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Reports linking the deinstitutionalisation of psychiatric care with homelessness and imprisonment have been published widely. To identify cohort studies that followed up or traced back long-term psychiatric hospital residents who had been discharged as a consequence of deinstitutionalisation. A broad search strategy was used and 9435 titles and abstracts were screened, 416 full articles reviewed and 171 articles from cohort studies of deinstitutionalised patients were examined in detail. Twenty-three studies of unique populations assessed homelessness and imprisonment among patients discharged from long-term care. Homelessness and imprisonment occurred sporadically; in the majority of studies no single case of homelessness or imprisonment was reported. Our results contradict the findings of ecological studies which indicated a strong correlation between the decreasing number of psychiatric beds and an increasing number of people with mental health problems who were homeless or in prison.

An enigmatic localized pneumonia escalated into a worldwide COVID-19 pandemic from Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). This review aims to consolidate the extensive biological minutiae of SARS-CoV-2 which requires decipherment. Having one of the largest RNA viral genomes, the single strand contains the genes ORF1ab, S, E, M, N and ten open reading frames. Highlighting unique features such as stem-loop formation, slippery frameshifting sequences and ribosomal mimicry, SARS-CoV-2 represents a formidable cellular invader. Hijacking the hosts translational engine, it produces two polyprotein repositories (pp1a and pp1ab), armed with self-cleavage capacity for production of sixteen non-structural proteins. Novel glycosylation sites on the spike trimer reveal unique SARS-CoV-2 features for shielding and cellular internalization. Affording complexity for superior fitness and camouflage, SARS-CoV-2 challenges diagnosis and vaccine vigilance. This review serves the scientific community seeking in-depth molecular details when designing drugs to curb transmission of this biological armament.

Smaller hippocampal volumes relative to controls are among the most replicated neuroimaging findings in individuals with unipolar but not bipolar depression. Preserved hippocampal volumes in most studies of participants with bipolar disorder may reflect potential neuroprotective effects of lithium (Li). To investigate hippocampal volumes in patients with bipolar disorder while controlling for Li exposure, we performed a meta-analysis of neuroimaging studies that subdivided patients based on the presence or absence of current Li treatment. To achieve the best coverage of literature, we categorized studies based on whether all or a majority, or whether no or a minority of patients were treated with Li. Hippocampal volumes were compared by combining standardized differences between means (Cohen d) from individual studies using random-effects models. Overall, we analyzed data from 101 patients with bipolar disorder in the Li group, 245 patients in the non-Li group and 456 control participants from 16 studies. Both the left and right hippocampal volumes were significantly larger in the Li group than in controls (Cohen d = 0.53, 95% confidence interval [CI] 0.18 to 0.88; Cohen d = 0.51, 95% CI 0.21 to 0.81, respectively) or the non-Li group (Cohen d = 0.93, 95% CI 0.56 to 1.31; Cohen d = 1.07, 95% CI 0.70 to 1.45, respectively), which had smaller left and right hippocampal volumes than the control group (Cohen d = −0.36, 95% CI −0.55 to −0.17; Cohen d = −0.38, 95% CI −0.63 to −0.13, respectively). There was no evidence of publication bias. Missing information about the illness burden or lifetime exposure to Li and polypharmacy in some studies may have contributed to statistical heterogeneity in some analyses. When exposure to Li was minimized, patients with bipolar disorder showed smaller hippocampal volumes than controls or Li-treated patients. Our findings provide indirect support for the negative effects of bipolar disorder on hippocampal volumes and are consistent with the putative neuroprotective effects of Li. The preserved hippocampal volumes among patients with bipolar disorder in most individual studies and all previous meta-analyses may have been related to the inclusion of Li-treated participants.

