Korsakoff’s syndrome (KS) is a chronic neuropsychiatric disorder characterised by severe anterograde amnesia and executive deficits. Theory of Mind (ToM) is the capacity to represent others’ mental states such as their knowledge, thoughts, feelings, beliefs, and intentions in order to explain and predict their behaviour. Surprisingly this topic has received hardly any attention in research on KS, although the severity of behavioural problems in KS suggest possible ToM difficulties. The aim of the present study was therefore to assess whether cognitive and affective ToM are impaired in patients with KS.

We examined 21 KS patients and 21 age- and gender-matched healthy controls on three standardised tests that assess cognitive and affective ToM, including the subtests of the mini-Social Cognition and Emotional Assessment battery and a specialised version of the Sally–Anne Test.

KS patients showed largely impaired cognitive and affective ToM compared to healthy controls, as reflected in large effect sizes on both cognitive and affective ToM tests. Executive deficits explained problems in emotion recognition, but not other ToM aspects.

KS patients have large impairments in both cognitive and affective aspects of social cognition. Their ability to recognise emotions, take the perspective of others, and understand socially awkward situations is vastly compromised. The impairments in ToM functioning are to a large degree functionally discrepant from executive disorders that are commonly present in KS. This study therefore highlights the importance to properly index ToM functioning in neuropsychological assessments for individuals with a possible KS diagnosis.

There is accumulating evidence that the error-related negativity (ERN), an event-related potential elicited after erroneous actions, is altered in different psychiatric disorders and may help to guide treatment options. Thus, the ERN is a promising candidate as a psychiatric biomarker. Basic methodological requirements for a biomarker are that their measurements are standardised and reliable. The aim of the present study was to establish ERN acquisition in a reliable, time-efficient and patient-friendly way for use in clinical practice.

Healthy subjects performed a speeded Eriksen Flanker Task that increases the number of errors. In a test–retest design (N = 14) with two sessions separated by 28 days we assessed the reliability of the ERN. To ensure external validity, we aimed to replicate previously reported correlation patterns of ERN amplitude with (A) number of errors and (B) negative affect. In order to optimise the clinical use of the task, we determined to which extent the task can be shortened while keeping reliability >0.80.

We found excellent reliability of the ERN (intraclass correlation coefficients = 0.806–0.947) and replicated ERN correlation patterns. The task can be halved to a patient-friendly length of 200 trials (recorded in 8 min) keeping reliability >0.80.

The modified task provides reliable and efficient recording of the ERN, facilitating its use as a psychiatric biomarker.

NMDA antagonists and nitric oxide synthase (NOS) inhibitors induce antidepressant-like effects and may represent treatment options for depression. The behavioural effects of NMDA antagonists seem to depend on Tyrosine kinase B receptor (TrkB) activation by BDNF and on mechanistic target of rapamycin (mTOR), in the medial prefrontal cortex (mPFC). However, it is unknown whether similar mechanisms are involved in the behavioural effects of NOS inhibitors. Therefore, this work aimed at determining the role of TrkB and mTOR signalling in the prelimbic area of the ventral mPFC (vmPFC-PL) in the antidepressant-like effect of NOS inhibitors.

Pharmacological treatment with LY235959 or ketamine (NMDA antagonists), NPA or 7-NI (NOS inhibitors), BDNF, K252a (Trk antagonist) and rapamycin (mTOR inhibitor) injected systemically or into vmPFC-PL followed by behavioural assessment.

We found that bilateral injection of BDNF into the vmPFC-PL induced an antidepressant-like effect, which was blocked by pretreatment with K252a and rapamycin. Microinjection of LY 235959 into the vmPFC-PL induced antidepressant-like effect that was suppressed by local rapamycin but not by K252a pretreatment. Microinjection of NPA induced an antidepressant-like effect insensitive to both K252a and rapamycin. Similarly, the antidepressant-like effects of a systemic injection of ketamine or 7-NI were not affected by blockade of mTOR or Trk receptors in the vmPFC-PL.

