Problematic smartphone use has been associated with altered reward and executive control network activity, yet potential sex differences in the underlying neural mechanisms remain insufficiently understood. We investigated sex-specific neural correlates of smartphone cue reactivity (CR) in 69 healthy young adult smartphone users (age range 18–30 years, female/male n = 45/24). Participants completed the Smartphone Addiction Inventory (SPAI) and underwent functional MRI during a smartphone CR paradigm. In addition, resting-state data were acquired to ensure that neural differences between female and male participants could be attributed to the CR paradigm rather than to sex differences in intrinsic neural activity. Whole-brain analyses revealed stronger activation in males compared to females in response to the presentation of smartphone cues within the right middle frontal gyrus (MFG), thalamus, cortical sensorimotor, parietal and occipital regions, whereas females showed no suprathreshold clusters compared to males. No overlap with resting-state amplitude of low-frequency fluctuation maps was observed with CR results, confirming task specificity. In males, right MFG correlated positively with SPAI-I total score, craving, and sleep interference scores, while in females, right parietal cortex activity correlated negatively with SPAI-I total score, daily life interference, and craving. Complementary cross-modal analyses showed that CR-related activation patterns were associated with several cortical excitatory and inhibitory neuronal and cellular markers, revealing subtle sex differences. These findings suggest sex-specific frontoparietal mechanisms underlying smartphone CR and highlight neurochemical pathways potentially linking excessive smartphone use to differential motivational and cognitive control processes in males compared to females. Males showed stronger smartphone cue-reactivity across frontoparietal, thalamic, sensorimotor, and occipital regions compared with females. Right middle frontal gyrus activation in males correlated positively with the extent of smartphone use, craving, and sleep interference. In females, right parietal cortex activation correlated negatively with the smartphone use levels, craving, and daily life interference. Cross-modal analyses pointed to shared excitatory and inhibitory neurochemical substrates, while revealing subtle sex-specific differences in how these neural markers relate to behavior. People use smartphones constantly, and for some individuals this can become difficult to control. One reason may be that certain smartphone-related cues, such as notifications or images of phones—trigger strong reactions in the brain. However, it is not well understood whether these reactions differ between females and males. In this study, we examined how the brains of 69 young adults respond to smartphone cues while lying in an MRI scanner. We also measured their usual smartphone use and collected resting-state brain data to make sure any differences we observed were truly related to the cue task. We found clear sex differences. When viewing smartphone cues, males showed stronger activity in brain regions involved in attention, decision-making, sensory processing, and visual perception, particularly in a frontal brain area linked to control of behavior. In contrast, females did not show stronger activity than males in any brain region, but instead showed a different pattern: activity in a parietal region was lower in those with more problematic smartphone use. These brain responses were specific to the cue task and not present in resting-state data. We also examined how these patterns relate to underlying brain chemistry. The activation seen during cue reactivity was connected to several markers of excitatory and inhibitory neural signaling, with subtle differences between females and males. Overall, our findings suggest that males and females engage different brain mechanisms when reacting to smartphone cues, which may help explain why excessive smartphone use affects them differently. These insights may support future strategies tailored to sex-specific motivational and self-control processes.

Altered intrinsic functional connectivity is a well-established marker of borderline personality disorder (BPD). However, recent research suggests that investigating brain dynamics may offer a more detailed perspective on the neural signatures of BPD-related symptoms. Resting-state fMRI data were analyzed in female patients with BPD (n = 47) and healthy controls (n = 28) to derive dynamic functional network connectivity (dFNC) indices using both meta-state and cluster-state approaches. Between-group comparisons assessed BPD-related dFNC alterations, while dimensional analyses explored associations between network dynamics and distinct symptom dimensions. Both meta-state and cluster-state analyses revealed strong associations between symptom dimensions and dynamic range and fluidity. Meta-state analysis indicated that greater emotion regulation difficulties corresponded to an expanded state repertoire, reflecting increased variability in large-scale network configurations. Cluster-state analysis showed that fewer state transitions were associated with heightened borderline symptom severity, greater childhood trauma exposure, and increased dissociative symptoms. Furthermore, childhood trauma and emotion regulation difficulties moderated the relationship between time spent in specific cluster-states and borderline symptom severity. These findings suggest that reduced dynamic flexibility but increased dynamic range in large-scale brain networks may contribute to core BPD symptoms, particularly in early trauma, emotion dysregulation as well as borderline symptom severity. The results highlight the association between aberrant dFNC and BPD and contribute to a more detailed characterization of neural dynamics relevant to the disorder.

