Chronic muscle pain is a very prevalent disorder, which affects some regions of the body more often than others. Andersson et al. (1) found that the most common location of chronic muscle pain was the shoulder and neck regions in which chronic muscle pain was reported by 30% of the general population, followed by low back pain affecting 23% of the population. Muscle pain from the shoulder and neck as well as from chewing and facial muscles probably plays an important role in tension-type headache, which may be the most common form of myofascial pain (6,10). Myofascial tissues are constructed to move; muscles need exercise, whereas change of position is necessary for joints and fasciae. Long-term immobilization or static posture affects these tissues and causes them to hurt. During normal functioning, there is a constant cross-talk between myofascial tissues and the central nervous system, eliciting the necessary changes in position and rest. In this way, the normal person is kept free of myofascial pain. Every time slight discomfort is felt from myofascial tissues there are afferent impulses in small-diameter myelinated Aδ-and unmyelinated C-fibers (nociception). This physiologically important afferent input, however, may be a latent source of pain, depending on the central modulation of nociception, which may explain why myofascial pain is so common.

But why is shoulder and neck pain and tension-type headache more common than myofascial pain from other areas in the body? One reason could be that pain thresholds to pressure are lower (increased sensitivity) in the cranium than in the extremities (19). Moreover, it was recently demonstrated that muscle pain sensitivity is higher in the trapezius than in the anterior tibial muscle, and that temporal summation of pain is higher in muscle than in skin in the trapezius, but not in the anterior tibial, region (3). Chewing and neck muscles are involved in emotional behavior, such as facial expression, aggression, and gnashing of teeth, as well as in stabilization of the head, and the head and face have a particular large cortical sensory representation. Pain perception is not a simple reflection of afferent noxious input, but a dynamic process that is highly influenced multiple factors, for example, past experience and emotional status. Liability to central sensitization in response to repetitive noxious input as well as the degree of descending inhibition may differ between input from extracranial and pericranial myofascial tissues (3). Thus, there are a multitude of factors that may explain the high prevalence of tension-type headache.

Because of the enormous prevalence and variability in frequency and severity of tension-type headache, any inheritance is almost certain to be polygenic. Sufferers of tension-type headache must by chance have many affected first-degree relatives. The population relative risk in relatives compared with normal controls has been calculated in a single study. In chronic tension-type headache, the risk was increased threefold, indicating a genetic predisposition (18). The transmission suggested complex inheritance. At present, we adopt the view that the great majority of the population, perhaps all, have the potential to develop
tension-type headache if exposed to sufficiently strong environmental factors.

Headaches are generally reported to occur in relation to emotional conflict and psychosocial stress, but the cause-effect relationship is not clear. Stress and mental tension are the most frequently reported precipitating factors, but they occur with similar frequency in tension-type headache and migraine (22). These findings are in correspondence with the findings of widely normal personality profiles in subjects with episodic tension-type headache, whereas studies of subjects with the chronic form often reveal higher frequency of depression and anxiety (9,16). As in other chronic pain disorders, psychological abnormalities in tension-type headache may be viewed as secondary rather than primary (9) and anxiety and depression are probably comorbid with chronic tension-type headache.

The origin of pain in tension-type headache has traditionally been attributed to increased contraction and ischemia of head and neck muscles. However, it has been demonstrated that muscle activity is normal or only slightly increased in tension-type headache (10), and that muscle lactate levels are normal during static muscle exercise in patients with chronic tension-type headache, ruling out muscle ischemia as cause of the pain (2). A large number of studies have consistently shown that the pericranial myofascial tissues are considerably more tender in patients with tension-type headache than in healthy subjects, and that the tenderness is positively associated with both the intensity and the frequency of tension-type headache. These findings are valid both for patients with episodic and for patients with chronic tension-type headache and both during and outside of headache (10,13). It has also been demonstrated that the consistency of pericranial muscles is increased (2).

The increased myofascial pain sensitivity in tension-type headache could be caused by release of inflammatory mediators resulting in excitation and sensitization of peripheral sensory afferents (6). This hypothesis was challenged in a recent study investigating in vivo interstitial concentrations of inflammatory mediators and metabolites in a tender point of patients with chronic tension-type headache (5). Ashina et al. (5) found no difference in these substances between patients and healthy controls during rest or in response to static exercise. The authors suggested that tender points are not sites of ongoing inflammation. Mork et al. infused a combination of endogenous substances into the trapezius muscle and reported that patients with frequent episodic tension-type headache developed more pain than healthy controls (17). Concomitant psychophysical measures indicated that a peripheral sensitization of myofascial sensory afferents was responsible for the muscular hypersensitivity in these patients.