Eye-tracking technology is a sensitive and direct method of measuring social-cognitive abilities regardless of language, causing minimal cognitive strain and with the advantage of its passive presentation of stimuli to participants, which allows observation without requiring verbal interaction nor explicit responses.

Our aim was to study variations in social attention among adults diagnosed with ASD, ADHD, comorbid ASD and ADHD, and non-clinical individuals using eye-tracking technology.

We recruited a total of 80 participants over the age of 18 from the Psychiatric External Ward of Vall Hebron University Hospital, resulting in approximately 20 participants in each group. Social attention was assessed using vignettes from the Autism Diagnostic Observation Schedule-2 (ADOS-2).

Preliminary results revealed significant statistical differences among the groups in the variables analyzed, indicating that individuals with ASD display distinct patterns of visual attention toward Areas of Interest (AOIs) containing social information compared to the other groups. No differences were found in the duration of fixation on the characters’ eyes among the groups. However, participants diagnosed with ASD and ASD+ADHD tended to spend more time looking at regions with lower social information density, such as the characters’ hands in the third vignette.

These findings shed light on social attention profiles across clinical and non-clinical populations, indicating specific patterns associated particularly with ASD, and highlight the importance of considering multiple aspects of social cognition. By employing eye-tracking technology, this study provides valuable insights into the underlying mechanisms of social attention across different neurodevelopmental conditions. Furthermore, the lack of significant differences in eye fixation duration on the eyes among clinical groups challenges conventional beliefs regarding social attention deficits in ADHD compared to ASD.

Using objective measures like eye-tracking can enhance our understanding of these complex neurodevelopmental conditions, potentially aiding in diagnosis and guiding the development of targeted interventions to address social cognition challenges in populations with neurodevelopmental disorders.

Our findings may contribute to a better understanding of social attention differences between ASD, ADHD, comorbid ASD+ADHD, and non-clinical individuals, paving the way for the design of more tailored and effective interventions.

None Declared

Using a ‘transdiagnostic’ paradigm for psychopathology, we review the evidence-base for the different treatment interventions for anger, aggression and violence (AAV). We aim to more accurately link the range of psychopathology associated with AAV to underlying brain structures and functional neurocircuitry. Building upon these findings, we propose a working model that may have greater clinical utility than reliance upon a purely ‘disorder-based’ paradigm for addressing AAV. This will permit greater understanding of when anger (which has also conferred evolutionary survival advantages) can become maladaptive and destructive. This comprehensive, ‘interventionist’ model will hopefully lead to better clinical conceptualization of AAV, especially since most AAV presents more commonly in the context of interpersonal/situational stressors and to non-forensically trained clinicians.

1. 1. To identify biological, cognitive, disorder-based, developmental and personality predispositions to AAV

2. 2. To link neuroanatomical and functional brain circuitry with onset and maintainence of AAV

3. 3. To identify how pharmacological and non pharmacological interventions work, and ‘where’ in the brain,

4. 4. To review the evidence-base supporting various treatment interventions

Database review of PUBMED, PsychINFO, Google Scholar and treatment guidelines dating back 15 years (review articles, treatment guidelines, meta-analyses and randomized controlled trials).

This will be visually depicted in an electronic slide (or >1 slide, if permitted) to identify:

1. 1) The inter-relationship between contextal factors, the psychopathology of AAV and undelying brain ‘circutry’

2. 2) The specific nature of the impulsive anger, ‘reactive’ aggression and violence response ‘cycle’ and where in this cycle various interventions can be effectively utlized

3. 3) Which patient populations respond best to which types of interventions

1. 1. AAV are hyperarousal states, with outcomes that can be successfully managed

2. 2. The evidence-base for the role of medications is more limited

3. 3. The evidence-base for the role of various psychotherapies is greater, with specific therapies being particularly useful across psychiatric disorders and populations

4. 4. Psychodynamic approches remain curently underutilized and underappreciated

5. 5. Both medications and therapy influence brain neuroplasticity separately and synergistically

None Declared

Lewy body dementia (LBD) is characterized by a range of complex neuropsychiatric symptoms that can initially mimic other psychiatric disorders, particularly melancholic depression. Failure to recognize these symptoms can lead to delayed diagnosis and inappropriate management.

This case report highlights the importance of a thorough evaluation of neuropsychiatric symptoms in the diagnosis of Lewy body dementia (LBD).

This case report was compiled through clinical observations, patient history from family members, and medical testing. Literature on LBD was reviewed to assess treatment strategies in light of this patient’s condition.

Mr. T.C., 75 years old, followed for hyperthyroidism and benign prostatic hyperplasia, was admitted for a severe depressive episode with melancholic features. Despite treatment with fluoxetine, mirtazapine, and olanzapine, his clinical condition did not improve. The patient exhibited food refusal, active suicidal ideation, and thoughts of incurability, along with a delusional syndrome. The Mini Mental State Examination (MMSE) revealed cognitive impairment with a score of 21/30. An initial brain MRI showed no abnormalities. The treatment was adjusted with the introduction of paroxetine alongside olanzapine and mirtazapine, but there was no significant improvement. A follow-up brain MRI revealed periventricular vascular leukoencephalopathy and moderate cortical atrophy, directing the diagnosis towards Lewy body dementia. The appearance of additional neuropsychiatric symptoms, including visual hallucinations, cognitive fluctuations, and mild parkinsonian signs, further supported the diagnosis of LBD. Treatment was then adjusted with the introduction of quetiapine, which is better tolerated in the context of LBD due to its favorable therapeutic profile.