The cerebellum has been implicated in schizophrenia-related structural and functional deficits, with posterior Crus I and II most consistently affected. Source-based morphometry (SBM) involves applying independent component analysis to gray matter volume to identify spatially distinct structural networks that covary across individuals. We applied SBM and voxel-based morphometry (VBM) to cerebellar structural imaging data to identify patterns of gray matter differences across individuals with schizophrenia (SZ), bipolar disorder with psychotic features (BDwP), and healthy controls (HC). Data were drawn from the Psychosis Human Connectome Project (P-HCP) and included 168 participants: 85 with SZ, 36 with BDwP, and 47 HC. T1-weighted images were processed using the ENIGMA Cerebellum Volumetrics Pipeline, and ICA decompositions were performed using the SBM module of the GIFT Toolbox. One independent component (IC) showed a significant diagnostic group effect (p < 0.05, Bonferroni-corrected), differentiating SZ from HC and BDwP. This cerebellar network included vermis VIIIa, bilateral Crus I, and right lobule IX with positive loadings, and bilateral Crus I and lobule IX with negative loadings. Voxel-based morphometry showed reduced GM volume in negatively loaded regions in SZ. Composite cognitive performance correlated with GM volume (r = 0.27, p < 0.001) and network loadings (r = -0.29, p < 0.001). Mediation analyses showed a strong direct diagnostic effect on IC loadings (-0.42), with small, nonsignificant indirect effects via cognition. These findings identify a cerebellar structural network that differentiates schizophrenia from bipolar disorder and controls, underscoring the cerebellum's unique contribution to the neurobiology of schizophrenia.

Auditory Verbal Hallucinations (AVH) are not exclusive to schizophrenia but also occur in other psychiatric disorders, including Borderline Personality Disorder (BPD). While AVH in SZ has been extensively studied, their neurobiological underpinnings in BPD remain poorly understood. Preliminary evidence suggests structural anomalies in auditory regions among BPD patients experiencing AVH, indicating potential neuroanatomical vulnerabilities. This study examined structural brain differences in female BPD patients with (BPD-AVH n = 20) and without (BPD-nAVH n = 27) a lifetime history of AVH, as well as healthy controls (HC, n = 30), using high-resolution structural MRI. Cortical thickness (CTh), gyrification (CG), and gray matter volume (GMV) were assessed in frontotemporal regions implicated in auditory and speech processing, including the inferior frontal gyrus and superior, middle, and transverse temporal gyri. Region-of-interest (ROI) analyses were performed via CAT12, with supplementary segmentation of Heschl’s gyrus using the TASH toolbox. Group comparisons were conducted using SPM12. Compared to both HC and BPD-nAVH, BPD-AVH patients showed significantly reduced CG in the right transverse temporal gyrus (rTTG), a region encompassing early auditory cortex. No significant group differences emerged in other ROI analyses, for GMV, CG or CTh. Reduced gyrification in the rTTG suggests aberrant cortical folding in early auditory regions among BPD patients with AVH. This may reflect disrupted neurodevelopmental processes that impair auditory signal encoding and internal vs. external sound source discrimination. These findings highlight the role of primary auditory cortex abnormalities in AVH and support transdiagnostic models emphasizing early sensory processing deficits.

