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In a randomized trial involving schizophrenic patients with acute psychosis, a new oral drug that does not have a dopamine D2-receptor–binding mechanism of action led to a greater reduction in the severity of overall symptoms than placebo over 4 weeks. The incidence of extrapyramidal symptoms was 3% with the new drug, a finding similar to that with placebo.

Abstract Cognitive dysfunction is a core feature of schizophrenia. The subtyping of cognitive performance in schizophrenia may aid the refinement of disease heterogeneity. The literature on cognitive subtyping in schizophrenia, however, is limited by variable methodologies and neuropsychological tasks, lack of validation, and paucity of studies examining longitudinal stability of profiles. It is also unclear if cognitive profiles represent a single linear severity continuum or unique cognitive subtypes. Cognitive performance measured with the Brief Assessment of Cognition in Schizophrenia was analyzed in schizophrenia patients (n = 767). Healthy controls (n = 1012) were included as reference group. Latent profile analysis was performed in a schizophrenia discovery cohort (n = 659) and replicated in an independent cohort (n = 108). Longitudinal stability of cognitive profiles was evaluated with latent transition analysis in a 10-week follow-up cohort. Confirmatory factor analysis (CFA) was carried out to investigate if cognitive profiles represent a unidimensional structure. A 4-profile solution was obtained from the discovery cohort and replicated in an independent cohort. It comprised of a “less-impaired” cognitive subtype, 2 subtypes with “intermediate cognitive impairment” differentiated by executive function performance, and a “globally impaired” cognitive subtype. This solution showed relative stability across time. CFA revealed that cognitive profiles are better explained by distinct meaningful profiles than a severity linear continuum. Associations between profiles and negative symptoms were observed. The subtyping of schizophrenia patients based on cognitive performance and its associations with symptomatology may aid phenotype refinement, mapping of specific biological mechanisms, and tailored clinical treatments.

Schizophrenia(SZ) classification and treatment response prediction hold substantial clinical application value. However, only a limited number of researchers have exploited the multi-feature information derived from resting-state functional magnetic resonance imaging (rs-fMRI) to achieve short-term drug-treatment SZ classification and treatment response prediction. We developed a multi-feature fusion recursive feature elimination random forest (RFE-RF) approach for SZ classification and treatment response prediction. Initially, we computed multiple features, such as regional homogeneity, fractional amplitude of low-frequency fluctuations, and functional connectivity. Subsequently, the RFE-RF method was employed to conduct SZ classification. Moreover, we utilized the rate of score reduction (RR) of the Positive and Negative Symptom Scale (PANSS) to forecast the treatment response of individual patients. Finally, we identified the neuroimaging biomarkers for SZ classification and drug-treatment response prediction. This method achieved the classification results (accuracy = 91.7%, sensitivity = 90.9%, and specificity = 92.6%), and the abnormalities in the visual and default mode networks emerged as potential neuroimaging biomarkers for differentiating SZ from healthy controls (HC). Additionally, we predicted the drug-treatment response of SZ patients in terms of their total PANSS scores, as well as negative and positive symptom scores after eight weeks of treatment. Specifically, the abnormalities in the visual network, sensorimotor network, and right superior frontal gyrus are crucial biomarkers for the short-term drug-treatment response of negative symptoms in SZ patients. Meanwhile, the abnormalities in the visual and default mode networks serve as important biomarkers of the short-term drug-treatment response of positive symptoms. There findings offer novel insights into the neural mechanisms underlying SZ following eight weeks of short-term drug treatment. With further clinical validation in the future, this research may provide potential biomarkers and intervention targets for personalized treatment of SZ.

Currently available laboratory procedures might provide additional information to psychiatric diagnostic systems for more valid classifications of mental disorders. To identify the correlative pattern of gray matter distribution that best discriminates schizophrenia patients from healthy subjects, we applied discriminant function analysis techniques using the multivariate linear model and the voxel-based morphometry. The first analysis was conducted to obtain a statistical model that classified 30 male healthy subjects and 30 male schizophrenia patients diagnosed according to current operational criteria. The second analysis was performed to prospectively validate the statistical model by successfully classifying a new cohort that consisted of 16 male healthy subjects and 16 male schizophrenia patients. Inferences about the structural relevance of the gray matter distribution could be made if the individual profile of pattern expression could be linked to the specific diagnosis of each subject. The result was that 90% of the subjects were correctly classified by the eigenimage, and the Jackknife approach revealed well above chance accuracy. The pattern of the eigenimage was characterized by positive loadings indicating gray matter decline in the patients in the lateral and medial prefrontal regions, insula, lateral temporal regions, medial temporal structures, and thalamus as well as the negative loadings reflecting gray matter increase in the patients in the putamen and cerebellum. When the eigenimage derived from the original cohort was applied to classify data from the second cohort, it correctly assigned more than 80% of the healthy subjects and schizophrenia patients. These findings suggest that the characteristic distribution of gray matter changes may be of diagnostic value for schizophrenia.

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) was published by the American Psychiatric Association (APA) in 2013, and the Work Group on the Classification of Psychotic disorders (WGPD), installed by the World Health Organization (WHO), is expected to publish the new chapter about schizophrenia and other primary psychotic disorders in 2017. We reviewed the available literature to summarize the major changes, innovations, and developments of both manuals. If available and possible, we outline the theoretical background behind these changes. Due to the fact that the development of ICD-11 has not yet been completed, the details about ICD-11 are still proposals under ongoing revision. In this ongoing process, they may be revised and therefore have to be seen as proposals. DSM-5 has eliminated schizophrenia subtypes and replaced them with a dimensional approach based on symptom assessments. ICD-11 will most likely go in a similar direction, as both manuals are planned to be more harmonized, although some differences will remain in details and the conceptual orientation. Next to these modifications, ICD-11 will provide a transsectional diagnostic criterion for schizoaffective disorders and a reorganization of acute and transient psychotic and delusional disorders. In this manuscript, we will compare the 2 classification systems.

