Schizophrenia Spectrum Disorder Patients Research Articles

Retinal structural alterations in chronic versus first episode schizophrenia spectrum disorders

Recent studies have found evidence of retinal thinning in schizophrenia spectrum disorder patients; however, it is not known whether retinal thinning is present at the first episode of psychosis or whether it is a result of the progression of the disease or related factors (e.g., emergence of medical comorbidities). We hypothesized that first episode patients (FEP) would not differ on any retinal variables when compared to age matched controls, while chronically ill patients would show evidence of retinal thinning compared to age matched controls. 15 first episode patients, 20 control subjects age-matched to the FEP group, 18 chronically ill patients, and 18 control subjects age-matched to the chronically ill group participated in Spectral Domain OCT scans. We collected data on retinal nerve fiber layer (RNFL) thickness, macula thickness and volume, and ganglion cell-inner plexiform layer (GCL-IPL) thickness as well as cup-to-disc ratio at the optic nerve head. No evidence of retinal structural change was found in the first episode group. In contrast, chronic schizophrenia and schizoaffective disorder patients were characterized by GCL-IPL thinning and overall macula thinning and volume reduction. No evidence of RNFL thinning was observed in the chronic group, however. These data suggest that retinal structure is unaffected very early in the course of schizophrenia spectrum disorders but that thinning is an aspect of illness progression, medical comorbidity, and/or long-term antipsychotic medication use in schizophrenia spectrum disorders. Among retinal indices, macula thickness and volume appear to be the most sensitive to the changes associated with illness chronicity.

A Neural Signature of Parkinsonism in Patients With Schizophrenia Spectrum Disorders: A Multimodal MRI Study Using Parallel ICA.

Motor abnormalities in schizophrenia spectrum disorders (SSD) have increasingly attracted scientific interest in the past years. However, the neural mechanisms underlying parkinsonism in SSD are unclear. The present multimodal magnetic resonance imaging (MRI) study examined SSD patients with and without parkinsonism, as defined by a Simpson and Angus Scale (SAS) total score of ≥4 (SAS group, n = 22) or <4 (non-SAS group, n = 22). Parallel independent component analysis (p-ICA) was used to examine the covarying components among gray matter volume maps computed from structural MRI (sMRI) and fractional amplitude of low-frequency fluctuations (fALFF) maps computed from resting-state functional MRI (rs-fMRI) patient data. We found a significant correlation (P = .020, false discovery rate [FDR] corrected) between an sMRI component and an rs-fMRI component, which also significantly differed between the SAS and non-SAS group (P = .042, z = -2.04). The rs-fMRI component comprised the cortical sensorimotor network, and the sMRI component included predominantly a frontothalamic/cerebellar network. Across the patient sample, correlations adjusted for the Positive and Negative Syndrome Scale (PANSS) total scores showed a significant relationship between tremor score and loadings of the cortical sensorimotor network, as well as between glabella-salivation score, frontothalamic/cerebellar and cortical sensorimotor network loadings. These data provide novel insights into neural mechanisms of parkinsonism in SSD. Aberrant bottom-up modulation of cortical motor regions may account for these specific motor symptoms, at least in patients with SSD.

A new genetic locus for antipsychotic-induced weight gain: A genome-wide study of first-episode psychosis patients using amisulpride (from the OPTiMiSE cohort).