Symptoms of fatigue, depression or anxiety are frequent in Crohn’s Disease (CD) and may relate to disturbed brain-gut interactions. While more prevalent in active disease, these symptoms are also experienced by many individuals with CD during remission. Little is known about neural networks underlying such extraintestinal symptoms in CD and their relationship with the current disease state. Using a data fusion approach for functional MRI, this study investigated spatiotemporal markers of resting-state brain activity and associations with neurotransmitter systems and symptoms of fatigue, depression or anxiety in an active disease state or remission. We examined n = 71 patients with CD in an active disease state (aCD; n = 47) or in remission (rCD; n = 24) and healthy controls (HC; n = 35). All participants underwent resting-state fMRI, completed symptom assessments for fatigue, depression and anxiety, and provided stool samples for analysis of faecal calprotectin (fCal; aCD and rCD only). Joint independent component analysis (jICA) of two resting-state brain activity parameters (temporal and spatial features) identified neural networks exhibiting disease-state-dependent alterations. Network connectivity strength was correlated with symptoms of fatigue, depression, and anxiety, as well as fecal calprotectin (fCal). We further explored associations of the networks with neurotransmitter receptor maps. JICA revealed three networks differentiating between disease states and/or between patients and controls. One network comprising affective orbitofrontal and temporal brain regions, exhibited reduced connectivity in active disease (HC vs. aCD: p = 0.003, pFDR = 0.01; aCD vs. rCD: p < 0.001, pFDR < 0.001) and was linked to serotonergic/dopaminergic transmission, fatigue, and fCal. Another network comprised sensorimotor brain regions and showed diminished connectivity in patients in remission (HC vs. rCD: p = 0.034, pFDR = 0.06; aCD vs. rCD: p = 0.003, pFDR = 0.01), correlating with depression, anxiety, and dopaminergic activity. The third network reflected the default-mode network topography and distinguished patients irrespective of disease status from controls (HC vs. aCD: p = 0.013, pFDR = 0.01; HC vs. rCD: p = 0.037, pFDR = 0.06), but showed no associations with symptoms. Resting-state brain network connectivity in patients with CD differed between active disease and remission, and was associated with symptoms of fatigue, depression, and anxiety. Alterations in sensorimotor networks were linked to depressive and anxiety symptoms, whereas affect-related networks were associated with fatigue. These observations suggest that distinct brain networks may contribute to specific neuropsychiatric symptom clusters in Crohn’s disease and underscore the role of brain–gut axis mechanisms in these manifestations.

Contemporary models of neural network function describe the brain as an “active system”, intrinsically generating patterns of activity that pre-structure top-down processing prior to extrinsic stimulation. In this context, self-relatedness is proposed to be one fundamental feature of this spontaneous brain activity. Self-relatedness has been postulated as a neuronal mechanism predominantly involving cortical midline regions ascribed to the so-called default mode network (DMN). This system essentially attributes the degree of self - or non-self -relevance to any interoceptive or exteroceptive stimuli (and by doing this, transforming stimuli in specific self - or non-self -like contents, possibly becoming objects in higher-level processes, particularly self-referential thinking). The focus of this paper is to demonstrate that the model of spontaneous brain activity has some important similarities to central aspects of transcendental philosophical theories of consciousness and subjectivity. For example, in German idealism the term ‘self’ or ‘ego’ refers to a spontaneous organisation capacity of the mind able to generate the very distinction between oneself and other , subject and object within the consciousness, pre-structuring mental processes prior to any specific function (e.g., sensory, cognitive processes). Furthermore, the processing of an informational content across multiple layers of consciousness corresponds to a logical sequence of different states (state of subject-object- undifferentiation , subject-object- differentiation , subject-object- integration ). We conclude, from the perspective of transcendental philosophy there must be a structural parallelism between these logical categories defining the essence of mental states, and their neuronal substrate. Otherwise, it would be hardly conceivable how a mapping of two different regional ontological domains, such as mental and neural processes, could occur.

Background Extraintestinal symptoms (EIS) in inflammatory bowel diseases, including fatigue, depression and anxiety, are highly prevalent, but poorly understood. Alterations of brain function may contribute to EIS, but their association with disease activity is unclear. This study analyzed intrinsic neural activity (INA) of individuals with Crohn's disease (CD) in different disease states and examined the relationship between INA and EIS.Methods Patients with CD (n = 92) and healthy controls (n = 41) underwent functional magnetic resonance brain imaging and completed symptom-specific psychometry. Temporal (amplitude of low-frequency fluctuations, ALFF) and spatial (regional homogeneity, ReHo) markers of INA were compared between CD and controls and between active (patients with active Crohn's disease [aCD]) versus remitted (rCD) disease. Regression analyses explored disease-state-dependent associations between INA and EIS.Results Patients exhibited aberrant INA in frontotemporal, occipital, and thalamic regions. Patients with aCD exhibited lower ALFF in left subcallosal cortex and inferior temporal gyri compared to rCD. Regional homogeneity in aCD was lower in left medial orbital gyrus and higher in right superior frontal, left inferior temporal, and left precentral gyrus. Compared to rCD, aCD showed higher ALFF predominantly in superior, ventro-, and dorsolateral prefrontal regions. Distinct associations between INA and EIS were detected in patients, particularly in the remitted state.Conclusions Intrinsic brain function in patients with CD varies by disease state, with prominent frontal cortex changes in active disease. These brain activity changes are at least partly related to the magnitude of neuropsychiatric symptoms and highlight a role of disturbed brain-gut interactions in the development of EIS especially in rCD. This study examined the intrinsic brain function of individuals with Crohn's disease in different disease states and healthy controls. Brain activity differed between patients and controls and between disease states and correlated with fatigue and depression in remitted disease only.

