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Evidence suggests that emotional memory plays a role in the pathophysiology of depression/anxiety disorders. Noradrenaline crucially modulates emotional memory. Genetic variants involved in noradrenergic signaling contribute to individual differences in emotional memory and vulnerability to psychopathology. A functional deletion polymorphism in the α-2B adrenoceptor gene (ADRA2B) has been linked to emotional memory and post-traumatic stress disorder. The noradrenaline reuptake inhibitor reboxetine attenuates enhanced memory for negative stimuli in healthy and depressed individuals. We examined whether the effect of reboxetine on emotional memory in healthy individuals would be moderated byADRA2Bgenotype.ADRA2Bdeletion carriers demonstrated enhanced emotional memory for negative stimuli compared with deletion noncarriers, consistent with prior studies. Reboxetine attenuated enhanced memory for negative stimuli in deletion noncarriers but had no significant effect in deletion carriers. This is the first demonstration of genetic variation influencing antidepressant drug effects on emotional processing in healthy humans.

Emotional enhancement of memory is a widely accepted phenomenon that, in addition to its adaptive role, may play a role in the evolution of psychiatric disorders. Hence a comprehensive understanding of its neurobiological basis is imperative. Whilst the pharmacological and neural mechanisms are well known, the contribution of genetic variation is not. Research suggests that two qualitatively different processes (recollection and familiarity) contribute to recognition memory. In this study, we examined the relative contribution of two common genetic polymorphisms, the deletion variant of the ADRA2B gene that codes the α2b adrenergic receptor and the val158met polymorphism of the COMT gene that codes the catechol-O-methyltransferase enzyme, to emotional enhancement of these two memory processes in 97 healthy male volunteers. There was a significant interaction between COMT genotype and emotional arousal in relation to recollection, but not familiarity, with the former being significantly elevated for emotionally arousing versus neutral pictures in carriers of the val158 allele compared with met158 carriers. There were no main effects or interactions in relation to ADRA2B genotype.

The COMT val(158) variant has been associated with impaired cognitive function compared to the Met(158) variant yet gene gene interactions are not well described. In this study we demonstrate an interaction between this COMT polymorphism and a deletion variant of ADRA2B, the gene encoding the alpha 2b-adrenergic receptor on episodic memory performance. Specifically, carriage of the ADRA2B deletion abolished the relative memory impairment in homozygous COMT val(158) carriers compared to Met(158) carriers.

Objective: We aimed to assess whether executive functioning improved over time in a sample of borderline personality disorder (BPD) subjects that took part in a quetiapine treatment trial. Methods: Performance on the following neurocognitive tasks was assessed at enrolment and at the end of the 12 weeks quetiapine treatment: Trail Making Task, Word Fluency Task and Tower of London Task. Forty-one BPD patients were recruited, of whom 32 completed the trial. An intention-to-treat analysis with a mixed linear model was applied. Results: The data show that participants significantly improved on most executive functioning measures. Patients' scores decreased significantly (mean [SD] difference; p-value) on the Trail Making Task Part A (11.7 [2.3];p < 0.0001), Part B (51.8 [9.2]; p < 0.0001) and 'B minus A' (40.1 [8.2]; p < 0.0001), on a Phonological (15.9 [1.6]; p < 0.0001) and Semantic (9.8 [1.1]; p < 0.0001) Verbal Fluency tasks, and on the Tower of London total correct score (2.5 [0.4]; p < 0.0001), total move score (29.5 [4.5]; p < 0.0001) and total time (172.9 [35.8]; p < 0.0001). Conclusions: In this study we have demonstrated that executive functioning in BPD is improved after treatment with quetiapine. Neurocognitive measures of executive functioning should be considered as valuable outcomes in the study of treatment efficacy in BPD. Copyright (C) 2009 John Wiley & Sons, Ltd.

