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Editorial

Editorial

Page 241 | Published online: 10 Oct 2011

Dear colleagues,

It is my great pleasure to welcome you to the fourth issue of 2011.

In our first article Duenas et al. investigated the question of sexual dysfunction during treatment with serotonin reuptake inhibitors (SSRIs) or duloxetine. The frequency of treatment-emergent sexual dysfunction (TESD) in patients with major depressive disorder (MDD) treated with duloxetine was comparable to that with SSRI monotherapy. However, a greater MDD effectiveness was found in favour of duloxetine.

Osorio and colleagues assessed the psychometric properties of the Brazilian Portuguese version of the Beck Anxiety Inventory (BAI) in a sample of university students with social anxiety disorder (SAD). The BAI was adequate for identifying anxiety symptoms, but its usefulness for screening SAD seems limited.

Matsunaga et al. sought to analyse the efficacy and safety of aripiprazole as augmentation agent for treatment-resistant obsessive compulsive disorder (OCD). The results suggest that adding aripiprazole to SSRIs can be a valid and effective strategy for treatment-resistant OCD patients.

Nazari and colleagues from Iran compared the efficacy of eye movement desensitization and reprocessing (EMDR) with citalopram during the treatment of OCD. It emerged that both EMDR and citalopram had significant effects in reducing OCD signs, while in the short term EMDR suggests better effects in the improvement of the final outcome of OCD.

Sansone et al. investigated the relationship between childhood trauma and borderline personality symptomatology in a non-psychiatric clinical population. They concluded that there appears to be a relationship between various forms of trauma (especially sexual abuse) and borderline personality symptoms, reinforcing the role of childhood trauma in borderline personality disorder.

The use of medication in the treatment of inpatients with borderline personality disorder (BPD) and clinicians’ views on the UK National Institute for Health and Clinical Excellence (NICE) Guideline on BPD were studied by Haw and Stubbs. They found that the use of psychotropics (especially clozapine), off-label prescribing and polypharmacy were common in patients with BPD. According to the view of the clinicians, the NICE BPD Guideline was helpful for managing community patients, but not for severe BPD inpatients.

Bravo-Ortiz and colleagues explored the quality of life and burden of Spanish patients with schizophrenia and their caregivers. It emerged that activities of daily life and anxiety/depression were the most relevant problems reported. Moreover, patients treated with risperidone long-acting injectable (LAI) had better quality of life outcomes and presented a lower burden to caregivers than patients treated with other types of antipsychotics.

Kapsali et al. from Greece examined the demographic, clinical and pharmacological factors associated with aggressive behaviour after abrupt discontinuation of medication in schizophrenic patients. The aggressive behaviour of 402 patients who were involuntarily hospitalised after abrupt discontinuation was assessed by using the Aggression Scale as well as the Discontinuation-Emergent Signs and Symptoms Checklist (DESS). Their findings suggest that abrupt drug discontinuation may lead to aggressive behaviour, being connected at least in the acute phase with particular demographic, clinical and pharmacological parameters.

Chiesa and colleagues addressed the questions whether d-amino acid oxidase activator (DAOA) variants were associated with schizophrenia and whether they could predict the clinical outcomes of patients treated with various antipsychotics. It emerged that rs7139958 and rs9558571 single- nucleotide polymorphisms may be associated with more severe baseline symptoms in schizophrenic patients.

Afonso et al. present a short report on the sleep promoting effect of endogenous melatonin in patients with schizophrenia compared to healthy controls. They concluded that increased sleep latency in schizophrenia may not be related to the reduced output of melatonin; however, further studies are needed to elucidate a possible disruption of its activity on somnogenic structures of the brain.

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