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Clinical features and genetics overlap in schizophrenia (SCZ) and bipolar disorder (BD). Identifying brain alterations associated with genetic vulnerability for SCZ and BD could help to discover intermediate phenotypes, quantifiable biological traits with greater prevalence in unaffected relatives (RELs), and early recognition biomarkers in ultrahigh risk populations. However, a comprehensive meta-analysis of structural and functional magnetic resonance imaging (MRI) studies examining relatives of patients with SCZ and BD has not been performed yet.We systematically searched PubMed, Scopus, and Web of Science for structural and functional MRI studies investigating relatives and healthy control subjects. A total of 230 eligible neuroimaging studies (6274 SCZ-RELs, 1900 BD-RELs, 10,789 healthy control subjects) were identified. We conducted coordinate-based activation likelihood estimation meta-analyses on 26 structural MRI and 81 functional MRI investigations, including stratification by task type. We also meta-analyzed regional and global volumetric changes. Finally, we performed a meta-analysis of all MRI studies combined.Reduced thalamic volume was present in both SCZ and BD RELs. Moreover, SCZ-RELs showed alterations in corticostriatal-thalamic networks, spanning the dorsolateral prefrontal cortex and temporal regions, while BD-RELs showed altered thalamocortical and limbic regions, including the ventrolateral prefrontal, superior parietal, and medial temporal cortices, with frontoparietal alterations in RELs of BD type I.Familiarity for SCZ and BD is associated with alterations in the thalamocortical circuits, which may be the expression of the shared genetic mechanism underlying both disorders. Furthermore, the involvement of different prefrontocortical and temporal nodes may be associated with a differential symptom expression in the two disorders.

A comprehensive assessment of catatonic symptoms is decisive for diagnosis, neuronal correlates, and evaluation of treatment response and prognosis of catatonia. Studies conducted so far used different cut-off criteria and clinical rating scales to assess catatonia. Therefore, the main aim of this study was to examine the frequency and distribution of diagnostic criteria and clinical rating scales for assessing catatonia that were used in scientific studies so far.We conducted a systematic review using PubMed searching for articles using catatonia rating scales/criteria published from January 1st 1952 (introduction of catatonic schizophrenia to first edition of the Diagnostic and Statistical Manual of Mental Disorders [DSM]) up to December 5th, 2022.1928 articles were considered for analysis. 1762 (91,39 %) studies used one and 166 (8,61 %) used ≥2 definitions of catatonia. However, 979 (50,7 %) articles did not report any systematic assessment of catatonia. As for clinical criteria, DSM criteria were used by the majority of studies (n = 290; 14.0 %), followed by International Classification of Diseases (ICD) criteria (n = 61; 2.9 %). The Bush-Francis Catatonia Rating Scale (BFCRS) was found to be by far the most frequently utilized scale (n = 464; 22.4 % in the respective years), followed by Northoff Catatonia Rating Scale (NCRS) (n = 31; 1.5 % in the respective years).DSM and ICD criteria as well as BFCRS and NCRS were most frequently utilized and can therefore be recommended as valid instruments for the assessment of catatonia symptomatology.

The specific role of white matter (WM) microstructure in parkinsonism among patients with schizophrenia spectrum disorders (SSD) is largely unknown. To determine whether topographical alterations of WM microstructure contribute to parkinsonism in SSD patients, we examined healthy controls (HC, n=16) and SSD patients with and without parkinsonism, as defined by Simpson-Angus Scale total score of ≥4 (SSD-P, n=33) or

While sensorimotor abnormalities in schizophrenia (SZ) are of increasing scientific interest, little is known about structural changes and their developmental origins that may underlie parkinsonism. This multimodal magnetic resonance imaging (MRI) study examined healthy controls (HC, n = 20) and SZ patients with (SZ-P, n = 38) and without (SZ-nonP, n = 35) parkinsonism, as defined by Simpson-Angus Scale total scores of ≥4 or ≤1, respectively. Using the Computational Anatomy Toolbox (CAT12), voxel- and surface-based morphometry were applied to investigate cortical and subcortical gray matter volume (GMV) and three cortical surface markers of distinct neurodevelopmental origin: cortical thickness (CTh), complexity of cortical folding (CCF) and sulcus depth. In a subgroup of patients (29 SZ-nonP, 25 SZ-P), resting-state fMRI data were also analyzed using a regions-of-interest approach based on fractional amplitude of low frequency fluctuations (fALFF). SZ-P patients showed increased CCF in the left supplementary motor cortex (SMC) and decreased left postcentral sulcus (PCS) depth compared to SZ-nonP patients (p 0.05, FWE-corrected at cluster level). In SMC, CCF was associated negatively with activity, which also differed significantly between the patient groups and between patients and HC. In regression models, severity of parkinsonism was associated negatively with left middle frontal CCF and left anterior cingulate CTh. These data provide novel insights into altered trajectories of cortical development in SZ patients with parkinsonism. These cortical surface changes involve the sensorimotor system, suggesting abnormal neurodevelopmental processes tightly coupled with cortical activity and subcortical morphology that convey increased risk for sensorimotor abnormalities in SZ.