Our data support the hypothesis that NMDA blockade induces an antidepressant-like effect that requires mTOR but not Trk signalling into the vmPFC-PL. The antidepressant-like effect induced by local NOS inhibition is independent on both Trk and mTOR signalling in the vmPFC-PL.

Depression is a common, serious, but under-recognised problem in multiple sclerosis (MS). The primary objective of this study was to assess whether a rapid visual analogue screening tool for depression could operate as a quick and reliable screening method for depression, in patients with MS.

Patients attending a regional MS outpatient clinic completed the Emotional Thermometer 7 tool (ET7), the Hospital Anxiety and Depression Scale – Depression Subscale (HADS-D) and the Major Depression Inventory (MDI) to establish a Diagnostic and Statistical Manual, 4th edition (DSM-IV) diagnosis of Major Depression. Full ET7, briefer subset ET4 version and depression and distress thermometers alone were compared with HADS-D and MDI. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and receiver operating characteristic (ROC) curve were calculated to compare the performance of all the screening tools.

In total, 190 patients were included. ET4 performed well as a ‘rule-out’ screening step (sensitivity 0.91, specificity 0.72, NPV 0.98, PPV 0.32). ET4 performance was comparable to HADS-D (sensitivity 0.96, specificity 0.77, NPV 0.99, PPV 0.37) without need for clinician scoring. The briefer ET4 performed as well as the full ET7.

ET are quick, sensitive and useful screening tools for depression in this MS population, to be complemented by further questioning or more detailed psychiatric assessment where indicated. Given that ET4 and ET7 perform equally well, we recommend the use of ET4 as it is briefer. It has the potential to be widely implemented across busy neurology clinics to assist in depression screening in this under diagnosed group.

Road traffic injuries are the leading cause of death among young people. Recognition of the contribution of impulsive behaviour may help novice drivers to behave more safely. Previously a brief intervention focusing on impulsive traffic behaviour conducted by psychologists in driving schools had been effective. The aim of this study was an independent re-evaluation of the effect of the intervention, as conducted by driving school teachers, and assessment of the potential associations with candidate genotypes.

Driving school students (mean age 22.5, SD=7.9) were divided into intervention (n=704) and control (n=737) groups. Driving school teachers were trained to administer the intervention which consisted of a lecture and group work (1.5 h in total) on impulsivity. Traffic offences and crashes were monitored during 3 years, using police and traffic insurance fund databases. Functional polymorphisms of the dopamine transporter (DAT) and serotonin transporter genes (DAT1 VNTR and 5-HTTLPR) were assessed.

The intervention significantly lowered general traffic risk and prevalence of traffic accidents. DAT1 VNTR 9R carriers, particularly males, had higher general traffic risk in the whole sample. Female 5-HTTLPR s’ allele carriers of the intervention group had the lowest general traffic risk. Intervention was most effective in female DAT1 VNTR 10R/10R homozygotes.

Brief impulsivity-centred intervention appears as a promising strategy for preventing risk-taking behaviour in novice drivers and can be fully integrated to driving school curriculum.

Patients with psychogenic non-epileptic seizures (PNES) may present with convulsive events that are not accompanied by epileptiform brain activity. Video-electroencephalography (EEG) monitoring is the gold standard for diagnosis, yet not all patients experience convulsive episodes during video-EEG sessions. Hence, we aimed to construct a predictive model in order to detect PNES from serum hormone levels, detached from an evaluation of patients’ convulsive episodes.

Fifteen female patients with PNES and 60 healthy female controls participated in the study, providing blood samples for hormone analysis. A binomial logistic regression model and the leave-one-out cross-validation were employed.

We found that levels of neuropeptide Y and adrenocorticotropic hormone were the optimal combination of predictors, with over 90% accuracy (area under the curve=0.980).

The ability to diagnose PNES irrespective of convulsive events would represent an important step considering its feasibility and affordability in daily clinical practice.