Imaging studies in patients with TTH have suggested a fundamental role for the anterior cingulate cortex and the insula, both areas recognized for contributing to the cognitive and affective processing of sensory information [
45,
46]. In this regard, stress remains one of the most commonly recognized precipitating psychosomatic factors in the onset of a TTH attack [
60‐
62]. Furthermore, it has been shown that cognitive stress can increase muscle pain in TTH patients compared to controls [
63]. Physiologically, stress can trigger or aggravate headache by increasing muscle contraction, releasing catecholamines and cortisol, peripherally sensitizing, and/or affecting central pain processing [
64]. The long-term release of corticosteroids in those patients with chronic stress could cause tissue damage and an increase in pain perception [
65,
66]. In TTH, stress has been shown to trigger higher rates of pericranial muscle pain compared to controls [
63]. However, and contrary to this theory, there are authors who have not found a relationship between stress and the alteration of the diffuse nociceptive inhibitory control [
67], so the pathophysiological mechanism by which stress can act as a trigger for TTH and its role with respect to the limbic system and supraspinal mechanisms has not yet been elucidated [
33]. Likewise, there is no evidence to support a relationship between stress and increased pericranial EMG activity in patients with TTH, so its role in the pathophysiology of TTH remains uncertain [
63,
68]. Therefore, the pathophysiological mechanism by which stress can act as a trigger for TTH and its role with respect to the limbic system and supraspinal mechanisms have not yet been elucidated [
33]. Likewise, there is no evidence to support a relationship between stress and increased pericranial EMG activity in patients with TTH, so its role in the pathophysiology of TTH remains uncertain [
63,
68]. Therefore, the pathophysiological mechanism by which stress can act as a trigger for TTH and its role with respect to the limbic system and supraspinal mechanisms have not yet been elucidated [
33]. Likewise, there is no evidence to support a relationship between stress and increased pericranial EMG activity in patients with TTH, so its role in the pathophysiology of TTH remains uncertain [
63,
68].
On the other hand, it has been seen that psychosomatic factors such as depression can increase sensitivity to the perception of pain [
34]. Population studies have shown that both depression and anxiety are more prevalent in individuals with TTH than in the general population without headache [
69‐
73]. Cross-sectional research suggests that depression and anxiety are also associated with the frequency and severity of TTH attacks [
74]. However, it is not possible to determine a causal relationship between psychosomatic factors and TTH based on cross-sectional data [
34]. A longitudinal study showed possible bidirectional effects between psychosomatic factors and the characteristic pain of patients with TTH [
75].
In this context, the correlation between depression/anxiety disorders and primary headache disorders, such as tension-type headache and migraine, has been extensively documented in clinical settings. Although psychiatric disorders rarely serve as the sole cause of headache symptoms, their comorbidity can significantly influence patient outcomes and treatment strategies [
76]. Particularly, individuals with primary headache disorders and concurrent multiple psychiatric disorders require thorough evaluation and proper management, especially in cases involving medication misuse or insufficient response to conventional headache treatments [
77].
In another longitudinal study conducted in patients with TTH, it was suggested that emotional factors play an important role in the perceived pain experience. Along the same lines, high levels of depression and neuroticism have been associated with increased sensitivity to pain in the cephalic and extracephalic regions both in individuals with TTH and in individuals with migraine [
69], which would corroborate that the way in which the fact that pain is faced or managed affects the perception and modulation of pain in patients with TTH [
75].