In the history of urban planning, the cognitive trend has been a well-established entity since the work of the American urban planner during the mid-’90s; Kevin Lynch. However, for a long time, urban planning has been deprived of the contribution of scientific knowledge from cognitive neurosciences, with a lack of operational recommendations for urban projects.

This study aims to reveal the role of embodiment theories in the revolution of urban design and urban projects through emerging findings in epigenetics and post-genomic biology.

We conducted an exhaustive review of the scientific literature to establish the relationship between embodied cognition and urban design through advances in epigenetics as well as potential applications of such finding. Our inquiry was to find out whether there was a scientific way to measure and quantify the performance of urban spaces.

Our review revealed that, epigenetics and epigenomics have provided new explanations and perspectives to certain debates on the theory of embodied cognition and that of enaction. Epigenetic marks constitute a bodily memory that enables cognition to emerge as a function of the level of adaptation to the environment. In fact, embodiment refers to thoughts, emotions and behaviors based on sensory experiences and bodily positions, while the enaction is a way of conceiving cognition that focuses on the way in which human organisms and minds organize themselves in interaction with the environment.

Cognition is the result of a level of adaptation to the environment determined by physiological parameters that confer possibilities of action depending on previous interactions with the environment. The regulation of epigenetic marks which are technically quantifiable is now recognized as the fundamental mechanism involved in the brain’s ability to create, dismantle or reorganize neural networks throughout life depending on various experiences including environmental ones.

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Neuropsychological disorders in patients with alcoholism intensively studied since the mid-70s of the last century. Research in this area divided into three groups: the study of premorbid neuropsychological features of alcohol dependence; study of neuropsychological disorders of chronic alcohol use; study of the prognostic value of neuropsychological disorders in patients suffering from alcohol dependence. In domestic neuropsychology, is the necessary information about the neuropsychological characteristics of patients suffering from alcohol dependence, neuropsychological manifestations in cognitive processes.

to identify neuropsychological features of patients suffering from alcohol dependence with a diagnosis of stage 2 alcoholic disease

A neuropsychological examination was carried out according to the method of A.R. Luria of 39 patients aged 29 to 68 years with a diagnosis of stage 2 alcoholic disease. The group of patients is divided into 3 subgroups of alcohol abuse: up to 10 years, 10-20 years; more than 20 years.

Disorders of higher mental functions identified in all subgroups. In chronic alcoholic encephalopathy, there is a tendency to increase cognitive deficits. According to the results of the neuropsychological examination, it was found that the greatest disorders in patients of the first subgroup occur in the implementation of successive processes (memory, thinking), arbitrary regulation of activity, and also relate to the regulatory aspects of memory, attention, thinking and speech.

In patients of the second subgroup, the most numerous in this sample, violations of visual object gnosis were revealed, as well as a violation of the synthesis of information necessary to endow the image of the object with a certain meaning In patients of the third subgroup, pronounced disorders inherent in the first and second subgroups were found, as well as distortions in the identification of emotions, that is, the inability to compare emotional objects with an emotional standard, which indicates signs affective-cognitive deficit in alcoholic disease of the second stage.

In the study, the dynamics of neuropsychological disorders in patients with alcohol disease of the second stage, depending on the experience of alcohol abuse, found

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Recent clinical and preclinical evidences suggested that neuroinflammation is a key factor which interacts with the neurobiological correlates of major depressive disorder, which are the (i) dysregulation of the hypothalamic-pituitary-adrenal axis, (ii) depletion of brain serotonin and (iii) alteration of neurogenesis in the dentate gyrus of the hippocampus.

The gut bacterial has major impact on the brain development, behaviour and host immune system through the microbiota-gut-brain axis.

The objective of the research is to establish the role inflammation induced by gut dysbiosis plays in behavioural changes of patients suffering from major depressive disorders.

Clinical data and preclinical experiments were used to elucidate the role gastrointestinal bacterial play in the development and functional physiology of the nervous system and because of the bidirectional communication between the enteric nervous system in the gut and the central nervous system, through the vagal plexus, blood circulation and endocrine system; it was discovered that the appropriate population of intestinal microbiota affect the immunological state of the brain.

The intestinal microbiota has been able to maintain the attenuation and regulation of pro-inflammatory biomarkers in the brain and such had assisted in the healthy state of the brain; however, a disruption of gastrointestinal organisms in a condition called dysbiosis could result in breakdown of protective gastrointestinal mucosa barrier resulting in leaky gut and consequently, the permeability of the gut lining and migration of some bacteria, to the brain through the vagal networks and other channels.

These pathophysiological cascades appear to be triggered or sustained and reinforced by chronic inflammatory condition involving increased circulating markers of inflammation, which are able to cross the blood brain barrier to activate the microglia.

Studies in depression suggest that inflammatory biomarkers such as C-reactive protein can be used to enrich samples for anti-inflammatory clinical trials for depression that target inflammation-related symptoms such as anhedonia and anxiety.

