Piotr Podwalski

Borderline personality disorder (BPD) is a severe and heterogeneous psychiatric condition characterized by emotional dysregulation, impulsivity, and interpersonal instability. Increasing evidence suggests that disruptions in white matter (WM) microstructure may contribute to its neurobiological underpinnings. Clarifying these findings is important because diffusion MRI studies in BPD remain heterogeneous in terms of age, symptom severity, comorbidity, medication status, trauma exposure, and analytic approach. This narrative review synthesizes current findings from diffusion tensor imaging (DTI) studies examining WM alterations in individuals with BPD and discusses key methodological considerations that influence the interpretation of results. Across studies, the most consistent abnormalities were observed in the corpus callosum, particularly the genu and body, which may reflect altered interhemispheric connectivity. Additional alterations were reported in fronto-limbic pathways, including the cingulum and fornix, as well as long association tracts such as the superior and inferior longitudinal fasciculi. These findings are consistent with the hypothesis that WM alterations in BPD may extend across large-scale structural networks that are anatomically connected to emotional and cognitive systems. However, results remain heterogeneous due to methodological variability, small sample sizes, and clinical heterogeneity. Differences in imaging techniques and analytical approaches further complicate comparisons across studies. Overall, WM alterations may represent one component of the neurobiological profile of BPD; however, their functional and clinical significance requires confirmation using advanced diffusion methods, longitudinal designs, and standardized protocols.

Stygmatyzacja i dyskryminacja osób ze względu na ich określone cechy to szeroko rozpowszechniony problem, zarówno w Polsce, jak i na świecie. Szczególnym jego rodzajem jest stygmatyzacja osób z zaburzeniami i chorobami psychicznymi. Chociaż zjawisko to swe korzenie ma już w starożytności i średniowieczu, a naukowo zostało opisane kilkadziesiąt lat temu to jest wciąż problemem aktualnym i nierozwiązanym. Stygmatyzacja może zachodzić na różnych poziomach i występować jako autostygmatyzacja, stygmatyzacja związana ze społecznościami i stygmatyzacja instytucjonalna. Przybiera różne postacie i wywiera zróżnicowane, negatywne skutki. Przeciwdziałanie tej sytuacji i likwidacja już powstałych jej efektów jest żywotną potrzebą społeczeństwa i aktywnością niezbędną dla zapewnienia lepszego funkcjonowania oraz leczenia osób chorych psychicznie. Wyzwania w tym zakresie stoją zarówno przed instytucjami państwowymi odpowiedzialnymi za system ochrony zdrowia, ale też podmiotami prywatnymi takimi jak organizacje pozarządowe, koncerny medialne czy firmy zatrudniające ludzi. Również indywidualne zaangażowanie wszystkich, pojedynczych osób jest istotne dla zapobiegania piętnowania osób dotkniętych chorobami psychicznymi i właściwej reakcji na tego typu działanie.

Virtual reality offers a promising avenue for the assessment of executive functioning in complex workplace environments. However, its use in schizophrenia remains limited. For that reason, we investigated the validity and test-retest reliability of the Jansari assessment of Executive Functions (JEF^©) in individuals with schizophrenia and its associations with competitive employment. A total of 69 participants with schizophrenia and 67 healthy controls completed JEF^© and standard tests. A subsample of 58 patients was retested after an 8-week interval. Individuals with schizophrenia performed more poorly than controls on JEF^© (p < 0.001) and standard tests (p < 0.05). JEF^© scores correlated with standard measures (p < 0.05), except inhibition tests, and with clinician-report of everyday problems (p < 0.001). Total score showed a good test-retest reliability and the practice adjusted RCI indicated 87.9% of patients remained stable over 8 weeks. In logistic regression, higher JEF^© total score significantly predicted competitive employment after adjusting for age (p = 0.004) and remained significant when years of education were added (p = 0.014). This comprehensive evaluation indicates that JEF^© is a valid and reliable tool assessing executive functions required in office work and offers an ecologically relevant complement to standard measures in schizophrenia.

Background/Objectives: Borderline personality disorder (BPD) is a serious psychiatric condition characterized by affective instability, impulsivity, and self-harming behaviors. Increasing evidence suggests that epigenetic mechanisms, especially DNA methylation, may mediate the interaction between genetic susceptibility and adverse environmental factors. This systematic review aimed to synthesize available findings on DNA methylation in BPD, including candidate gene studies and epigenome-wide association studies (EWAS). Methods: We conducted a systematic search of PubMed, Embase, and Scopus databases following PRISMA guidelines. Eligible studies (N = 19) included original research examining DNA methylation in individuals with BPD, assessed either through candidate gene approaches or genome-wide platforms. Data were extracted regarding study design, sample characteristics, psychometric instruments, genes, CpG sites analyzed, and main findings. Results: Inconsistent associations were found between BPD and altered methylation of several candidate genes, such as NR3C1, FKBP5, BDNF, DRD2, HTR2A, and COMT. Differential methylation was often linked to early-life adversities and symptom severity. EWAS also identified new loci, including APBA3, MCF2, PXDN, and OPRK1. Across studies, methodological heterogeneity and small sample sizes limited definitive conclusions. Conclusions: Evidence for DNA methylation alterations in BPD is mixed, and current findings do not allow firm conclusions about their mechanisms or clinical relevance. Larger and longitudinal studies are required to clarify whether these epigenetic changes contribute meaningfully to BPD.