This case emphasizes the importance of accurately diagnosing neuropsychiatric disorders in Lewy body dementia. Appropriate management, based on a thorough clinical evaluation, can prevent treatment errors and improve the patient’s quality of life.

None Declared

The lack of accessible plasma biomarkers to identify target populations limits the promise of precision medicine for Alzheimer’s Disease (AD). Amnestic mild cognitive impairment (aMCI) is an important risk for AD and often occurs years before the onset of AD.

Based on an emerging mechanistic model of mitochondrial mechanisms of brain plasticity, we studied the role of acetylcarnitine and free-carnitine levels assayed in plasma as potential markers of cognitive dysfunction in subjects with aMCI or early-AD.

We used available samples from two independent cohorts well characterized for clinical and neuropsychological characteristics together with ultraperformance liquid chromatography-tandem mass spectrometry and computational approaches. Cerebrospinal fluid (CSF) measures of b-amyloid accumulation and t-Tau levels were also available and used in computational modeling.

Within the primary cohort, our data showed decreased levels of carnitine in relation to cognitive function as assessed by using the Mini Mental Status Exam (MMSE) in women but not men with CI as compared to age- and sex-matched HC. Furthermore, the magnitude of carnitine deficiency reflected the severity of cognitive dysfunction in a sex-specific manner (women: p = 0.015; men: p = 0.441). Our data also replicated the prior finding of decreased LAC levels in both women and men with AD, supporting the robustness of the study samples assayed in our new study. Using computational approaches, we found that the integration of these mitochondrial measures with canonical CSF biomarkers improves diagnostic accuracy. A second cohort provides a validation of the sex-specific relationship between free-carnitine deficiency and the severity of cognitive dysfunction.

Taken together with prior mechanistic studies in rodents, the current findings support future research on the development of individualized treatment models targeting sex-specific changes in mitochondrial metabolism.

None Declared

Impulsivity implies difficulties in control, leading to non-premeditated actions, and troubles resisting distraction and remaining focused on a goal. It is a transdiagnostic construct that is associated with several disorders, including Attentional Deficit and Hyperactivity Disorder (ADHD), Borderline Personality Disorder and Obsessive-Compulsive Disorder (OCD). It is possible to divide impulsivity between impulsive actions, associated with the ability to inhibit actions, and choice impulsivity, that involves decision-making. It is also common to differentiate between trait impulsivity, that involves more stable characteristics, and state impulsivity, in which the impulsive behavior is more transient.

To investigate the association between action impulsivity as a trait (using self-report measures) and as state (using different level of analysis in a computerized task, i.e., behavioral and neuroimaging measures).

52 university students (mean age = 21.4; standard deviation = 3.33) filled the BIS-11 self-report questionnaires and completed a Stroop-matching/stop-signal task while they had their behavioral and hemodynamic brain activity collected using Functional Near- Infrared Spectroscopy (fNIRS). The Stroop-matching/stop-signal task had three conditions varying the inhibitory demands: Congruent/Unrelated; Incongruent/Unrelated and Incongruent/Related. Spearman correlations were performed between scores of the BIS-11 subscales (Attentional, Motor and Non-planning impulsivity) and the reaction time (RT) and hemodynamic responses (β) of the Stroop-matching/stop-signal task. Alpha level = 0.05.

RTs in all conditions of the task were positively correlated with Motor Impulsivity scores (Congruent/Unrelated, rho = .31, p = .025; Incongruent/Unrelated, rho = .27, p = .049; Incongruent/Related, rho = .38, p = .005). Brain activity in the left temporoparietal region was positively correlated with Attention Impulsivity scores (rho = .29, p = .033).

Motor and attentional aspects of trait impulsivity can be differently correlated with behavioral and neurophysiological measures of state impulsivity. In this study, motor impulsivity was correlated with more peripherical measures of inhibition (reaction times) while attentional impulsivity was correlated with activity in temporoparietal regions commonly associated with inhibition of distractive stimuli. Greater levels of motor and attentional impulsivity were associated with slower responses and greater brain activity, respectively.

None Declared

Atypical antipsychotics (APs) are the drugs of choice for the treatment of the acute episodes and for relapse prevention in schizophrenia (SZ) and psychosis. Nevertheless, these drugs have side effects and particularly increase the risk to develop metabolic syndrome. Moreover, it has been reported that first-episode psychosis (FEP) patients have significant trends to insulin resistance, a higher body mass index and a higher rate of obesity, compared to the healthy subjects. Changes in gut microbiome have been linked to increased systemic inflammation, which could be associated with metabolic disturbances and the development of SZ. In this context, some previous studies have explored the efficacy of probiotic supplementation in SZ, showing benefits in gut regulation and in improving the metabolic effects of APs.

