Dopamine involvement in the migraine attack Fanciullacci M, Alessandri M, Del
Rosso A Department of Internal Medicine, Headache Centre, University of
Florence, Italy
Chat-logomini
Clinical evidence and recent genetic findings seem to indicate an
involvement of dopamine in the pathophysiology of the migraine attack.
Prodromal symptomatology (mood changes, yawning, drowsiness, food craving),
accompanying symptoms (nausea, vomiting, hypotension) and postdromal symptoms
(mood changes, drowsiness, tiredness) may be related to dopaminergic
activation. The dopaminergic system could also play a role in the headache
phase, either by taking part in nociception mechanisms, or by regulating
cerebral blood flow. A body of pharmacological findings seems to support this
involvement. Migraine patients, between attacks, show a higher responsiveness
to acute administration of dopaminergic agents. Apomorphine administration
induces in migraineurs more yawns as well other dopaminergic symptoms e.g.
nausea, vomiting, dizziness. Migraine has been associated with hypotension
and, occasionally, with syncope. Bromocriptine causes severe orthostatic
syndrome in migraine patients. Both piribedil and apomorphine markedly
increase cerebral blood flow of migraine patients, thus indicating enhanced
responsiveness of dopamine receptors which are involved in cerebral blood
flow regulation. Interictal dopaminergic hypersensitivity has also been
demonstrated by means of neuroendocrine tests. Altered dopaminergic control
of prolactin secretion exists in migrainous women. L-deprenyl, a MAO-B
inhibitor, is significantly more effective in reducing prolactin levels in
migraineurs than in controls. Taken together, these findings support the view
that hypersensitivity of peripheral and central dopaminergic receptors is a
specific migraine trait. Finally, a high density of lymphocytic D5 receptors
has been found in migraine sufferers, thus suggesting their upregulation.
Therefore, the hypothesis that dopaminergic activation is a primary
pathophysiological component in certain subtypes of migraine, namely those
characterised by marked dopaminergic symptomatology, has been advanced. From
this perspective, a blockade of dopaminergic hyperresponsive receptors can be
considered as a rationale for the therapy of migraine. Introduction : The
pathogenetic factors underlying migraine have not yet been completely
elucidated. However, migraine is also regarded as a disease related to
dysfunction of central and peripheral "master neurotransmitter systems"
controlling cephalic pain and vasomotility and other autonomic functions.
Serotonin has historically played an important role in migraine pathogenesis;
however, the serotonin system may represent only one facet of the monoamine
involvement in migraine. In this context, dopamine (DA) is able to modulate
nociception, autonomic responses and vasoregulation, all of these functions
being involved in migraine pathophysiology.
In past decades, a body of clinical evidence indicated a role of DA
pathways in the chain of successive events which result in a migraine attack.
These observations led to the idea that migraine was linked to a DA receptor
hypersensitivity in certain brain and peripheral regions related to migraine
attack. This notion has attracted renewed interest after the emergence of
genetic data showing an increased frequency of certain alleles of the DA
receptor gene in migraine patients. The present paper focuses on data
indicating that alterations in DA neurotransmission occur in migraine and
provides a rationale for a DA avenue in the treatment of migraine.
POSSIBLE DOPAMINERGIC MECHANISMS IN THE MIGRAINE ATTACK
Although headache remains the nucleus of migraine episodes, five distinct
migrainous phases have been proposed by Blau: prodrome, aura, headache,
resolution, postdrome (recovery). The symptoms of each phase have their own
characteristics and the tempo of symptoms during each phase suggests d
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