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.

Major depressive disorder (MDD) and schizophrenia (SCZ) share neurobiological and clinical commonalities. Altered functional connectivity of large-scale brain networks has been associated with both disorders. Electroconvulsive therapy (ECT) has proven to be an effective treatment in severe forms of MDD and SCZ. However, the role of ECT on the modulation of the dynamics of brain networks is still unknown. In this study, we used resting state functional magnetic resonance imaging (rs-fMRI) to investigate functional connectivity in 16 pharmacoresistant patients with SCZ or MDD and a matched group of normal controls. Patients were scanned before and after right-sided unilateral ECT. Group spatial independent component analysis was carried out with a multiple analysis of covariance (MANCOVA) approach to estimate the effects of ECT treatment on intrinsic components (INs). Functional network connectivity (FNC) was calculated between pairs of INs. Patients had reduced connectivity within a striato-thalamic network in the thalamus as well as increased low frequency oscillations in a striatal network. ECT reduced low frequency oscillations (LFOs) on a striatal network along with increasing functional connectivity in the medial prefrontal cortex within the DMN. Following ECT treatment, the FNC of the executive network was reduced with the DMN and increased with the salience network, respectively. Our findings suggest transnosological effects of ECT on the connectivity of large-scale networks as well as at the level of their interplay. Furthermore, they support a transnosological approach for the investigation not only of the neural correlates of the disease but also of the brain mechanism of treatment of mental disorders.

There is strong neuroimaging evidence that cortical alterations represent a core pathophysiological feature of major depressive disorder (MDD). Differential contributions of cortical features of neurodevelopmental origin, which may distinctly contribute to MDD vulnerability, disease-onset, or symptom expression, are unclear at present.We investigated distinct markers of cortical neurodevelopment, i.e. local cortical gyrification (LGI) and thickness (CT) in patients with MDD (n = 38) and healthy controls (HC, n = 22) using 3 T structural magnetic resonance imaging data and surface-based data analysis techniques. CT and LGI were computed using the Computational Anatomy Toolbox (CAT12). Analyses were performed for the entire cortical surface followed by a complementary regions-of-interest approach.MDD patients showed significantly greater LGI in frontal, cingulate, parietal, temporal, and occipital regions compared to HC (FDR-corrected at p 0.05 using threshold-free cluster enhancement). No significant differences of CT were found. In the MDD-group, correlations were found between duration of illness in years and number of depressive episodes and LGI of frontal, temporal, and parietal regions (p 0.05).Main limitations are the relatively modest sample size and a cross-sectional study design. We did not control for early environmental factors potentially influencing neurodevelopment, such as childhood trauma. We report associations uncorrected for multiple comparisons.The data suggest different local trajectories of cortical change in MDD. In addition, our data support the notion that aberrant cortical development may serve as a vulnerability marker of MDD, as well as a potential predictor of disease course.

Although genuine motor abnormalities (GMA) are frequently found in schizophrenia, they are also considered as an intrinsic feature of bipolar, obsessive-compulsive, and neurodevelopmental disorders with early onset such as autism, ADHD, and Tourette syndrome. Such transnosological observations strongly suggest a common neural pathophysiology. This systematic review highlights the evidence on GMA and their neuroanatomical substrates in bipolar, obsessive-compulsive, and neurodevelopmental disorders. The data lends support for a common pattern contributing to GMA expression in these diseases that seems to be related to cerebello-thalamo-cortical, fronto-parietal, and cortico-subcortical motor circuit dysfunction. The identified studies provide first evidence for a motor network dysfunction as a correlate of early neurodevelopmental deviance prior to clinical symptom expression. There are also first hints for a developmental risk factor model of these mental disorders. An in-depth analysis of motor networks and related patho-(physiological) mechanisms will not only help promoting Research Domain Criteria (RDoC) Motor System construct, but also facilitate the development of novel psychopharmacological models, as well as the identification of neurobiologically plausible target sites for non-invasive brain stimulation.

In schizophrenia temporal cortical volume loss differs between patients presenting with persistent auditory verbal hallucinations (pAVH) in contrast to those without hallucinatory symptoms (nAVH). However, it is unknown whether this deficit reflects a neural signature of neurodevelopmental origin or if abnormal temporal cortical volume is reflective of factors which may be relevant at later stages of the disorder. Here, we tested the hypothesis that local gyrification index (LGI) in regions of the temporal cortex differs between patients with pAVH (n=10) and healthy controls (n=14), and that abnormal temporal LGI discriminates between pAVH and nAVH (n=10). Structural magnetic resonance imaging at 3T along with surface-based data analysis methods was used. Contrary to our expectations, patients with pAVH showed lower LGI in Broca´s region compared to both healthy persons and nAVH. Compared to nAVH, those individuals presenting with pAVH also showed lower LGI in right Broca's homologue and right superior middle frontal cortex, together with increased LGI in the precuneus and superior parietal cortex. Regions with abnormal LGI common to both patient samples were found in anterior cingulate and superior frontal areas. Inferior cortical regions exhibiting abnormal LGI in pAVH patients were associated with overall symptom load (BPRS), but not with measures of AVH symptom severity. The pattern of abnormal cortical folding in this sample suggests a neurodevelopmental signature in Broca's region, consistent with current AVH models emphasizing the pivotal role of language circuits and inner speech. Temporal cortical deficits may characterize patients with pAVH during later stages of the disorder.