Neurological soft signs (NSS) are subtle sensorimotor abnormalities that have been observed in various mental disorders with neurodevelopmental origin. While NSS have been extensively examined in patients with schizophrenia (SZ), preliminary evidence also suggests that NSS are also present in patients with borderline personality disorder (BPD). However, a transdiagnostic examination of the severity of NSS in BPD compared to SZ is still lacking. Here, NSS were examined with the Heidelberg NSS scale (HNSS) in three groups of female subjects: BPD (n = 45), SZ (n = 30) and healthy controls (HC) (n = 32). Multivariate analysis of variance (MANOVA) was conducted jointly for BPD, SZ, and HC and HNSS subscores. Post hoc tests were performed using linear discriminant analysis (LDA). In the BPD group, partial Spearman correlations (with age and medication as covariates) were performed between NSS scores and depressive symptoms (HAMD-21), impulsivity (BIS-11), dissociative symptoms (DTS), childhood trauma (CTQ), and borderline symptoms (BSL-23). BPD showed significantly higher NSS levels compared to HCs. For the BPD, significant associations between NSS and childhood trauma and depressive symptoms were found. MANOVA showed a significant group difference, LDA differentiated between HC, and patients with SZ and BPD, but not between the patient groups. Patients with BPD have significantly higher NSS levels than HC. NSS in BPD showed significant associations with childhood trauma, supporting a “two-hit” model. Importantly, patients with BPD and SZ may show similar NSS patterns, suggesting that sensorimotor dysfunction is a transdiagnostic phenomenon.

Dieser Beitrag schlägt unter dem programmatisch gewählten Titel „Neuro-History“ einen Brückenschlag zwischen naturwissenschaftlich betriebener neurologischer Forschung und der Geschichtswissenschaft vor. Ältere Ansätze – vor allem die Psychohistorie – verfolgten eine Verbindung von psychoanalytischen Überlegungen auf das historische Quellenmaterial, über dessen Nachprüfbarkeit aufgrund der Probleme der nur indirekten Kenntnis historischer Persönlichkeiten durch die Quellen gestritten werden kann. Der hier skizzierte Weg einer „Neuro-History“ eröffnet hingegen einen Dialog, bei dem beide Wissenschaften bei ihrem Kernbereich – der historischen Quellenkritik und der experimentellen Neurologie – bleiben, aber in der Abgleichung beider Perspektiven neue Einsichten gewinnen. Am Beispiel mystischer Erfahrungsberichte des Spätmittelalters, die mit den Erkenntnissen zu subklinischen psychotischen Erfahrungen kontrastiert werden, zeigt sich die Selektion und Einseitigkeit der erhaltenen Schriftquellen, aber auch die kulturelle Rahmung gegenwärtiger neurologischer Forschung. Die positive Wertung psychotischer Erlebnisse im spätmittelalterlichen Kloster steht im Kontrast zur modernen Pathologisierung und eröffnet so eine neue Sichtweise sowohl der spätmittelalterlichen Mystik als auch der aktuellen neurowissenschaftlichen Forschung. Der Artikel möchte damit zu einem weiteren, fruchtbaren Dialog über die Fachgrenzen hinweg anregen.

