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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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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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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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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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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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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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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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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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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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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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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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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Panksepp paved the way for neuropsychoanalysts to better delineate the differences between emotions, feelings, and affect, and their evolutionary purposes. Affect pertains to an individual’s capacity to engage in emotional responses to stimuli, events, memories, and thoughts, while feelings denote the conscious perceptions of emotions, which are primarily social in nature.

Feelings are personal and biographical, while affect remains largely impersonal. Panksepp’s theory of basic affective systems in mammals, dividing emotions into positive and negative categories, is another major contribution to neuropsychoanalysis. Three primary emotions -joy, fear, and disgust- have been identified in humans, which are associated with specific peptides and monoamines (e.g., dopamine and endorphins for joy, norepinephrine and CRH for fear, serotonin and substance P for disgust). These basic emotions are thought to have evolved to address basic life tasks in a phylogenetic and ontogenetic primary stage.

This study aims to provide an overview of Jaak Panksepp’s theories and assertions on the journal Neuropsychoanalysis.

The authors employed a neuropsychoanalytic approach to analyse articles published in the Neuropsychoanalysis journal between 2015-2023.

Emotions primarily function to maintain homeostasis and protect the organism, as in fight or flight responses. In social animals, emotions can sometimes be recognized among individuals of the same and different species. The neurobiological basis of emotional transfer and empathy-like behaviors shed light on cross-species emotion transfer.

The facial feedback hypothesis and the interoceptive inference theory are also discussed as examples of theories for the recognition of emotions as well as the neural mechanisms involved in emotion perception and recognition.

Jaak Panksepp’s valuable insights shed light on the mysteries of human affect, and lay the foundation for future work in the field.

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The modern understanding of AD allows us to consider it through the constructs of “vulnerability” and “stability” of the brain in relation to the pathological effects of neurodegeneration. To describe the resistance of the brain to a developing lesion due to a pathological process, the concept of “reserve” is proposed.

A systematic review of scientific studies was conducted.

The review includes an analysis of full-text literature sources.

Resilience models based on reserves are described, which can be broadly divided into cerebral and cognitive reserve models. The quality of the brain substrate underlies the cerebral reserve. Its role and power are determined by the ratio of healthy/affected neurons, the integrity of synaptic connections, and the size of the brain/ It seems to us that the conditions that promote or hinder the functioning of the brain should also be taken into account when characterizing the cerebral reserve. Cognitive reserve is determined by the phenomena of mental processes and functions. It includes the individual’s involvement of the individual in various cognitively stimulating activities throughout life. Cognitive reserve plays a decisive role when it comes to determining the effectiveness of the activation of additional areas or the implementation compensatory strategies, behaving more flexibly and dynamically than the passive threshold. Brain and cognitive reserve models cannot be considered mutually exclusive. They reflect different categorical levels: substrate and functional. The cerebral reserve system is the morphological basis of the cognitive reserve. In fact, we can talk about a single cerebral-cognitive reserve.

The reserve concept states that there are individual differences in the adaptability of the functional processes of the brain that allow some people to cope with age-related and disease-related brain changes better than others. The reserve plays a protective role, postponing clinical manifestations and ensuring that adequate cognitive functioning is maintained. There is a transition from the protective role of the reserve to the compensatory function. Even after anatomical signs of brain damage are observed, the time to clinical conversion can be modulated depending on the volume of the reserve. The protection mechanisms underlying the reserve concept are partially controllable, which allows building strategies for correcting cellular homeostasis, brain functions, behavioral and cognitive patterns. Understanding the mechanisms of aging and the determinants of life expectancy will help reduce age-related morbidity and promote healthy aging.

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Age-related changes of brain functional connectivity, in contrast to brain structure, are understudied in schizophrenia. Importantly, patients with schizophrenia demonstrate an increased difference between the brain-predicted age and chronological age indicating that brain structural aging may be accelerated in this mental disorder (Constantinides et al. Mol Psychiatry 2023; 28 1201-1209). Research on functional connectivity correlates of this process seems to be fruitful.

