Orally Inhaled Dihydroergotamine: Improving a Classic
Orally Inhaled Dihydroergotamine: Improving a Classic
Migraine is an evolving and dynamic phenomenon, both in terms of pathophysiology and treatment targets. Migraine pathophysiology has transitioned from the purely vascular theory to the neurovascular theory. The vascular theory of migraine stated that focal neurologic symptoms were caused by vasoconstriction, while pain resulted from subsequent vasodilation. However, the current neurovascular theory of migraine suggests that migraine aura and neurologic symptoms do not represent arterial vasospasm, but rather are caused by spreading cortical depression affecting cortical neurons themselves as well as other neuronal changes in the brainstem, and that the vascular alterations are under neuronal control. We know that there are many complex processes involved and unrecognized therapeutic targets are likely present throughout the neuronal connections of the brainstem, cortex and cerebral vasculature. Migraine treatment will continue to evolve based on new discoveries in our understanding of pathophysiology. Ultimately, migraine therapeutics will better target additional, unrecognized receptors and pathways, while limiting interactions at receptors associated with the known adverse effects and contraindications of current medications.
Future Perspective
Migraine is an evolving and dynamic phenomenon, both in terms of pathophysiology and treatment targets. Migraine pathophysiology has transitioned from the purely vascular theory to the neurovascular theory. The vascular theory of migraine stated that focal neurologic symptoms were caused by vasoconstriction, while pain resulted from subsequent vasodilation. However, the current neurovascular theory of migraine suggests that migraine aura and neurologic symptoms do not represent arterial vasospasm, but rather are caused by spreading cortical depression affecting cortical neurons themselves as well as other neuronal changes in the brainstem, and that the vascular alterations are under neuronal control. We know that there are many complex processes involved and unrecognized therapeutic targets are likely present throughout the neuronal connections of the brainstem, cortex and cerebral vasculature. Migraine treatment will continue to evolve based on new discoveries in our understanding of pathophysiology. Ultimately, migraine therapeutics will better target additional, unrecognized receptors and pathways, while limiting interactions at receptors associated with the known adverse effects and contraindications of current medications.
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