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Figure 1. The pathophysiology of migraine headache. A = Cortical spreading depression (CSD); B = release of NO,CGRP, prostaglandins, or ions leading to vasodilatation of dural blood vessels; C = activation of primary afferents of trigeminal nerve; D = direct activation of second order neurons of the trigeminal nerve; E = activation of primary afferents causes release of substance P and calcitonin-gene related peptide, which leads to neurogenic inflammation or further vasodilatation of dural blood vessels; F = neurogenic inflammation and vasodilatation lead to primary afferent conduction; G = excitation of second order neurons of the trigeminal nerve; H = ascending signals from the second order neurons of the trigeminal nerve are modulated by the LC and DR and later synapse in the thalamus before relaying the signal to the cortex. (Adapted from Cutrer FM, Limmroth V, Moskowitz M: Possible mechanisms of valproate in migraine prophylaxis. Cephalalgia 17:93-100, 1997; and Wynn D: The scientific basis of migraine. Postgraduate Medicine pp 4-9, 2000; with permission.) (See also page 914, Fig. 1 in article by Martin and Behbehani.) Figure 2. Possible sites of action of the various triggers. Stress = hypothalamus and limbic regions; Food = dural blood vessel, presynaptic terminals of sympathetic nerves that innervate the blood vessels or release of factors from mast cells near the blood vessels; Smell = cortex, amygdala, thalamus; Sleep = hypothalamus, LC, DR; Light = cortex, hypothalamus, thalamus or brainstem modulatory pathways (LC, DR). (Adapted from Cutrer FM, Limrnroth V, Moskowitz M: Possible.mechanisms of valproate in migraine prophylaxis. Cephalalgia 17:93-100, 1997; and Wynn D: The scientific basis of migraine. Postgraduate Medicine pp 4-9, 2000; with permission.) (See also page 934, Fig. 2 in article by Martin and Behbehani.)
Figure 2.
Figure 1. The pathophysiology of migraine headache. A = Cortical spreading depression (CSD); B = release of NO,CGRP, prostaglandins, or ions leading to vasodilatation of dural blood vessels; C = activation of primary afferents of trigeminal nerve; D = direct activation of second order neurons of the trigeminal nerve; E = activation of primary afferents causes release of substance P and calcitonin-gene related peptide, which leads to neurogenic inflammation or further vasodilatation of dural blood vessels; F = neurogenic inflammation and vasodilatation lead to primary afferent conduction; G = excitation of second order neurons of the trigeminal nerve; H = ascending signals from the second order neurons of the trigeminal nerve are modulated by the LC and DR and later synapse in the thalamus before relaying the signal to the cortex. (Adapted from Cutrer FM, Limmroth V, Moskowitz M: Possible mechanisms of valproate in migraine prophylaxis. Cephalalgia 17:93-100, 1997; and Wynn D: The scientific basis of migraine. Postgraduate Medicine pp 4-9, 2000; with permission.) (See also page 914, Fig. 1 in article by Martin and Behbehani.) Figure 2. Possible sites of action of the various triggers. Stress = hypothalamus and limbic regions; Food = dural blood vessel, presynaptic terminals of sympathetic nerves that innervate the blood vessels or release of factors from mast cells near the blood vessels; Smell = cortex, amygdala, thalamus; Sleep = hypothalamus, LC, DR; Light = cortex, hypothalamus, thalamus or brainstem modulatory pathways (LC, DR). (Adapted from Cutrer FM, Limrnroth V, Moskowitz M: Possible.mechanisms of valproate in migraine prophylaxis. Cephalalgia 17:93-100, 1997; and Wynn D: The scientific basis of migraine. Postgraduate Medicine pp 4-9, 2000; with permission.) (See also page 934, Fig. 2 in article by Martin and Behbehani.)
Figure 2.