We aimed to search for the brain regions whose resting-state whole-brain functional connectivity is differently associated with brain-predicted age in schizophrenia patients compared to healthy controls.

Eighty-three male patients with schizophrenia (age range 17.3 – 52.3; mean age 32.1 ± 10.5) and eighty-seven male healthy individuals (age range 18.3 – 53.6; mean age 31.7 ± 10.0) underwent structural MRI and resting-state fMRI (Philips Ingenia 3T scanner). Brain-predicted age was individually estimated using a model trained on independent data based on 68 measures of cortical thickness and surface area, 7 subcortical volumes, lateral ventricular volumes, and total intracranial volume, all derived from T1-weighted MRI scans (Han et al. Mol Psychiatry 2021; 26 5124-39). The associations between the brain-predicted age and the whole-brain global correlation (GCOR) were compared between groups; t-contrasts were calculated (one-way ANCOVA covariate interaction via CONN; RRID:SCR_009550; www.nitrc.org/projects/conn). The chronological age was a covariate of no interest.

Schizophrenia patients had a higher difference between brain-predicted age and chronological age (T(168) = 2.1; p = .036; Cohen’s d = 0.32; 95% CI 0.02-0.63). Greater brain-predicted age in schizophrenia patients, compared to controls, was associated with lower functional connectivity of a region in the right Heschl’s gyrus, planum temporale, as well as central opercular and insular cortex with the rest of the brain (p < .001 voxelwise, p[FDR] < .05 clusterwise; Figure 1).

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Our results coincide with earlier findings on accelerated brain structural aging in schizophrenia. To the best of our knowledge, the present study is the first to indicate that this process is coupled with a decline of the whole-brain functional connectivity of a region located in the right temporal, insular, and parietal cortices, and this effect is not driven by chronological age. Further studies are needed to clarify the clinical and cognitive correlates of this decline of functional connectivity.

The study was supported by RSF grant project 22-25-00706.

None Declared

Impulsivity and compulsivity are natural behaviors controlled by brain mechanisms that are essential for survival in all species. Understanding these brain mechanisms may lead to targeted treatment strategies for these symptom domains when impulsivity and compulsivity become dysfunctional.

Pathological impulsivity and compulsivity characterise a broad range of mental disorders.

This study aimed to synthesise the latest evidence about the conceptualization of the impulsivity-compulsivity spectrum.

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

The concept of impulsivity can be defined as a predisposition toward rapid, unplanned reactions to internal or external stimuli without regard to the negative consequences of these reactions to the impulsive individual or to others. However, impulsivity is not always unplanned. Impulsive behaviours can be conceptualised as the core symptoms of a broad range of psychiatric disorders.

In contrast, compulsivity refers to repetitive behaviours that are performed according to certain rules or in a stereotypical fashion. Compulsivity is a tendency to repeat the same, often purposeless acts, which are sometimes associated with undesirable consequences.

Impulsivity and compulsivity may be viewed as diametrically opposed, or alternatively, as similar, in that each implies a dysfunction of impulse control. Each involves alterations within a wide range of neural processes, including attention, perception, and coordination of motor or cognitive responses.

The neurobiology of impulsivity and compulsivity may involve inhibitory neurotransmitters, excitatory neurotransmitters, the prefrontal cortex, and/or limbic dysfunction.

Impulsive and compulsive features may present at the same time or at different times during the same illness. Although both compulsive and impulsive disorders may be related to prefrontal cortex dysfunction, compulsive disorders would be related to hyperactivity and impulsive disorders to hypoactivity of the prefrontal cortex. Compulsiveness appears to be associated with increased frontal lobe activity, while impulsiveness may be associated with reduced frontal lobe activity.

