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PURPOSE: Family members of patients who die in the intensive care unit (ICU) may experience symptoms of stress, anxiety, depression, posttraumatic stress disorder (PTSD), and/or prolonged grief. We evaluated whether grief symptoms were alleviated if the physician and the nurse in charge at the time of death sent the closest relative a handwritten condolence letter.METHODS: Multicenter randomized trial conducted among 242 relatives of patients who died at 22 ICUs in France between December 2014 and October 2015. Relatives were randomly assigned to receiving (n = 123) or not receiving (n = 119) a condolence letter. The primary endpoint was the Hospital Anxiety and Depression Score (HADS) at 1 month. Secondary endpoints included HADS, complicated grief (ICG), and PTSD-related symptoms (IES-R) at 6 months. Observers were blinded to group allocation.RESULTS: At 1 month, 208 (85.9%) relatives completed the HADS; median score was 16 [IQR, 10-22] with and 14 [8-21.5] without the letter (P = 0.36). Although scores were higher in the intervention group, there were no significant differences regarding the HADS-depression subscale (8 [4-12] vs. 6 [2-12], mean difference 1.1 [-0.5 to 2.6]; P = 0.09) and prevalence of depression symptoms (56.0 vs. 42.4%, RR 0.76 [0.57-1.00]; P = 0.05). At 6 months, 190 (78.5%) relatives were interviewed. The intervention significantly increased the HADS (13 [7-19] vs. 10 [4-17.5], P = 0.04), HADS-depression subscale (6 [2-10] vs. 3 [1-9], P = 0.02), prevalence of depression symptoms (36.6 vs. 24.7%, P = 0.05) and PTSD-related symptoms (52.4 vs. 37.1%, P = 0.03).CONCLUSIONS: In relatives of patients who died in the ICU, a condolence letter failed to alleviate grief symptoms and may have worsened depression and PTSD-related symptoms. Trial registration Clinicaltrials.gov Identifier: NCT02325297.

Purpose The prevalence of parental burnout, a condition that has severe consequences for both parents and children, varies dramatically across countries and is highest in Western countries characterized by high individualism. Method In this study, we examined the mediators of the relationship between individualism measured at the country level and parental burnout measured at the individual level in 36 countries (16,059 parents). Results The results revealed three mediating mechanisms, that is, self-discrepancies between socially prescribed and actual parental selves, high agency and self-directed socialization goals, and low parental task sharing, by which individualism leads to an increased risk of burnout among parents. Conclusion The results confirm that the three mediators under consideration are all involved, and that mediation was higher for self-discrepancies between socially prescribed and actual parental selves, then parental task sharing, and lastly self-directed socialization goals. The results provide some important indications of how to prevent parental burnout at the societal level in Western countries.

Aging is accompanied by a drop in the level of health and autonomy, within Western countries more and more people being cared for in nursing homes (NH). The nutritional data in NH in France remain poor, not exhaustive and not representative. The objective of the study was to assess the nutritional status, dementia and mobility patterns among residents of NH in the Limousin territory of France. The study was cross-sectional, descriptive and exhaustive, conducted with the residents of 13 voluntary NH. Undernutrition was identified using French High Authority for Health criteria, and obesity if Body Mass Index >30, in the absence undernutrition criterion. The Mini Mental State examination scores was used for dementia assessment at the threshold of 24. The Mini Nutritional AssessmentTM was used for mobilitity assessment. The statistics were significant at the 5% threshold. 866 residents (70.6% women) included with an average age of 85.3 ± 9.3 years. Undernutrition was 27.5%, obesity 22.9%, dementia 45.7% and very low mobility 68.9%. Women were older than men, more often undernourished, more often demented and more often had very low mobility (p<0.01). Undernutrition (p<0.0001) and low mobility (p<0.0001) were significantly higher among those with dementia versus those without dementia. Very low mobility was higher among undernourished (p<0.05). Undernutrition and obesity are important problems in NH in France. Being a woman, having dementia and having a very low mobility may induce undernutrition.

