The prevalence of psychiatric disorders in people with epilepsy is as high as 43% and, among them, psychoses represent a severe comorbidity.

This is a narrative review discussing the interplay between epilepsy and psychosis and identifying challenges in diagnosing and managing psychotic symptoms in epilepsy, focusing on the past 10 years.

Articles published between June 2014 and December 2024 were identified through searches in PubMed using the search terms ‘psychosis’, ’seizure, epilepsy and convulsion’, ‘epile*’, ’seizure*’ and ‘convuls*’.

The association between epilepsy and psychosis was shown to be bidirectional, with people with psychosis being at increased risk of epilepsy. In epilepsy, psychotic symptoms may occur in three clinical scenarios, with clinical presentation and management varying in relationship to these: seizure-related (peri-ictal), treatment-related or independent of the former.

There are no guidelines for the management of psychotic symptoms in epilepsy, but it is possible to apply policies for the treatment of psychoses, taking into account the peculiarities and needs of people with epilepsy.

Complex post-traumatic stress disorder (cPTSD) is a newly recognized condition characterized by core PTSD symptoms and disturbances in self-organization (DSO) that has been associated with psychotic-like experiences (PLEs). This study employs two psychopathology network approaches to identify which post-traumatic symptoms are related to PLEs in a sample of late adolescents. We propose that cPTSD symptoms play a crucial role in explaining the co-occurrence of trauma and PLEs.

A sample of 1010 late adolescents provided measures of post-traumatic symptomatology and PLEs. We estimated the Gaussian graphical network structure of PTSD/cPTSD symptoms and PLEs and assessed their bridge centrality indices. Bayesian network analysis was then used to estimate a directed acyclic graph (DAG). Gender was set as a moderator in both Gaussian and Bayesian models.

Results show that affect dysregulation, a cPTSD domain, presented the highest bridge connection with the PLE cluster. Bayesian network analysis identified a pathway going from cPTSD items of worthlessness and relational dysregulation, to PLE items of paranoia and social anxiety. Additionally, we found relevant gender differences in network connectivity, with females showing higher connectivity compared to males.

Our findings highlight the central role of affect dysregulation and negative self-concept in linking cPTSD to PLE symptoms, with specific differences according to gender. These insights underscore the need for targeted, gender-sensitive approaches in the prevention and treatment of PLEs among adolescents, emphasizing early intervention and tailored treatment strategies.

Social health (SH) markers, including marital status, contact frequency, network size, and social support, have been linked with increased cognitive capability. However, the underlying mechanisms remain poorly understood. We aim to investigate whether depression symptoms and inflammatory biomarkers mediate associations between SH and cognitive outcomes.

We used data from waves 1-9 of the English Longitudinal Study of Ageing, involving 7,136 participants aged 50 or older at baseline. First, we examined associations between SH (wave 1) and depression and inflammatory biomarkers (C-reactive protein (CRP) and fibrinogen) (wave 2) using linear regression models. Second, we tested associations between a) SH and b) depression and inflammation with subsequent standardised verbal fluency and memory in wave 3 and change between waves 3-9, indexed using slopes derived from multilevel models. We adjusted for age, sex, socio-economic position, cardiovascular disease, basic and instrumental activities of daily living, health behaviours, and baseline depression symptoms and cognition. We will also conduct causal mediation analysis.

All SH markers, except contact frequency, were associated with lower subsequent depression, but not inflammatory biomarkers. Greater contact frequency (e.g. once-twice a week vs <once per year: β=0.18 [0.01, 0.36]) and less negative support (β=0.02 [0.00, 0.03]) were associated with higher verbal fluency. Larger network size (>6 people vs none: β=0.007SD/year [0.001, 0.012]), less negative (β=0.001SD/year [0.001, 0.002]) and more positive support (β=0.001SD/year [0.000, 0.001]) were linked with slower memory decline, and more positive support predicted slower verbal fluency decline (β=0.001SD/year [0.000, 0.001]). Depression symptoms were associated with lower memory and verbal fluency, and faster memory decline (β=-0.001SD/year [-0.001, -0.000]) and verbal fluency (β=-0.001SD/year [-0.001, -0.000]). CRP was associated with lower verbal fluency (β=-0.02 [-0.04, 0.00]), whereas fibrinogen was linked with faster memory decline (β=-0.001SD/year [-0.003, -0.000]).