Background:Antipsychotic-induced weight gain is a common and debilitating side effect of antipsychotics. Although genome-wide association studies of antipsychotic-induced weight gain have been performed, few genome-wide loci have been discovered. Moreover, these genome-wide association studies have included a wide variety of antipsychotic compounds.Aims:We aim to gain more insight in the genomic loci affecting antipsychotic-induced weight gain. Given the variable pharmacological properties of antipsychotics, we hypothesized that targeting a single antipsychotic compound would provide new clues about genomic loci affecting antipsychotic-induced weight gain.Methods:All subjects included for this genome-wide association study (n=339) were first-episode schizophrenia spectrum disorder patients treated with amisulpride and were minimally medicated (defined as antipsychotic use <2 weeks in the previous year and/or <6 weeks lifetime). Weight gain was defined as the increase in body mass index from before until approximately 1 month after amisulpride treatment.Results:Our genome-wide association analyses for antipsychotic-induced weight gain yielded one genome-wide significant hit (rs78310016; β=1.05; p=3.66 × 10−08; n=206) in a locus not previously associated with antipsychotic-induced weight gain or body mass index. Minor allele carriers had an odds ratio of 3.98 (p=1.0 × 10−03) for clinically meaningful antipsychotic-induced weight gain (⩾7% of baseline weight). In silico analysis elucidated a chromatin interaction with 3-Hydroxy-3-Methylglutaryl-CoA Synthase 1. In an attempt to replicate single-nucleotide polymorphisms previously associated with antipsychotic-induced weight gain, we found none were associated with amisulpride-induced weight gain.Conclusion:Our findings suggest the involvement of rs78310016 and possibly 3-Hydroxy-3-Methylglutaryl-CoA Synthase 1 in antipsychotic-induced weight gain. In line with the unique binding profile of this atypical antipsychotic, our findings furthermore hint that biological mechanisms underlying amisulpride-induced weight gain differ from antipsychotic-induced weight gain by other atypical antipsychotics.

Neurocognitive variability in schizophrenia spectrum disorders: relationship to real-world functioning

Neurocognitive variability exists within the schizophrenia spectrum disorder (SSD) population, with subgroups performing at the same level as healthy samples Here we study the relationship between different levels of neurocognitive responding and real-world functioning. The participants were 291 SSD patients and 302 healthy controls that were assessed with a comprehensive neurocognitive battery. In addition, the patients were assessed with the Specific Level of Functioning Scale (SLOF). The results showed that the mean neurocognitive test responses of the SSD group were significantly below that of the control group. However, there was considerable overlap between the cognitive scores of the two groups, with as many as 24% of the patients performing above the mean healthy score for some domains. Moreover, the patients with the highest level of neurocognitive functioning reached the highest levels of practical and work-related functioning outcome skills. There was no significant relationship between neurocognitive and social function skills. The large differences in cognitive performance and their associations with functional outcome within the patient group are rarely addressed in clinical practice, but indicate a clear need for individualized treatment of SSD. Early identification of cognitive risk factors for poor real-life functional outcome is necessary in order to alert the clinical and rehabilitation services about patients in need of extra care.

Study protocol of a randomised clinical trial testing whether metacognitive training can improve insight and clinical outcomes in schizophrenia

BackgroundAlthough insight in schizophrenia spectrum disorders (SSD) has been associated with positive outcomes, the effect size of previous treatments on insight has been relatively small to date. The metacognitive basis of insight suggests that metacognitive training (MCT) may improve insight and clinical outcomes in SSD, although this remains to be established.MethodsThis single-center, assessor-blind, parallel-group, randomised clinical trial (RCT) aims to investigate the efficacy of MCT for improving insight (primary outcome), including clinical and cognitive insight, which will be measured by the Schedule for Assessment of Insight (Expanded version) (SAI-E) and the Beck Cognitive Scale (BCIS), respectively, in (at least) n = 126 outpatients with SSD at three points in time: i) at baseline (T0); ii) after treatment (T1) and iii) at 1-year follow-up (T2). SSD patients receiving MCT and controls attending a non-intervention support group will be compared on insight level changes and several clinical and cognitive secondary outcomes at T1 and T2, whilst adjusting for baseline data. Ecological momentary assessment (EMA) will be piloted to assess functioning in a subsample of participants.DiscussionTo the best of our knowledge, this will be the first RCT testing the effect of group MCT on multiple insight dimensions (as primary outcome) in a sample of unselected patients with SSD, including several secondary outcomes of clinical relevance, namely symptom severity, functioning, which will also be evaluated with EMA, hospitalizations and suicidal behaviour.Trial registrationClinicalTrials.gov: NCT04104347. Date of registration: 26/09/2019 (Retrospectively registered).

