is independent from the CGRP signaling pathway. Here, we investigate PACAP38 signaling pathways in relation to glyceryl trinitrate (GTN), levcromakalim and sumatriptan. ⋯ Based on the findings in our mouse model of migraine using migraine-inducing compounds and anti-migraine drugs, we suggest that PACAP acts via a distinct pathway. Using PACAP38 antagonism may be a novel therapeutic target of interest in a subgroup of migraine patients who do not respond to existing therapies.