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The riots of November 2005 among minority ethnic youths in the banlieues of France exposed a racism that scores deep into the French nation. Emergency law was invoked, curfews imposed and thousands of police were deployed. In the process, both the riots and the response to them brought into the open an aspect of France's secular republicanism that often lies hidden; an explosive mix of poverty, discrimination and Islamophobia. French assimilation is seen to have failed, yet the acceptance of multiculturalism as a social fact is viewed with suspicion.

The passing of a recent referendum in Switzerland, proposed by the Swiss People's Party (SVP) in order to halt 'mass immigration', is being lauded by Europe's far Right as a victory for 'direct democracy'. Here the authors argue that the form of participatory democracy that allowed the referendum to take place has brought about the institutionalisation of xeno-racism, rolling back over forty years of anti-racist reform and leaving migrant workers from other EU countries in the same vulnerable conditions that workers from southern Europe and the Balkans endured in Switzerland in the years following the second world war: with no rights to settlement, they were open to exploitation. The authors warn that the SVP's victory is a sign of the growing tendency across Europe of populist politicians to push centre parties further rightwards.

Alterations in reward processes may underlie motivational and anhedonic symptoms in depression and schizophrenia. However it remains unclear whether these alterations are disorder-specific or shared, and whether they clearly relate to symptom generation or not. We studied brain responses to unexpected rewards during a simulated slot-machine game in 24 patients with depression, 21 patients with schizophrenia, and 21 healthy controls using functional magnetic resonance imaging. We investigated relationships between brain activation, task-related motivation, and questionnaire rated anhedonia. There was reduced activation in the orbitofrontal cortex, ventral striatum, inferior temporal gyrus, and occipital cortex in both depression and schizophrenia in comparison with healthy participants during receipt of unexpected reward. In the medial prefrontal cortex both patient groups showed reduced activation, with activation significantly more abnormal in schizophrenia than depression. Anterior cingulate and medial frontal cortical activation predicted task-related motivation, which in turn predicted anhedonia severity in schizophrenia. Our findings provide evidence for overlapping hypofunction in ventral striatal and orbitofrontal regions in depression and schizophrenia during unexpected reward receipt, and for a relationship between unexpected reward processing in the medial prefrontal cortex and the generation of motivational states. ; Supported by a MRC Clinician Scientist award (G0701911), a Brain and Behaviour Research Foundation Young Investigator, and an Isaac Newton Trust award to Dr Murray; an award to Dr Segarra from the Secretary for Universities and Research of the Ministry of Economy and Knowledge of the Government of Catalonia and the European Union; by the University of Cambridge Behavioural and Clinical Neuroscience Institute, funded by a joint award from the Medical Research Council and Wellcome Trust (G1000183 and 093875/Z/10Z respectively); by awards from the Wellcome Trust (095692) and the Bernard Wolfe Health Neuroscience Fund to Professor Fletcher, and by awards from the Wellcome Trust Institutional Strategic Support Fund (097814/Z/11) and Cambridge NIHR Biomedical Research Centre. The authors are grateful for the help of clinical staff in CAMEO, in the Cambridge Rehabilitation and Recovery service and Pathways, and in the Cambridge IAPT service, for help with participant recruitment. ; This is the final version of the article. It first appeared from Nature Publishing Group via http://dx.doi.org/10.1038/npp.2015.370

[EN] High doses of antipsychotics have been associated with loss in cortical and total gray matter in schizophrenia. However, previous imaging studies have not taken benzodiazepine use into account, in spite of evidence suggesting adverse effects such as cognitive impairment and increased mortality. In this Northern Finland Birth Cohort 1966 study, 69 controls and 38 individuals with schizophrenia underwent brain MRI at the ages of 34 and 43 years. At baseline, the average illness duration was over 10 years. Brain structures were delineated using an automated volumetry system, volBrain, and medication data on cumulative antipsychotic and benzodiazepine doses were collected using medical records and interviews. We used linear regression with intracranial volume and sex as covariates; illness severity was also taken into account. Though both medication doses associated to volumetric changes in subcortical structures, after adjusting for each other and the average PANSS total score, higher scan-interval antipsychotic dose associated only to volume increase in lateral ventricles and higher benzodiazepine dose associated with volume decrease in the caudate nucleus. To our knowledge, there are no previous studies reporting associations between benzodiazepine dose and brain structural changes. Further studies should focus on how these observations correspond to cognition and functioning. ; This study was supported by the University of Oulu Scholarship Foundation, the Jalmari and Rauha Ahokas foundation, the Orion Research Foundation sr, the Scholarship Fund of the University of Ouu - Tyyni Tani Found, the Foundation for Psychiatric Research, the Sigrid Juselius Foundation, the Academy of Finland (#132071, #268336 and #278286), the Brain & Behavior Research Foundation, Northern Finland Health Care Support Foundation, the Universidad Carlos III de Madrid, the European Union's Seventh Framework Programme for Research, Technological Development and Demonstration under Grant agreement no. 600371, el Ministerio de ...

Objective: Current research does not provide a clear explanation for why some patients with Parkinson's Disease (PD) develop psychotic symptoms. The 'aberrant salience hypothesis' of psychosis has been influential and proposes that dopaminergic dysregulation leads to inappropriate attribution of salience to irrelevant/non-informative stimuli, facilitating the formation of hallucinations and delusions. The aim of this study is to investigate whether non-motivational salience is altered in PD patients and possibly linked to the development of psychotic symptoms. Methods: We investigated salience processing in 14 PD patients with psychotic symptoms, 23 PD patients without psychotic symptoms and 19 healthy controls. All patients were on dopaminergic medication for their PD. We examined emotional salience using a visual oddball fMRI paradigm that has been used to investigate early stages of schizophrenia spectrum psychosis, controlling for resting cerebral blood flow as assessed with arterial spin labelling fMRI. Results: We found significant differences between patient groups in brain responses to emotional salience. PD patients with psychotic symptoms had enhanced brain responses in the striatum, dopaminergic midbrain, hippocampus and amygdala compared to patients without psychotic symptoms. PD patients with psychotic symptoms showed significant correlations between the levels of dopaminergic drugs they were taking and BOLD signalling, as well as psychotic symptom scores. Conclusion: Our study suggests that enhanced signalling in the striatum, dopaminergic midbrain, the hippocampus and amygdala is associated with the development of psychotic symptoms in PD, in line with that proposed in the 'aberrant salience hypothesis' of psychosis in schizophrenia. ; This study was supported by a MRC Clinician Scientist [G0701911] and an Isaac Newton Trust award to G.K.M., and by the Cambridge NIHR Biomedical Research Centre; and by the European Union's Horizon 2020 to F.K. [754462]. T.W.R. discloses consultancy with Cambridge Cognition, Unilever and Greenfield Bioventures; he receives royalties from Cambridge Cognition, research grants from Shionogi & Co and GlaxoSmithKline, and editorial honoraria from Springer Nature and Elsevier. None of these conflict with the findings reported in this manuscript. None of the other authors report any conflicts of interest. R.A.B. discloses consultancy with Living Cell Technologies; Novo Nordisk; BlueRock Therapeutics; Fujifilm Cellular Dynamics Inc; Aspen Neuroscience and UCB pharma and editorial honoraria from Springer Nature. None of these conflict with the findings reported in this manuscript.