Abstract
Clinical, pathophysiological, pharmacological, and biochemical evidence support the concept that the prostanoid system may be involved in migraine. As a local defence system prostaglandins may best be linked with hyperalgesia and vascular events. The response to potent inhibitors of PG-synthesis like tolfenamic acid further supports the involvement of prostaglandins in the “inflammatory-like” aspects of migraine pain. The prostanoid system may be closely coupled with the monoaminergic mechanism; e.g. in stress reactions plasma thromboxane correlates with adrenaline levels. The possible participation of leukotrienes in migraine is only speculative. However, in cerebral hypoxia lipid peroxidation is increased and leukotrienes might participate in the cerebrovascular reactions. Prostaglandins may inhibit the formation of free radicals, antagonize some actions of leukotrienes and protect the tissues. The interplay between leukotrienes and prostaglandins may give new aspects to some cerebrovascular abnormalities in migraine.
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