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Body dysmorphic disorder (BDD) was considered an anxiety disorder in the DSM-IV, but in the DSM-V was added to the obsessive-compulsive and related disorders category. BDD is a psychiatric disorder characterised by an excessive, persistent, and distressful preoccupation with a perceived defect in appearance. These perceived defects are slight and are unnoticed by others. People with BDD usually have poor insight and are preoccupied with a perceived physical defect which causes them to check on it repeatedly. This leads to an impairment in psychosocial functioning, depression, and an increase in suicide risk.

Review how dismorphophobia (BDD) and obsessive compulsive syndrome intersect, the differences they present in symptomatology, prevalence and treatment.

Presentation of a patient’s case and review of existing literature, in regards to body dysmorphic syndrome and its similarities and differences with respect to obsessive compulsive syndrome.

There are common features between both disorders, which are genetic overlap, physical past traumatic events, sex ratio, trait of perfectionism and body image disturbance.

Studies have found the prevalence of BDD in patients with OCD in a large patient sample was 8.7% to 15% compared to 3% in non-OCD.

The risk of comorbidity of OCD-BDD is three times higher in samples with a primary diagnosis of BDD compared to those with a primary diagnosis of OCD with 27.5% and 10.4%, respectively.

BDD as well as OCD must be managed with pharmacological and psychotherapy treatment. A selective serotonin reuptake inhibitor is the recommended first-line medication for BDD, even if appearance beliefs are delusional in nature.

Serotonin reuptake inhibitor (SRI) doses and trial durations are similar to those used for OCD; higher doses and a longer treatment trial are recommended than those typically used for depression and most other disorders. Cognitive-behavioral therapy that is specifically tailored to BDD is the psychosocial treatment of choice. Simply treating BDD as if it were OCD is not recommended.

There are limitations included a restricted number of studies overall, an absence of studies comparing biological parameters, and the frequent inclusion of participants with comorbid body dysmorphic disorder and obsessive-compulsive disorder. The current nosological status of body dysmorphic disorder is somewhat tenuous and requires further investigation, with particular focus on dimensional, biological and aetiological elements.

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In recent years, there has been a growing interest in the potential consequences of disruptions in the inflammatory and immune systems on the onset of obsessive-compulsive disorder (OCD) and associated conditions, such as Paediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infection (PANDAS) and Tourette syndrome (TS). While this area of inquiry is undeniably captivating, the available data remain somewhat controversial and limited in scope.

The aim of this paper is to conduct an exhaustive examination and evaluation of the existing body of literature concerning aberrations in inflammatory and immune system processes within the context of OCD, PANDAS, and TS.

This narrative review entailed a comprehensive search of English language papers on PubMed and Google Scholar from January 1985 to July 31, 2023.

The data collected up to this point suggest that the underlying mechanisms at play may differ depending on the age of the patients and the specific disorder being investigated. Notably, PANDAS seems to have a stronger connection with infections that trigger autoimmunity, which may not necessarily be limited to those resulting from Group A beta-haemolytic streptococcal (GABHS) infections, as previously assumed. In the case of TS, autoimmunity appears to play a significant role, especially when combined with individual susceptibilities stemming from both genetic and environmental factors. As for adult OCD, while the available data are somewhat scattered and occasionally based on relatively small groups of patients, they do indicate that the immune system and inflammatory processes are involved in the disorder’s pathophysiology. However, it remains uncertain whether these processes are primary driving forces or secondary reactions.

In summary, when viewed collectively, the current research findings unveil promising avenues for exploring the underlying causes of OCD and related disorders. They also hold the potential for the development of innovative therapeutic approaches that go beyond the current pharmacological paradigms.

None Declared

Obsessive-compulsive disorder (OCD) has a high prevalence and causes a significative reduction in functionality and quality of life.

First and second line treatment is ineffective in a variable percentage of patients. In such cases transcranial magnetic stimulation (TMS) may be considered.

The goal of this study is to evaluate the impact of TMS treatment on obsessive-compulsive, anxious and depressive symptomatology in patients with OCD.