Although, still at the developmental stages, imaging of neuroinflammation will help establish a target in the brain to further facilitate the testing of anti-inflammatory therapies for depression.

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Discriminating between bipolar disorder (BD) and behavioral variant Frontotemporal Dementia (bvFTD) is a clinical challenge as it is still based on clinical judgement, which often leads to misdiagnosis. This challenge is particularly pronounced in cases involving the C9orf72 hexanucleotide expansion, a genetic factor responsible for a substantial portion of familial FTD cases, as in these patients the development of late psychoses is particularly frequent. Moreover, individuals with C9orf72 bvFTD are also characterized by behavioral changes that resemble those seen in late-life BD, especially during the early stages of the disease. This raises questions about whether the clinical similarities between BD and bvFTD are rooted in specific alterations within the brain networks involved in cognitive processing or in selective genetic and epigenetic mutations. In light of this, our recently published neuroimaging study has shed light on the presence of distinctive structural and metabolic characteristics in elderly individuals with BD and bvFTD. These findings offer valuable neurobiological insights that may lead to differentiate between bvFTD and elderly BD patients.

Building on our previous research, this study further explores the existence of similar epigenetic expression patterns in plasma neural derived extra cellular vesicles (NDEs), such as miRNA and lncRNA, and seeks to correlate these epigenetic data with shared or distinct biological markers obtained through structural Magnetic Resonance Imaging and [18F]-fluorodeoxyglucose (FDG)-Positron Emission Tomography (PET).

We will plan to conduct statistical analyses on epigenetic and neuroimaging data on C9orf72 and sporadic bvFTD as well as on late-and early-onset BD patients and on healthy controls. Additionally, A PET study will be also performed on a subpopulation of these patients.

Our hypothesis posits that selective epigenetic modifications may impact the brain’s structure and function, in a way that can change the glutamatergic neurotransmission in prefrontal regions, with subsequent indirect effects on subcortical areas.

Our findings will not only help identifying the specific biological signatures of BD and bvFTD, which might have important implications not only in prevention but also in differential diagnosis and treatment, but also offer insights into potential targets for slowing the onset and progression of the structural alterations characterizing these disorders.

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Tourette’s syndrome (TS) is a disorder characterized by repetitive, involuntary movements, and vocalizations known as tics. While there are existing treatment options, there is a growing need for novel pharmacological approaches to manage the symptoms of TS effectively. This study delves into the emerging field of using cannabinoids as a potential treatment for Tourette’s syndrome.

The primary objectives of this review are to examine the current evidence base for the use of cannabinoids in the treatment of Tourette’s syndrome, to assess the biological rationale supporting the use of cannabinoids in managing tic severity, to provide insights into the results of existing clinical trials involving cannabinoids and Tourette’s syndrome, and to draw conclusions regarding the potential efficacy and safety of cannabinoid-based treatments for TS.

Narrative review of the available scientific literature.

There is a strong biological rationale for how cannabinoids could impact tic severity. The endocannabinoid system plays a crucial role in regulating various physiological processes, including motor control and neurotransmitter release. Activation of cannabinoid receptors in the brain may modulate these processes, potentially reducing tics. While limited, two small randomized, placebo-controlled trials of THC have been conducted in TS patients. These trials suggested potential benefits of cannabis-derived agents in reducing tic frequency and severity. Self-report and examiner rating scales demonstrated significant improvements in tic symptoms. The trials indicated that THC treatment did not result in significant adverse effects in TS patients.

The exploration of cannabinoids as a treatment option for Tourette’s syndrome is promising but requires further investigation. The biological mechanisms through which cannabinoids may affect tic severity in TS are sound, suggesting their potential as a therapeutic option. Existing trials with THC have shown encouraging results, demonstrating a reduction in tics without significant adverse effects. However, the limited number of trials warrants caution in drawing definitive conclusions. Despite the promising findings, the overall efficacy and safety of cannabinoid-based treatments remain largely unknown. Further trials are essential to address dosing, active ingredients, optimal administration, and potential long-term effects. Clinical use should be approached with caution. While early evidence is encouraging, additional rigorous studies are needed to establish the safety and efficacy of cannabinoid-based treatments for this disorder.

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Vitamin B12 deficiency gives rise to a wide spectrum of hematological, gastrointestinal, psychiatric, and neurological disorders. Notable among the neuropsychiatric symptoms are mood disturbances, cognitive decline, and psychotic manifestations.

We present a case of a woman with neuropsychiatric symptoms linked to vitamin B12 deficiency to highlight certain organic aetiologies with psychiatric symptoms in the foreground.

We discussed through a clinical case and a literature review, the relationship between neuropsychiatric symptoms and vitamine B12 deficiency in the context of biermer’s disease.

