"intermittent intravenous therapies: fluids, dopamine antagonists (e.g. chlorpromazine), corticosteroids, sodium valproate, magnesium sulphate"
"Migraine may have polygenic risk factors, but there are rare instances of monogenic migraine, such as familial hemiplegic migraine due to mutations in the CACNA1A, ATP1A2 or SCN1A genes 8,12."
"CACNA1A-related disorders"
"retinal dystrophy, optic nerve oedema, splenomegaly, anhidrosis, and migraine headache (ROSAH) syndrome"
"symptoms are often subtle, such as increased yawning, emotional lability, food cravings, neck stiffness, bowel changes, etc."
"Routine MRI obtained when an individual is not having a migraine is essentially normal in most patients. In up to 40% of patients with migraine 4,5, there may be non-specific T2 hyperintensities in the white matter of the centrum semiovale, not dissimilar to small-vessel deep white matter ischaemic change. These alterations typically present as ovoid, round, or slightly elongated foci"
"increased risk of cerebral infarction in patients with migraine with aura; association in patients without aura is less convincing 14"
"It is hypothesised that cortical spreading depression and subsequent activation of the trigeminovascular system (composed of peripheral axons from the trigeminal ganglion that innervate the meninges and peripheral intracranial blood vessels), leading to release of neuropeptides such as calcitonin gene-related peptide (CGRP), a powerful vasodilator 8,16. The trigeminovascular system and the trigeminocervical complex are widely connected to the brainstem (e.g. periaqueductal grey matter and locus coeruleus) and diencephalon (e.g. hypothalamus and thalamus) 16."
"Migraine may have polygenic risk factors, but there are rare instances of monogenic migraine, such as familial hemiplegic migraine due to mutations in the CACNA1A, ATP1A2 or SCN1A genes 8,12."
"demyelination (e.g. multiple sclerosis)"
"other primary headache disorders (e.g. cluster headache)"