Peripheral Factors

Individuals who have been exposed to static or repetitive work for long periods of time may develop pericranial muscle tenderness and tension-type headache. Therefore, for many years the research on the mechanisms that lead to tension-type headache focused on peripheral or muscular factors. Increased pericranial myofascial tissue tenderness to manual palpation is the most prominent abnormal finding in patients with chronic tension-type headache.^11–13 Painful impulses from these tissues may be referred to the head and perceived as headache, and myofascial mechanisms may therefore play a major role in the pathophysiology of tension-type headache.¹⁴ Possible excessive pericranial muscle contraction, ischemia, and inflammation have been extensively studied in tension-type headache; however, electromyography with surface electrodes failed to demonstrate significantly increased activity.^15–17

A microdialysis study reported altered blood flow regulation in tender skeletal muscles of patients with chronic tension-type headache during static work.¹⁸ The authors found no difference in locally increased interstitial lactate between patients and control subjects. This seems to rule out the presence of ischemia in the tender points of chronic tension-type headache patients during static exercise. It was hypothesized that increased excitability of neurons in the central nervous system may affect the regulation of muscle blood flow during static work.¹⁸ The microdialysis study also demonstrated that the interstitial concentration of inflammatory mediators in tender muscle did not differ between patients with chronic tension-type headache and healthy subjects.¹⁹ These data indicate that tender points are not sites of ongoing inflammation.

In summary, firm evidence for peripheral muscle pathology as a cause of muscle pain and chronic headache in tension-type headache is still lacking.

Central Factors

Since the mid-1990s, there has been increasing interest in the role of central factors in tension-type headache. It has been shown that pressure pain detection and thresholds of tolerance of mechanical stimuli were decreased in chronic tension-type headache sufferers.^20,21 Furthermore, Bendtsen and colleagues²² demonstrated that patients with chronic tension-type headache had a qualitatively altered pain perception. On the basis of these findings and data from basic pain research,²³ it has been suggested that the central sensitization, and therefore the chronic pain state, in patients with chronic tension-type headache may result from sensitization at the level of the spinal dorsal horn, the trigeminal nucleus, or both, induced by prolonged nociceptive input from pericranial myofascial tissues.⁶ The hypothesis of central sensitization in tension-type headache is supported by experimental pharmacological studies. Animal studies have shown that sensitization of pain pathways may be caused by or associated with activation of nitric oxide synthase and the generation of nitric oxide.²⁴ To test the hypothesis of central sensitization in tension-type headache, the antinociceptive effect of nitric oxide synthase inhibitors^25,26 and the nociceptive effect of nitric oxide donor²⁷ were investigated in patients with chronic tension-type headache. The nitric oxide synthase inhibitor N^G-monomethyl-L-arginine hydrochloride reduced headache and pericranial myofascial tenderness and hardness. Furthermore, the nitric oxide donor glyceryl trinitrate induced tension-type headache in these patients.²⁷ These data suggest that nitric oxide plays an important role in the pathophysiology of chronic tension-type headache⁵ and that inhibition of nitric oxide synthase may become a novel principle in the treatment of this disorder.

In summary, clinicians are beginning to understand some of the complex mechanisms leading to tension-type headache. It is hoped that this will lead to the development of more effective and specific treatment modalities.