The purpose of this study is to evaluate the effectiveness of an add-on postbiotic to Aps on metabolic disturbances and psychopathological variables in patients diagnosed with FEP or schizophrenia spectrum disorder (SSD). , as well as to determine whether the addition of postbiotics can improve biomarkers related to compensatory immunity and the endocannabinoid system.

A randomized, double-blind, placebo-controlled clinical trial, in which postbiotic or placebo will be administered for 12 weeks as add-on APs. The study comprises two branches: FEP branch, patients recently diagnosed with first psychotic episode; and SSD branch, patients with long-standing psychotic disorder. Five follow-up appointments will be conducted along the 12 weeks to carry on clinical assessments. Patients will be monitoring with a glucose sensor, and blood and microbiota will be analysed.

This is a study protocol that is currently underway. No results are available at this time.

Over the past few decades, it has been abundantly evident how important the human microbiota is to both short-term and long-term human health. In this regard, postbiotics seem to have higher benefitial effects and lower risk than probiotics and they offer a promising approach to improve metabolic disturbances and amelioration of psychopathological symptoms in FEP and SSD patients.

None Declared

Patients of depression and psychotic disorders are often troubled by unsatisfactory interpersonal relationships. While an inability to maintain a stable sense of self restricts one’s understanding another’s emotional state, whether disrupted self-versus-other referential processing is a transdiagnostic predictor of increased emotion misreading across diagnostic groups has not been explicated.

We tested whether weakened differential learning between self and other may account for impoversihed emotion recognition accross mood and psychotic disorders.

Inpatients admitted for major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SCZ; ns = 59, 32, and 43) and 40 healthy controls were recruited. Aside from ratings of depressive and schizophrenic symptoms by psychiatrists, participants were assessed on self- versus other- referential learning, emotion recognition, emotion sharing.

Regression analysis indicates lower effectiveness of self-other tagging to be a predictor independent from symptom severity for increased emotion misrecognition across MDD, BD and SCZ (F(8, 160) = 8.52, p < 0.001). Clinical groups showed lower accuracy for other-referential recall and emotion recognition, but comparable emotion sharing and self-prioritization to healthy controls.

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Heightened emotion misrecognition in MDD, CD, and SCZ patients can be traced back to the weakened ability in coordinating self- and other-representations according to task-demands. Future examinations on whether interventions on brain regions pertaining to self-versus-other learning might enhance emotion recognition in different patient groups would be clinically relevant.

None Declared

Hypericin and hyperforin, key secondary metabolites of Hypericum spp., commonly known as St. John’s Wort, are known for their ability to modulate neurotransmitter systems in the mammalian brain. These compounds, which evolved as plant defense chemicals, have significant implications for their interaction with mammalian neurobiology, particularly concerning serotonin, dopamine, and norepinephrine pathways.

This review aims to elucidate the precise molecular mechanisms by which hypericin and hyperforin influence mammalian brain function. The focus is on understanding how these compounds interact with neurotransmitter transporters and receptors, and how these interactions may lead to both therapeutic and adverse neurobiological outcomes.

A comprehensive review of neurobiological and pharmacological literature was conducted, focusing on studies that detail the molecular interactions of hypericin and hyperforin with key components of neurotransmitter systems in mammals. in vitro binding assays, in vivo neuropharmacological studies, and molecular dynamics simulations were reviewed to understand these compounds’ binding affinities, receptor modulation, and downstream signaling effects.

Hypericin, with its planar polycyclic structure, exhibits a strong affinity for serotonin transporters (SERT), where it acts as a non-competitive inhibitor, leading to increased synaptic levels of serotonin. This mechanism mirrors that of selective serotonin reuptake inhibitors (SSRIs) but also introduces the potential for serotonin syndrome when combined with other serotonergic agents. Additionally, hypericin’s ability to generate reactive oxygen species (ROS) under light exposure contributes to neurotoxicity, particularly in regions of the brain exposed to higher oxidative stress.

Hyperforin, characterized by its phloroglucinol core and multiple prenyl groups, exerts its effects primarily through modulation of synaptic vesicle function and ion channel activity. It non-selectively inhibits the reuptake of several neurotransmitters, including serotonin, dopamine, and norepinephrine, through a mechanism involving transient receptor potential (TRP) channels. This broad-spectrum inhibition can lead to significant changes in synaptic plasticity and neurotransmission, impacting mood regulation, anxiety, and cognition.

The interaction of hypericin and hyperforin with mammalian neurotransmitter systems underscores their potential as both therapeutic agents and neurotoxins. The molecular mechanisms by which these compounds modulate neurotransmitter transporters and receptors reveal a delicate balance between beneficial and adverse effects. Understanding these mechanisms is critical for evaluating the safety and efficacy of Hypericum extracts in clinical contexts, particularly regarding their impact on brain function and the potential for neurotoxicity.

None Declared

Chronic mental illness is a significant risk factor for developing neurocognitive disorders. Advanced molecular imaging techniques, such as amyloid PET and FDG-PET, provide critical insights into the neurobiological mechanisms that link psychiatry and neurology, enhancing our understanding of the continuum between these fields.