Cognitive validation of cross-diagnostic cognitive subgroups on the schizophrenia-bipolar spectrum

BackgroundCognitive heterogeneity in schizophrenia spectrum disorders (SSD) and bipolar disorder (BD) has been explored using clustering analyses. However, the resulting subgroups have not been cognitively validated beyond measures used as clustering variables themselves. We compared the emergent cross-diagnostic subgroups of SSD and BD patients on measures used to classify them, and also across a range of alternative cognitive measures assessing some of the same constructs. MethodDomain scores from the Matrics Consensus Cognitive Battery were used in a cross-diagnostic clustering analysis of 86 patients with SSD (n = 45) and BD (n = 41). The emergent subgroups were then compared to each other and healthy controls (n = 76) on these and alternative measures of these domains, as well as on premorbid IQ, global cognition and a proxy of cognitive decline. ResultsA three-cluster solution was most appropriate, with subgroups labelled as Globally Impaired, Selectively Impaired, and Superior/Near-Normal relative to controls. With the exception of processing speed performance, the subgroups were generally differentiated on the cognitive domain scores used as clustering variables. Differences in cognitive performance among these subgroups were not always statistically significant when compared on the alternative cognitive measures. There was evidence of global cognitive impairment and putative cognitive decline in the two cognitively impaired subgroups. LimitationsFor clustering analysis, sample size was relatively small. ConclusionsThe overall pattern of findings tentatively suggest that emergent cross-diagnostic cognitive subgroups are not artefacts of the measures used to define them, but may represent the outcome of different cognitive trajectories.

Anatomical integrity within the inferior fronto-occipital fasciculus and semantic processing deficits in schizophrenia spectrum disorders

The core symptoms of schizophrenia spectrum disorders (SSD) include abnormal semantic processing which may rely on the ventral language stream of the human brain. Thus, structural disruption of the ventral language stream may play an important role in semantic deficits observed in SSD patients.Therefore, we compared white matter tract integrity in SSD patients and healthy controls using diffusion tensor imaging combined with probabilistic fiber tractography. For the ventral language stream, we assessed the inferior fronto-occipital fasciculus [IFOF], inferior longitudinal fasciculus, and uncinate fasciculus. The arcuate fasciculus and corticospinal tract were used as control tracts. In SSD patients, the relationship between semantic processing impairments and tract integrity was analyzed separately. Three-dimensional tract reconstructions were performed in 45/44 SSD patients/controls (“Bern sample”) and replicated in an independent sample of 24/24 SSD patients/controls (“Basel sample”).Multivariate analyses of fractional anisotropy, mean, axial, and radial diffusivity of the left IFOF showed significant differences between SSD patients and controls (p(FDR-corr) < 0.001, ηp2 = 0.23) in the Bern sample. Axial diffusivity (AD) of the left UF was inversely correlated with semantic impairments (r = −0.454, p(FDR-corr) = 0.035). In the Basel sample, significant group differences for the left IFOF were replicated (p < .01, ηp2 = 0.29), while the correlation between AD of the left IFOF and semantic processing decline (r = −0.376, p = .09) showed a statistical trend. No significant effects were found for the dorsal language stream.This is direct evidence for the importance of the integrity of the ventral language stream, in particular the left IFOF, in semantic processing deficits in SSD.

Interaction of Cannabis Use Disorder and Striatal Connectivity in Antipsychotic Treatment Response.

Antipsychotic (AP) medications are the mainstay for the treatment of schizophrenia spectrum disorders (SSD), but their efficacy is unpredictable and widely variable. Substantial efforts have been made to identify prognostic biomarkers that can be used to guide optimal prescription strategies for individual patients. Striatal regions involved in salience and reward processing are disrupted as a result of both SSD and cannabis use, and research demonstrates that striatal circuitry may be integral to response to AP drugs. In the present study, we used functional magnetic resonance imaging (fMRI) to investigate the relationship between a history of cannabis use disorder (CUD) and a striatal connectivity index (SCI), a previously developed neural biomarker for AP treatment response in SSD. Patients were part of a 12-week randomized, double-blind controlled treatment study of AP drugs. A sample of 48 first-episode SSD patients with no more than 2 weeks of lifetime exposure to AP medications, underwent a resting-state fMRI scan pretreatment. Treatment response was defined a priori as a binary (response/nonresponse) variable, and a SCI was calculated in each patient. We examined whether there was an interaction between lifetime CUD history and the SCI in relation to treatment response. We found that CUD history moderated the relationship between SCI and treatment response, such that it had little predictive value in SSD patients with a CUD history. In sum, our findings highlight that biomarker development can be critically impacted by patient behaviors that influence neurobiology, such as a history of CUD.