We presented a patient aged 51-years-old without neurological or psychiatric history, she was hospitalised in a psychiatry department for behavioral disturbances, hetero-aggression, and incoherent speech. The psychiatric examination revealed distant contact, inappropriate affects, disorganized speech with persecutory delusions, memory problems, and poor insight. Neurological et physical examinations were normal, and cerebral magnetic resonance imaging (MRI) showed no abnormalities. First, haloperidol 25mg was prescribed, however, there was only partial improvement. Complete blood counts revealed macrocytic anemia (Hemoglobin: 8 g/dL, mean corpuscular volume: 106 fL). Her serum B12 assay was 48.19 pmol/L.Given these results we proceed to a Fundic biopsy, performed by fibroscopy, that revealed fundic atrophy and intestinal metaplasia compatible with Biermer’s disease. Vitamin B12 replacement therapy began with hydroxocobalamin at 1000 μg/day intramuscularly for 15 days, followed by 1000 μg every 15 days for one month. Subsequently, there was a remarkable improvement in psychotic symptoms and cognitive function. Follow-up assessments demonstrated a return to baseline functioning.

This case, coupled with prior studies, emphasizes the importance of considering vitamin B12 deficiency in the differential diagnosis of neuropsychiatric symptoms. Therefore, prompt diagnosis and treatment of vitamin B12 deficiency are imperative in preventing potential irreversible neurological damage.

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Olfactory loss (including short-term) initiates neural reorganization processes in the brain, but the central mechanisms of this largely remain unknown.

We aim to conduct a neurophysiological study of neocortical mechanisms for the effects of olfactory sensation on functional activity of human brain under temporary obstruction of nasal breathing.

123 healthy volunteers (76 female and 47 male students aged 18 to 23 years)participated in this study.EEG was registered during the rest state (5 min), olfactory blockage (5 min), under odor stimulation with the lemon essential oil (5 min) and renewal of nasal breathing (5 min). We estimated the spectral power density and the levels of coherence of all the frequencies from 0.2 to 35 Hz.

The onset of orthonasal olfactory sensory blockage was accompanied by an increase in the power of processes of local synchronization of beta frequency in the caudal regions of the brain, with simultaneous enhancement of the coherence of the theta band in parietal-occipital zones and a certain enhancement of the interfrontal and intrahemispherical left-side and right-side interactions in the beta2-subband. Thus, the sudden cessation of olfactory detection led to activation of thalamo-cortical loops and top-down control systems (search for the olfactory signal): that is an active orienting process (triangle of increase in F4-T4-P4 connections) with emotional coloring (the caudal localization of the coherence changes in the theta band). The prolongation of the nasal blockage, despite the possibility of activation of the retronasal route of odor perception and odorized air, was accompanied by a definite inhibition of distant interactions in the posterior regions of the brain in the theta-band and a significant decrease in right-brain long-distant and parietooccipital beta2-subband functional connectivity. Restoration of nasal breathing and olfactory perception is accompanied by sufficiently powerful activation of interhemispheric long and short distance information interactions in the theta1,2 and beta1 frequency bands.

Our data indicated that cessation and restoration of olfactory perception lead to an increase cognitive activity, the development of memory processes, the current sensory and cognitive-emotional control of behavioral reactions, focusing attention, assessment of the significant stimulus.

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Hyperprolactinemia (HPL) is a condition associated with disturbing consequences. Antipsychotic medications are one of the main causes of nontumoral hyperprolactinemia. Prolactin release in the hypothalamic tuberoinfundibular tract is increased through dopaminergic inhibition, which occurs more frequently with high- potency typical antipsychotics (40%–90%). Less commonly than typical antipsychotics, atypical antipsychotics can also result in hyperprolactinemia. In the presence of symptoms, clinicians frequently struggle with the decision of whether to stop using the suspected offending agent, lower the dosage, switch to another medication, or even add a full or partial dopamine agonist to the patient's current treatment. The issue is exacerbated by the fact that finding a suitable agent for each patient is sometimes a challenging task.

Due to the partial D2 receptor agonistic activity of aripiprazole, there is enough dopaminergic tone to continue the inhibition of prolactin release. Aripiprazole has been recommended in literature either as an adjunctive treatment in low doses or as a switch in therapy.

In the Psychiatric clinic of the General Hospital of Corfu, a low-dose (5mg/day) of aripiprazole is being used as adjunctive therapy in patients with antipsychotic-induced hyperprolactinemia. More specifically in total 42 subjects, 19 male and 22 female, with a mean prolactin level of 862ng/ml, were introduced to the prior therapy. We whereupon conducted prolactin measurements to evaluate the response at the first, the third, and the sixth month of treatment.

Of the 42 subjects, 38 responded with an average reduction of prolactin to the level of 530ng/ml (mean reduction 38,5%).

Having noticed the beneficial effect of low-dose Aripiprazole in patients with antipsychotic-induced hyperprolactinemia, we consider it appropriate that the literature recommendations concerning this additional use of aripiprazole should not be overlooked in clinical practice.

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Personality neuroscience employs a broad range of methods to identify the neurobiological mechanisms of complex psychological phenomena. The role of the insula is often associated with its involvement in emotion processing.

The study aims to identify the associations between neural activity in the anterior insula cortex (AInC) and self-stigma (or its components) in a scoping review.