BACKGROUND:Auditory verbal hallucinations are a major burden for patients with schizophrenia spectrum disorder and are often resistant to pharmacological and psychotherapeutic interventions. Repetitive transcranial magnetic stimulation (rTMS) of the temporo-parietal cortex has been proposed as a treatment for persistent auditory verbal hallucinations. We aimed to compare the efficacy and safety of bilateral continuous theta burst stimulation (cTBS), a brief and efficient form of rTMS, in adults with auditory verbal hallucinations versus sham cTBS. METHODS:This multicentre, randomised, sham-controlled, triple-blind phase 3 clinical trial was conducted at seven German psychiatric university hospitals and followed a planned two-stage adaptive design. Eligible patients were aged 18-65 years, had experienced persistent auditory verbal hallucinations at least once per week for a minimum of 3 months, and scored 3 points or higher on item P3 (hallucinatory behaviour) of the clinician-rated Positive Scale of the Positive and Negative Syndrome Scale (PANSS). 138 adults with treatment-persistent auditory verbal hallucinations and schizophrenia spectrum disorder were randomly assigned (1:1) to receive 15 sessions of active (n=70) or sham cTBS (n=68) administered sequentially as 600 pulses to the left and 600 pulses to the right temporo-parietal cortex over a 3-week period. The primary outcome was the change in the auditory hallucinations subscale of the Psychotic Symptom Rating Scales (PSYRATS-AH) from baseline to the end of treatment at 3 weeks, analysed in the intention-to-treat population, which included all randomly assigned patients who received at least one stimulation session. Safety was assessed in all patients who received at least one stimulation session. Follow-up assessments were performed at 1, 3, and 6 months after the end of treatment. People with lived experience were not involved in the study. This trial was registered at ClinicalTrials.gov, NCT02670291. FINDINGS:Between Oct 24, 2015, and May 1, 2023, 2583 patients were screened for eligibility, of whom 138 patients were randomly assigned to active cTBS (n=70; 32 [46%] females and 38 [54%] males) or sham treatment (n=68; 24 [35%] females and 44 [65%] males). Race and ethnicity data were not collected. The primary intention-to-treat analysis (66 patients in the active cTBS group; 64 patients in the sham cTBS group), combining stages 1 and 2, showed patients in the active cTBS group had a significantly greater decrease in the PSYRATS-AH score at end of treatment than did patients in the sham cTBS group (-6·36 [SD 7·97] vs -3·74 [SD 5·79]; adjusted difference -2·36 [95% CI -4·71 to -0·01]; p=0·042). Overall, 85 adverse events (43 in the active cTBS group; 42 in the sham cTBS group) were reported in 22 (33%) of 66 patients in the active cTBS group and 21 (33%) of 64 patients in the sham cTBS group. Headache was the most common adverse event in both groups (n=13 active cTBS group vs n=17 sham cTBS group). One serious adverse event occurred in the active group. INTERPRETATION:Sequential bilateral temporo-parietal cTBS over 3 weeks was safe and effective for reducing auditory verbal hallucinations in adults with schizophrenia spectrum disorder. This trial establishes cTBS as a treatment option for the care of these patients. Further research is needed to evaluate maintenance strategies, identify treatment predictors, and assess long-term efficacy. FUNDING:German Research Foundation.

Problematic smartphone use (PSU) has been associated with withdrawal-like symptoms and altered intrinsic neural activity (INA). While previous studies suggest that PSU affects brain function, little is known about how INA is modulated by smartphone restriction. This longitudinal fMRI study investigated group- and timedependent changes in resting-state INA following short-term smartphone deprivation. 36 participants (aged 18-29; 22 female) were categorized into PSU (n = 19) and non-PSU (n = 17) groups using the Smartphone Addiction Scale-Short Version (SAS-SV). Resting-state fMRI scans were obtained before and after a 72-hour period of smartphone restriction. Psychometric measures included the Mannheim Craving Scale (MaCS) and the Smartphone Addiction Inventory (SPAI). A significant group-by-time interaction revealed INA changes in the left inferior frontal gyrus, bilateral posterior cingulate cortex, right middle frontal and precentral gyri, and left calcarine cortex. INA increased over time in the non-PSU group but decreased in the PSU group in prefrontal and cingulate areas. In contrast, sensorimotor and occipital regions showed increased INA over time in PSU individuals. Associations between neural activity and MaCS scores indicated that greater craving was linked to reduced INA in the posterior cingulate cortex. Within the PSU group, higher smartphone-use severity, as measured by the SPAI, was associated with altered INA in occipital, parietal, and cerebellar regions. These findings suggest PSU is linked to distinct and state-dependent neurofunctional alterations that may reflect withdrawal-related processes and maladaptive reward and cognitive control mechanisms.