Memory dysfunction occurs in a number of neuropsychiatric disorders. Therapeutic psychopharmacological agents may exacerbate such memory impairment. Detailed characterisation of drug-induced memory impairment is therefore important. We recently showed that the D2/D3antagonist amisulpride quantitatively impairs emotional memory in a randomised placebo-controlled study of 33 healthy volunteers. Current evidence suggests that two qualitatively different processes (recollection and familiarity) contribute to recognition memory and can be investigated using a Dual-Process Signal Detection model. Using such a model, we found that amisulpride levels at encoding were significantly inversely correlated with recollection estimates for emotional but not neutral stimuli or familiarity estimates in healthy male volunteers. This suggests that dopamine antagonism at encoding preferentially impairs the recollection component of emotional memory, relative to the familiarity component. This was supported by receiver operating characteristic analysis. We also found a significantly increased false recognition rate, associated with significantly shorter reaction times for emotional but not neutral stimuli in the amisulpride group. These findings have important implications for our understanding of recognition memory processes, as well as the interpretation of neuropsychological findings in medicated patients.

Background: Catechol-O-methyltransferase (COMT) metabolizes catecholamines in the prefrontal cortex (PFC). A common polymorphism in the COMT gene (COMT val158met) has pleiotropic effects on cognitive and emotional processing. The met allele has been associated with enhanced cognitive processing but impaired emotional processing relative to the val allele. Methods: We genotyped healthy, white men in relation to the COMT val158met polymorphism. They were given a single 4 mg dose of the selective noradrenaline reuptake inhibitor (NRI) reboxetine or placebo in a randomized, double-blind between-subjects model and then completed an emotional memory task 2 hours later. Results: We included 75 men in the study; 41 received reboxetine and 34 received placebo. In the placebo group, met/met carriers did not demonstrate the usual memory advantage for emotional stimuli that was observed in val carriers. Reboxetine restored this emotional enhancement of memory in met/met carriers, but had no significant effect in val carriers. Limitations: We studied only men, thus limiting the generalizability of our findings. We also relied on self-reported responses to screening questions to establish healthy volunteer status, and in spite of the double-blind design, participants were significantly better than chance at identifying their intervention allocation. Conclusion: Emotional memory is impaired in healthy met homozygotes and selectively improved in this group by reboxetine. This has potential translational implications for the use of reboxetine, which is currently licensed as an antidepressant in several countries, and edivoxetine, a new selective NRI currently in development.

It is basically a primarily legal philosophical and political problem whether or not mentally disordered persons “belong” in prison. Countries applying the construct of criminal responsibility or incompetence to stand trial can prevent mentally disordered persons from being imprisoned. Secure confinement can then be ordered in a forensic psychiatric institution, if necessary. Of course this principle does not prevent people from becoming mentally unwell when put in a prison environment, nor does the presence or a history of mental disorder automatically result in the absence of criminal responsibility. The still high prevalence of mental disorders in prisoners has been impressively demonstrated in more recent surveys. In a systematic review of 62 surveys from 12 different western countries including 22,790 prisoners (mean age 29 years, 81% men), 3.7% of the men had psychotic illnesses, 10% major depression, and 65% a personality disorder, while 4% of women had psychotic illnesses, 12% major depression, and 42% a personality disorder. In comparison to the general population, prisoners have an increased risk of suffering from a mental disorder that transcends countries and diagnoses. Psychotic disorders increase the risk of suicide, which as a rule is considerably higher in prisoners than in the general population. Suicide is the leading cause of death in penal institutions, especially during the early stages of confinement.

The Republic of Belarus (ROB) covers 207 600 km2 and has a population of about 10 million (Ministry of Statistics and Analysis, 2005). It was a member state of the former Soviet Union until it gained independence in 1991. Belarus is located between Poland, Lithuania and Latvia in the west, Russia in the east, and Ukraine in the south. Seventy-two per cent of the population live in an urban environment and 28% in rural areas. The average life span for men is 63 years and for women 75 years (Ministry of Public Health, 2005).

Individual differences in emotional processing are likely to contribute to vulnerability and resilience to emotional disorders such as depression and anxiety. Genetic variation is known to contribute to these differences but they remain incompletely understood. The serotonin transporter (5-HTTLPR) and alpha(2B)-adrenergic autoreceptor (ADRA2B) insertion/deletion polymorphisms impact on two separate but interacting monaminergic signalling mechanisms that have been implicated in both emotional processing and emotional disorders. Recent studies suggest that the 5-HTTLPR s allele is associated with a negative attentional bias and an increased risk of emotional disorders. However, such complex behavioural traits are likely to exhibit polygenicity, including epistasis. This study examined the contribution of the 5-HTTLPR and ADRA2B insertion/deletion polymorphisms to attentional biases for aversive information in 94 healthy male volunteers and found evidence of a significant epistatic effect (p < 0.001). Specifically, in the presence of the 5-HTTLPR s allele, the attentional bias for aversive information was attenuated by possession of the ADRA2B deletion variant whereas in the absence of the s allele, the bias was enhanced. These data identify a cognitive mechanism linking genotype-dependent serotonergic and noradrenergic signalling that is likely to have implications for the development of cognitive markers for depression/anxiety as well as therapeutic drug effects and personalized approaches to treatment.