We searched in PubMed (MEDLINE), PsychINFO, EMBASE via the Ovid platform through September 21st, 2022. Included studies had to use fMRI to assess neurophysiological markers in AInC, and to include a measure of association between fMRI results and a measure of self-stigma and/or its components as assessed by a scale or questionnaire in participants aged 18-65 y.o. The PRISMA-ScR checklist was used.

After full-text screening 10 of 206 original researches were chosen for the final analysis (Table 1).Table 1:

Included studies in the analysis.

In 5 studies, the results were presented with MNI-space coordinates. Figure 1 illustrats the regions of local activity change maxima according to MNI-space coordinates based on the results of the included studies in the analysis.

Neural activation in the regions of the AInC was positively associated with greater levels of social rejection sensitivity and other components of self-stigma in 9 studies. Reduced activity was observed in only one study (Lindner et al., PLoS One. 2014; 9(1): e85014) among highly self-stigmatized patients with schizophrenia. This finding may reflect a biological manifestation of deficits in self-awareness and affective processing in schizophrenia.

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Associations between neural activity changes in specific brain regions and levels of self-stigma and/or its components, as reported in included neuroimaging studies, have the potential to shed light on the neurobiological mechanisms underlying such a complex psychological phenomenon as stigma.

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The sense of agency (SoA) indicates a person’s ability to feel her/his own motor acts as actually being her/his, and through them to exert control over the course of external events. Disruptions in SoA may profoundly affect the individual’s functioning, as observed in several neuropsychiatric disorders.

This is the first article to systematically review studies that investigated intentional binding (IB), a quantitative proxy for SoA measurement, in neurological and psychiatric patients.

Eligible were studies of IB involving patients with neurological and/or psychiatric disorders. The research adhered to the guidelines outlined in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA).

We included 15 studies involving 692 individuals. Risk of bias was low throughout studies. Eligible studies dealt with data from 357 patients with neuropsychiatric disorders matched with 335 HCs. Of included patients, 95 were with schizophrenia (SCZ), 30 with a putative prodromal psychosis (PP), 21 with borderline personality disorder (BPD), 66 with Parkinson’s disease (PD), 38 with an autism spectrum disorder (ASD), 29 with functional movement disorders (FMDs), 25 with Gilles de la Tourette syndrome (GTS), 52 with anorexia nervosa (AN; 22 with active disorder and 30 after they had recovered), and 10 with Cortico-Basal syndrome (CBS).

Temporal binding was calculated in eleven studies using variations of the experimental procedure introduced by Haggard et al. (Haggard et al. Nat Neurosci 2002;5 382-385)(Figure 1, A), while four studies utilized a different paradigm named interval estimation (IE)(Figure 1, B).

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Abnormally increased action-outcome binding was found in schizophrenia and in patients with Parkinson’s disease taking dopaminergic medications or reporting impulsive-compulsive behaviours. A decreased IB effect was observed in Tourette’s disorder and functional movement disorders whereas increased action-outcome binding was found in patients with cortico-basal syndrome. The extent of IB deviation from healthy control values correlated with the severity of symptoms in several disorders. Inconsistent effects were found for autism spectrum disorders, anorexia nervosa, and borderline personality disorder. Findings pave the way for treatments specifically targeting SoA in neuropsychiatric disorders where IB is altered.

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Autism Spectrum Disorders (ASD) is diagnosed when an individual displays irregularity in three key domains: social development, communication, and repetitive behavior/obsessive interests.

The theory of mind-blindness in ASD suggests that individuals on the autism spectrum exhibit deficiencies in the typical empathic process, relative to their mental age.

Empathy comprises two primary components: firstly, the capacity to attribute mental states to both oneself and others, and secondly, experiencing an emotional response that aligns with the mental state of the other person.

This study aimed to synthetase the latest evidence about the neuropsychiatric basis of empathy in ASD.

A review was conducted, drawing on reputable sources (PubMed and Web of Science databases).

A neural basis of empathy has built on a model first proposed by Brothers. It was suggested that social intelligence was a function of three regions: the amygdala, the orbitofrontal and medial frontal cortex, and the superior temporal sulcus and gyrus - the “social brain”. Abnormalities in autism have been found in the amygdala, the orbito and the medial frontal cortex.

Amygdala has been implicated primarily in fear perception of facial expressions, as well as in the recognition of other emotions such as sadness and “social” emotions. In addition to fear perception, the amygdala has also been implicated in related processes including eye gaze, affective memory, olfactory learning, and social judgment.

To date, findings on amygdala structure in autism have been mixed, with studies indicating reduced and increased volumes, as well as nonsignificant differences.

ASD is one of the most heterogeneous neurodevelopmental disorders, and cognitive theories as well as structural findings have linked likely frontal lobe abnormalities to the social and cognitive profiles of autism.

Future studies may elucidate existing data by taking advantage of new and infrequently used data acquisition technologies such as Transcranial Magnetic Stimulation.