This study aims to describe the clinical history of chronic mental illness in a sample of patients with diagnosis of dementia, using molecular imaging to investigate the relationship between psychiatric history and neurodegenerative pathology.

We conducted a retrospective, descriptive analysis of patients who underwent amyloid PET imaging at the Neurology Department of Infanta Leonor University Hospital from January 2019 to October 2024. Inclusion criteria mandated a documented history of chronic mental illness, irrespective of psychiatric hospitalization. Collected data included demographic variables (age, sex), cardiovascular risk factors, psychiatric diagnoses according to DSM-5, years of mental illness, neurological diagnoses, and results from FDG and amyloid PET imaging. Ethical approval was obtained, and statistical analyses were performed using SPSS 22.0.

A total of 25 patients were included. The main characteristics of the sample are shown in Table 1.

Among those with a chronic mental illness history exceeding ten years (N=8), the diagnostic distribution was as follows: 20% Alzheimer’s disease, 20% Lewy body dementia, 20% major depressive disorder, 10% post-traumatic stress disorder, and 10% indeterminate. Notably, 75% of Alzheimer’s patients and 66.6% of those with Lewy body dementia had a history of major depressive disorder. Patients with frontotemporal dementia often presented with neurocognitive behavioral disorders or obsessive-compulsive disorder. Among four patients with psychiatric hospitalization, only one received a definitive neurological diagnosis (frontotemporal dementia).

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These findings highlight the importance of considering chronic mental illness histories in the cognitive assessment of patients. The neurobiological links between depressive disorders and Alzheimer’s disease emphasize the need for interdisciplinary approaches in clinical practice. Molecular imaging serves as a pivotal tool in refining diagnostic accuracy, complementing both psychiatric and neurological perspectives, and enabling therapeutic strategies to improve patients’ quality of life.

None Declared

Centropontine myelinolysis (CPM) is an acute demyelinating neurological disorder that primarily affects the central bridge and is frequently associated with rapid correction of hyponatremia. Common clinical manifestations of CPM include spastic quadriparesis, dysarthria, pseudobulbar palsy and encephalopathy of varying degrees. In addition, CPM could be accompanied by neuropsychiatric manifestations, such as personality changes, thymic symptoms, acute psychosis, paranoia, hallucinations or catatonia, usually associated with additional brain damage, described as extrapontine myelinolysis (EPM).

Study the nature of comorbidity between CPM and mood disorders, particularly depression.

We present the case of a patient hospitalized in the psychiatry department B of the Hedi Chaker hospital in Sfax in July 2024. He was been admitted at the request of a third party for behavioral disorders such as agitation and refusal of treatment.

This is Mr. S.BH aged 68, with a psychiatric family history of follow-up for unspecified psychiatric disorders in a niece. He has no psychiatric history, but has a somatic history, unmonitored high blood pressure as well as chronic constipation causing hyponatremia, which was quickly corrected 1 month ago. The latter was responsible for CPM objectified on the brain MRI requested by a free practice neurologist who consulted him for agitation. Our patient is married. He has been retired for a few months and previously worked as a farmer for 35 years. According to the family, the history of his illness dates back to March 2024, following professional stressors when he began to present multiple somatic complaints, with anorexia and weight loss as well as a tendency towards isolation. Since June 2024, following the CPM, he believed that the police wanted to harm him. As a result, he became anxious and agitated. At the interview: Slowed down on the psychomotor level, the contact was superficial, the mood was sad, his speech was provoked, poor and conveyed in a low voice verbalizing anhedonia, he presents congestive disorders and he refuses treatment and diet at the beginning. The patient obtained a score of 12 on < < the Geriatric Depression Scale GDS >> and a score of 12 on < <the mini-mental state examination MMSE >>.

This case demonstrates that depression might represent the main manifestation of CPM, especially in the early stages of the disease, which should be taken into consideration when evaluating patients with acute abnormalities of sodium metabolism.

None Declared

Background: Lifestyle factors are linked to differences in brain aging and risk for Alzheimer’s disease, underscored by concepts like ‘cognitive reserve’ and ‘brain maintenance’. The Resilience Index (RI), a composite of 6 factors (cognitive reserve, physical and cognitive activities, social engagement, diet, and mindfulness) provides such a holistic measure.

This study aims to examine the association of RI scores with cognitive function and assess the mediating role of cortical atrophy.

Baseline data from 113 participants (aged 45+, 68% female) from the Healthy Brain Initiative were included. Life course resilience was estimated with the RI, cognitive performance with Cognivue®, and brain health using a machine learning derived Cortical Atrophy Score (CAS). Mediation analysis probed the relationship between RI, cognitive outcomes, and cortical atrophy.

In age and sex adjusted models, the RI was significantly associated with CAS (β= -0.25, p = 0.006) and Cognivue® scores (β= 0.32, p < 0.001). The RI-Cognivue® association was partially mediated by CAS (β= 0.07; 95% CI [0.02, 0.14]).

Findings revealed that the collective effect of early and late-life lifestyle resilience factors on cognition are partially explained by their association with less brain atrophy. These findings underscore the value of comprehensive lifestyle assessments in understanding the risk and progression of cognitive decline and Alzheimer’s disease in an aging population.