Introduction: Impulsivity is one of the overlapping symptoms common to borderline personality disorder (BPD) and attention deficit hyperactivity disorder (ADHD), but the neurobiological basis of these disorders remains uncertain. This systematic review aims to identify abnormalities in the gray and white matter associated with impulsivity in BPD and ADHD. Methods: We conducted a systematic search of the PubMed, Embase, and SCOPUS databases, adhering to PRISMA guidelines. Studies that investigated gray and white matter alterations in BPD or ADHD populations and their relationship with impulsivity were included. We reviewed information from 23 studies involving 992 participants, which included findings from structural MRI and DTI. Results: The review identified various nonhomogeneous changes associated with impulsivity in BPD and ADHD. BPD was mainly associated with abnormalities in the prefrontal cortex (PFC) and limbic areas, which correlated negatively with impulsivity. In contrast, impulsivity associated with ADHD was associated with structural changes in the caudate nucleus and frontal–striatal pathways. Despite the overlapping symptoms of impulsivity, the neurobiological mechanisms appeared to differ between the two disorders. Conclusions: These findings emphasize the distinct neurostructural correlates of impulsivity in BPD and ADHD. While both disorders show impulsivity as one of their main symptoms, the fundamental brain structures associated with this trait are different. BPD is primarily associated with abnormalities in the prefrontal cortex and limbic system, whereas the alterations seen in ADHD tend to focus on the caudate nucleus and frontostriatal pathways. Further research is needed to clarify these differences and their implications for treatment.

Cel pracy: Dowody sugerują, że zmniejszone wydzielanie dopaminy w szlakach mezokortykolimbicznych może predysponować do zwiększonej podatności na uzależnienie od substancji psychoaktywnych. Zaproponowano zdefiniowanie takiego zjawiska jako zespołu deficytu nagrody (ang. reward deficiency syndrome, RDS). Badania wskazują, że zmniejszenie stymulującej transmisji glutaminergicznej w układzie dopaminergicznym może stanowić alternatywny fenotyp RDS. Potencjalnym źródłem tego typu nieprawidłowości jest wychwyt zwrotny glutaminianu, który zależy od funkcji transporterów aminokwasów pobudzających (ang. excitatory amino acid transporter, EAAT). Celem zaprezentowanego badania była ocena związku wariantów rs4354668 genu dla EAAT2 z ryzykiem wystąpienia zaburzeń związanych z używaniem substancji psychoaktywnych.Metoda: Przeanalizowaliśmy materiał genetyczny i dane psychometryczne 125 młodych dorosłych (n = 125) pod kątem wpływu polimorfizmu rs4354668 genu SLC1A2 dla EAAT2 na ryzykowne lub szkodliwe używanie narkotyków (ang. risky or harmful drug use, RHDU). Po analizie eksploracyjnej wykorzystaliśmy modele regresji logistycznej do oceny prawdopodobieństwa wystąpienia RHDU w poszczególnych grupach.Wyniki: W ostatecznym modelu wariant T/T rs4354668 był istotnie powiązany z niższym prawdopodobieństwem wystąpienia RHDU w porównaniu z wariantem G/G (OR: 0.021; 95% CI: 0.001 – 0.275; p = 0.009). Innymi istotnymi predyktorami RHDU były palenie tytoniu oraz ryzykowne lub szkodliwe picie alkoholu.Wnioski: Uzyskane wyniki mogą wskazywać na możliwy związek ryzyka szkodliwego używania narkotyków z wariantami polimorfizmu rs4354668 genu SLC1A2 dla EAAT2. Osoby z wariantem T/T tego polimorfizmu wydają się być mniej narażone na rozwój zaburzeń związanych z używaniem narkotyków.

This study compared cognitive domains between deficit schizophrenia (DS) and non-deficit schizophrenia (NDS) patients and healthy controls (HC), analyzing relationships between psychopathological dimensions and cognitive domains. A total of 29 DS patients, 45 NDS patients, and 39 HC subjects participated. Cognitive domains were measured using the Measurement and Treatment Research to Improve Cognition in Schizophrenia Battery. Psychopathological symptoms were evaluated with the Positive and Negative Syndrome Scale. Clinical groups performed poorer than HC groups in regards to speed of processing, attention/vigilance, working memory, verbal and visual learning and memory, reasoning and problem solving, and social cognition. DS patients scored poorer than NDS patients in terms of all cognitive domains and the overall score, except for reasoning and problem solving. Positive, negative, disorganization, and resistance symptoms were related to cognitive functions only in NDS patients. Our findings suggest that the MCCB battery is sensitive to detecting cognitive dysfunctions in both deficit and non-deficit schizophrenia.