Data on the efficacy of quetiapine in borderline personality disorder (BPD) are still scarce. We aimed to investigate the efficacy of quetiapine for impulsivity and a broad range of affective symptoms in BPD. In this 12-week open-label study, we included individuals with BPD who presented to psychiatric in- and outpatient services. After a gradual titration of quetiapine, a flexible dose (range, 100-800 mg) was administered. The main outcome measures consisted of the scores on patient-rated questionnaires (Barratt Impulsiveness Scale, Buss-Durkee Hostility Inventory, Affective Lability Scale, Spielberger State and Trait Anxiety Inventory, Spielberger State and Trait Anger Inventory, and Beck Depression Inventory) and on neurocognitive tasks related to impulsivity (Stroop Color Word Task and IOWA Gambling Task). A mixed linear model, correcting for age, sex, antidepressant use, and weeks in psychotherapy, was applied. Forty-one patients (34 females and 7 males; mean [SD] age, 27.0 [9.0] years) were enrolled in the study, 32 of which completed the trial. Patients' scores decreased significantly (mean [SD] difference; P value) on the Barratt Impulsiveness Scale (19.7 [2.0]; P < 0.0001), Buss-Durkee Hostility Inventory (11.5 [1.4]; P < 0.0001), Affective Lability Scale (0.75 [0.08]; P < 0.0001), Beck Depression Inventory (25.0 [1.7]; P < 0.0001), Spielberger State and Trait Anxiety Inventory state (19.9 [1.9]; P < 0.0001) and trait (20.8 [1.7]; P < 0.0001) subscale, and Spielberger State and Trait Anger Inventory state (7.3 [1.1]; P < 0.0001) and trait (10.1 [1.0]; P < 0.0001) subscale. In addition, patients showed significantly less inference on the Stroop Color Word Task and had more 'good choices' on the IOWA Gambling Task. These results suggest that quetiapine may be efficacious in the treatment of impulsivity and affective symptoms in BPD.

Vomiting and retching are behaviours that are part of the clinical manifestation of several disorders. Rarely, vomiting is actually tic and, when not recognized, may mislead physicians and other caregivers to erroneously diagnose a medical or psychiatric disorder without considering a tic-disorder. We report on an 18 year old male patient who demonstrated vomiting as main symptom. Initially, he was diagnosed with an eating disorder, bulimia nervosa purging type (DSM-IV TR). Firstly, he was not very able to suppress his vomiting, but later the vomiting became forced by putting fingers in his throat. This self-induced vomiting had a compulsive component and was performed after almost every meal. Psychiatric assessment disclosed a specific sequence of a premonitory epigastric feeling preceding the vomiting and relief after vomiting. History taking revealed that he had a childhood onset of motor tics (copropraxia which consisted of grabbing his genitalia, bilateral facial grimacing and sudden movements of the head) and phonic tics (sniffing and gargling). Furthermore, he had been treated with methylphenidate for a childhood diagnosis of Attention Deficit and Hyperactivity Disorder and suffered from obsessive-compulsive symptoms (OCS). His vomiting was considered a tic in the course of a Tourette syndrome. His score on the Yale Global Tic Severity Scale dropped from 74 at the first assessment to a score of 50 at week 4 of treatment with risperidone 0,5 mg/day and sertralin 25 mg/day. Sedation and sexual dysfunction occurred as adverse events. Vomiting as a tic is rare clinical manifestation, but this possibility should be considered when patients have a history of tics.