Semantic Memory Impairment Across the Schizophrenia Continuum: A Meta-Analysis of Category Fluency Performance

Abstract Semantic memory (SM) impairments are a core feature of schizophrenia and are present along the psychosis continuum. It is, however, unclear whether the degree of SM impairments vary along this continuum and if demographic and clinical factors affect impairment severity. This study performed meta-analyses of category fluency task performance (a task commonly used to assess SM) in 4 groups along the schizophrenia continuum: high schizotypes (HSZT), first-degree relatives (FDR), recent-onset patients (≤2 y; ROP) and chronic patients (CSZ). Electronic databases were searched for relevant studies published up to October 2019 resulting in the inclusion of 48 articles. The main analyses assessed fluency productivity scores in 2978 schizophrenia spectrum disorder patients, 340 first-degree relatives of schizophrenia spectrum disorder patients, and 3204 healthy controls. Further analyses assessed errors, mean cluster size, and switching data that were available in the CSZ group only. Results revealed significant impairments in fluency productivity were present in the FDR, ROP, and CSZ groups relative to healthy controls, but not in HSZT. In the CSZ group, significant differences relative to healthy controls were also observed in non-perseverative errors, mean cluster size, and number of switches. The findings collectively suggest that SM deficits are present at each stage of the continuum and are exacerbated post-illness onset. They also support the centrality of SM impairments in schizophrenia and most elevated risk groups. Future studies with more diverse measures of SM function are needed to replicate and extend this research.

Leptin Serum Levels are Associated With GLP-1 Receptor Agonist-Mediated Effects on Glucose Metabolism in Clozapine- or Olanzapine-Treated, Prediabetic, Schizophrenia Patients

Abstract Background We previously demonstrated that the glucagon-like peptide-1 receptor agonist (GLP-1RA) liraglutide significantly reduced glucometabolic disturbances and body weight vs placebo in prediabetic, overweight, or obese schizophrenia-spectrum disorder patients treated with clozapine or olanzapine. Here, we aimed to identify potential biomarkers of prediabetes and the GLP-1RA-induced effects on glucose tolerance in schizophrenia patients treated with clozapine or olanzapine. Methods Multiplexed immunoassays were used to measure 8 proteins (adiponectin, C-reactive protein, interleukin-1 receptor antagonist, leptin, macrophage migration inhibitory factor, prolactin, receptor for advanced glycation end products, and vascular endothelial growth factor [VEGF]) in fasting prediabetic and non-prediabetic patients with schizophrenia-spectrum disorder, the prediabetic patients receiving 16-week randomized treatment with liraglutide or placebo. Results Serum adiponectin (P = .004) and VEGF (P = .019) levels were significantly lower in prediabetic (n = 81) than non-prediabetic schizophrenia-spectrum disorder patients (n = 32). Adiponectin levels increased significantly (P = .022) and leptin levels decreased significantly (P = .017) following treatment with liraglutide (n = 39) vs placebo (n = 42). Importantly, patients receiving liraglutide who had higher baseline leptin levels showed significantly larger reductions in the primary endpoint, the 75-g oral glucose tolerance test value, than patients with lower baseline leptin levels (P = .009). Conclusion These results provide new evidence for metabolic alterations associated with prediabetes and GLP-1RA treatment in the context of schizophrenia. They suggest that leptin may be a valuable biomarker predicting GLP-1RA-induced improvement in glucose tolerance in overweight or obese schizophrenia-spectrum disorder patients with prediabetes treated with clozapine or olanzapine. These findings require further validation in larger numbers of individuals.

