We report on a patient with tardive dyskinesia (TDK) treated with aripiprazole, a third-generation antipsychotic with partial D2 agonist-antagonist activity at both the dopamine and serotonin receptors. The patient’s condition improved with administration of a combination of tetrabenazine, botulinum toxin, and clozapine, which has previously not been used. We suggest that this treatment combination may have potential benefits for patients with TDK. After aripiprazole discontinuation, the patient was treated with clozapine (150 mg/day) and biperiden (8 mg/day). Due to a lack of improvement, we administered 300 units (intramuscularly; IM) of botulinum toxin into the paravertebral muscles every 3 months and 1,000 units IM every 4 months in addition to tetrabenazine (75 mg/day) and biperiden (8 mg/day). The patient stopped this treatment, at which point TDK reappeared. After starting a treatment regimen of clozapine (100 mg/day), tetrabenazine (75 mg/day), and botulinum toxin (300 units IM), the patient’s symptoms remitted.

Despite being clinically underestimated, sexual dysfunction (SD) is one of the most frequent and lasting adverse effects associated with antidepressants. Desvenlafaxine is an antidepressant (AD) with noradrenergic and serotonergic action that can cause a lower SD than other serotonergic ADs although there are still few studies on this subject. Objective: To check the frequency of SD in two groups of depressive patients: one group was desvenlafaxine-naïve; the other was made up of patients switched to desvenlafaxine from another AD due to iatrogenic sexual dysfunction. A naturalistic, multicenter, and prospective study of patients receiving desvenlafaxine (50–100 mg/day) was carried out on 72 patients who met the inclusion criteria (>18 years old and sexually active), who had received desvenlafaxine for the first time (n = 27) or had switched to desvenlafaxine due to SD with another AD (n = 45). Patients with previous SD, receiving either drugs or presenting a concomitant pathology that interfered with their sexual life and/or patients who abused alcohol and/or drugs were excluded. We used the validated Psychotropic-Related Sexual Dysfunction Questionnaire (PRSexDQ-SALSEX) to measure AD-related sexual dysfunction and the Clinical Global Impression Scale for psychiatric disease (CGI-S) and for sexual dysfunction (CGI-SD) at two points in time: baseline and three months after the commencement of desvenlafaxine treatment. Results: In desvenlafaxine-naïve patients, 59.2% of the sample showed moderate/severe sexual dysfunction at baseline, which was reduced to 44% at follow-up. The PSexDQ-SALSEX questionnaire total score showed a significant improvement in sexual desire and sexual arousal without changes in orgasmic function at follow-up (p < 0.01). In the group switched to desvenlafaxine, the frequency of moderate/severe SD at baseline (93.3%) was reduced to 75.6% at follow-up visit. Additionally, SD significantly improved in three out of four items of the SALSEX: low desire, delayed orgasm, and anorgasmia at follow-up (p < 0.01), but there was no significant improvement in arousal difficulties. The frequency of severe SD was reduced from 73% at baseline to 35% at follow-up. The CGI for psychiatric disease and for sexual dysfunction improved significantly in both groups (p < 0.01). There was a poor tolerability with risk of treatment noncompliance in 26.7% of patients with sexual dysfunction due to another AD, this significantly reduced to 11.1% in those who switched to desvenlafaxine (p = 0.004). Conclusion: Sexual dysfunction improved significantly in depressed patients who initiated treatment with desvenlafaxine and in those who switched from another AD to desvenlafaxine, despite this, desvenlafaxine treatment is not completely devoid of sexual adverse effects. This switching strategy could be highly relevant in clinical practice due to the significant improvement in moderate/severe and poorly tolerated SD, while maintaining the AD efficacy.