A possible link between prenatal exposure to the selective serotonin reuptake inhibitors (SSRIs) and development of autism spectrum disorders (ASDs), previously suggested by two case-control studies, was not confirmed by a recent cohort study that followed for 5–10 years more than 600,000 births. However, this study failed to demonstrate that SSRI exposure during pregnancy is safe in terms of child development outcomes, as an increased risk of ASDs cannot be completely ruled out. In the present article, the main strengths and weaknesses of this study are briefly analysed, including a possibility of confounding by indication.

Psychostimulants are the first choice medication in children with attention-deficit/hyperactivity disorder (ADHD). Despite the proven high efficacy of psychostimulants, at least in the short term, for ADHD core symptoms, concerns continue to be raised on their adverse effects, including putative increased risk of substance use disorders (SUDs). A recent multicentre, case–control, longitudinal, prospective, European study by Groenman and colleagues found that treatment with psychostimulants in children with ADHD lowered the risk of SUDs in adolescence. However, this finding is at odds with other recent evidence concluding that ADHD children with and without medication treatment history did not significantly differ on any subsequent SUDs rates. In the present paper, we discuss the study by Groenman and colleagues in view of its methodological strengths and limitations, and we suggest possible implications for day-to-day clinical practice.

This editorial focuses on discordant twins as a valuable epidemiological design for psychiatric aetiological research. First, we summarise the advantages and strengths of this design over the classical matched case-control study. Then, we draw attention to the use of this method in bipolar disorder, revising previous discordant-twin studies. A future greater use of discordant twins is desirable to gain further relevant insights in the aetiology of bipolar disorder.

According to a recent cross-sectional study, some antidepressants, including amitriptyline, citalopram and escitalopram, are associated with QTc prolongation. However, the magnitude of this association is relatively small, and the clinical implications uncertain. In this article, the main strengths and weaknesses of this cross-sectional study are briefly analysed alongside recent warnings issued by regulatory authorities. Implications for research and practice are discussed.

Impairment of cognitive functions is a core feature of schizophrenia with relevant consequences on patients' psychosocial functioning. Cognitive remediation techniques have been recently developed with the aim to restore or compensate for such impairments and improve the functional outcome of the disease. There is now convincing evidence of the efficacy of many of these techniques, especially when delivered in the context of a comprehensive treatment programme. Whether the application of these techniques in the early phases of the disease could modify the disease course and outcome and how they could affect brain plasticity and the trajectory of brain disease of schizophrenia is still under scrutiny.

According to a recently published population study conducted in France, exposure to benzodiazepines may be associated with an approximately 50% increase in the risk of dementia in the elderly. However, the clinical interpretation of this finding raised some concerns. A causal link between benzodiazepine use and diagnosis of dementia may be real, but it is nevertheless possible that the increased risk might be due to other confounding factors. In this article, the main strengths and weaknesses of this study are briefly analysed, including the possibility of reverse causation. Implications for research and current practice are discussed.

This brief review encompasses the key findings of structural Magnetic Resonance Imaging (sMRI) research on amygdala volume in autism spectrum disorders (ASD). We also highlight the possible correlation between the autistic behavioural phenotype and amygdala alteration.