The role of schizotypal traits and the OXTR gene in theory of mind in schizophrenia: A family-based study.

There is consistent evidence that theory of mind (ToM) is impaired in schizophrenia (SZ); however, it remains unclear whether such deficits are trait- or state-dependent. We evaluated ToM in patients with schizophrenia spectrum disorders (SSDs), their healthy first-degree relatives, and controls to test its suitability as an endophenotypic marker. We also studied the modifying effect of markers of clinical and genetic liability to SZ (schizotypy and genetic variability in the oxytocin receptor gene: OXTR) on ToM in healthy individuals. The sample included 38 stable SSD patients, 80 unaffected first-degree relatives, and 81 controls. ToM was assessed using the Hinting Task (HT) and schizotypy via the Schizotypal Personality Questionnaire-Brief (SPQ-B), which generates interpersonal (SPQ-IP), cognitive-perceptual (SPQ-CP), and disorganization (SPQ-D) scores. The polymorphism rs53576 of OXTR was genotyped. Patients presented poorer HT performance than relatives and controls (p=0.003 and p<0.001). High SPQ-IP and SPQ-CP scores correlated with poorer ToM performance in relatives (p=0.010 and p=0.030), but not in controls. OXTR was not associated with HT scores, but it showed a modifying effect within controls; high SPQ-CP was related to HT poorer performance conditional to GG genotype (p=0.007). ToM deficits were present in patients but not in unaffected relatives or controls. However, our data indicate the usefulness of clinical and genetic liability markers to characterize differences in ToM abilities within healthy individuals. Then, the observed link between ToM and SZ liability suggests the putative role of ToM as an endophenotypic marker. Nevertheless, new analyses in larger samples are needed.

PMH49 PERSONALIZED HEALTHCARE EPISODE IDENTIFICATION IN SCHIZOPHRENIA SPECTRUM DISORDER USING HEALTHCARE CONSUMPTION TRAJECTORIES

Background: Schizophrenia Spectrum Disorder (SSD) patients have repeated symptomatic relapses during their life course. A clear definition of such episodes is required to enable building patient level models describing episode patterns. In current literature, the definitions of relapse and episodes in SSD are mostly based on hospitalisation and occasionally on symptom scales. Hospitalisation rates are affected by deinstitutionalization, hence definitions of episodes should rather depend on healthcare intensity. We present a method for grouping healthcare consumption trajectories into episodes based on individual patterns of healthcare use. Methods: Administrative data describing the daily healthcare consumption of 13155 SSD patients in the Northern Netherlands is available for research. Data was collected between the years 2000 and 2012. Healthcare use costs are calculated using unit costs from a costing manual. We use Exponentially Weighted Moving Average (EWMA) control charts to distinguish two states of healthcare consumption based on intensity. Daily healthcare use weighted by cost is used as healthcare intensity. State transitions are determined on a patient level. The chart is restarted after a detected structural change. The approach is validated by determining the association between the Global Assessment of Functioning (GAF) scale and the episode state. Results: The mean number of episodes was 0.63 per patient per year. For the subsample without hospitalisations this was also 0.63. Average episode durations were similar with 235 and 245 days for the full- and subsample respectively. GAF scores have an inverse relationship with the episode state indicator. Conclusions: The Repeated Exponentially Weighted Moving Average Control Chart (REWMACC), using a daily healthcare intensity signal, is a feasible and promising tool in quantifying patient level SSD healthcare episodes, useful in health economic models to support prevention based healthcare. The results in the subgroup without hospitalizations show that the method is robust towards changes in health care policy.