Depression symptoms and SH showed associations with subsequent cognitive capability and change. SH was linked with lower depression, but not inflammatory biomarkers. Findings highlight the potential for depression to underpin associations between SH and cognition, a pathway which we will test using causal mediation analysis. We will also examine whether findings replicate in the Swedish National Study of Aging and Care in Kungsholmen.

Although the COVID-19 pandemic has affected depression, evidence of the role of pre-pandemic history of depression remains limited.

We investigated how long-term trajectories of depressive symptomatology before the COVID-19 pandemic were related to depression during the pandemic, over and above the latest pre-pandemic depression status. Furthermore, we examined whether those experiencing depression closer to the pandemic were at higher risk during the pandemic.

Employing data from waves 4–9 of the English Longitudinal Study of Ageing (2008–2009 to 2018–2019), we used group-based trajectory modelling on 3925 English older adults aged 50+ years to identify distinctive trajectories of elevated depressive symptoms (EDS). Fully adjusted logistic models were then used to examine the associations between trajectories and depression during the COVID-19 pandemic (June–July and November–December 2020).

We identified four classes of pre-pandemic trajectories of EDS. About 5% were classed as ‘enduring EDS’, 8% as ‘increasing EDS’, 10% as ‘decreasing EDS’ and 77% as ‘absence of EDS’. Compared with respondents with absence of EDS, those with EDS history were more likely to have depression during the COVID-19 pandemic, particularly those with enduring or increasing EDS in the previous 10 years. Moreover, the frequency of EDS was more crucial in predicting the risks of depression during the pandemic than the timing of the latest episode.

Trajectories of depressive symptomatology are an important risk factor for older adults’ mental health, particularly in the context of crisis. Older people with enduring or increasing EDS should receive particular attention from policy makers when provisioning post-pandemic well-being support.

Different electrophysiological (EEG) indices have been investigated as possible biomarkers of schizophrenia. However, these indices have a very limited use in clinical practice, as their associations with clinical and functional outcomes remain unclear. This study aimed to investigate the associations of multiple EEG markers with clinical variables and functional outcomes in subjects with schizophrenia (SCZs).

Resting-state EEGs (frequency bands and microstates) and auditory event-related potentials (MMN-P3a and N100-P3b) were recorded in 113 SCZs and 57 healthy controls (HCs) at baseline. Illness- and functioning-related variables were assessed both at baseline and at 4-year follow-up in 61 SCZs. We generated a machine-learning classifier for each EEG parameter (frequency bands, microstates, N100-P300 task, and MMN-P3a task) to identify potential markers discriminating SCZs from HCs, and a global classifier. Associations of the classifiers’ decision scores with illness- and functioning-related variables at baseline and follow-up were then investigated.

The global classifier discriminated SCZs from HCs with an accuracy of 75.4% and its decision scores significantly correlated with negative symptoms, depression, neurocognition, and real-life functioning at 4-year follow-up.

These results suggest that a combination of multiple EEG alterations is associated with poor functional outcomes and its clinical and cognitive determinants in SCZs. These findings need replication, possibly looking at different illness stages in order to implement EEG as a possible tool for the prediction of poor functional outcome.

Symptoms of depression are transdiagnostic heterogenous features frequently assessed in psychiatric disorders, that impact the response to first-line treatment and are associated with higher suicide risk. This study assessed whether severe mental pain could characterize a specific phenotype of severely depressed high-risk psychiatric patients. We also aimed to analyze differences in treatments administered.

2,297 adult patients (1,404 females and 893 males; mean age = 43.25 years, SD = 15.15) treated in several Italian psychiatric departments. Patients were assessed for psychiatric diagnoses, mental pain, symptoms of depression, hopelessness, and suicide risk.

More than 23% of the patients reported high depression symptomatology and high mental pain (HI DEP/HI PAIN). Compared to patients with lower symptoms of depression, HI DEP/HI PAIN is more frequent among females admitted to an inpatient department and is associated with higher hopelessness and suicide risk. In addition, HI DEP/HI PAIN (compared to both patients with lower symptoms of depression and patients with higher symptoms of depression but lower mental pain) were more frequently diagnosed in patients with personality disorders and had different treatments.

