The Pathophysiology of Migraine
The sensation of pain in migraine is attributed to activation of the CNS pathway that transmits noxious sensory inputs from the cerebral blood vessels to higher brain centers (Goadsby et al, 2002). This pathway is known as the trigeminovascular system (Figure 1) and has three main components:

• Trigeminal nerves with their cell bodies in the trigeminal ganglion transmit noxious sensory input caused by distension of the blood vessels of the dura and meninges. The peripheral terminals of these neurons also release potent neuropeptide vasodilators, Substance P and Calcitonin Gene Related Peptide (CGRP), causing dilation of dural blood vessels and further activation of the sensory neurons.
• Sensory input from the trigeminal nerves is conveyed from the trigeminal ganglia to the brainstem trigeminal nucleus caudalis (TNC), an important pain relay station for the head and neck region.
• From the TNC, higher brain centers are activated in the thalamus and cerebral cortex, resulting in the perception of headache pain.

Figure 1: Activation of Trigeminovascular Pathway During Migraine Headache