Childhood trauma and hippocampal subfield volumes in first-episode schizophrenia and healthy controls

Childhood trauma and schizophrenia are both associated with neuroanatomical abnormalities in the hippocampus, a stress-sensitive structure vulnerable to developmental insults. However, few studies have evaluated the effects of childhood trauma exposure on hippocampal morphometry in minimally treated first-episode schizophrenia patients. Here we aim to investigate the associations of childhood trauma with hippocampal subfield volumes in a cohort of antipsychotic-naive or minimally treated first-episode schizophrenia spectrum disorder patients and matched controls. 79 patients with first-episode schizophrenia spectrum disorder and 82 matched controls completed the childhood trauma questionnaire and underwent MRI assessment. Hippocampal subfields were reconstructed using FreeSurfer 6.0. We considered inter-correlations between the various subfields, by entering them as dependent variables into a multivariate analysis of co-variance (MANCOVA), modeling for interactions between diagnosis, childhood trauma total score and gender while controlling for substance use, scanner sequence and age. MANCOVA revealed a significant interaction between sex, childhood trauma total scores and diagnosis across hippocampal sub-regions (p = 0.012). Bonferroni corrected post-hoc analysis revealed a significant sex*diagnosis*childhood trauma score interaction for the hippocampal fissure (F(1,161) = 9.485,p = .002). Hippocampal fissure size showed a positive relationship with CA structures as well as whole hippocampal size in the larger sample. Findings from the present study suggest that childhood trauma exposure exerts illness-specific effects on hippocampal structures in female patients with first-episode schizophrenia, consistent with increased stress sensitivity in this group.

Adverse childhood experiences and clinical severity in bipolar disorder and schizophrenia: A transdiagnostic two-step cluster analysis

BackgroundAdverse childhood experiences (ACEs) are risk factors for psychiatric disorders, but evidence about their relationship with clinical severity is limited. We aimed to classify patients according to ACEs and to compare these clusters with regards to the clinical severity. MethodsSeventy-four patients with Bipolar Disorder (BD) and 91 patients with a diagnosis within the Schizophrenia Spectrum Disorders (SSDs) were interviewed. The Childhood Experience of Care and Abuse scale (CECA) and the Positive and Negative Symptoms Scale (PANSS) were administered. A two-step cluster analysis was run to identify clusters according to ACEs. PANSS average scores were compared between clusters. ResultsThree clusters emerged; significant differences in ACEs distribution were evident. Cluster 1 was characterized by very low frequency of ACEs. ACEs related to lack of support/isolation were more frequent within Cluster 2, instead ACEs related to abuse/neglect were over represented in Cluster 3. The comparison of PANSS through ANOVA demonstrated that Cluster 3 not only had significantly higher scores in all dimensions than Cluster 1 and 2 but also a higher average number of ACEs. LimitationsCECA is a self-report scale and is subject to recall bias. ConclusionsSpecific ACEs are related to clinical severity among BD and SSD patients. Early life adversities related to abuse and neglect are associated to greater symptomatic severity than those related to lack of support/isolation. Our findings suggest that a history of ACEs could be used to identify patients at higher risk of unfavorable clinical features.

Gender differences in early onset of chronic physical multimorbidities in schizophrenia spectrum disorder: Do women suffer more?

The association between various physical illnesses and schizophrenia spectrum disorder (SSD) is well-established. However, the role of gender remains unclear. The present study explored the gender-based differences in the prevalence and early onset of chronic physical multimorbidities (CPM) in patients with SSD and the general population (GEP). We recruited 329 SSD patients and 837 GEP controls in this nested cross-sectional study. The primary outcome was the prevalence of the chronic physical multimorbidities, especially in the youngest age group (<35 years). Women with SSD had more than double the odds for having CPM than men (OR = 2.47; 95% CI 1.35-4.50), while the gender-related burden of chronic diseases in controls was nearly the same (OR = 0.89; 95% CI 0.65-1.22). Furthermore, the prevalence of chronic disease in younger women patients was significantly higher than in controls (P = .002), while younger men did not seem to experience this increased comorbidity burden. This study suggests that women with SSD are at increased physical comorbidity risk compared to men, particularly early in the course of psychiatric illness. Tailored and individualized treatment plans must consider this, aiming to deliver holistic care and effective treatment outcomes.

