## 4 Discussion  
The current study has identified three subgroups of patients with TTH by using, for the first time, the SC algorithm. This analysis identified one cluster including all patients with CTTH (cluster 2) and two clusters including most patients with FETTH (clusters 0 and 1). In general, patients with CTTH (cluster 2) showed worse scores in all outcomes as compared to those with FETTH (clusters 0-1); however, the SC analysis identified a subgroup of patients with FETTH exhibiting widespread pressure pain hypersensitivity (cluster 0) in a similar proportion than those with CTTH (cluster 2). This study using SC supports the clinical classification commonly used by the International Headache Society establishing 15 days per month as a potential cut-off value for differentiating between CTTH and FETTH [6,14]. In addition, SC analysis also supports the presence of worse clinical presentation and widespread pressure pain hypersensitivity in patients with CTTH (cluster 2) than in those with FETTH (clusters 0 and 1). The presence of widespread sensitivity to pressure pain is a clinical manifestation of central sensitization in CTTH. In fact, a recent meta-analysis concluded that sensitivity to pressure pain seems to be widespread in CTTH and confined to the head and cervical spine in FETTH [38], supporting those findings identified by the current SC analysis. There is evidence supporting that development of central sensitization is a continuous process related to an increase in the frequency of headache [39]. Interestingly, the current SC analysis found two subgroups of patients with FETTH, one group with less widespread pain sensitivity to pressure pain (cluster 1) and other group (cluster 0) with a similar widespread pain hyperalgesia than CTTH patients (cluster 2). This subclassification could potentially help to identify individuals with FETTH at a higher risk for developing central sensitization and a potentially quicker transition from the episodic to the chronic form of the disease. It is also possible that this subgroup of FETTH patients with higher levels of central sensitization would be more susceptible for developing widespread pain symptoms representing the 35-44% of TTH patients suffering from co-morbid fibromyalgia syndrome [40]. This hypothesis is supported by the presence of widespread symptoms in this group (cluster 0) experienced by lower scores in the bodily pain domain of the health-related quality of life questionnaire [41]. Although the most accepted theories agree that the episodic form is more peripherally related whereas the chronic form is more centrally related [6], SC has been able to identify a group of patients with FETTH exhibiting a more central component (cluster 0) which could be at a higher risk of chronification. Current findings are clinically relevant since identification of this subgroup of individuals with FETTH showing greater sensitization could lead to earlier therapeutic strategies for preventing chronification of the headache. The fact that one group of patients with FETTH exhibited higher widespread pain sensitization may suggest different mechanisms underlying this subgrouping of the patients. It is accepted that prolonged nociception from peripheral tissues are the main responsible for triggering centralized sensitization mechanisms [42] and, hence, they promote the evolution from episodic to chronic TTH [6]. In this sensitization process, muscle tissues, particularly trigger points, have received particular attention in the last decades [43]. In fact, it has been postulated that the pain referral elicited by active TrPs (those reproducing the headache pain features) could be one of the main responsible of TTH-related pain and sensitization [44]. Interestingly, the SC analysis found that the subgroup of patients with FETTH with sensitization (cluster 0) presented a higher number of active TrPs than those FETTH patients with less sensitization (cluster 1), but, most importantly, in a similar proportion to those with CTTH (cluster 2).