A trigger is an integral part of any acute migraine attack. In this article, the author argues that triggers, identifiable or not, must be present in all attacks of migraine headache. It is hypothesized that triggers, internal or external, induce the onset of cortical spreading depression (CSD) in a pre-existing hyper-excitable cortex of a migraine brain, initiating the process of pain generation. The author hypothesizes on a second site of action of triggers at the level of trigeminal nuclear complex (TNC) in brain stem, the cell station of second order neuron pathway for migraine pain transmission to the sensory cortex. The author suggests existence of a hypothetical 'gate' at TNC level where incoming trigeminal migraine pain impulses would 'compete' with descending inhibitory signals from brain stem pain modulatory neurons, to get entry into the central nervous system. The author draws analogy with the 'gate control' mechanism operative at the dorsal horn level for spinally transmitted somatic and visceral pain. It is suggested that the hypothetical 'gate' at TNC level is controlled by activity of 5HT receptors, thus supporting the concept of an additional site of action of triptans in aborting acute migraine pain. The suggested hypothesis on mechanism of action of triggers, offers theoretical basis for efficacy of currently available pharmacologic and non-pharmacologic therapies for abortive and prophylactic treatment of migraine.