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SYNOPSIS

In the stereotyped, transient and paroxysmal triad of autonomic, vascular and nociceptive dysfunction, precipitated by non-specific factors, known as the migraine attack certain biochemical mediators appear to occupy key-positions in the chain of pathomechanic events occurring at the neural and humoral interface.Of these are reviewed: histamine and serotonin (inhibitory at the microvascular level), substance P and the kinins (excitatory at the nociceptive neural level), tyramine as an a-adrenergic activator, and prostaglandins as humoral agents acting on certain cell-membranes. Anatomical, clinical and biochemical arguments are marshalled to bring the neurogenic origin of the migraine attack into focus, in particular at hypothalamic level.