To estimate the cumulative incidence of diagnostic conversion from psychotic unipolar depression to bipolar and psychotic disorders in Sweden.
Data from Swedish national registers were used to identify incident cases of psychotic unipolar depression between 2005 and 2011. To minimize the risk of misclassification, patients with a prior history of psychotic disorders, bipolar disorders, or manic episodes were excluded. Patients were followed until the first occurrence of a diagnostic change, death, or December 31, 2021. The cumulative incidence of diagnostic change was estimated using a competing risk model.
A total of 7836 patients diagnosed with psychotic depression between 2005 and 2011 were included. The median age at index diagnosis of psychotic depression was 49 years (interquartile range: 35–65), and 56.7% were women. By the end of follow-up, 28.8% (95% CI: 27.7–29.9) of patients had undergone a diagnostic change to either a psychotic or bipolar disorder. The cumulative incidence of conversion was higher to psychotic disorders (17.5%, 95% CI: 16.6–18.4) than to bipolar disorders (14.7%, 95% CI: 13.8–15.5). In a sensitivity analysis requiring at least two recorded diagnoses separated by ≥ 1 year, the overall incidence of diagnostic change decreased to 19.0% (95% CI: 18.1–20.0), with corresponding rates of 10.0% (95% CI: 9.3–10.7) to psychotic disorders and 9.8% (95% CI: 9.1–10.5) to bipolar disorders. Diagnostic conversion was more common among younger individuals.
Approximately 20%–30% of patients diagnosed with psychotic depression in secondary care in Sweden are expected to receive a subsequent diagnosis of a bipolar or psychotic disorder within 17 years. This has important clinical implications, as prognosis and treatment strategies differ between these conditions. Further research is needed to identify risk factors for diagnostic conversion to improve early detection and management.
R. Nudel, M. Da Re, and M. E. Benros, “Systematic Multi-Trait Study of Genetic Correlation and Causality Relationships Between General Medical Conditions and Mental Disorders,” Acta Psychiatrica Scandinavica 152, no. 3 (2025): 236–249, https://doi.org/10.1111/acps.13825.
Since the publication of our article, we have discovered that the R script that was used to merge pairs of summary statistics datasets for analyses with LCV (ExampleRealdataScript.R, downloaded from the LCV GitHub) did not handle strand flips across the two datasets correctly; the instructions within the script recommend using summary statistics munged by LDSC (which we did, with munge_sumstats.py, removing ambiguous SNPs and checking for potential allele mismatches using the same reference file with merge-alleles for all sets of summary statistics in the study), but the R script does not take into account strand flips; in LDSC, these are handled during the LDSC analysis (hence the genetic correlation analyses were not affected). While some pairs of traits did not have this issue, mostly when they were from the same cohort (e.g. when both traits had GWASs done in iPSYCH), and, otherwise, only a relatively small number of SNPs were affected for other pairs of traits, we have repeated all the LCV analyses after modifying this script to take strand flips into account and re-merging sets of summary statistics.
This had a minor effect on the results, and the main conclusions of our study did not change. Nonetheless, the results for the pairs of traits in Table 3 in the article would change to the ones in the new Table 3 here. Only for the association between obsessive-compulsive disorder and irritable bowel syndrome do we see a change of sign for the GCP, even though the absolute size of the change was small, and the GCP is still close to zero. This result thus remains weak evidence for genetic causality for this pair of traits. We have also updated Supplementary Table S4 with the full results of the new LCV analyses after the reprocessing of the summary statistics datasets. Across all analyses, the mean of the absolute value of the difference in GCP was < 0.01. No associations that were not significant previously (q ≤ 0.05) became significant or vice versa.
Supplementary Table S4 has been replaced in the published article, together with further checks for one of the main results from the LCV analyses.
We apologize for this error.
A. M. Fernandes, E. S. de Lima, T. C. Ferreira, G. C. Pardi, F. G. de Matos e Souza, and L. W. Bisol, “In the Assessment of Childhood Maltreatment and Cognitive Function in Bipolar Disorder All Variables Should Be Taken Into Consideration,” Acta Psychiatrica Scandinavica 152, no. 5 (2025): 397–398, https://doi.org/10.1111/acps.70009.
The reference 1 was incorrect.
The correct reference 1 should be: “Fares-Otero, N.E., Pérez-Ramos, A., Lopez-Escribano, R., Martin-Parra, S., Alameda, L., Halligan, S.L., Miskowiak, K.W. and Vieta, E. (2025), Childhood Maltreatment and Cognitive Functioning in Bipolar Disorder: A Systematic Review and Meta-Analysis. Acta Psychiatr Scand. https://doi.org/10.1111/acps.13813”.
Thank you for the opportunity for the correct the information.
The mortality gap between people with mental disorders and the general population is well established. This study aims to comprehensively investigate how mortality rates for people with mental disorders and their mortality gap have changed over time.
We conducted a population-based cohort study using nationwide administrative data, including all people aged 1–99 years living in Denmark at some point between 2010 and 2023. Mental disorders were identified in the Danish hospital registers and classified into 10 groups. Information on mortality was obtained from population registers, and causes of death were categorized into 11 groups within the broad categories of natural causes and external causes. For each specific mental disorder, we estimated mortality rates for those diagnosed and for the general population via direct standardization using the distribution of sex and age (5-year age categories) of those diagnosed. All analyses were performed for five calendar periods (2010–2012, 2013–2015, 2016–2018, 2019–2021, and 2022–2023).