OBJECTIVE:Delusional disorders (DD) are among the most debilitating mental disorders in the elderly. Persistent monothematic delusions frequently include paranoid and persecutory beliefs, as well as various forms of somatic delusions, including delusions of being infested by pathogens. So far, little is known about the neural correlates of DD. Yet, particularly in elderly patients, white-matter lesions (WML) are thought to play an important pathophysiological role. METHODS:To investigate regional WML in patients with DD, structural MRI was used, followed by automated lesion segmentation methods to facilitate WML load (WMLL) comparisons between healthy controls (HC, n = 28) and patients with distinct types of DD, that is, somatic (n = 16) versus non-somatic DD (n = 17). Patients with somatic DD presented with specific delusional content, that is, beliefs of delusional infestation (DI), whereas individuals with non-somatic DD (non-DI) showed predominantly paranoid and persecutory content. RESULTS:Regions with higher WMLL in both DI and non-DI patients compared to HC included the anterior cingulate and lateral prefrontal regions located in the middle frontal gyrus. Regions with higher WMLL in DI patients versus both HC and non-DI patients were predominantly located in the sensorimotor areas of the frontal lobe. CONCLUSION:The data suggest distinct patterns of regional WMLL in elderly patients with DI versus non-DI. The anatomical distribution of WMLL supports a neuromechanistic model that emphasises the importance of brain areas that drive the internal bodily focus of somatic delusions versus the externalised cognitive distortions that can be observed in non-somatic delusions.

Growing evidence suggests problematic smartphone use can lead to impaired mental health and quality of life. We conducted a 60-day longitudinal smartphone tracking study using an app capturing daily smartphone use. 186 individuals were enrolled and classified as problematic (PSUs, n = 86) or unproblematic smartphone users (USUs, n = 100), based on the Smartphone Addiction Scale - Short Version (SAS-SV). Sociodemographic data, mental health and quality of life were assessed at baseline. Using linear mixed effects models (LMMs), primary analyses examined the effects of time, group (PSU vs. USU), gender, and time x group interactions on daily total smartphone and app category use i.e. communication, social and gaming apps. Overall, participants used their smartphones for 3.7 h per day, with higher daily use in PSUs (4.2 h) compared to USUs (3.3 h). These group differences were also present in daily use of communication and social apps, alongside a significant effect of gender on daily total use of any app (F(1,189) = 5.06, p = 0.026). Secondary gender-stratified analyses showed that male PSUs used their smartphones significantly more than USUs in both total (F(1,106.15) = 12.06, p < 0.001) and social app use (F(1,105.44) = 9.23, p = 0.003). In females, the only group difference found was in the communication app category, with higher daily use in PSUs (F(1,97.34) = 6.50, p = 0.012). Nevertheless, PSUs of both genders reported lower quality of life and higher levels of depressiveness at baseline, which significantly correlated with PSU severity (all r > 0.22, all p < 0.041).

Background and Hypothesis Parkinsonism, psychomotor slowing, negative and depressive symptoms show evident phenomenological similarities across different mental disorders. However, the extent to which they interact with each other is currently unclear. Here, we hypothesized that parkinsonism is an independent motor abnormality showing limited associations with psychomotor slowing, negative and depressive symptoms in schizophrenia spectrum (SSD), and mood disorders (MOD).Study Design We applied network analysis and community detection methods to examine the interplay and centrality (expected influence [EI] and strength) between parkinsonism, psychomotor slowing, negative and depressive symptoms in 245 SSD and 99 MOD patients. Parkinsonism was assessed with the Simpson-Angus Scale (SAS). We used the Positive and Negative Syndrome Scale (PANSS) to examine psychomotor slowing (item #G7), negative symptoms (PANSS-N), and depressive symptoms (item #G6).Study Results In SSD and MOD, PANSS item #G7 and PANSS-N showed the largest EI and strength as measures of centrality. Parkinsonism had small or no influence on psychomotor slowing, negative and depressive symptoms in SSD and MOD. In SSD and MOD, exploratory graph analysis identified one community, but parkinsonism showed a small influence on its occurrence. Network Comparison Test yielded no significant differences between the SSD and MOD networks (global strength p value: .396 and omnibus tests p value: .574).Conclusions The relationships between the individual domains followed a similar pattern in both SSD and MOD highlighting their transdiagnostic relevance. Despite evident phenomenological similarities, our results suggested that parkinsonism is more independent of negative and depressive symptoms than psychomotor slowing in both SSD and MOD.