Patterns of co‐altered brain structure and function underlying neurological soft signs in schizophrenia spectrum disorders

Neurological soft signs (NSS) comprise a broad range of subtle neurological deficits and are considered to represent external markers of sensorimotor dysfunction frequently found in mental disorders of presumed neurodevelopmental origin. Although NSS frequently occur in schizophrenia spectrum disorders (SSD), specific patterns of co-altered brain structure and function underlying NSS in SSD have not been investigated so far. It is unclear whether gray matter volume (GMV) alterations or aberrant brain activity or a combination of both, are associated with NSS in SSD. Here, 37 right-handed SSD patients and 37 matched healthy controls underwent motor assessment and magnetic resonance imaging (MRI) at 3 T. NSS were examined on the Heidelberg NSS scale. We used a multivariate data fusion technique for multimodal MRI data-multiset canonical correlation and joint independent component analysis (mCCA + jICA)-to investigate co-altered patterns of GMV and intrinsic neural fluctuations (INF) in SSD patients exhibiting NSS. The mCCA + jICA model indicated two joint group-discriminating components (temporoparietal/cortical sensorimotor and frontocerebellar/frontoparietal networks) and one modality-specific group-discriminating component (p < .05, FDR corrected). NSS motor score was associated with joint frontocerebellar/frontoparietal networks in SSD patients. This study highlights complex neural pathomechanisms underlying NSS in SSD suggesting aberrant structure and function, predominantly in cortical and cerebellar systems that critically subserve sensorimotor dynamics and psychomotor organization.

Utilization of somatic healthcare in Croatian patients with schizophrenia spectrum disorder, major depression, PTSD and the general population

BackgroundUtilization of somatic healthcare services is highly predictive of the development of chronic physical illnesses and increased mortality risks. The objective of this study was to assess the differences in healthcare utilization among patients with schizophrenia spectrum disorders (SSD), major depressive disorder (MDD) and posttraumatic stress disorder (PTSD) and the general population in Croatia.MethodsWe enrolled 566 Croatian participants from the general population, 282 with SSD, 178 with MDD, and 86 with PTSD. The primary outcome was a self-reported specialist consultation for non-psychiatric (e.g., somatic) causes within the previous 12 months.ResultsAlthough SSD patients with chronic physical illnesses were significantly more often hospitalized for physical illness than the general population, the proportion of patients who had a specialist consultation were equal in SSD and the general population. MDD and PTSD patients had significantly higher adjusted odds for specialist consultation than the general population and SSD patients (MDD compared to SSD: OR = 2.14; 95% CI 1.27–3.59; PTSD compared to SSD: OR = 2.03; 95% CI 1.00–4.10).ConclusionsSSD patients’ utilization of somatic healthcare is equal to the general population, despite their increased healthcare needs. However, their utilization is lower than in MDD and PTSD patients and, therefore, probably not adequate.Trial registrationThe study protocol was registered at ClinicalTrials.gov (NCT02773108) on May 16, 2016.

Use of Long-Acting Injectable Antipsychotic in an Inpatient Unit of a Community Teaching Hospital.

Background Individuals with Schizophrenia Spectrum Disorders (SSD) often experience significant impairment in educational, occupational, and psychosocial functioning. The clinical benefit of long-acting injectable antipsychotics (LAIs) in the management of patients with SSD is well established. SSD patients who are nonadherent to treatment have lower disease relapse and readmission rates when prescribed a LAI, compared to oral antipsychotics. Despite the reported advantages of LAIs, their prescription rates in clinical settings remain low. This pilot study aimed to determine the pattern of LAI prescription in psychiatric inpatients of a teaching community hospital in Brooklyn, New York. Methods A retrospective review of the charts of patients discharged from the psychiatric units of the hospital from September 1, 2017, through September 30, 2017, was conducted. Frequencies and proportions for demographic and disease-related characteristics were calculated. Pertinent continuous variables were recoded into categorical variables. Chi-square-tests or Fisher's exact tests were performed for categorical variables. The one-sample Shapiro-Wilk test (for sample size < 50) was used to check for the normality of distribution of continuous variables. Statistical significance was defined as p ≤ 0.05. Results Forty-three (70%) of the patients discharged from the inpatient unit during the study period had SSD and were eligible for a LAI. Their ages ranged from 20 to 71 years (mean = 41 years), and more than two-thirds were male. Less than half of the eligible patients (n = 19; 44%) were prescribed a LAI, most of whom were male (n=16; 84%). An association between age group (patients aged 41 years or younger) and LAI use was observed (p < 0.05), while gender, employment status, living arrangement, length of hospital stay, recent hospitalization, and cooccurring substance use disorder were not. Conclusion LAI prescription rate at the inpatient psychiatric unit of the hospital was marginally higher than those reported in most studies. Age appears to influence LAI use during the study period. Initiatives that increase LAI prescription rate for all eligible patients admitted to inpatient psychiatric unit should be encouraged.

