Pathophysiology of migraine and tension-type headache

Migraine and tension-type headache are common in general population. Recent progress in basic and clinical research has increased our understanding of pathophysiology of these headaches. New treatment modalities and drugs for the treatment of these headaches are emerging. Migraine is a neurovascular headache with complex pathophysiology, which has not been fully clarified. Genes for both migraines, with and without aura, are being identified. Current research indicates importance of cortical spreading depression and abnormal brain stem activity in the pathophysiology of migraine with aura. The migraine headache most likely originates in the sensory fibers innervating intracranial and extracranial blood vessels. Peripheral and central sensitization of trigeminovascular nociceptive pathways may develop during migraine attacks. Central sensitization of second- and third-order trigeminovascular nociceptive neurons may lead to transformation of episodic migraine to chronic migraine. Pericranial myofascial pain sensitivity is increased in patients with tension-type headache and may be of importance in the pathophysiology of this headache. Sensitization of second-order neurons at the level of the spinal dorsal horn or trigeminal nucleus, sensitization of supraspinal neurons, and decreased descending inhibition from supraspinal structures play a major role in the pathophysiology of chronic tension-type headache.