Esketamine had been rised as a potential treatment for Resistant Depression, becoming an alternative for the use of Electroconvulsive Therapy. In Spain since 2020, it has been applied for compassionate use but is not widely used. Although Esketamine is defined safe and effective in preliminary studies, there are common side effects which could reduce it use.

Increasing blood pressure has been found commonly in ederly population treated with Esketamine Nasal. Studies showed as very common side effect (10% or more) increasing systolic and diastolic blood pressure which is higher in elderly people. Our aim is to show that esketamine is well tolerated and safe in ederly people without increasing blood pressure, although is combinate with oral antidepressant therapy.

Presenting female 65-year-old with 4 years of treatment maintaining a moderate-severe symptoms. Althougt numerous pharmacological strategies have been attempted, with optimal time and maximum doses, which have been progressively withdrawing showing lack of efficacy or appearance of adverse effects. Among the drugs used we find; 11 antidepressants, 3 antipsychotics, benzodiazepines and even lithium, without response after 6 weeks of treatment. Futhermore, patient refusal to receive Electro-Convulsive Therapy. Treating with Esketamine nasal and applying the established guidelines.

Assess the response to Esketamine Nasal with Montgomery-Asberg depression scale (MADRS) we found that decrease the initial score in 26 points. Evaluating blood pressure before and after each time with no increased value.

Concluding esketamine is well tolerated and safe in ederly people without increasing blood pressure. These findings and results should be confirmed with futher studies.

Previous studies of patients with unipolar depression have shown that early decrease of prefrontal EEG cordance in theta band can predict clinical response to various antidepressants. We have now examined whether decrease of prefrontal quantitative EEG (QEEG) cordance value after 1 week of venlafaxine treatment predicts clinical response to venlafaxine in resistant patients.

We analyzed 25 inpatients who finished 4-week venlafaxine treatment. EEG data were monitored at baseline and after 1 week of treatment. QEEG cordance was computed at three frontal electrodes in theta frequency band. Depressive symptoms and clinical status were assessed using Montgomery–Åsberg Depression Rating Scale (MADRS), Beck Depression Inventory-Short Form (BDI-S) and Clinical Global Impression (CGI).

Eleven of 12 responders (reduction of MADRS ≥50%) and only 5 of 13 non-responders had decreased prefrontal QEEG cordance value after the first week of treatment (p = 0.01). The decrease of prefrontal cordance after week 1 in responders was significant (p = 0.03) and there was no significant change in non-responders. Positive and negative predictive values of cordance reduction for response were 0.7 and 0.9, respectively.

The reduction of prefrontal theta QEEG cordance value after first week of treatment might be helpful in the prediction of response to venlafaxine.

Current studies suggest that improvement of depressive symptoms after 2 weeks of treatment could predict the subsequent response. The aim of our study was to compare the predictive effect of early improvement (EI) after 1 and 2 weeks of treatment in patients who had failed to respond to previous antidepressant treatments (≥1 unsuccessful antidepressant trial).

Seventy-one subjects were treated (≥4 weeks) with various antidepressants chosen according to the judgment of attending psychiatrists. We used three definitions of EI (MADRS reduction ≥20, 25, 30%) at both time points. Areas under curve (AUC) were calculated to compare predictive effect of EI.

We found lower MADRS scores in weeks 1 and 2 in responders (≥50% reduction of MADRS, n = 35) compared to nonresponders. AUCs of MADRS reduction for response prediction at week 1 and 2 were not significantly different (0.73 vs 0.8; p = 0.24).

The results indicate that improvement of depressive symptoms in the treatment of resistant patients may occur after the first week of treatment. The predictive potential might be comparable to that found after the second week of antidepressant intervention and be clinically meaningful.

The purpose of present study was to evaluate the efficacy of the addition of reboxetine in patients that had not previously responded, or had done so only partially, over 6 weeks of conventional pharmacological treatment with venlafaxine.

This open-label, prospective and multicentric study included 40 outpatients diagnosed with major depressive disorder according to the DSM-IV criteria. Efficacy was assessed using the 21-item Hamilton Depression Rating Scale (HAMD) and the Clinical Global Impression-Improvement (CGI-I). Safety was evaluated by recording spontaneously reported adverse events. Data were analysed on an intent-to-treat basis, using the last-observation-carried-forward method.

Mean HAMD reduction was 34.9% (P < 0.0001). The percentages of responders (≥50% reduction in HAMD) and patients considered as benefiting from complete remission (HAMD ≤ 10 points) at week 6 were 27.5 and 12.5%, respectively. By the end of the treatment, the score of CGI-I decreased 24.8% (P < 0.0001). Percentage of patient improving (CGI < 4 points) was 47.5%. The most common non-serious adverse events were constipation, nervousness, anxiety and insomnia.

These findings suggest that the combined treatment of reboxetine and venlafaxine, in venlafaxine-resistant patients, may be an effective and well-tolerated strategy.