Few studies have examined the consumption trajectories of inmates after entry to prison. The aim of this study was to assess the changes in the consumption of psychoactive substance between the period before detention and during incarceration and to characterize the profiles of prisoners with similar consumption trajectories during incarceration. A multicenter, cross-sectional study was performed in all of the prisons from one region of France. All prisoners incarcerated during their 3rd months, over 18 years old, and with a sufficient level of French fluency to participate in the study were recruited over a period of 12 months. A total of 800 prisoners were recruited. All prisoners were interviewed face-to-face by a trained interviewer. A majority of prisoners had used at least one psychoactive substance in the weeks prior to incarceration. During incarceration, a substantial reduction in alcohol and illicit drug consumption was observed. The initiation of consumption and an increase in consumption were primarily related to medications. Five different profiles of consumption before incarceration were identified. These profiles all had a high probability of migrating to a similar profile during detention, characterized by less severe consumption of psychoactive substances. Based on their consumption profile prior to incarceration, most prisoners would benefit from a specific medical evaluation as soon as possible following entry into detention. Prison could be an opportunity for reduced consumption and/or the initiation of treatment for the majority of prisoners, despite the pejorative development observed for a minority of prisoners during incarceration.

Youths with severe and persistent irritability have a particularly high rate of school failures and learning difficulties. The aim of this study was to determine whether inpatient adolescents with Disruptive Mood Dysregulation Disorder (DMDD) have more motor and/or language impairments compared to patients with other psychiatric disorders. A retrospective chart review of all consecutive cases admitted in two adolescent inpatient units between January 2017 and December 2018 was conducted (N = 191). All patients received multi-disciplinary clinical and developmental assessments. For a subtest of subjects, additional standardized tests were used to document motor and language impairments. In this clinical chart 53 adolescents with a DMDD (mean age 13.6 ± 1.5, min 12, max 16, 70% males) were compared to patients with a major depressive disorder (MDD, n = 64, mean age 15.3 ± 1.6, 52% males) and patients with a non-mood disorder (NMD, n = 61, mean age 14.4 ± 1.55, 59% males). Among inpatients with DMDD, 71% had an associated motor and/or language disorder, with combined forms in around two-thirds of cases. Compared to youths with MDD, participants with DMDD were more likely to have an associated developmental coordination disorder (67% vs. 22%, OR = 4.7) and a written language disorder (35% vs. 10%, OR = 4.6). While 31% of inpatients with DMDD had an associated communication/oral language disorder, this rate was not statistically different from those observed in the MDD group (11%, OR = 3.2). The frequencies of motor and language impairments were not statistically different between participants in the DMDD group and in the NMD group. The high rate of motor and written language disorders found in DMDD patients may partly account for their academic difficulties. Such finding, if confirmed, supports systematic screening of motor and written language impairments in youths with chronic irritability and suggests remediation potential.

Lewy body disease (LBD) is a neurodegenerative disease resulting in dementia. It shares clinical and pathological features with Parkinson disease (PD), the most frequent synucleinopathy, Parkinson disease dementia (PDD), and Alzheimer disease (AD), a tauopathy. Even though the diagnostic criteria for these neurodegenerative diseases are clearly established, and recently revised for LBD, their precise clinical diagnosis is often difficult because LBD, PD, PDD, and AD share epidemiological, clinical, and pathological characteristics. This manuscript discusses current understanding of overlapping symptoms and the particular features of LBD, PD, and AD. It also describes features that could facilitate the diagnosis of each of these diseases. We concluded that the concept of neurodegenerative “overlap” syndrome, which includes the accepted diagnosis of LBD, may be taken in account and should contribute to clarifying LBD and definitions of close differential diagnoses. This should allow clinicians to suspect LBD at an earlier stage and provide better patient care.