A prospective observational study was conducted, including all patients diagnosed with OCD who underwent TMS in the Psychiatry department of Centro Hospitalar Universitário de São João since March 2023.

Symptomatology was assessed using the Yale Brown Obsessive-Compulsive Scale (Y-BOCS), the Hamilton Anxiety Rating Scale (HAM-A) and the Hamilton Depression Rating Scale (HAM-D) before and after treatment.

Statistical analysis was performed using the SPSS-Statistics program. A significance level of 0.05 was considered.

As of October 31, 2023, nine individuals with OCD completed treatment with TMS, 33% male and with a median age of 40 years (range 33-57).

The median Y-BOCS score pre-TMS was 30 (range 20-33) and post-TMS 28 (range 16-34). The median difference was 2.5 (range -5-14) and was not statistically significant (p=0.128).

The median score on the HAM-A pre-TMS was 21 (range 9-41) and post-TMS 18 (range 11-24). The median difference was 0 points (range -4-21) and was not statistically significant (p=0.345).

The median HAM-D score pre-TMS was 26 (range 14-40) and post-TMS 19 (range 10-32). The median difference was 2.5 (range -3-20) and was not statistically significant (p=0.225).

Preliminary findings suggest that the impact of TMS on obsessive-compulsive, anxious, and depressive symptomatology in patients with OCD does not appear to be clinically or statistically significant.

Further results are necessary to confirm this trend.

None Declared

Obsessive-compulsive disorder (OCD) is a chronic condition characterized by time-consuming and distressing obsessions and/or compulsions, often accompanied by avoidance behaviours. It is a highly prevalent and incident disorder that results in considerable disability and quality of life reduction.

Current pharmacological treatments are hindered by their delayed onset and the limited evidence on how to approach first and second line treatment-resistant patients.

Recent research showcased the involvement of glutamatergic pathways in the pathophysiology of OCD prompting research into the potential therapeutic use of ketamine, which binds to the N-methyl-D-aspartic acid receptor and acts as a non-competitive antagonist of glutamate.

The aim of this study is to conduct a literature review on the use of ketamine and its enantiomers as a treatment for OCD and report a clinical case involving an OCD patient who experienced significant improvement following ketamine use.

A search was performed on PubMed using a combination of keywords and Medical Subject Headings terms, including “Ketamine”, “Esketamine” and “Obsessive-Compulsive Disorder”. Only studies that involved patients with OCD aged ≥18 years who had received ketamine or its enantiomers as an intervention and that reported treatment response using a validated scale were included.

Nine studies were included, 4 case reports, 3 open-label trials and 2 randomized controlled trials, totalling 71 patients. Ketamine was administered intravenously in 7 studies and intranasally in the remaining 2. The results were heterogeneous, with some studies reporting no effect on obsessive-compulsive (OC) symptoms and others demonstrating significant and rapid improvement, albeit some only transitorily.

We present the case of a 42-year-old man who experienced OC symptoms since the age of 20 but was only formally diagnosed with OCD 3 years ago. During his first consultation, the patient described obsessive thoughts related to contamination and dirtiness, accompanied by handwashing rituals and avoidance behaviours (e.g., avoiding touching handles and switches). His Yale-Brown Obsessive Compulsive Scale (Y-BOCS) score was 29. Escitalopram was initiated with a progressive dose titration, resulting in partial improvement (Y-BOCS 23). In a follow-up appointment, the patient disclosed that he had purchased and self-administered a single intravenous dose of 2g of ketamine 2 months earlier for recreational use. This led to an immediate and significant improvement of his OC symptoms. Subsequent re-evaluation 4 months later confirmed that he remained asymptomatic (Y-BOCS 2).

Ketamine may be a therapeutic alternative for OCD patients who are treatment resistant due to its rapid anti-obsessional effect. Further studies with improved designs and larger sample sizes are warranted to better assess the efficacy of ketamine in OCD treatment.

None Declared