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Attention-deficit/hyperactivity disorder (ADHD) is one of the most prevalent neurodevelopment disorders in the world. Clinical guidelines for ADHD recommend multimodal treatment approaches, with current evidence suggesting that medication, including methylphenidate and various amphetamine formulations, in conjunction with psychosocial treatment are most effective in the short-term and long term. Over the last decade, an increasing number of studies investigating non-pharmacological treatments have been published, such as cognitive therapy, Neurofeedback (NF), Transcranial direct current stimulation with the aim of treating ADHD patients.

We comprehensively reviewed literature searching for studies on the effectiveness and specificity of NF for the treatment of ADHD. The aim of this review is to understand if there is scientific evidence in using of electroencephalogram (EEG)-Neurofeedback for treating patients with ADHD.

We did a non systemathic review using pubmed and google schoolar databases in order to analyze the influence and effects of therapy in patients diagnosed with ADHD and under treatment based on EEG Neurofeedback. We analyzed 18 systhematic reviews and metha-analysis and 2 case control studies.

Accourding to the systhematic reviews results showed positive and significant effects in the visual memory, attention and visual recognition (spatial working memory). EEG also showed improvement in upper alpha activity in a resting state (open-eyed) measured from the occipital area, which similarly indicated improvement in the cognitive domain (attention). Compared to non-active control treatments, NF appears to have more durable treatment effects, for at least 6 months following treatment.

In conclusion, it is possible to affirm that a neuromodulating effect of the therapy positively influences cognitive processes, mood, and anxiety levels in patients with ADHD and is associated with significant long-term reduction in symptoms. Though limitations exist regarding conclusions about the specific effects of NF, the review documents improvements in school, social, and family environments. However, future efforts should focus on implementing standard neurofeedback protocols, ensuring learning, and optimizing clinically relevant transfer and more studies are needed for a properly powered comparison of follow-up effects between NF and active treatments and to further control for non-specific effects.

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There is strong evidence that delusions are associated with cortical and subcortical structural alterations. However, whether these abnormalities differ in different types of delusions within schizophrenia spectrum disorders remains unclear.

We aimed at exploring structural neural patterns underlying influence/persecutory delusions across diagnostic categories within the schizophrenia-spectrum disorders.

Twenty six right-handed patients with delusional disorder (n=7) and schizophrenia (n=19), presenting with delusions were divided in two clinical subgroups. The first one was presented with persecutory delusions (n=12, 20.2-55.4 years, mean age 36.0±11.6, 2 females) and the second with delusions of influence (n=14, 21.2-47.6 years, mean age 36.7±8.4, 2 females). The control group consist of 26 matched healthy controls (20.2-53.6 years, mean age 36.3±9.9, 4 females). All participants underwent structural MRI at 3T scanner. MRI images were processed via FreeSurfer 6.0 to quantify cortical thickness (CTh) and volumes for subcortical and brainstem (midbrain, pons, superior cerebellar peduncle and medulla) structures.

Compared to healthy controls, patients with delusions of influence showed decreased gray matter thickness in 17 cortical regions (Figure, A), and decreased volumes of thalamus bilaterally (left: F(1,35)=9.0, p=0.005; Cohen’s d=−0.8; right: F(1,35)=8.0, p=0.008; Cohen’s d=−0.8), left hippocampus (F(1,35)=8.8, p=0.005; Cohen’s d=−0.8), midbrain (F(1,35)=11.0, p=0.002; Cohen’s d=−0.9) and pons (F(1,35)=8.2, p=0.007; Cohen’s d=−0.8). Conversely, patients with delusions of persecution showed decreased thickness only in 4 cortical regions of the right hemisphere (figure, B) and no alterations in subcortical volumes compared to healthy controls.

No differences in cortical or subcortical measures between two clinical subgroups survived corrections for multiple comparisons. No correlations between structural alterations and total PANSS or BABS scores were found in either clinical groups.

Figure. Clusters of decreased cortical thickness according to atlas of Desikan et al. (2006) in delusions of influence (A) and delusions of persecution (B) subgroups compared to healthy controls.

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The findings suggest that patients with delusions of influence have more pronounced cortical, subcortical and brainstem structural deficit as compared to patients with delusions of persecution. However, the limited sample size and the lack of correlations with clinical scores do not allow to conclude definitely whether the revealed structural abnormalities underlies delusions of influence, which should be elucidated via further research.

This study was supported by RFBR grant 21-515-12007

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Autobiographical memory is known to be disturbed in schizophrenia. In addition, a leading theory of auditory hallucinations (AVH) is that they are intrusive – typically negative – autobiographical memories that are misinterpreted as perceptions.

The aim of this study was to examine the brain functional correlates of recall of negatively emotionally valanced autobiographical memories in patients with schizophrenia, with a longer term aim of comparing patients with and without AVH.

11 patients meeting DSM-5 criteria for schizophrenia or schizoaffective disorder and 10 age, sex and estimated premorbid IQ-matched healthy controls have so far taken part.