Appetite and drug addiction Disruptions in dopamine signalling have been implicated in psychiatric disorders, such as schizophrenia and drug addiction. The phosphoprotein DARPP-32 is a prominent mediator of dopamine signalling in the striatum, a part of the brain where dopaminergic activation has been linked to reward and learning. Now a novel signal transduction cascade involving nuclear accumulation of DARPP-32 has been discovered, induced by both drugs of abuse and natural stimuli such as food. Disruption of this cascade alters the behavioural effects of the drugs and decreases motivation for food, suggesting a role for this mechanism in the in vivo actions of dopamine signalling. Dopamine orchestrates motor behaviour and reward-driven learning. Perturbations of dopamine signalling have been implicated in several neurological and psychiatric disorders, and in drug addiction. The actions of dopamine are mediated in part by the regulation of gene expression in the striatum, through mechanisms that are not fully understood. Here we show that drugs of abuse, as well as food reinforcement learning, promote the nuclear accumulation of 32-kDa dopamine-regulated and cyclic-AMP-regulated phosphoprotein (DARPP-32). This accumulation is mediated through a signalling cascade involving dopamine D1 receptors, cAMP-dependent activation of protein phosphatase-2A, dephosphorylation of DARPP-32 at Ser 97 and inhibition of its nuclear export. The nuclear accumulation of DARPP-32, a potent inhibitor of protein phosphatase-1, increases the phosphorylation of histone H3, an important component of nucleosomal response. Mutation of Ser 97 profoundly alters behavioural effects of drugs of abuse and decreases motivation for food, underlining the functional importance of this signalling cascade.

In the current literature, two distinct and opposite models are suggested to explain the consciousness disorders in schizophrenia. The first one suggests that consciousness disorders rely on a low-level processing deficit, when the second model suggests that consciousness disorders rely on disruption in the ability to consciously access information, with preserved unconscious processing. The current study aims to understand the mechanisms associated with visual consciousness disorder in order to pave the road that will settle the debate regarding these hypotheses. During a functional magnetic resonance imaging session, 19 healthy participants (HC) and 15 patients with schizophrenia (SCZ) performed a visual detection task to compare the neural substrates associated with the conscious access to the visual inputs. The visual detection threshold was significantly higher in SCZ than in HC [t(32) = 3.37, p = 0.002]. Whole-brain ANOVA demonstrated that around the visual detection threshold patients with SCZ failed to activate a large network of brain areas compared to HC. (1) During conscious vision, HC engaged more the left cuneus and the right occipital cortex than patients with SCZ, (2) during unconscious vision, HC engaged a large network that patients with SCZ failed to activate, and finally, (3) during the access to consciousness process, patients with SCZ failed to activate the anterior cingulate cortex. These results suggest that the consciousness disorders in schizophrenia rely on specific dysfunctions depending on the consciousness stage. The disorders of the conscious vision are associated with dysfunction of occipital areas while the ones associated with unconscious vision rely on a large widespread network. Finally, the conscious access to the visual inputs is impaired by a dysfunction of the anterior cingulate cortex. The current study suggests that none of the two suggested models can explain consciousness disorders in schizophrenia. We suggest that there is an alternative model supporting that the conscious access to visual inputs is due to a disengagement of the supragenual anterior cingulate during the unconscious processing of the visual inputs associated with a sensory deficit.

Traumatic events are associated with increased risk of psychotic experiences, but it is unclear whether this association is explained by mental disorders prior to psychotic experience onset. To investigate the associations between traumatic events and subsequent psychotic experience onset after adjusting for post-traumatic stress disorder and other mental disorders. We assessed 29 traumatic event types and psychotic experiences from the World Mental Health surveys and examined the associations of traumatic events with subsequent psychotic experience onset with and without adjustments for mental disorders. Respondents with any traumatic events had three times the odds of other respondents of subsequently developing psychotic experiences (OR = 3.1, 95% CI 2.7-3.7), with variability in strength of association across traumatic event types. These associations persisted after adjustment for mental disorders. Exposure to traumatic events predicts subsequent onset of psychotic experiences even after adjusting for comorbid mental disorders.

Purpose of Review Several reviews and metanalyses have shown that sleep disturbances, such as insomnia and nightmares, can predict suicidal ideations and behaviors. Common physio-pathological pathways may explain this relationship. However, only in recent years, some research groups have tried to apply this knowledge in the quest for a reliable tool of suicide risk prediction. We aim to describe in this paper the results of studies using ecological or quasi-ecological assessment methods that connect sleep disturbances and suicide risk. Recent Findings Our review confirms the paucity of studies on this topic. The few studies that we could analyze suggest the interest of ecological methods of sleep assessment since sleep disturbances predicted the onset or worsening of suicidal ideations and behaviors. Summary Ecological assessment of sleep can help to understand how sleep disturbances contribute to the emergence of suicidal ideations and behaviors. Sleep disturbances appear as a promising “real-life” marker of risk, but further studies are needed to determine if sleep monitoring could guide preventive interventions.