The number of neuroimaging studies on movement disorders, sensorimotor, and psychomotor functioning in schizophrenia spectrum disorders (SSD) has steadily increased over the last two decades. Accelerated by the addition of the “sensorimotor domain” to the Research Domain Criteria (RDoC) framework in January 2019, neuroscience research on the role of sensorimotor dysfunction in SSD has gained greater scientific and clinical relevance. To draw attention to recent rapid progress in the field, we performed a triennial systematic review (PubMed search from January 1st, 2018 through December 31st, 2020), in which we highlight recent neuroimaging findings and discuss methodological pitfalls as well as challenges for future research. The identified magnetic resonance imaging (MRI) studies suggest that sensorimotor abnormalities in SSD are related to cerebello-thalamo-cortico-cerebellar network dysfunction. Longitudinal and interventional studies highlight the translational potential of the sensorimotor domain as putative biomarkers for treatment response and as targets for non-invasive neurostimulation techniques in SSD.

Popularity of smartphones has dramatically increased in the past years, accompanied by increased concerns regarding potentially adverse effects on physical and mental health. Addictive behavior associated with excessive smartphone use, frequently referred to as "smartphone addiction" (SPA), has attracted increased scientific interest. However the neural correlates of SPA are unknown. We used functional magnetic resonance imaging at 3T to investigate the neural correlates of cue reactivity (CR) in individuals with SPA (n = 21) compared to controls (n = 21). SPA was assessed using the Smartphone Addiction Inventory (SPAI), and neural activity was measured by a modified CR task. Contrasts of images of smartphones vs. neutral stimuli and stimuli including active vs. inactive smartphones (p 0.001, uncorrected for height, followed by correction for spatial extent) were analyzed. In the first contrast, group differences in medial prefrontal (MPFC), occipital, temporal, and anterior cingulate (ACC) cortices, in temporoparietal regions, and cerebellum were found. For active vs. inactive smartphones, group differences were found in frontal operculum/anterior insula and precentral gyrus. Negative correlations were found between MPFC, ACC, precuneus, and precentral gyrus and specific SPAI subscores, i.e. compulsive behavior, functional impairment and withdrawal. This study suggests spatial similarities of CR-related brain activation between addictive smartphone use and other well-known addictive disorders.

Patients with psychiatric disorders of significant neurodevelopmental origin, such as schizophrenia and autism frequently experience genuine motor abnormalities, such as neurological soft signs (NSS). Previous MRI studies in patients with schizophrenia have shown that NSS are associated with abnormal cortical, thalamic and cerebellar structure and function. So far, however, no neuroimaging study focused on the role of the local gyrification index (LGI) in the pathophysiology of NSS. This study sought to explore the relationship between NSS and folding patterns of the cerebral cortex that are thought to be established during early brain development. In this study, whole brain high-resolution magnetic resonance imaging (MRI) at 3 Tesla was used to investigate the LGI in 33 patients with recent-onset schizophrenia. Cortical reconstruction was performed with the Freesurfer image analysis suite. NSS were examined on the Heidelberg Scale and related to LGI. Age, gender, years of education and medication were considered as potential confounding variables. In summary, higher NSS scores were positively associated with morphological changes of LGI predominantly in parietal and occipital areas. Our results confirm the hypothesis of a significant relationship between LGI changes and the NSS expression in schizophrenia. Investigation of LGI may help to explain subtle motor symptoms such as NSS in schizophrenia.

Background Previous structural neuroimaging studies linked cerebellar deficits to neurological soft signs (NSS) in schizophrenia. However, no studies employed a methodology specifically designed to assess cerebellar morphology. In this study, we evaluated the relationship between NSS levels and abnormalities of the human cerebellum in patients with recent-onset schizophrenia and healthy individuals using an exclusive cerebellar atlas. Methods A group of 26 patients with recent-onset schizophrenia and 26 healthy controls were included. All participants underwent a high-resolution T1-weighted MRI scan on a 3 Tesla scanner. We used a voxel-based morphometry (VBM) approach utilizing the Spatially Unbiased Infratentorial (SUIT) toolbox to provide an optimized and fine-grained exploration of cerebellar structural alterations associated with NSS. Results Compared with healthy controls, patients had significantly smaller cerebellar volumes for both hemispheres. In the patients' group, we identified a significant negative correlation between NSS levels and gray matter volume in the left lobule VI and the right lobule VIIa, corrected for multiple comparisons. Further, NSS performance was significantly associated with white matter volume in the left midbrain and corpus medullare and the right lobule VIIa. In contrast, no significant associations between NSS scores and cerebellar subregions in healthy subjects arose. Conclusion Our results demonstrate the benefits of SUIT when investigating cerebellar correlates of NSS. These results support the view that distinct parts of sensorimotor and cognitive cerebellum play an important role in the pathogenesis of NSS in schizophrenia.