Preventing relapse is an important goal in treating patients with schizophrenia or schizoaffective disorder. This study compared risperidone, a newer, atypical antipsychotic medication, and haloperidol, an older, conventional neuroleptic drug, for the prevention of relapse in clinically stable adult outpatients. Patients treated with risperidone had a lower risk of relapse. Patients treated with risperidone had a lower risk of relapse. Schizophrenia is a chronic illness with a lifetime prevalence of 0.7 percent in the United States 1 and with serious physical, social, and economic consequences. 2 The economic burden of schizophrenia on society was estimated as $33 billion in the United States in 1990. 3 Much of this cost was attributed to the consequences of psychotic relapse. 4 The course of schizophrenia varies, 5 but most patients have a chronic course with frequent relapses, typically characterized by exacerbation of psychosis and rehospitalization. Successive relapses can reduce the degree and duration of the next remission, worsen disability, and increase refractoriness to future treatment. 6 To prevent relapse, . . .

Abstract We can trace, with high congruence, the clinical syndromes of depression and mania as described over the 20th century in psychiatric textbooks back to 1880 and to the earliest writing of Kraepelin published in 1883. However, this is not the case for Kraepelin’s 2 delusional syndromes central to his overall nosology: Dementia Paranoides (later paranoid schizophrenia) and Paranoia. A detailed examination of 28 textbook descriptions of delusional psychoses from 1880 to 1900 reveals a diverse and partially overlapping set of syndromes with an admixture of symptoms and signs that would later be considered indicative of Dementia Paranoides and Paranoia. A similar pattern in seen in Kraepelin’s own description of “Primäre Verrücktheit” from the first edition of his textbook (1883). No clear prototypes emerged in these textbooks or in Kraepelin’s early writings for the 2 distinct delusional syndromes that would later evolve in his mature writings. Rather, the nosologic approach taken in these writings was symptom based and assumed that a viable diagnostic category could be constituted by including all delusional patients once those suffering from organic or mood disorders were excluded. While Kraepelin used the historical syndromes of mania and depression, with no appreciable change, as building blocks for his category of manic-depressive insanity, his nosologic system for the psychotic disorders—the syndromes of Dementia Praecox and Paranoia—was more innovative and without clear precedent in the prior psychiatric literature.

While the roots of mania and melancholia can be traced to the 18th century and earlier, we have no such long historical narrative for dementia praecox (DP). I, here, provide part of that history, beginning with Kraepelin’s chapter on Verrücktheit for his 1883 first edition textbook, which, over the ensuing 5 editions, evolved into Kraepelin’s mature concepts of paranoia and paranoid DP. That chapter had 5 references published from 1865 to 1879 when delusional-hallucinatory syndromes in Germany were largely understood as secondary syndromes arising from prior episodes of melancholia and mania in the course of a unitary psychosis. Each paper challenged that view supporting a primary Verrücktheit as a disorder that should exist alongside mania and melancholia. The later authors utilized faculty psychology, noting that primary Verrücktheit resulted from a fundamental disorder of thought or cognition. In particular, they argued that, while delusions in mania and melancholia were secondary, arising from primary mood changes, in Verrücktheit, delusions were primary with observed changes in mood resulting from, and not causing, the delusions. In addition to faculty psychology, these nosologic changes were based on the common-sense concept of understandability that permitted clinicians to distinguish individuals in which delusions emerged from mood changes and mood changes from delusions. The rise of primary Verrücktheit in German psychiatry in the 1860–1870s created a nosologic space for primary psychotic illness. From 1883 to 1899, Kraepelin moved into this space filling it with his mature diagnoses of paranoia and paranoid DP, our modern-day paranoid schizophrenia.

The subtype system for categorising presentations of schizophrenia will be removed from International Classification of Diseases 11th Revision. In its place will be a system for rating six domains of psychotic disorder pathology: positive symptoms, negative symptoms, depressive symptoms, manic symptoms, psychomotor symptoms and cognitive symptoms. This paper outlines the rationale and description of the proposed symptom rating scale, including current controversies. In particular, the scale could adopt either a 4-point severity rating or a 2-point presence/absence rating. The 4-point scale has the advantage of gathering more information, but potentially at the cost of reliability. The paper concludes by describing the field testing process for evaluating the proposed scale.

Accumulating evidence from both genetic and clinico-pharmacological studies suggests that D -serine, an endogenous coagonist to the NMDA subtype glutamate receptor, may be implicated in schizophrenia (SZ). Although an association of genes for D -serine degradation, such as D -amino acid oxidase and G72, has been reported, a role for D -serine in SZ has been unclear. In this study, we identify and characterize protein interacting with C-kinase (PICK1) as a protein interactor of the D -serine synthesizing enzyme, serine racemase (SR). The binding of endogenous PICK1 and SR requires the PDZ domain of PICK1. The gene coding for PICK1 is located at chromosome 22q13, a region frequently linked to SZ. In a case–control association study using well-characterized Japanese subjects, we observe an association of the PICK1 gene with SZ, which is more prominent in disorganized SZ. Our findings implicating PICK1 as a susceptibility gene for SZ are consistent with a role for D -serine in the disease.