R. Ezzeddine: None Declared, D. Oshea: None Declared, S. Camacho: None Declared, L. Besser: None Declared, M. Tolea: None Declared, J. Galvin Employee of: Cognivue (Chief Scientific Officer of Cognivue). Cognivue devices are used for research conducted at the center., C. Galvin: None Declared, L. Wang: None Declared, G. Gibbs: None Declared

Children with Noonan syndrome, the most prevalent RASopathy, exhibit a characteristic neurocognitive phenotype. Specific difficulties in learning, memory, and executive function are among the most frequently observed manifestations documented in the scientific literature.

The present study aimed to measure specific learning difficulties and intelligence in children with RASopathies.

A total sample of 47 patients (55.3% male) aged 3–16 years (M = 8.6, S.D. = 3.1) was recruited from various Spanish regions (Murcia, Alicante, Gandía, Valencia, Castellón de la Plana, Tarragona, Cantabria, Asturias, Zaragoza, Madrid, Badajoz, Huelva, Sevilla and Cádiz), within the framework of The Grey Matter project. Most patients were diagnosed with Noonan syndrome, and some had Cardiofaciocutaneous syndrome. The most frequent mutations were PTPN11 (72.3%), RIT1 (6.4%), and unknown mutations in 12.8% of patients. Patients were assessed using the Spanish version of the Wechsler Preschool and Primary Scale of Intelligence, Fourth Edition (WPPSI-IV) or the Wechsler Intelligence Scale for Children, Fifth Edition (WISC-V) according to age; the Spanish Reading Processes Evaluation Battery (PROLEC) according to the appropriate age range (from 6 years); and the Spanish Writing Processes Evaluation Battery (PROESC), from 8 years.

On the one hand, 32.3% presented with severe difficulty in reading words. In turn, 30% of the children showed severe difficulty in reading comprehension of texts when they were read by an examiner, and 29% after reading by themselves. On the other hand, 56% of the children presented severe orthographic difficulty in writing words and 50% presented severe difficulty in written expressions. Finally, regarding intelligence, the mean total IQ of the children was 84.7 points (S.D. = 15.1), with better scores on the Verbal Comprehension Index (M = 89.4; S.D. = 16), Visual Spatial Index (M = 87.7; S.D. = 13.8), and Fluid Reasoning Index (M = 88.6; S.D. = 11.9), in contrast with the Working Memory Index (M = 84.3; S.D. = 13.2), and the Processing Speed Index (M = 83.2; S.D. = 14.4). In turn, 42.6% of children had low global intelligence scores (IQ ≤ 79).

In conclusion, children with RASopathies, particularly those diagnosed with Noonan syndrome, need educational support to compensate for all these significant academic difficulties.

None Declared

Paediatric patients with severe diseases awaiting solid organ or haematopoietic stem cell transplantation are known to experience cognitive impairments, particularly in executive functioning. Neuropsychological pre-transplant evaluation serves as a baseline for identifying executive functioning deficits that may affect the medical and psychosocial aspects of care. This is clinically relevant because patients with poorer executive functioning may show decreased adherence to medical treatments, face greater challenges in coping with their illness, and be more likely to require educational adaptations, including curricular or methodological adjustments based on pedagogical criteria.

This study aimed to assess everyday executive functioning in paediatric patients awaiting transplantation using an ecologically valid measure.

A total of 49 patients (59.2% male) aged between 6 and 18 years (M = 11.4, S.D. = 3.5) were recruited from La Paz University Hospital (Madrid, Spain). Patients were awaiting for various types of organ transplants (kidney: 26, heart: 4, lung: 4, hepato-renal: 3, or liver: 2 patients) or haematopoietic stem cells (10 patients). Patients were assessed using the Spanish parent-reported version of the Behavior Rating Inventory of Executive Function, Second Edition (BRIEF-2) with age- and sex-adjusted norms from the Spanish general population. The three BRIEF-2 composite scores were analysed (the Cognitive, Emotional and Behavioral Regulation Indexes), and clinically relevant scores were set at T ≥ 65 points.

Clinically significant levels of executive deficits were observed in 33.3% of patients regarding cognitive regulation problems, in 32.7% regarding emotional regulation difficulties and in 26.5% regarding behavioural regulation problems.

Between 1 in 4 and 1 in 3 patients have shown some type of executive regulation difficulties. The early identification of executive functioning deficits in paediatric transplant candidates is crucial. Incorporating standardised ecologically valid measures, such as the BRIEF-2, into routine assessments can help detect neuropsychological impairments at an early stage, allowing timely therapeutic or preventive interventions (e.g., psychological prehabilitation). This approach can improve medical outcomes and quality of life and guide educational adaptations to support academic performance.

None Declared

The association between cannabis use and cognitive functioning in individuals experiencing a first episode of psychosis (FEP) is inconsistent, with some studies reporting deterioration (Bogaty et al. J Psychiatr Res 2018; 99:22-32), others indicating improved performance (Rodríguez-Sánchez et al. Schizophr Res 2010; 124:142-151), and some finding no difference.