A total of 7,133,833 individuals were followed up for 78.0 million person-years. The mortality rate for 2010–2023 for individuals with mental disorders was 19.8 deaths (95% CI: 19.8–19.9) per 1000 person-years, while the standardized mortality ratio (SMR) was 2.15 (2.14–2.16). Mortality rates decreased for both the general population and those with mental disorders over time, while SMRs decreased from 2.47 (2.44–2.50) in 2010–2012 to 2.32 (2.28–2.36) in 2022–2023. However, these improvements were only observed in males, and only for some disorders (including depression and anxiety), and not for others (including schizophrenia or substance use disorders).
Despite improvements in the mortality rates of people with mental disorders, these have not been sufficient to close the mortality gap with the general population, especially for the most severe disorders. More initiatives are needed and existing initiatives need to be strengthened.
Posttraumatic stress disorder (PTSD) is a mental disorder resulting from exposure to traumatic events. Evidence suggests that ketamine may be efficacious in treating PTSD, however, ketamine's mechanisms in treating PTSD remain unclear. Herein, this review aims to evaluate the clinical outcomes of ketamine treatment in persons with PTSD and investigate the possible neurobiological mechanisms underlying ketamine's therapeutic effect in PTSD.
A systematic search was conducted on PubMed and OVID (MEDLINE, Embase, PsychINFO) from inception until September 2025. Randomized controlled trials reporting on the effects of intravenous ketamine to treat PTSD were included.
Seven studies with a total of 323 participants were included in this review. Ketamine administration meaningfully improved PTSD symptoms in two trials as evidenced by significant improvement on the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5) and the Impact of Event Scale-Revised (IES-R) compared to control/placebo. Multi-infusion administration schedules achieved greater clinical outcomes when compared to single-dose administration schedules. Preliminary evidence suggests that repeated lower doses (0.2mg/kg) of ketamine were more efficacious in sustaining treatment effects than standard doses (0.5mg/kg). For persons receiving ketamine, an association was observed between top-down inhibition of the amygdala originating in the ventromedial prefrontal cortex (vmPFC) and symptom improvement.
Our results suggest that intravenous ketamine may be efficacious in the treatment of PTSD. Subsequent studies should attempt to evaluate the additive effect of combining ketamine with psychotherapeutic interventions as well as determining mechanistic pathways mediating symptom relief in persons with PTSD.
Psychotic symptoms are frequent during acute episodes of bipolar disorder (BD), particularly in mania, and are traditionally considered a marker of greater severity and worse prognosis. However, data comparing psychotic and nonpsychotic mania remain limited and inconsistent.
This study aimed to retrospectively examine clinical, therapeutical and 3-year outcome differences between patients hospitalized for mania with and without psychotic symptoms.
We included all patients admitted for a manic episode to the acute psychiatry unit at Hospital Clínic of Barcelona between 2015 and 2019 (n = 277). Data were extracted from medical records. Patients were followed for 3 years to assess psychiatric emergency department (PED) visits and readmissions. Functional outcomes were also analyzed in the BD subgroup (n = 234). Descriptive statistics and survival analyses were used.
Psychotic symptoms were present in 73.6% of the patients and were associated with younger age (p < 0.001), earlier onset (p = 0.020), poorer insight (p < 0.001), higher cannabis use (p = 0.018) and manic predominant polarity (p = 0006). Non-psychotic patients had more previous admissions for depressive episodes (p = 0.003), more previous mixed episodes (p = 0.006) and suicide attempts (p = 0.002). No significant differences were found in PED visits or readmissions in the next 3 years. Logistic regression identified the number of previous mixed-episode-related admissions as a significant predictor of readmissions (p = 0.041), while psychotic symptoms were not associated with either outcome.
While psychotic and non-psychotic mania show clinical and therapeutical differences, psychosis may not predict short- to medium-term outcomes. Non-psychotic mania—which is associated with depressive polarity, mixed features and suicidal behaviour—may indicate a clinically relevant and therapeutically challenging but underrecognized subgroup. These findings call for a nuanced comprehension of the impact of psychosis in mania and multidimensional approaches.
Robust evidence associates immunoinflammatory dysfunction and bipolar disorder (BD), with immune dysregulation present in patients newly diagnosed with BD. This suggests that anti-inflammatory agents, like low-dose aspirin (LDA), might be repurposed in the treatment of early-stage BD. Building on pharmacoepidemiologic and meta-analytic evidence, we conducted the first randomised controlled trial (RCT) testing the effects of add-on LDA in patients with newly diagnosed BD. We hypothesised that add-on treatment with LDA would reduce mood instability (MI), activity instability (AI), and depression severity.
In this parallel group, triple-blind, superiority RCT, patients newly diagnosed with BD, recruited from a public outpatient mood disorder clinic in the Capital Region of Denmark, were randomised 1:1 to 150 mg acetylsalicylic acid or placebo by an independent third party. The primary outcome was average MI at 6-month follow-up, assessed by the Root Mean Square of Successive Differences (RMSSDs) method. Secondary outcomes included average AI, assessed by the RMSSD method, and change in depressive symptoms, assessed with the 6-item Hamilton Depression Rating Scale, at 6 months. Tertiary outcomes included sleep variability, cognition, manic symptoms and questionnaires at 6 months.
Two hundred fifty patients were randomised from January 20, 2022, to May 30, 2024, with the last follow-up on November 18, 2024. Analyses included data from 240 patients (120 received placebo; 120 LDA), with a mean of 108 (SD = 57) daily mood registrations. The estimated treatment difference for MI was 0.022 (95% CI: −0.056 to 0.1, p = 0.58) for LDA compared to placebo, indicating no clinically relevant difference. No beneficial effects of LDA were found across secondary or tertiary outcomes. Methodologically, randomisation and blinding were successful, and serum-thromboxane B2 levels confirmed high adherence to LDA.
Low-dose aspirin did not demonstrate any benefit on MI or on secondary or tertiary outcomes in patients with newly diagnosed BD.
Clinicaltrials.gov registration number: NCT05035316
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