## 4 Discussion  
A multidimensional protocol based on transcranial Direct Current Stimulation (tDCS), cognitive-attentional therapy and therapeutic exercise was applied to a BMS-affected woman with a 45-day follow-up. TDCS was used previously in other cranial pain conditions with good results [32]. The most common target for stimulation in pain has been M1, but DLPFC has also shown good effects in chronic pain conditions [33]. As [PERSON] et al. [7] showed the effectiveness of DLPFC stimulation specifically in BMS, we chose this target for our protocol. In our case, there was an improvement in the subjective perception of pain with changes in VNPRS scores, but the effect disappeared at 45 days during the follow-up period (Figure 1). Large effect sizes were found in pain questionnaires (BPI, PCS and LANSS) and disability (IDDC, OHIP), and all except LANSS continued to improve after the end of the intervention. All of the changes persisted at 45 days of follow-up. Figure 1: Results of the visual analogue scale during therapy and follow up. These results are in line with those of [PERSON] et al. [7], who applied 10 sessions of rTMS on DLPFC and found an improvement in pain intensity immediately; as in our study, they found a worsening at one month of follow-up, but in their study, an improvement was seen 2 months later. We could not prove this further improvement as our follow-up period was limited to 45 days. According to [PERSON] et al., these results suggest that the analgesic and antidepressant effects of non-invasive transcranial stimulation may act independently and suggest that inhibitory activation as a consequence of DLPFC stimulation by rTMS, used in their study, could be due to an improvement of limbic system dysfunction in patients with BMS. Although tDCS on the left Dorsolateral Prefrontal Cortex has been shown to be effective in improving affective symptoms [34], there were no changes in the anxiety and depression scales in our case, which may mean that there are effects beyond emotional improvement justifying the effects of this protocol. Although the action mechanisms of tDCS are not yet fully understood, it has been suggested that the modulation of cortical excitability induces an activation of descending inhibitory pain systems [35]; surprisingly, in our case, there were no changes in objective pain measurements (widespread mechanical hyperalgesia and temporal summation) at any point. Contrarily to what was expected, Conditioned Pain Modulation significantly worsened when measured immediately after finishing the 10 sessions of the treatment protocol, returning to the baseline at day 45. These changes may be justified by the studies by [PERSON] et al. [36], which found that the daily application of tDCS may produce a neuroinflammatory effect that conditions the results of objective pain measurements just after completing the protocol. The transient worsening of CPM may be seen also seen as part of the nocebo effect that may have been caused by the end of the protocol [37]. CPM has been shown to decrease with aging [38]. Considering that CPM possibly predicts exercise-induced analgesia [39], therapeutic exercise may not have been a crucial factor on the effects of our protocol. On the other hand, the cognitive effects of the protocol show an improvement in processing speed and executive control as well as sustained attention (improvements on TMT A and B task and Stroop-word) that persisted at one month of follow-up. Due to the relationship between executive function and pain, the improvement in pain perception may be explained in part by the improvement in the tasks that mediate the executive function [40]. Unexpectedly, an improvement in the MoCA score was also observed, improving from mild cognitive impairment to performance within normal limits; this may be due to the attention improvement on the performance of certain tasks of the test as the TMT-B.