This study aims to evaluate the effect of cannabis use on cognitive functioning among individuals diagnosed with FEP.

A cross-sectional study was conducted on FEP patients enrolled in the ITPCan Program (Santander, Spain) between January 2020 and July 2024. A total of 207 participants (57 cannabis users and 145 non-users) with a FEP diagnosis were included. A descriptive-univariate analysis was performed on clinical, analytical, and cognitive variables. A Student’s t-test compared baseline cognitive performance between cannabis users and non-users, while a multivariate general linear model (GLM) assessed differences related to cannabis consumption, adjusting for sex, age, and educational level. Statistical analyses were performed using SPSS.

Out of the 207 FEP participants, 53.6% were women, with an average age of 36.8 years. Cannabis users comprised 28.1% of the group, and present at baseline a lower mean age at intake (27 years; p < 0.001). Cannabis users exhibited significantly higher scores in mania and positive psychotic symptoms. Cognitive assessments, completed by 148 patients (39 users and 108 non-users), revealed that cannabis users performed better than non-users on “processing speed” task; however, after adjusting for sex, age, and educational level, these differences were attributed to educational level and sex.

In consonance with some previous studies (Sánchez-Gutiérrez et al. Eur Psychiatry 2020; 63(1)), cannabis use does not appear to be a determining factor in cognitive performance in early psychosis.

None Declared

HIV infection can lead to neurological and psychiatric disorders by affecting the central nervous system. Toxoplasma gondii can cause encephalitis in immunocompromised individuals, particularly damaging brain regions such as the frontal cortex and basal ganglia. These neuroanatomical disruptions can influence dopaminergic and serotonergic neurotransmitter pathways, resulting in severe neuropsychiatric symptoms like behavioral disinhibition, personality changes, and psychotic manifestations (Vidal JE. J Int Assoc Provid AIDS Care 2019; 18:2325958219867315).

This case seeks to demonstrate the neuropsychiatric effects of HIV and Toxoplasma gondii infections on neuronal function and behavior, emphasizing the importance of continuous assessment and integrated treatment approaches.

A 49-year-old male patient, with no known medical history, developed Toxoplasma gondii encephalitis after being diagnosed with HIV. Following discharge from the infectious disease ward, the patient exhibited increased irritability, impulsivity, hypersexuality, visual hallucinations, disorganized speech, and risky behaviors, along with cognitive dysfunction and social norm violations. The patient’s symptoms partially improved with a treatment regimen of 15 mg olanzapine and 1000 mg valproic acid. However, the patient’s ongoing course, parkinsonism symptoms emerged, prompting the discontinuation of valproic acid and the consideration of quetiapine. The patient’s follow-up treatment is ongoing.

HIV and Toxoplasma gondii disrupt neuronal function through inflammatory responses and microglial activation in the central nervous system. HIV does not directly damage neurons, but inflammation from cytokines released by microglia can lead to neurodegenerative conditions. Dopaminergic dysfunction is linked to psychotic symptoms, while serotonergic disruptions contribute to depression and anxiety. Frontal lobe and basal ganglia damage impair executive functions (planning, decision-making, impulse control), causing increased impulsivity, risky behaviors, emotional dysregulation, irritability, lack of empathy, behavioral disinhibition, hypersexuality, and cognitive dysfunction. These changes are tied to structural damage in the frontal cortex, necessitating long-term follow-up and comprehensive treatment. Diagnostic imaging often shows white matter lesions, basal ganglia damage, and frontal cortex atrophy. Treatment involves antiretroviral therapy, low-dose antipsychotics, mood stabilizers for managing symptoms (Bartolomé Del Pino LE et al. Actas Esp Psiquiatr 2024; 52(2):149-60).

HIV and Toxoplasma gondii infections induce significant central nervous system impairment, leading to neuropsychiatric disorders. This case illustrates their impact on neurotransmitter systems, manifesting as psychosis, cognitive dysfunction, and behavioral disturbances. Continued monitoring and comprehensive treatment are essential.

None Declared

Activity of the glutamate neurotransmitter system contribute to the development of many mental disorders, in particular of depression and schizophrenia. While the glutamate is the principal excitatory neurotransmitter in the brain there are poor data on its relationships with EEG.

The aim of the study was to search for possible relationships between parameters of EEG and glutamate dehydrogenase (GDH) activity in patients with depressive-delusional disorders.

The study involved 28 female in-patients aged 16-35 years (mean age 22.0 ± 8.1 years) with depressive-delusional disorders in the frames of schizophrenia (F20.01, by ICD-10). Pre-treatment multichannel resting EEG recordings with spectral power analysis in narrow frequency sub-bands were performed in all patients. Patients were divided into two groups with relatively “normal” (n=18) and “slow” (n=10) EEGs. “Slow EEG” group statistically differed (p<0.05) from “normal EEG” group by greater spectral power values in theta2 (6-8 Hz) EEG sub-band in frontal-central-temporal regions of the left hemisphere. GDH enzymatic activity was measured in platelets’ extracts from blood samples by spectrophotometric kinetic method and was assessed by the rate of NAD•H absorption decrease at 340 nm. The descriptive statistics and the rank correlation analysis (Spearman) were used for statistical processing of EEG and neurochemical data.