Multimodal Magnetic Resonance Imaging Data Fusion Reveals Distinct Patterns of Abnormal Brain Structure and Function in Catatonia

Catatonia is a nosologically unspecific syndrome, which subsumes a plethora of mostly complex affective, motor, and behavioral phenomena. Although catatonia frequently occurs in schizophrenia spectrum disorders (SSD), specific patterns of abnormal brain structure and function underlying catatonia are unclear at present. Here, we used a multivariate data fusion technique for multimodal magnetic resonance imaging (MRI) data to investigate patterns of aberrant intrinsic neural activity (INA) and gray matter volume (GMV) in SSD patients with and without catatonia. Resting-state functional MRI and structural MRI data were collected from 87 right-handed SSD patients. Catatonic symptoms were examined on the Northoff Catatonia Rating Scale (NCRS). A multivariate analysis approach was used to examine co-altered patterns of INA and GMV. Following a categorical approach, we found predominantly frontothalamic and corticostriatal abnormalities in SSD patients with catatonia (NCRS total score ≥ 3; n = 24) when compared to SSD patients without catatonia (NCRS total score = 0; n = 22) matched for age, gender, education, and medication. Corticostriatal network was associated with NCRS affective scores. Following a dimensional approach, 33 SSD patients with catatonia according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision were identified. NCRS behavioral scores were associated with a joint structural and functional system that predominantly included cerebellar and prefrontal/cortical motor regions. NCRS affective scores were associated with frontoparietal INA. This study provides novel neuromechanistic insights into catatonia in SSD suggesting co-altered structure/function-interactions in neural systems subserving coordinated visuospatial functions and motor behavior.

Differential contributions of brainstem structures to neurological soft signs in first- and multiple-episode schizophrenia spectrum disorders

Neurological soft signs (NSS) are frequently found in patients with schizophrenia spectrum disorders (SSD) at any stage of the disease. Brainstem structures are crucial for motor control, integration of sensory input and coordination of automatic motor actions. It is unclear whether disease duration has an impact on NSS/brainstem volume relationships. We tested the hypothesis that volumes of brainstem structures differ between first-episode psychosis (FEP) and multiple-episodes psychosis (MEP) patients with SSD, and that alterations of these structures are associated with NSS. T1-weighted structural MRI data at 3 T were obtained from 92 right-handed SSD patients (27 FEP and 65 MEP). FreeSurfer vers. 6.0 was used for segmentation of brainstem structures including the medulla oblongata, pons, superior cerebellar pedunculus (SCP), and midbrain. Multiple regression analyses were used to describe the relationship between brainstem structures and distinct NSS subdomains. In FEP, pons volume had a significant effect on NSS total score (p = 0.001, Bonferroni corr.). Further, medulla oblongata (p = 0.001, Bonferroni corr.) and pons (p = 0.001, Bonferroni corr.) volumes had a significant effect on NSS motor coordination score. In MEP, significant associations between brainstem structures and NSS levels were not found. The present data support the notion that brainstem structures play an important role in the expression of NSS in SSD individuals with FEP, in contrast to individuals with MEP. Our study also emphasizes the need of better characterizing episode-specific brainstem correlates of NSS in SSD.