Abstract Background In IBD, extraintestinal symptoms (EIS) such as fatigue, depression and anxiety are a major burden on the patients’ quality of life (QoL). These EIS are more prevalent in active disease but can persist in remission. A deleterious effect of depression and anxiety on the course of disease has already been confirmed in longitudinal studies, but to our knowledge the relevance and nature of fatigue symptoms in this regard have not been addressed longitudinally. We examined patients with Crohn’s disease (CD) in an active disease state and followed them up after 3-6 months to evaluate the presence, course and relationships of EIS. Methods We recruited patients with CD in active disease and healthy controls (HC). Patients were instructed to complete self-report questionnaires to measure clinical activity (HBI), fatigue (WEIMuS), anxiety and depressive symptoms (HADS-A, -D) and QoL (IBDQ) before a change of therapy (T1, n=49) and 3-6 months later (T2, n=46). HCs (n=25) answered the same questionnaires except IBDQ. We compared EIS scores between PAT and HC, as well as between T1 and T2, and evaluated EIS changes in PAT with regard to response vs. non-response at T2. Finally, we explored the influence of EIS on clinical activity at T2. Results At both visits and in each of the questionnaires analysed, patients showed higher scores for EIS compared to HC (all pcorr<0.004, FDR 0.05). In patients, fatigue scores were significantly lower at T2 compared to T1 (pcorr=0.034). Patients’ QoL improved (pcorr=0.003), while depression and anxiety didn’t change significantly between T1 and T2. When comparing remitted vs non-remitted CD at T2 (see Table 1), remitted patients had larger differences in EIS scores from T1 to T2 (all pcorr=0.012). Also, remitted patients showed significantly higher and more positive changes in QoL compared to non-remitted patients (pcorr=0.005). In multiple regression analysis, BMI, HADS-D and WEIMuS at T1 were positive predictors for the HBI at T2 (all pcorr<0.019). In contrast, HADS-A at T1 was a negative predictor for HBI at T2 with pcorr=0.002 (see Figure 1). Conclusion As expected, EIS were higher in CD compared to HC. Patients who responded to therapy changes showed higher decrease of fatigue, depression and anxiety and higher increases of QoL compared to non-responders. Higher BMI, depressive and fatigue symptoms at T1 were associated with non-response, higher anxiety at T1 could be associated with response. These findings need to be confirmed in larger studies but indicate the importance of successful induction of remission to improve not only intestinal inflammation and QoL, but also fatigue and affective symptoms.

Background Understanding the relationship between psychopathology and major domains of human neurobehavioral functioning may identify new transdiagnostic treatment targets. However, studies examining the interrelationship between psychopathological symptoms, sensorimotor, cognitive, and global functioning in a transdiagnostic sample are lacking. We hypothesized a close relationship between sensorimotor and cognitive functioning in a transdiagnostic patient sample. Methods We applied network analysis and community detection methods to examine the interplay and centrality [expected influence (EI) and strength] between psychopathological symptoms, sensorimotor, cognitive, and global functioning in a transdiagnostic sample consisting of 174 schizophrenia spectrum (SSD) and 38 mood disorder (MOD) patients. All patients ( n = 212) were examined with the Positive and Negative Syndrome Scale (PANSS), the Heidelberg Neurological Soft Signs Scale (NSS), the Global Assessment of Functioning (GAF), and the Brief Cognitive Assessment Tool for Schizophrenia consisted of trail making test B (TMT-B), category fluency (CF) and digit symbol substitution test (DSST). Results NSS showed closer connections with TMT-B, CF, and DSST than with GAF and PANSS. DSST, PANSS general, and NSS motor coordination scores showed the highest EI. Sensory integration, DSST, and CF showed the highest strength. Conclusions The close connection between sensorimotor and cognitive impairment as well as the high centrality of sensorimotor symptoms suggests that both domains share aspects of SSD and MOD pathophysiology. But, because the majority of the study population was diagnosed with SSD, the question as to whether sensorimotor symptoms are really a transdiagnostic therapeutic target needs to be examined in future studies including more balanced diagnostic groups.