“Slow EEG” and “normal EEG” groups did not statistically differ (p>0.05) in age, HDRS and PANSS scores, while the clinical severity was somewhat greater in “slow EEG” group. Nevertheless, “slow EEG” and “normal EEG” groups apparently differed in correlation structure between EEG and GDH activity parameters. Thus, in “slow EEG” group values of GDH activity correlated positively (p<0.05÷0.01) with values of spectral power in delta (2-4 Hz), theta1 (4-6 Hz) and theta2 (6-8 Hz) EEG sub-bands. In “normal EEG” group values of GDH activity did not correlate with any studied EEG parameters.

Greater GDH activity in “slow EEG” group of patients with depressive-delusional disorders have to provoke the glutamate mediated excitation deficit reflected in EEG slowing. The predominance of this phenomenon in the left hemisphere may underlie some features of the clinical conditions in these patients and need further studying.

None Declared

Preclinical stages of Alzheimer’s disease (AD) are characterized by structural and neurochemical abnormalities in temporal lobe and temporoparietal junction (T-TPJ; Popuri et al. Hum Brain Mapp 2020; 41 4127-4147; Jagust. Nat Rev Neurosci 2018; 19 687-700). However, the role of functional characteristics of T-TPJ in conversion to AD is understudied.

Our aim was to clarify whether any patterns of functional connectivity (FC) within T-TPJ differentiate patients with amnestic mild cognitive impairment (aMCI) and future conversion to AD from stable aMCI and healthy controls.

Patients with aMCI and future conversion to dementia due to AD (converters, n = 15; mean age 74.31 ± 7.86), patients with stable aMCI (non-converters, n = 12; mean age 66.77 ± 9.54), and healthy individuals without cognitive deficits (n = 29; mean age 64.17 ± 11.30) underwent resting-state fMRI (3T Philips Ingenia scanner). Eighteen T-TPJ cortical ROIs in each hemisphere were defined according to Harvard-Oxford atlas (Desikan et al. Neuroimage 2006; 31 968-980). FC between these ROIs was compared between groups separately for each hemisphere (one-way ANCOVA with connection threshold p[FDR] < 0.05 and post hoc between-group comparisons). Age, sex, and number of outlier scans due to motion were included into the models as covariates of no interest. The analyses were implemented via CONN (RRID:SCR_009550; www.nitrc.org/projects/conn).

FC between the posterior parts of left middle and inferior temporal gyri was different between converters, non-converters, and healthy individuals (p[FDR] = .0256). Converters demonstrated an increased FC between these regions compared to other groups (p = .0003 for both tests). We also observed a trend for inverse correlation between this FC and delayed recall of words (MoCA) in the entire sample (p = .055).

An increased FC between the temporal brain regions may reflect either pathological processes that have already started, or compensatory mechanisms, or both in future converters to AD. The posterior part of left middle temporal gyrus is critical for auditory verbal memory, whereas the posterior inferior temporal cortex in the left hemisphere stores visual images associated with a word. The observed trend-like correlation might indicate that patients with worse auditory verbal memory rely on visual images associated with a word, however, this assumption should be supported in further studies.

The study was supported by RSF grant 24-15-00220.

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In depressive disorders caused by chronic psychological stress, cognitive decline is produced by neuroinflammatory and neurodegenerative changes in the brain. M2-type macrophages possess high pronounced regenerative potential due to high production of neurotrophic, neuroprotective and angiogenic factors. We have previously shown that M2 macrophage-derived soluble factors (M2-SFs) edit stress-induced depressive-like behavior.

The aim of the study was to investigate the central effects of soluble factors derived from human macrophages, polarized to M2 phenotype (M2-SFs) involved in the mechanisms underlying the editing of depressive-like behavior.

Human macrophages were polarized polarised to M2 phenotype under serum deprivation conditions. Stress-induced depression-like male mice were undergoing intranasal administration of M2-SFs during 7 days. After which an immunohistochemical analysis was performed assessing the expression of the microglial marker Iba1. The levels of brain-derived neurotrophic factor (BDNF) and cytokines in separate structures of the brain were assessed by ELISA. For histological examination Nissl staining was applied.

Depressive-like behavior editing after the M2-SFs administration was registered against the background of some structural and functional changes in the brain. It was found an increase in the density of pyramidal neurons in the frontal cortex and augmented level of BDNF in this brain structure and also in the hippocampus. After the introduction of the M2-SFs in depressive-like mice the decreased expression of the microglial marker Iba1, accompanied with decreased levels of pro-inflammatory cytokines IL-1β, IL-6, TNF-α, INF-γ in pathogenetically significant structures of the brain was also observed.

The data obtained indicate that the depressive-like behavior-editing effect of M2 macrophage-derived soluble factors is mediated by stimulating neurogenesis, neuroplasticity and reducing neuroinflammation.

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Negative symptoms and cognitive deficits in schizophrenia (SZ) significantly affect patients’ quality of life and functionality, but show limited response to antipsychotic treatment.

