Substance dependence disorder is a chronically relapsing condition characterised by neurobiological changes leading to loss of control in restricting a substance intake, compulsion and withdrawal syndrome. In the past few years, (endo)cannabinoids have been raised as a possible target in the aetiology of drug addiction. On the other hand, although the exact mechanisms of the genesis of addiction remain poorly understood, it is possible that neuroinflammation might also play a role in the pathophysiology of this condition. Studies demonstrated that (endo)cannabinoids act as immunomodulators by inhibiting cytokines production and microglial cell activation. Thus, in the present review, we explore the possible role of neuroinflammation on the therapeutic effects of cannabinoids on drug addiction.

We conducted an evidence-based review of the literature in order to assess the role of cannabinoids on the neuroinflammatory hypothesis of addiction (terms: addiction, cannabinoids and inflammation). We searched PubMed and BioMedCentral databases up to April 2014 with no date restrictions.

In all, 165 eligible articles were included in the present review. Existing evidence suggests that disruption in cannabinoid signalling during the drug addiction process leads to microglial activation and neuroinflammation.

The literature showed that inflammation and changes in endocannabinod signalling occur in drug abuse; however, it remains uncertain whether these changes are causally or coincidentally associated with addiction. Additional studies, therefore, are needed to elucidate the contribution of neuroinflammation on the behavioural and neuroprotective effects of cannabinoids on drug addiction.

Impaired social functioning and autistic symptoms are characteristics of schizophrenia. The social hormones oxytocin (OT) and arginine-vasopressin (AVP) both modulate social interaction and therefore may be involved in the pathogenesis of schizophrenia. We investigated whether men with schizophrenia show altered OT and AVP levels compared with healthy controls (HC) and whether autism symptoms are associated with OT levels.

Forty-one men with non-acute schizophrenia and 45 matched HC were enroled. Schizophrenia was assessed with the Positive and Negative Syndrome Scale (PANSS). Blood samples were collected on 2 days, and plasma OT and AVP levels were measured by ELISA immunoassay.

The schizophrenia patients had significantly lower plasma OT levels than the HC; a similar trend was found for AVP. Plasma OT levels were associated with severe life events, fewer important attached persons, and a higher score on the PANSS negative scale; the most dominant PANSS items were ‘preoccupation’, ‘emotional withdrawal’, and ‘passive/apathetic social withdrawal’.

These findings support an association between the social hormones OT and AVP and schizophrenia. We suggest that OT metabolism may be altered in schizophrenia, but other possible causes for decreased plasma OT levels in schizophrenia patients include decreased OT synthesis, mRNA expression, and translation. Especially the ‘autistic’ symptoms of schizophrenia seem to be closely linked to an altered metabolism of OT, the ‘attachment’ hormone.

Brain-derived neurotrophic factor (BDNF) plays a critical role in brain plasticity processes and serum levels have been demonstrated to be altered in patients with different mental disorder including suicidal behaviour. The objective of this study was to examine the association between serum BDNF levels as a possible peripheral indicator of suicide behaviour in subjects suffering from depression, personality disorders (PDs) and adjustment disorders (ADs) with or without suicide attempt.

The research included 172 randomly selected individuals suffering from recurrent depressive disorder (RDD; F 33.2), emotionally unstable PD (F 60.3) and AD (F 43.2), with or without attempted suicide according to the criteria of the ICD-10 (International Statistical Classification of Diseases and Related Health Problems 10th Revision) and 60 phenotypically health control subjects. In the group of patients, 73% subjects took some form of psychopharmacotherapy. Serum BDNF levels were measured by enzyme linked immunosorbent assay.

Subjects with PD and AD with suicide attempts had significantly lower serum BDNF levels than those without suicide attempts. In groups of subjects with PD and AD, those taking psychopharmacotherapy had higher serum BDNF levels. In the group of subjects with RDD, there were no differences with respect to suicide attempts or psychopharmacotherapy. Logistical regression analysis was indicated that psychopharmcotherapy and serum BDNF levels statistically correlated with suicide attempts.

The lower levels of BDNF in subjects suffering from PD and AD with suicide attempts, suggest that the serum BDNF level is a potential marker of suicidal behaviour, independent of mental disorders.

The aim of this study was to evaluate the validity of a new apathy rating scale in predicting the ability to return to work (RTW) in patients with depression or anxiety a year after discharge from a psychiatric hospital.

We evaluated 56 patients with depression or anxiety, who participated in an on-going randomised clinical trial using RTW as primary outcome. The degree of apathy was measured by the Diagnostic Apathia Scale, which contains six items covering the following neuropsychological symptoms: concentration/memory problems, difficulties in decision making, lassitude, tiredness/fatigue, insomnia, and reduced ability to work and engage in personal interests. The scale was analysed for psychometric validity (scalability) and for its ability to predict RTW. Finally, the predictive validity of the Diagnostic Apathia Scale regarding RTW was compared with scales measuring severity of depression/anxiety symptoms, disability, and psychological well-being.

The Diagnostic Apathia Scale displayed sufficient scalability, that is, the total score was a psychometrically valid measure of apathy. Only the Diagnostic Apathia Scale, and not the scales measuring severity of symptoms, disability, or psychological well-being, had predictive validity regarding RTW. Thus, 76% with ‘clinically significant apathy’ at baseline were unable to RTW versus 50% of the patients without apathy (p<0.05).

The Diagnostic Apathia Scale was found to have an acceptable predictive validity in terms of patients’ ability to RTW 1 year after discharge from hospitalisation for depression or anxiety.

Shared decision making (SDM) is an essential component of patient-centered care, but there is little information about its use in the psychiatric care.

To measure to what extent psychiatric patients feel they were involved in the process and steps of decision making about treatment choice and to analyse the influence of socio-demographic, clinical, and psychological processes on this perception.

Cross-sectional survey involving 1100 consecutive psychiatric outpatients invited to complete the nine-item Shared Decision-Making Questionnaire (SDM-Q-9), health locus of control and control preferences, self-efficacy and drug attitude scales, as well as a questionnaire including socio-demographic and clinical variables.

A high response rate of 77% was registered, resulting in a sample of 846 psychiatric outpatients. SDM-Q-9 total score indicate a moderately low degree of perceived participation, with differing perceived implementation of the individual the SDM process steps. Patient diagnosis evidenced significant differences in SDM perception. Patients’ perception of SDM was explained by four main variables: the older the patient, the lower self-reported SDM; having a diagnosis of schizophrenia increases the likelihood of lower SDM; a positive attitude towards psychiatric drugs favors greater SDM, as well as a higher level of self-efficacy.

The result of this study suggests that SDM is currently not widely practiced in psychiatric care. Further research is needed to examine if the low level of participation self-reported is justified by psychiatric patients’ decisional capacity.

Deep brain stimulation is currently an experimental treatment for major depressive disorder. Information is lacking, however, on how sham responding may affect efficacy. This article applies exploratory meta-analysis to address that topic.

Data on benefits of deep brain electrical stimulation come from a recent review. Stimulated brain regions included subgenual cingulate, capsular interna, nucleus accumbens, and medial forebrain bundle. Expert opinion plus random number software was used to generate hypothetical values for sham responding.

An effect size of 1.71 (95% CI: 1.47–1.96) was obtained for deep brain stimulation versus sham treatment in patients suffering from long-term treatment-resistant depression.

Preliminary findings on deep brain electrical stimulation suggest that the procedure may be 71% more effective than sham treatment. Expressing these findings as patients-needed-to-treat, deep brain electrical stimulation is required by 2.9 patients with long-term treatment-resistant depression in order for one of them to benefit.