Since January 1st 2022, catatonia is (again) recognized as an independent diagnostic entity in the 11th revision of the International Classification of Diseases (ICD-11). This is a relevant time to systematically review how the concept of catatonia has evolved within the 19th century and how this concept changed under the influence of a wide variety of events in the history of psychiatry. Here, we systematically reviewed historical and modern German and English texts focusing on catatonic phenomena, published from 1800 to 1900. We searched five different electronical databases (https://archive.org, www.hathitrust.org, www.books.google.de, https://link.springer.com and PubMed) and closely reviewed 60 historical texts on catatonic symptoms. Three main findings emerged: First, catatonic phenomena and their underlying mechanisms were studied decades before Karl Ludwig Kahlbaum's catatonia concept of 1874. Second, Kahlbaum not only introduced catatonia, but, more generally, also called for a new classification of psychiatric disorders based on a comprehensive analysis of the entire clinical picture, including the dynamic course and cross-sectional symptomatology. Third, the literature review shows that between 1800 and 1900 catatonic phenomena were viewed to be 'located' right at the interface of motor and psychological symptoms with the respective pathophysiological mechanisms being discussed. In conclusion, catatonia can truly be considered one of the most exciting and controversial entity in both past and present psychiatry and neurology, as it occupies a unique position in the border territory between organic, psychotic and psychogenic illnesses.

Patients with catatonia often show serious motor, affective and behavioral symptoms, behind which the subjective experience often remains hidden. Therefore, this study disseminates our own systematic empirical investigation of the subjective experience of catatonia patients to a German-speaking audience of clinicians and researchers. Based on current evidence and the clinical experience of the authors, the self-report questionnaire Northoff Scale for Subjective Experience in Catatonia (NSSC) was modified, extended and validated and now consists of 26 items capturing the subjective experience of catatonia in its clinical diversity. A total of 46 patients with catatonia according to the International Classification of Diseases (11th revision, ICD-11) were asked about their subjective experience during the acute phase of the disease using the NSSC. The NSSC showed high internal consistency (Cronbach's alpha = 0.91). The NSSC total score was significantly associated with the Northoff Catatonia Rating Scale (NCRS; r = 0.46; p < 0.05), the total score of the Positive and Negative Syndrome Scale (PANSS; r = 0.30; p < 0.05), the Brief Psychiatric Rating Scale (BPRS; r = 0.33; p < 0.05), and Trait Anxiety (STAI; r = 0.64; p < 0.01), supporting its validity. Preliminary validation of the NSSC revealed good psychometric properties. The NSSC is a useful instrument for routine clinical use to assess the subjective experience of patients with catatonia in order to provide tailored psychotherapeutic interventions.

In the 19th century, postmortem brain examination played a central role in the search for the neurobiological origin of psychiatric and neurological disorders. During that time, psychiatrists, neurologists, and neuropathologists examined autopsied brains from catatonic patients and postulated that catatonia is an organic brain disease. In line with this development, human postmortem studies of the 19th century became increasingly important in the conception of catatonia and might be seen as precursors of modern neuroscience. In this report, we closely examined autopsy reports of eleven catatonia patients of Karl Ludwig Kahlbaum. Further, we performed a close reading and analysis of previously (systematically) identified historical German and English texts between 1800 and 1900 for autopsy reports of catatonia patients. Two main findings emerged: (i) Kahlbaum's most important finding in catatonia patients was the opacity of the arachnoid; (ii) historical human postmortem studies of catatonia patients postulated a number of neuroanatomical abnormalities such as cerebral enlargement or atrophy, anemia, inflammation, suppuration, serous effusion, or dropsy as well as alterations of brain blood vessels such as rupture, distension or ossification in the pathogenesis of catatonia. However, the exact localization has often been missing or inaccurate, probably due to the lack of standardized subdivision/nomenclature of the respective brain areas. Nevertheless, Kahlbaum's 11 autopsy reports and the identified neuropathological studies between 1800 and 1900 made important discoveries, which still have the potential to inform and bolster modern neuroscientific research in catatonia.