The present study aims to investigate the acute (n=32) and one-month (n=25; active-tDCS:13 vs. sham-tDCS:12) effects of repeated transcranial Direct Current Stimulation (tDCS) on negative symptoms and executive attention in recent-onset SZ.

In this study, 32 clinically stable SZ patients (age:24.7±4.5, 65% male) with a disease duration under 5 years were included in a single-blind, randomized sham-controlled trial. Patients received 10 sessions of either active-tDCS (n=17) or sham-tDCS (n=15) (anode: left dorsolateral prefrontal cortex, DLPFC; cathode: right orbitofrontal region) at 2 mA for 20 minutes, twice daily, across 5 consecutive days and were followed up after the 10th tDCS on day 5 (acute effect), and at weeks 2 and 4. Pre- and post-tDCS assessments included the Brief Negative Symptom Scale (BNSS), Brief Psychiatric Rating Scale (BPRS), Calgary Depression Scale for SZ (CDSS), Global Assessment of Functioning (GAF), Clinical Global Impression Scale, Verbal Fluency Test (VFT), and the Penn Computerized Neurocognitive Battery’s Letter N-Back and Continuous Performance Test (CPT). One-way ANCOVA was used to assess between-group changes over time, controlling for pre-tDCS measurements, while mixed-design ANOVA explored time × tDCS-group interactions, followed by repeated measures ANOVA to assess within-group effects. Pairwise comparisons over time within each group were examined using a post-hoc Bonferroni test.

The active-tDCS group showed significant acute improvements in Avolition-Apathy (AA) (F(1,29)=13.55, p<0.001, pη²=0.319) and Expressive Deficit (EXP) (F(1,29)=4.66, p=0.039, pη²=0.138) domains, BNSS-total (F(1,29)=25.12, p<0.001, pη²=0.464), BPRS-General Psychopathology (F(1,29)=19.68, p<0.001, pη²=0.404), CDSS (F(1,29)=8.16, p=0.008, pη²=0.22) scores, VFT-phonemic fluency (F(1,29)=11.98, p=0.002, pη²=0.292) and CPT (F(1,29)=5.29, p=0.029, pη²=0.154) performances compared to sham-tDCS. Time-group interactions were significant in BNSS-AA domain (F(1,21)=16.44, p<0.001, pη²=0.701), BNSS-total (F(1,21)=15.77, p<0.001, pη²=0.693), and BPRS-General Psychopathology (F(1,21)=6.42, p=0.003, pη²=0.479). Following the mixed-design ANOVA, repeated measures analyses showed significant score decreases over time in the active-tDCS, while the sham group showed no significant changes or a slight increase (only for BNSS-total scores) (Fig. 1).

Image 1:

The present results suggest that anodal tDCS over the left DLPFC may be effective in alleviating negative symptoms, reducing general psychopathology severity, and acutely enhancing complex attention functions and working memory in recent-onset SZ.

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The presentation of psychotic symptoms in adults requires a global medical assessment, especially in cases of atypical presentations or if warning signs are present. The presence of cognitive symptoms and behavioral changes requires screening for various neurological diseases.

Underline the importance of neurological evaluation in atypical psychotic conditions with cognitive and behavioral symptoms. Describe Brain Sagging Dementia as a possible etiology of these conditions.

Presentation of clinical case and bibliographic review.

The clinical case of a 59-year-old female patient brought to the emergency department for psychiatric evaluation due to behavioral alterations is described. During the evaluation, paranoid symptoms were detected, with marked suspicion towards her family, which led to her admission for psychiatric hospitalization. During observation, the clinical history was completed, revealing marked changes in behavior, apathy, perseveration, and decreased functionality for more than five years. Neuropsychological tests were performed, where cognitive and visuospatial alterations were evident. A consultation with the neurology service was requested, who initially considered the diagnosis of behavioral-variant frontotemporal dementia.

Given the history of orthostatic headaches secondary to cerebrospinal fluid hypotension due to a dorsal fistula, a new brain MRI was performed, which found evidence of cerebrospinal fluid hypotension without frontotemporal atrophy. Given all the clinical and radiological findings, a possible diagnosis of Brain Sagging Dementia was considered.

Brain Sagging Dementia is a rare syndrome caused by spontaneous intracranial hypotension (SIH), which mimics the behavioral clinical findings of frontotemporal dementia (bvFTD), excluding it due to the absence of frontotemporal atrophy. It is insidious in nature, with gradual cognitive and behavioral alterations.

The first-line treatment is an epidural blood patch, with partial resolution of symptoms in up to 81% of cases and complete resolution in up to 67%.

In this case presented, the patient is awaiting evaluation by neurosurgery.

In case of suspected neurological origin of psychiatric symptoms, a complete evaluation is essential with special attention to potentially reversible causes.

It is important to keep in mind the neuropsychiatric manifestations that can occur in dementia and other neurology conditions, to avoid delaying a correct diagnosis. These include behavioral alterations, psychotic symptoms, eating disorders, as well as affective disorders ranging from apathy and depression to expansiveness with signs of disinhibition.

Brain sagging dementia is a reversible condition with symptoms of bvFTD, whose early diagnosis and treatment significantly improve the medical prognosis.

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