Patients reporting severe symptoms of depression and high mental pain presented a mixture of particular dangerousness (high trait hopelessness and the presence of suicide ideation with more frequency and less controllability and previous suicide behaviors). The presence of severe mental pain may act synergically in expressing a clinical phenotype that is likewise treated with a more complex therapeutic regime than that administered to those experiencing symptoms of depression without mental pain.

During the COVID-19 pandemic, older and clinically vulnerable people were instructed to shield or stay at home. Policies restricting social contact and human interaction pose a risk to mental health, but we know very little about the impact of shielding and stay-at-home orders on the mental health of older people.

To understand the extent to which shielding contributes to poorer mental health.

We used longitudinal data from wave 9 (2018/2019) and two COVID-19 sub-studies (June/July 2020; November/December 2020) of the English Longitudinal Study of Ageing, and constructed logistic and linear regression models to investigate associations between patterns of shielding during the pandemic and mental health, controlling for sociodemographic characteristics, pre-pandemic physical and mental health, and social isolation measures.

By December 2020, 70% of older people were still shielding or staying at home, with 5% shielding throughout the first 9 months of the pandemic. Respondents who shielded experienced worse mental health. Although prior characteristics and lack of social interactions explain some of this association, even controlling for all covariates, those shielding throughout had higher odds of reporting elevated depressive symptoms (odds ratio 1.87, 95% CI 1.22–2.87) and lower quality of life (β = −1.28, 95% CI −2.04 to −0.52) than those who neither shielded nor stayed at home. Shielding was also associated with increased anxiety.

Shielding seems associated with worse mental health among older people, highlighting the need for policy makers to address the mental health needs of those who shielded, both in the current pandemic and for the future.

People with severe mental illnesses (SMI) have a mortality rate two times higher compared to the general population, with a decade of years of life lost. In this randomized controlled trial (RCT), we assessed in a sample of people with bipolar disorder, major depressive disorder, and schizophrenia spectrum disorder, the efficacy of an innovative psychosocial group intervention compared to a brief psychoeducational group intervention on patients’ body mass index (BMI), body weight, waist circumference, Framingham and HOMA-IR indexes.

This is a multicentric RCT with blinded outcome assessments carried out in six Italian university centers. After recruitment patients were randomized to receive a 6-month psychosocial intervention to improve patients’ physical health or a brief psychoeducational intervention. All recruited patients were assessed with standardized assessment instruments at baseline and after 6 months. Anthropometric parameters and blood samples have also been collected.

Four-hundred and two patients with a diagnosis of bipolar disorder (43.3%), schizophrenia or other psychotic disorder (29.9%), or major depression (26.9%) were randomly allocated to the experimental (N = 206) or the control group (N = 195). After 6 months, patients from the experimental group reported a significant reduction in BMI (odds ratio [OR]: 1.93, 95% confidence intervals [CI]: 1.31–2.84; p < 0.001), body weight (OR = 4.78, 95% CI: 0.80–28.27, p < 0.05), and waist circumference (OR = 5.43, 95% CI: 1.45–20.30, p < 0.05). Participants with impaired cognitive and psychosocial functioning had a worse response to the intervention.

The experimental group intervention was effective in improving the physical health in SMI patients. Further studies are needed to evaluate the feasibility of this intervention in real-world settings.

The COVID-19 pandemic has disrupted lives and livelihoods, and people already experiencing mental ill health may have been especially vulnerable.

Quantify mental health inequalities in disruptions to healthcare, economic activity and housing.

We examined data from 59 482 participants in 12 UK longitudinal studies with data collected before and during the COVID-19 pandemic. Within each study, we estimated the association between psychological distress assessed pre-pandemic and disruptions since the start of the pandemic to healthcare (medication access, procedures or appointments), economic activity (employment, income or working hours) and housing (change of address or household composition). Estimates were pooled across studies.