OBJECTIVE: Cognitive models suggest that biased processing of emotional information may play a role in the genesis and maintenance of psychotic symptoms. The role of dopamine and dopamine antagonists in the processing of such information remains unclear. The authors investigated the effect of a dopamine antagonist on perception of, and memory for, emotional information in healthy volunteers. METHOD: Thirty-three healthy male volunteers were randomly assigned to a single-blind intervention of either a single dose of the dopamine D(2)/D(3) antagonist amisulpride or placebo. An attentional blink task and an emotional memory task were then administered to assess the affective modulation of attention and memory, respectively. RESULTS: A significant interaction was observed between stimulus valence and drug on recognition memory accuracy; further contrasts revealed enhanced memory for aversive-arousing compared with neutral stimuli in the placebo but not the amisulpride group. No effect of amisulpride was observed on the perception of emotional stimuli. CONCLUSIONS: Amisulpride abolished the enhanced memory for emotionally arousing stimuli seen in the placebo group but had no effect on the perception of such stimuli. These results suggests that dopamine plays a significant role in biasing memory toward emotionally salient information and that dopamine antagonists may act by attenuating this bias.

Background: Few attempts have been made to examine the relationship between amygdala abnormalities and specific symptoms in psychosis. The present study explored the relationship between amygdala morphology and mood congruent and mood incongruent delusional beliefs. Methods: Amygdala volumes were measured in 43 patients presenting with delusional beliefs in the context of their first episode of psychosis and 43 healthy volunteers matched for age and gender. Results: Left-greater-than-right-asymmetry of the amygdala varied as a function of gender and mood congruence of delusional beliefs, due to asymmetrical enlargement of the left amygdala in women presenting with predominantly mood incongruent delusions. However, there was no difference in amygdala volumes across groups. Conclusions: Amygdala abnormalities in women may be associated with aberrant emotional processing that Could contribute to the development of mood incongruent delusional beliefs. Sexually dimorphic changes in the amygdala may contribute to differential phenotypic illness expression in men and women

PURPOSE OF REVIEW: Compelling evidence suggests that a small group of men who develop schizophrenia display a stable pattern of antisocial behaviour from childhood onwards, causing considerable suffering to victims and to themselves and imposing a significant financial burden on society. We reviewed the literature on the neurobiological correlates of antisocial behaviour and violence to further the understanding of this subgroup of persons with schizophrenia and develop testable hypotheses for future research. RECENT FINDINGS: Few studies have been conducted, sample sizes are small and measures vary greatly. Taken together, the results suggest that among men with schizophrenia, those who have displayed a stable pattern of antisocial and aggressive behaviour since childhood, as compared with those with no such history, perform better on neuropsychological tests tapping specific executive functions and more poorly on assessments of orbitofrontal functions. We hypothesize that individuals in this subgroup are less compromised neurologically and display structural brain abnormalities in the amygdala-orbitofrontal system and in the prefrontal cortex and hippocampus. SUMMARY: A better understanding of the distinctive neurobiological characteristics of this subgroup of men with schizophrenia will contribute to developing treatments tailored to their needs, to prevent antisocial behaviours and to reduce the symptoms of schizophrenia. Language: en

SummaryBelgium has become one of the few countries in the world where euthanasia is legally allowed within a specific juridical framework. Even more unique is the inclusion of grounds for requesting euthanasia on the basis of mental suffering. Further refinement of the legal, medical and psychiatric approach to the issue is required in order to clear up essential practical and ethical matters. Psychiatrists and their professional organisations need to play a greater role in this ongoing debate and contribute from a clinical, scientific and ethical point of view.

Men and women who develop schizophrenia are at increased risk, compared with the general population, to engage in violence toward others. The reasons for this robust finding remain obscure. We undertook a review of studies comparing neuropsychological test performance, neurological soft signs, and structural brain images of persons with schizophrenia with and without a history of violence. Our search identified 17 studies. The results are inconsistent and contradictory, mainly due to varying definitions of violence, differences in sample characteristics, and the use of diverse measures to tap the neurobiological correlates of violent behavior. The results suggest, however, that among men with schizophrenia, those who have displayed a stable pattern of antisocial and aggressive behavior since childhood, as compared with those with no such history, perform better on neuropsychological tests tapping specific executive functions and more poorly on assessments of orbitofrontal functions, show fewer neurological soft signs, and display larger reductions in volume of the amygdalae, more structural abnormalities of the orbitofrontal system, more abnormalities of white matter in the amygdala-orbitofrontal system, and smaller reductions in volumes of the hippocampus.