## 4 Discussion
In turn, increased neuronal activity would also require some neurovascular coupling adaptations mediated by brain perfusion [24]. Contradictory to the present findings, an fNIRS-based study of local cerebral oxygenation during tDCS in patients with mild traumatic brain injury found that tDCS leads to a decrease in the local brain oxygenation values on the anodal side of between 8 and 12 min in 3-5 days post-injury [25]. Conversely, another study showed that anodal tDCS did not elicit any consistent, instantaneous, or dose-dependent cerebral blood flow increases in the specific targeted hand primary motor cortex at conventional intensity ranges [26]. On the other hand, a study showed that tDCS had positive effects on people with depression with cerebral vascular impairments compared to sham controls [27]. This particular type of depression is often less responsive to drug treatment. The results showed that 58% of inpatients achieved remission when receiving two daily sessions of tDCS. The same group had a response rate of 68%, whereas the sham group had no response at all. Conversely, a systematic review with meta-analysis showed improved cognitive performance and increased HbO in response to tDCS intervention [24], although some potential confounders had to be pointed out, such as the moderate heterogeneity for HbO responses and the large variation in the tasks used to assess cognitive performance. Another study applied tDCS 1 mA bilaterally on the prefrontal cortex (anode left on Fp1 and cathode right on Fp2) [28]. The results showed a peak of HbO in the bilateral prefrontal region 4 min after the end of stimulation and before returning to baseline levels. The effect was more pronounced under the left anode when 15 min of stimulation was preferred over 10 min. The present baseline hemodynamic response of the group with depression showed lower levels of SatO\({}_{2}\) and HbO compared to controls, suggesting that people with depression have marked abnormalities of the prefrontal cortex oxygenation. A recent case-control meta-analysis and meta-regression showed decreased cerebral blood flow in the inferior frontal gyrus, insula, middle occipital gyrus, and bilateral superior temporal gyrus in all patients with major depressive disorder [29]. Another study compared controls with no prior history of psychiatric disorder to a database of SPECT scans of suicidal patients, all diagnosed with the major depressive disorder [30]. The results showed hypoperfusion bilaterally in the superior/medial prefrontal cortex in the cohort of completed suicides compared to controls. Depression is considered a strong comorbid factor, with potential deficits in tasks associated with this region, including attention, memory, and executive function. Finally, in accordance with the present findings, another previous study showed the abnormal resting state of corticolimbic blood flow in unmedicated patients with depression [30]. In this particular cited study, the resting blood flow in patients with depression was correlated with the severity of depression based on [PERSON]'s scale scores. Some limitations must be addressed. The present study was designed to produce immediate results in a specific cohort of patients and controls. Distinct baseline characteristics, such as the level of impairment, age, and sex distribution, may alter the observed outcomes. The present study also lacked a sham group. The groups were not age-homogeneous. Nevertheless, when age was applied as a covariate, no changes were detected in the present results. The findings were restricted to the assessed prefrontal area. Thus, other interactions among cortical areas were not considered in discussing the results. The electrode positioning was the same for all patients. The 10-20 system was the only adopted setting to account for skull variability. Procedures such as neuro navigation or computational modeling were not available in the laboratory's facilities.