It is unclear whether there is a direct link between economic crises and changes in suicide rates. The Lopez-Ibor Foundation launched an initiative to study the possible impact of the economic crisis on European suicide rates. Data was gathered and analysed from 29 European countries and included the number of deaths by suicide in men and women, the unemployment rate, the gross domestic product (GDP) per capita, the annual economic growth rate and inflation. There was a strong correlation between suicide rates and all economic indices except GPD per capita in men but only a correlation with unemployment in women. However, the increase in suicide rates occurred several months before the economic crisis emerged. Overall, this study confirms a general relationship between the economic environment and suicide rates; however, it does not support there being a clear causal relationship between the current economic crisis and an increase in the suicide rate.

Objective Converging evidence suggests that the subgenual cingulate (SGC) is implicated in regulation of mood and in the pathophysiology of mood disorders. Our objective was to carry out the first meta-analysis of SGC volumes in patients with mood disorders. Methods We reviewed 10 volumetric magnetic resonance imaging studies of SGC volumes in patients with unipolar depression and bipolar disorders. For meta-analysis, we used standardized differences between means (SDMs) and random effects models. In the search for sources of heterogeneity, we subdivided the studies on the basis of diagnosis and presence of family history. Results The volumes of left and right SGC in patients with mood disorders were significantly reduced relative to healthy control subjects (SDM –0.38, 95% confidence interval [CI] –0.67 to –0.1 and SDM –0.2, 95% CI –0.4 to –0.007, respectively). There were significant SGC volume reductions in patients with unipolar (left SGC SDM –0.5, 95% CI –0.92 to –0.07; right SGC SDM –0.33, 95% CI –0.64 to –0.02,), but not bipolar, disorder. Patients with a positive family history of mood disorders showed significant left SGC volume decrease (SDM –0.52, 95% CI –0.96 to –0.07), which was not present among subjects without family history of mood disorders. There was no association between age and SGC volumes. Conclusion The available evidence suggests the existence of left and less robust right SGC volumetric reductions in patients with mood disorders, predominantly in those with unipolar depression. The effect size of this difference was moderate and increased in more homogeneous subgroups of patients with a positive family history. The clustering of SGC abnormalities in patients with a family history, their presence early in the illness course and their lack of progression with age make SGC a candidate for a primary vulnerability marker, although studies in unaffected high-risk subjects are missing.

Aberrant amygdala reactivity to affective stimuli represents a candidate factor predisposing patients with bipolar disorder (BD) to relapse, but it is unclear to what extent amygdala reactivity is state-dependent. We evaluated the modulatory influence of mood on amygdala reactivity and functional connectivity in patients with remitted BD and healthy controls. Amygdala response to sad versus neutral faces was investigated using fMRI during periods of normal and sad mood induced by autobiographical scripts. We assessed the functional connectivity of the amygdala to characterize the influence of mood state on the network responsible for the amygdala response. We included 20 patients with remitted BD and 20 controls in our study. The sad and normal mood exerted opposite effects on the amygdala response to emotional faces in patients compared with controls (F1,38 = 5.85, p = 0.020). Sad mood amplified the amygdala response to sad facial stimuli in controls but attenuated the amygdala response in patients. The groups differed in functional connectivity between the amygdala and the inferior prefrontal gyrus (p ≤ 0.05, family-wise error–corrected) of ventrolateral prefrontal cortex (vlPFC) corresponding to Brodmann area 47. The sad mood challenge increased connectivity during the period of processing sad faces in patients but decreased connectivity in controls. Limitations to our study included long-term medication use in the patient group and the fact that we mapped only depressive (not manic) reactivity. Our results support the role of the amygdala–vlPFC as the system of dysfunctional contextual affective processing in patients with BD. Opposite amygdala reactivity unmasked by the mood challenge paradigm could represent a trait marker of altered mood regulation in patients with BD.