Participants underwent functional MRI in a 3T scanner while performing a task requiring them to recall autobiographical memories in response to individually tailored pairs of cue words. The cue words were based on autobiographical memories previously elicited in an interview with each patient and were designed to evoke the same memory. The cue words were presented in 10 20-second blocks interspersed with blocks where the subjects viewed cue words that did not evoke autobiographical memories. Brain activations were examined in three contrasts of interest: memory evoking words vs baseline, neutral words vs baseline and memory evoking vs neutral words.

Pre-processing and analysis were carried out with the FEAT module included in the FSL software. Statistical analysis was performed by means of a General Linear Model (GLM) approach.

In the memory evoking vs baseline contrast the patients showed hypoactivation in the medial frontal cortex compared to the healthy controls (Figure 1). There were no differences in activation between the patients and the controls comparing the memory evoking and neutral cues.

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The finding of hypoactivation in the medial frontal cortex compared to low level baseline in patients with schizophrenia suggests dysfunction in the default mode network, which is known to activate during recall of autobiographical memories.

These preliminary results suggest that recall of negative autobiographical memories in patients with schizophrenia is associated with reduced activity in the default mode network. A planned larger sample of patients and controls will be used to examine activations in patients with and without AVH.

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Nonsuicidal self-injury (NSSI) is defined as deliberate and direct damage to one’s body tissues without any suicidal intent. NSSI is now recognized as a major risk factor for suicide and is prevalent among adolescents, with prevalence rates ranging from 7.5% to 46.5%, leading to increased interest in the pathophysiology of NSSI. This study aimed to examine cortical gyrification morphology, a neurobiological index of cortical folding and patterning, among unmedicated individuals with NSSI, which is prevalent in adolescents and young adults.

The main objective of this study is to compare cortical morphological abnormalities between individuals with NSSI and controls in terms of the local gyrification index (LGI), the ratio of the smooth cortical surface area at each vertex to the corresponding sulcal folds. In addition, we hypothesized that the LGI, a stable neurodevelopmental marker of cortical and subcortical circuit intergrity, would correlate with clinical measures in youth with NSSI.

A total of 101 individuals with NSSI and 100 age-, gender-, and handedness-matched controls completed self-report questionnaires and structural magnetic resonance imaging (MRI) data were acquired on a 3T Siemens scanner. A surface-based analysis was conducted using the Computational Anatomy Toolbox (CAT12) in Statistical Parametric Mapping (SPM12). Partial correlation analysis was also performed using R software to investigate the association between the LGI values extracted from the region of interest (ROI) and clinical symptoms, including depression, anxiety, emotion dysregulation, and anhedonia in individuals with NSSI.

Individuals with NSSI showed significantly increased LGI in the right insula sulcus and left superior temporal sulcus (STS), along with decreased LGI in the right calcarine and left superior parietal sulcus (SPS), compared to controls (5000 permutation correction, threshold-free cluster enhancement with a threshold of p < .05). In addition, higher LGI in left STS was correlated with greater scores of the Beck Anxiety Inventory (r = 0.22, p < .05) and of the Impulse Control Difficulties subscale of the Difficulties in Emotion Regulation Scale (r = 0.34, p < .001). Conversely, reduced LGI of the right calcarine was associated with a higher score on the Anhedonia subscale of the Beck Depression Inventory (r = -0.23, p < .05) within individuals with NSSI.

This study identified hypergyria in the right insular and left STS and hypogyria in the right calcarine and left SPS in individuals with NSSI. The former pattern was associated with anxiety and impulse control difficulties, and the latter was with anhedonia. This study is the first to alter distinct neurodevelopmental patterns of local gyrification and their correlations with clinical manifestations in individuals with NSSI.

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Vocal and motor tics are characteristic for Tic disorders (TD) and Tourette’s syndrome (APA 2022) . Because of the pathophysiology of the disorders not being fully understood and the presence of the externally measurable symptoms; great attention has been paid to the cortico-striatal regions of patients with TD . In addition to the alterations in motor symptoms patients can experience a premonitory urge (PU) which can be felt before a tic (Reese et al. Behav. Ther. 2014; 45 177–186) . Previous studies found an impact of these urges on sensory perception, attention and social cognition as well as an involvement of the brain regions insula, anterior cingulate cortex (ACC) and the temporoparietal junction (TPJ) (Seeley J. Neurosci. 2019; 39 9878–9882, Kucyi et al. J. Neurophysiol. 2012; 108 3382–3392, Uddin et al. Brain Topogr. 2019; 32 926–942) . These findings lead to the idea of altered functional connectivity of the salience network (SN) in patients with TD.

This study aims to investigate the connectivity changes of the SN in patients with TD. We examined functional resting-state scans of patients with TD and searched for possible correlations between the tic and PU severity and the connectivity of the SN.

