To review the available literature on obsessive–compulsive symptom (OCS)/obsessive–compulsive disorder (OCD) in patients with schizophrenia.

Electronic searches were carried out to locate studies reporting various aspects of OCS/OCD in patients with schizophrenia.

Available evidence suggests that prevalence of OCS/OCD in patients with schizophrenia is much higher than prevalence in general population and it is seen in all the stages of schizophrenia, starting from at risk mental state to chronic/stabilisation/deficit phases. Symptom profile of OCS/OCD in schizophrenia is similar to that seen in patients with OCD only. Presence of OCS/OCD is associated with higher severity of symptoms of schizophrenia and more negative outcome. At present there is very limited data on the efficacy/effectiveness of various pharmacological measures and psychological interventions, for management of OCS/OCD in patients with schizophrenia. There is some evidence pointing towards beneficial effect of certain antipsychotics, antidepressants and cognitive behaviour therapy. Management of OCS/OCD in patients with schizophrenia involves proper assessment. If the OCS/OCD is related to use of particular antipsychotic use, initial attempt must be made to reduce the dose of antipsychotics, however, if this is not effective, than addition of a selective serotonin reuptake inhibitor (SSRIs) must be considered. If the OCS/OCD is not related to the use of antipsychotic medication, than depending up on the severity of psychotic symptoms, addition of SSRIs must be considered.

This review suggests that OCS/OCD is highly prevalent among patients with schizophrenia and there is limited good quality evidence to make any specific recommendations for management.

The aim of this paper was to provide a systematic review and update on the available longitudinal studies on the impact of prenatal alcohol exposure (PAE) on language, speech and communication development, as well as associated potential environmental confounders during the preschool period.

A literature search was restricted to English, full‐text, peer‐reviewed, longitudinal studies in from 1970 until present: PUBMed, Scopus, Web of Science {C-e Collection, Biological Abstracts, KCI-Kean Journal Database, Russian Science Citation Index, SciELO Citation Index, Zoological Rec-d}, Academic Search Premier (Africa-Wide Information, CINAHL, MEDLINE, PsycINFO. Keywords included: prenatal alcohol exposure (PAE); speech or language or communication outcomes; neurocognitive or neurodevelopment or neurobehavioral or neurobehavioural; infant or baby or toddler or preschooler; longitudinal or follow-up. The inclusion criteria included (i) longitudinal cohorts with at least 2 time-points; (ii) association of light, moderate or heavy PAE on language, speech or communication delay, development or disorder; (iii) environmental confounders; (iv) infants up to preschool age.

Six studies satisfied the threshold for inclusion. Three studies reported that PAE was significantly associated with receptive or expressive delay. These studies demonstrated lower scores on either receptive or expressive communication in the alcohol group in comparison to the non-alcohol group, even after controlling for environmental factors up to 36 months.

Evidence from the longitudinal studies reviewed suggest that PAE influenced delays in receptive and expressive communication up to 36 months. Contextual risk factors played a significant role in language development over time and especially as children approached school age.

Individual biological predispositions should play a role in risky driving behaviour. Platelet monoamine oxidase (MAO) activity, dopamine transporter gene (DAT1) and neuropeptide S receptor 1 (NPSR1) gene polymorphisms have been identified as markers of impulsivity, alcohol use and excessive risk-taking. We aimed to find out how this knowledge on neurobiology of impulsivity applies to drunk driving and traffic behaviour in general.

We have longitudinally examined the behaviour of drunk drivers (n = 203) and controls (n = 211) in traffic, in association with their alcohol-related problems, personality measures and the three biomarkers. We analysed differences between the subjects based on whether they had committed driving while impaired by alcohol (DWI) violation in a 10-year time period after recruitment or not and investigated further, what kind of predictive value do the different biomarkers have in committing DWI and other traffic violations and accidents.

The original drunk drivers group had lower platelet MAO activity but further DWI was not significantly associated with this measure. Being a NPSR1 T-allele carrier contributed to the risk of repeatedly committing DWI. DAT1 9R carriers in contrast were involved in more traffic accidents by their own fault (active accidents), compared to 10R homozygotes in the whole sample. All groups with DWI also had significantly more alcohol-related problems and higher scores in maladaptive impulsivity compared to controls without DWI.

Established biological markers of alcohol use and impulsivity can be reliably associated with everyday traffic behaviour and help in contributing to the understanding of the need for more personalized prevention activities.

Genetic and environmental factors interact in the development of major depressive disorder (MDD). While neurobiological correlates have only partially been elucidated, altered levels of calcitonin gene-related peptide (CGRP)-like immunoreactivity (LI) in animal models and in the cerebrospinal fluid of depressed patients were reported, suggesting that CGRP may be involved in the pathophysiology and/or be a trait marker of MDD. However, changes in CGRP brain levels resulting from interactions between genetic and environmental risk factors and the response to antidepressant treatment have not been explored.

We therefore superimposed maternal separation (MS) onto a genetic rat model (Flinders-sensitive and -resistant lines, FSL/FRL) of depression, treated these rats with antidepressants (escitalopram and nortriptyline) and measured CGRP-LI in selected brain regions.

CGRP was elevated in the frontal cortex, hippocampus and amygdala (but not in the hypothalamus) of FSL rats. However, MS did not significantly alter levels of this peptide. Likewise, there were no significant interactions between the genetic and environmental factors. Most importantly, neither escitalopram nor nortriptyline significantly altered brain CGRP levels.

Our data demonstrate that increased brain levels of CGRP are present in a well-established rat model of depression. Given that antidepressants have virtually no effect on the brain level of this peptide, our study indicates that further research is needed to evaluate the functional role of CGRP in the FSL model for depression.

To investigate oxidative stress parameters [total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), paraoxonase (PON), arylesterase (ARE) and thiol-disulphide homeostasis] in patients who were diagnosed as having somatic symptom disorder in accordance with Diagnostic and Statistical Manual of Mental Disorders-5.

The study included 41 medication-free patients with somatic symptom disorder and 47 age, sex, and sociodemographic-matched healthy individuals. The patients were administered the Patient Health Questionnaire-15, Somatic Symptom Amplification Scale, Beck Depression Inventory, and Beck Anxiety Inventory. TOS, TAS, OSI, PON, ARE thiol, disulphide levels, and routine biochemical parameters were compared between the two groups.

TOS, OSI, disulphide levels, disulphide/native thiol, and disulphide/total thiol ratios were found significantly higher in the patient group compared with the control group (p < 0.001). There was no significant difference in PON, ARE, and TAS parameters between the two groups (p > 0.05).

This study showed that the level of oxidants increased and oxidative balance was impaired in somatic symptom disorder. Oxidative stress may play a role in the aetiopathogenesis of this disorder. This is the first study to report an association between oxidative stress and somatic symptom disorder.

The present study explores the relationship between neuroactive hormones and religious commitment. We hypothesised that religious commitment is mediated by neuropeptide Y and oxytocin. These neurohormones have a well-established role in general well-being, anxiety regulation, stress-resilience, social affiliation and spirituality.

Sixty healthy women (median age 21) participated in the study and completed the Religious Commitment Inventory and other psychometric surveys. Blood was sampled from each participant and serum levels of neuropeptide Y were measured using radioimmunoassay. Oxytocin, stress and sex hormones were measured using enzyme-linked immunosorbent assay. Correlations were tested using non-parametric statistical methods.

We found a positive correlation between serum neuropeptide Y levels and religious commitment, but not between oxytocin and religious commitment.

The present study provides preliminary evidence that neuropeptide Y is a biological correlate of religious commitment.