Abstract Methamphetamine is a potent and highly addictive psychostimulant, and one of the most widely used illicit drugs. Over recent years, its global usage and seizure have been on a rapid rise, with growing detrimental effects on mental and physical health, and devastating psychosocial impact pressing for intervention. Among the unwanted effects of methamphetamine, acute and long-term sleep impairments are of major concern, posing a significant therapeutic challenge, and a cause of addiction relapse. Unraveling mechanisms and functional correlates of methamphetamine-related sleep and circadian disruption are, therefore, of key relevance to translational and clinical psychiatry. In this article, we review the mounting evidence for the acute and long-term impairements of sleep–wake behavior and circadian activity caused by single or recurring methamphetamine usage and withdrawal. Factors contributing to the severity of sleep loss and related cognitive deficit, with risks of relapse are discussed. Key molecular players mediating methamphetamine-induced dopamine release and neuromodulation are considered, with wake-promoting effects in mesolimbic circuits. The effects on various sleep phases and related changes in dopamine levels in selected subcortical structures are reviewed and compared to other psychostimulants with similar action mechanisms. A critical appraisal is presented of the therapeutic use of modafinil, countering sleep, and circadian rhythm impairments. Finally, emerging knowledge gaps and methodical limitations are highlighted along with the areas for future research and therapeutic translation.

Escitalopram is the S-enantiomer of the selective serotonin reuptake inhibitor (SSRI) citalopram, which contains equal amounts of the S- and R-forms in a racemic mixture. Escitalopram is the most selective SSRI, with almost no significant affinity to other tested receptors. It has been demonstrated that it is escitalopram that carries the therapeutic potential of citalopram, and has statistically superior and clinically relevant properties compared with citalopram. Escitalopram is at least as effective in the treatment of depression and anxiety as other SSRIs, as well as venlafaxine, bupropion and duloxetine. Owing to multiple metabolic degrading pathways, the clinically relevant interactions of escitalopram with other drugs are minimal. Compared with other antidepressants, escitalopram is generally better tolerated, its onset of action is relatively fast, and its use may have cost-effectiveness and cost-utility advantages. Escitalopram is an effective first-line option in the management of patients with major depression, including severe forms, and various anxiety disorders.

A common limitation of neuroimaging studies is their small sample sizes. To overcome this hurdle, the Enhancing Neuro Imaging Genetics through Meta-Analysis (ENIGMA) Consortium combines neuroimaging data from many institutions worldwide. However, this introduces heterogeneity due to different scanning devices and sequences. ENIGMA projects commonly address this heterogeneity with random-effects meta-analysis or mixed-effects mega-analysis. Here we tested whether the batch adjustment method, ComBat, can further reduce site-related heterogeneity and thus increase statistical power. We conducted random-effects meta-analyses, mixed-effects mega-analyses and ComBat mega-analyses to compare cortical thickness, surface area and subcortical volumes between 2897 individuals with a diagnosis of schizophrenia and 3141 healthy controls from 33 sites. Specifically, we compared the imaging data between individuals with schizophrenia and healthy controls, covarying for age and sex. The use of ComBat substantially increased the statistical significance of the findings as compared to random-effects meta-analyses. The findings were more similar when comparing ComBat with mixed-effects mega-analysis, although ComBat still slightly increased the statistical significance. ComBat also showed increased statistical power when we repeated the analyses with fewer sites. Results were nearly identical when we applied the ComBat harmonization separately for cortical thickness, cortical surface area and subcortical volumes. Therefore, we recommend applying the ComBat function to attenuate potential effects of site in ENIGMA projects and other multi-site structural imaging work. We provide easy-to-use functions in R that work even if imaging data are partially missing in some brain regions, and they can be trained with one data set and then applied to another (a requirement for some analyses such as machine learning). •ENIGMA studies commonly conduct meta-analysis or mixed-effects mega-analyses.•We tested if ComBat can better address site effects and increase statistical power.•We compared MRI data between 2897 individuals with schizophrenia and 3141 controls.•ComBat increased the statistical power and significance.•We provide easy-to-use functions in R that work even if there are missing data.