21 Patients (mean age: 30.9 years ± 10.0 [range = 19–57], 6 females) diagnosed with TD, and 20 healthy controls (mean age: 29.7 years ± 8.9 [range = 18–50], 5 females) underwent a resting-state fMRI scan. Functional and anatomical images were conducted on a 3T Siemens Prisma fit MRI scanner. PU and tic severity were measured by the Premonitory Urges for Tics Scale (PUTS) and the Yale Global Tic Severity Scale (YGTSS). The connectivity analysis of the resting-state scans was done using the CONN toolbox v21.a. After pre-processing and de-noising steps, a whole-brain seed-based connectivity analysis was carried out with the seeds being the major cortical nods of the SN. For the correlation analysis a linear regression of the YGTSS score/PUTS score and the brain connectivity of the seed regions was conducted.

The PUTS score was 25.3±5.4 (range 10-33) and the YGTSS total tic score was 23.1±7.9 (range 10-38) for the patients. The connectivity analysis revealed a significant difference in connectivity between the groups for the ACC, the right insula and the TPJ. A negative correlation between the YGTSS scores and the connectivity of the left insula and the right superior frontal gyrus (SFG) was shown in the correlation analysis. No significant correlation was found for the PUTS scores in the investigated seed regions.

The right SFG mediates motor urgency and inhibitory control. Since we found a negative correlation between the insula and the right SFG regarding to higher YGTSS scores of the patients, our results might shed some light on the pathophysiology regarding lower inhibitory control in patients which experience higher tic severity.

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Major Depressive Disorder (MDD) stands as a prevalent psychiatric condition within the general population. Despite extensive research efforts, the identification of definitive diagnostic biomarkers for depressive disorders remains elusive. Currently, machine learning methods are gaining prominence in the diagnosis of medical illnesses.

This study aims to construct a machine learning-based prediction model for Major Depressive Disorder (MDD) by harnessing diffusion tensor imaging (DTI) data.

The DTI datasets comprising MDD (N=83) and Healthy Control (N=70) groups were procured from the cohort study of Anxiety and Depression conducted at the National Center for Mental Health in South Korea. A machine learning method using a decision tree algorithm was employed to select relevant brain regions and establish a robust diagnostic model. Features associated with white matter (WM) tracts were chosen through recursive feature elimination.

Demographic characteristics, including age, sex, and handedness, displayed no significant differences between the MDD and Healthy Control groups. However, the total score of the Beck Depression Inventory was notably higher in individuals with MDD compared to Healthy Controls. A diagnostic model was crafted using the decision tree algorithms to distinguish between the two groups. The model demonstrated the following classification performance metrics: accuracy (65.6% ± 8.5), sensitivity (66.6% ± 12.5), and specificity (64.7% ± 13.6). Furthermore, through recursive feature elimination, specific neuroanatomical features tied to brain structures such as the inferior cerebellar peduncle, posterior thalamic radiation, cingulum (hippocampus), uncinate fasciculus, and tapetum were identified.

Despite of limited performance of classification, a machine learning-based approach could provide insights into the development of a diagnostic model for MDD using neuroimaging data. Furthermore, these features, derived from DTI-derived data, may have implications for understanding the neural underpinnings of major depressive disorder.

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The fNIRS is an optical brain monitoring technique which uses near-infrared spectroscopy for the purpose of functional neuroimaging. Using fNIRS, brain activity is measured by using near-infrared light to estimate cortical hemodynamic activity which occurs in response to neural activity. In the aspect of psychiatry fNIRS is a tool that can potentially facilitate the clinical diagnostic process and identify stages of psychiatric illnesses by providing objective and quantifiable evidences of brain changes. However, this will require specific cerebral haemodynamic patterns to be validated in larger clinical populations with specific psychiatric disorders.

Our team decided to set a fNIRS system to find out the difference in prefrontocortical (PFC) activity pattern between healthy and anhedonic population. This abstract has been created for introduce our first findings about the difference in PFC activity under emotionally positively or negatively coloured stimuli in healthy population.

We have measured 5 healthy adults, non-anhedonic participants under emotionally different visual and acustic stimuli with the use of NIRX/NIRScout system with the view of our prefronto-temporo-parietal montege.

Fig 1 We devided our experimental tools into 4 individual 20 second long parts:

Passive neutral visual or acustic stimuli for baseline (watching a black dot or scilence)

Passive visual stimuli (watching a single picture)

Active visual stimuli (choosing from photo collage) to detect contrast of cortical background activation

Passive acustic stimuli (listening sounds)

In total, we defined emotionally, two neutral, four positive and four negative stimuli in our experimental setting.

Softwares: We used HOMER3 for analyzing our datas and estimate hemodinamic reponse factor (HRF) using general linear matrix (GLM) regression. We used AtlasViewer for reconstructing HRF image onto the Colin27 digitalised brain model. And we also used SPSS for statictical analysis between stimuli types and HRF means.

Fig 2 Significant HRF differences were measured in the dominant hemisphere dorsolateral prefrontal cortex (DLPFC) between the influence of each emotionally negative and positive stimuli (p<0.001). The level of DLPFC activity was positively influenced by emotionally positive stimuli (p<0.001).