Across the analysed data-sets, 28% to 77% of participants experienced at least one disruption, with 2.3–33.2% experiencing disruptions in two or more domains. We found 1 s.d. higher pre-pandemic psychological distress was associated with (a) increased odds of any healthcare disruptions (odds ratio (OR) 1.30, 95% CI 1.20–1.40), with fully adjusted odds ratios ranging from 1.24 (95% CI 1.09–1.41) for disruption to procedures to 1.33 (95% CI 1.20–1.49) for disruptions to prescriptions or medication access; (b) loss of employment (odds ratio 1.13, 95% CI 1.06–1.21) and income (OR 1.12, 95% CI 1.06 –1.19), and reductions in working hours/furlough (odds ratio 1.05, 95% CI 1.00–1.09) and (c) increased likelihood of experiencing a disruption in at least two domains (OR 1.25, 95% CI 1.18–1.32) or in one domain (OR 1.11, 95% CI 1.07–1.16), relative to no disruption. There were no associations with housing disruptions (OR 1.00, 95% CI 0.97–1.03).

People experiencing psychological distress pre-pandemic were more likely to experience healthcare and economic disruptions, and clusters of disruptions across multiple domains during the pandemic. Failing to address these disruptions risks further widening mental health inequalities.

One in six adolescents suffers from mental health problems. Despite the presence of general information on Italian adolescents' mental health, researches conducted with standardized assessment tools are scarce in the literature. We evaluated the prevalence of self-reported behavioral and emotional problems in a group of Italian adolescents and examined their relation to socio-demographical variables.

This population-based sampling survey was conducted on high school students aged 14–18 from urban areas of Rome and Latina. Participants completed Youth Self-Report (YSR) and a socio-demographic schedule to collect information on age, gender, type of school attended, socio-economic status, urbanicity.

Final sample consisted of 1400 adolescents (38.61% male, mean age 16 years, s.d. 1.42). Prevalence of Internalizing Problems, Externalizing Problems and Total Problems was 29.55%, 18.34% and 24.13%. In our multivariable model, Internalizing Symptoms were not explained by sociodemographic variables while Externalizing Symptoms were explained by Male Gender [OR = 1.53 (1.14–2.06)], older age [OR = 2.06 (1.52–2.79)] and attending a Technical and Professional Institute [OR = 2.15 (1.53–3.02)], with an adjusted R2 = 4.32%. Total Problems were explained by School Type [Technical and Professional Institutes and Art and Humanities v. Grammar and Science School; OR respectively 1.93 (1.40–2.67) and 1.64 (1.08–2.47)], adjusted R2 = 1.94.

The study provides, for the first time, evidence of a great prevalence of self-reported behavioral and emotional problems in a large sample of Italian adolescents, highlighting the role of different socio-demographic variables as risk factors for externalizing behaviors. Our results emphasize the urgent need for implementing prevention programs on mental health in adolescence.

Rasd2 is a striatal GTP-binding protein that modulates Akt and mTOR signaling cascades, well known to be highly vulnerable pathways in psychiatric disorders.

We investigated the association of Rasd2 and its genetic variation with a series of prefronto-striatal phenotypes related to psychosis in rodents and humans.

We want to provide evidence that Rasd2 controls the vulnerability to schizophrenia-related behavior induced by psychothomimetic drugs in mice. Moreover, we aim to find genetic variations within the Rasd2 gene that influence a series of brain schizophrenia-related phenotypes in human.

Rasd2 knockout mice were employed to evaluate schizophrenia-like behaviors induced by psychotomimetic drugs like amphetamine and phencyclidine. Furthermore, we investigated if RASD2genetic variations in humans are associated with mRNA expression in post-mortem prefrontal cortex, as well as prefrontal and striatal grey matter volume and physiology during working memory as measured with MRI in healthy subjects. Finally, we assessed RASD2mRNA expression levels in post-mortem brains of patients with schizophrenia and bipolar disorder.

We found that both psychotomimetics triggered greater vulnerability to motor stimulation and to prepulse inhibition deficits in Rasd2 mutants. In humans, we found that a genetic variation (rs6518956) within RASD2 predicts prefrontal mRNA expression as well as prefrontal grey matter volume and prefronto-striatal activity during working memory. Finally, we reported that RASD2 mRNA expression is slightly reduced in post-mortem prefrontal cortex of patients with schizophrenia.

Collectively, our data suggests that RASD2represents a gene of potential interest in psychiatric disorders for its ability to modulate prefronto-striatal phenotypes related to schizophrenia.

The authors have not supplied their declaration of competing interest.