The relationship between TTH and pericranial muscle disorders has been discussed in the literature since 1940, but there is no conclusion as to whether muscle disorders are a cause or a consequence of TTH, or just one of the factors in the pathogenesis of TTH. Peterson et al. (1995) investigated the site specificity of painful muscles in the head during headache in a group of TTH patients by using a subjective self-report rating of five muscles, including the frontalis, temporalis, masseter, cephalicus and trapezius muscles. Although detailed quantitative observations were made for each muscle, no significant relationship was found between muscle pain and muscle tension and electromyographic activity levels. Jensen et al. (1998) observed that in patients with CTTH with pericranial muscle disorders, the tenderness was significant and the pain response to mechanical stimulation was hypersensitive, i.e. the more significant the tenderness, the more sensitive the response to mechanical stimulation, and the electromyographic activity was significantly increased, but the threshold for thermal pain stimulation was not abnormal, while in patients with ETTH, none of the above changes were significant. In recent years, Bansevicius et al. (1999) studied the correlation between muscle pain, tension and electromyographic response in patients with TTH, and used visual analog scale (VAS) to record the pain level in the forehead, right and left temporalis, neck and right and left shoulder muscles, and also recorded the superficial electromyographic activity in these areas. Tension and fatigue were also recorded by the VAS method, and the patients were asked to self-assess. There was no correlation between electromyographic activity and pain, between electromyographic activity and fatigue, and between tension and fatigue, so the authors concluded that the role of tension in TTH was not prominent. 2. The relationship between TTH and psychological changes Catheart et al. (1998) did an experimental biopsychological study on the relationship between arousal-related mood (ARM) and ETTH, and they used the activation-deactivation adjective check list (ADACL) They found that the tension level of ETTH patients was higher than that of the control group, even when they did not have headache, and the tension level was significantly lower in the non-headache period than in the headache period. Therefore, it is believed that there is a relationship between tension and headache. 3. The relationship between TTH and vascular headache Since it can be found that tension-type headache and migraine occur in the same patient at the same time, and some patients initially present with migraine, and when the frequency of attacks gradually increases, they present with ETTH, which can then be converted to CTTH, the relationship between these two types of headache has been reported quite a lot, for example, Tackeshima et al (1998) in reviewing the literature For example, Tackeshima et al. (1998), in reviewing the literature, pointed out that myoclonic headache and migraine have many common features, such as the clinical symptoms and features of both can overlap with each other, platelet 5-HT can be decreased and plasma 5-HT can be increased in both, sympathetic function of the peripheral autonomic nervous system can be low in both, and genetic studies found that there are both migraine and myoclonic headache patients in the same family, etc. Recently, Hannerz et al. 1998) proposed whether CTTH is a vascular headache? In their experimental study, patients with CTTH were first placed in supine position, and sublingual nitroglycerin and head lowering were used to induce headache. Therefore, the authors concluded that the occurrence of headache in CTTH patients was closely related to cranial hemodynamics, and since the headache decreased slowly at the end of head-down position, it was thought that the headache was caused by insufficient intracranial venous return or venous dilatation. The headache is thought to be caused by insufficient intracranial venous return or dilated veins. For example, Oishi et al. (1998) examined the levels of plasma platelet factor 4, β-thromboglobulin and 11-dehydrothromboxane B2 and found that the levels of these three substances in ETTH patients were significantly higher than those in CTTH group and control group, and concluded that the headache and platelet dysfunction in ETTH patients were particularly close. Mishima et al. (1997) found that serum platelet magnesium ion levels were reduced in TTH patients and suggested that it might be related to enhanced platelet function, Martinez et al. (1994) found that plasma 5-hydroxytryptamine levels were higher and catecholamine levels were lower in TTH patients than in controls, that plasma dopamine levels were positively correlated with headache duration, and In addition, it was found that monoamine levels did not correlate with the degree of depression. These results suggest that there are changes in the function of the central monoaminergic nervous system in TTH patients, and that such changes are not related to the ensuing depression, but to the pathophysiological mechanism by which the headache occurs. Marukawa et al. (1996) found a significant increase in substance P and 5-hydroxytryptamine in the saliva of TTH patients during headache attacks and suggested that substance P is released by the nociceptive system. In conclusion, the above examples show that the pathogenesis of TTH is still being studied from various aspects, including the relationship between headache and muscles, the relationship between headache and depression, and even the concept of whether “tension” refers to muscular tension or psychosomatic tension.