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Fig 3 Our fNIRS experimental system is a suitable tool to measure and model the pattern of prefrontal cortical activity.

Based on the measured hemodynamic values, we detected a significant activity difference in the dominant hemisphere DLPFC during emotionally positive and negative stimuli, the extent of which is positively influenced by emotionally positive stimuli.

The left DLPFC appears to be a promising target for our next studies of anhedonia.

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It is still being discussed whether treatment-resistant schizophrenia (TRS) is a biological subtype which differs from non-treatment-resistant schizophrenia or is it a more severe condition that affects brain worse than non-treatment-resistant schizophrenia. However, there are few and heterogeneous studies and the etiology of TRS remains quite unclear.

This study aimed to explore cortical and subcortical morphometric characteristics in TRS patients and its associations with the clinical features. The pilot stage comprises the comparison to the mentally healthy subjects.

21 right-handed male patients (mean age 28.99 ± 8.08 years) fulfilling TRS criteria and 21 matched healthy controls (mean age 29.35 ± 7.41 years) underwent T1-weighted structural MRI at 3T Philips scanner and clinical examination. Images were processed using FreeSurfer 7.1.1. Cortical thickness and area, volumes of subcortical structures and separately volumes of the amygdala nuclei and hippocampal subregions were compared between groups. The morphometry data, PANSS (Positive and Negative Syndrome Scale), CDSS (Calgary Depression Scale for Schizophrenia) and daily chlorpromazine equivalent doses of antipsychotics were included in correlational analysis. Results were considered significant if they retained significance after correction for multiple comparisons.

Compared to healthy controls, TRS patients showed decreased gray matter thickness in frontal, temporal, parietal, occipital, cingulate and insular regions (Figure 1). The temporal lobe showed the most prominent thinning of the cortex. The volumes of the amygdala, hippocampus (Figure 2) and nucleus accumbens, a number of amygdala nuclei and hippocampal subregions bilaterally were also decreased in TRS patients. The volume of the right globus pallidus, on the contrary, was increased (Figure 2). No correlations between altered cortical thickness, PANSS (positive, negative, general psychopathology scales and total score), CDSS and chlorpromazine equivalent doses of antipsychotics were found.

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The widespread gray matter cortical and subcortical loss in TRS finds confirmation in the literature. The increased globus pallidus volume is an unexpected and intriguing result. Other studies demonstrated conflicting results on that point. Some studies reported possible therapy influence, others suggested possible associations with symptoms. We did not find any correlations with psychometric or therapy characteristics. It is possible that there are non-linear relationships or relationships that exist only at a certain stage of the disease. As for therapy, patients took individual medication, consisting of various antipsychotics and drugs from other pharmacological groups, and such heterogeneity could affect the results of the study. Further research is going to be carried out.

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There is growing evidence of excitation / inhibition (E/I) balance abnormalities in schizophrenia, which might be associated with abnormal gamma frequency oscillations and glutamate concentrations. However, to the best of our knowledge, only one multimodal study have examined such associations between EEG and metabolite characteristics in patients at clinical-high risk of psychosis (CHR) so far.

We aimed to investigate potential associations between GLX (glutamate + glutamine) levels and resting-state gamma-band power in CHR individuals and healthy controls (HC).

Twenty right-handed male patients (16-27 years, mean age 19.9 ± 2.7) fulfilling CHR criteria and 19 healthy male controls (16-27 years, mean age 21.6 ± 3.6) underwent resting-state EEG (16 leads; 10−20 system) and MR spectroscopy at 3T MRI scanner with voxels of 30×30×30mm located in left and right medial prefrontal cortex. Spectral analysis with estimation of gamma-band power (30-45 Hz) were conducted. MEGA-PRESS acquisitions were analyzed with jMRUi (ver. 5.1 Alpha), levels of GLX were calculated as a ratios to creatine + phosphocreatine (GLX/Cr). Gamma-band (30-45 Hz) spectral power and GLX/Cr were compared between groups. Correlations between EEG and metabolite data were analyzed with regression model including age and chlorpromazine equivalents as covariates.

Compared to healthy controls, patients showed reduced spectral gamma-band power in 6 leads (Table). No alterations in GLX/Cr were detected. Positive correlations between altered gamma-power in all leads (except Cz) and GLX/Cr in left medial prefrontal cortex were revealed in CHR (F3: r=0.51, p=0.006; F8: r=0. 54, p=0.004; C3: r=0.37, p=0.037; Pz: r=0.51, p=0.039; P4: r=0.56, p=0.009). No correlations in HC group were found. Chlorpromazine equivalents did not correlate with GLX/Cr of gamma power in CHR group.Table.

Results of between-group comparisons corrected for multiple comparisons

The findings suggest that clinical-high risk of psychosis is associated with widespread alterations in resting-state gamma-band power. Positive correlations of such alterations with GLX/Cr and absence of such correlations in HC group are presumably indicative of disturbances in the excitation / inhibition balance in CHR individuals.

This study was supported by RFBR grant 19-29-10040

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