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Recent studies on tension-type headache indicate that the nociceptive input to the central nervous system may be increased as a result of activation or sensitization of peripheral sensory afferents. Moreover, pain perception studies and pharmacologic studies strongly suggest that the central nervous system is sensitized in patients with chronic tension-type headache. The barrage of nociceptive impulses from the periphery may be responsible for the sensitization of second- and third-order neurons in the central nervous system. In this way, sensitization may play a role in the initiation and maintenance of tension-type headache. Studies have demonstrated that treatment with drugs that counteract sensitization has an analgesic effect on tension-type headache. Targeting this mode of action seems to be a promising way of improving the treatment for this prevalent disorder.

The tenderness of pericranial myofascial tissues and number of myofascial trigger points are considerably increased in patients with tension-type headache (TTH). Mechanisms responsible for the increased myofascial pain sensitivity have been studied extensively. Peripheral activation or sensitization of myofascial nociceptors could play a role in causing increased pain sensitivity, but firm evidence for a peripheral abnormality still is lacking. Peripheral mechanisms are most likely of major importance in episodic TTH. Sensitization of pain pathways in the central nervous system due to prolonged nociceptive stimuli from pericranial myofascial tissues seem to be responsible for the conversion of episodic to chronic TTH. Treatment directed toward muscular factors include electromyography biofeedback, which has a documented effect in patients with TTH, as well as physiotherapy and muscle relaxation therapy, which are most likely effective. Future studies should aim to identify the source of peripheral nociception.

Tension-type headache is the most prevalent type of primary headache but is frequently forgotten by the patient and doctor. This article summarizes the present knowledge about tension-type headache and discusses some of the problematic aspects. Most patients in specialized headache clinics suffer from several different primary and secondary headaches at the same time and deserve a careful characterization before a rational therapy can be initiated. In particular, it is of utmost importance to increase focus on clinical and basic research in order to develop effective treatment strategies for the most neglected and most costly type of headache.

Tension-type headache is one of the most common primary headache disorders. Advances in basic pain and clinical research have improved our understanding of pathophysiologic mechanisms of tension-type headache. Increased excitability of the central nervous system generated by repetitive and sustained pericranial myofascial input may be responsible for the transformation of episodic tension-type headache into the chronic form. Studies of nitric oxide (NO) mechanisms suggest that NO may play a key role in the pathophysiology of tension-type headache and that the antinociceptive effect of nitric oxide synthase inhibitors may become a novel principle in the future treatment of chronic headache. Future studies should focus on investigation of the source of peripheral nociception, the role of descending pain modulation, and the development of an animal model of tension-type headache to support the pathophysiologic importance of central sensitization in tension-type headache.