Psychotic Symptoms In Schizophrenia Research Articles

Longitudinal analysis of astrocyte-derived protein levels in the blood of drug-naive and relapsed patients with schizophrenia

The potential influence of astrocytes on neuronal circuitry and psychotic symptoms in schizophrenia have recently been highlighted. Human postmortem studies have observed reduced astrocyte numbers in schizophrenia, but whether this pathology is present at disease onset or accumulates progressively with further psychotic episodes remains unclear.Therefore, we analysed serum levels of the astrocyte-derived proteins glial fibrillary acidic protein (GFAP) and fatty acid-binding protein 7 (FABP7) in acutely ill first-episode (n = 60) and relapsed (n = 34) schizophrenia patients compared to 94 matched controls. Measurements were taken before and 6 weeks after antipsychotic treatment. We found significantly lower levels of GFAP (p < 0.001) and FABP7 (p < 0.001) in patients compared to controls, with no significant differences between first-episode and relapsed patients or changes after treatment. FABP7 negatively correlated with age in controls (r = −0.319, p = 0.002), but not in patients (r = −0.251, p = 0.015). In contrast, GFAP showed no correlation with age.Our findings suggest that lowered GFAP and FABP7 may serve as trait markers of astrocyte pathology in schizophrenia, even prior to antipsychotic treatment. The absent correlation between FABP7 and age in schizophrenia patients, in contrast to controls, may be related to premature brain aging in schizophrenia. Long-term studies are needed to explore the relationship between chronic disease and astrocyte pathology in schizophrenia.

Neuregulin-1 immunoreactivity in peripheral plasma is associated with rs6982890 polymorphism-mediated psychotic symptoms in schizophrenia

ObjectivesNeuregulin 1 (NRG1) is a risk gene for schizophrenia and involved in neurodevelopment and synaptic plasticity. Polymorphisms in NRG1 may affect psychotic symptoms in schizophrenia. This study investigated the effects of the single nucleotide polymorphism (SNP) rs6982890 on peripheral plasma NRG1 immunoreactivity, clinical symptoms and cognitive functions in schizophrenia patients. Material and methodsWe recruited subjects from the Han population of northern China from 2010 to 2022. We first genotyped and analyzed 6 NRG1 SNPS in 1304 patients with schizophrenia and 871 healthy controls. Then, 91 patients with schizophrenia and 40 healthy controls were selected to detect the peripheral plasma NRG1 immunoreactivity by ELISA. Among them, 84 patients were divided into rs6982890 genotypes to analyze the correlation between NRG1 immunoreactivity and clinical symptoms. ResultsRs6982890 allelic frequencies were statistically significant between patients and controls. Baseline peripheral plasma NRG1 immunoreactivity in patients were significantly lower than controls. NRG1 immunoreactivity in patients were significantly increased after 8 weeks of antipsychotic treatment and significantly correlated with clinical symptoms and cognitive function. Genotyping of patients with SNP rs6982890 indicated NRG1 immunoreactivity in CC genotype increased significantly after treatment, while CT genotype had no significant change. Baseline NRG1 immunoreactivity with the CT genotype were significantly higher than CC genotype. ConclusionsNRG1 SNP rs6982890 is significantly associated with schizophrenia in the Han population of northern China, and it may affect the effect of antipsychotic drug treatment by regulating the peripheral plasma NRG1 immunoreactivity.

Kappa opioid receptor availability predicts severity of anhedonia in schizophrenia.

The kappa opioid receptor (KOR) and its endogenous agonist dynorphin have been implicated in multiple psychiatric conditions including psychotic disorders. We tested the hypotheses that kappa expression is elevated and associated with psychotic symptoms in schizophrenia. We measured kappa expression in unmedicated patients with schizophrenia (7 female, 6 male) and matched controls (7 female, 6 male) with positron emission tomography (PET). We also acquired a measurement of cumulative dopamine activity over the life span in the same subjects using neuromelanin sensitive MRI. We hypothesized that neuromelanin accumulation would be higher in patients than controls and that in patients there would be a positive association between KOR availability and neuromelanin accumulation. Fourteen patients and thirteen controls were enrolled. Whole brain dynamic PET imaging data using the KOR selective tracer [18F]LY245998 were acquired. Distribution volume (VT) was measured with region of interest analysis in 14 brain regions. Neuromelanin accumulation in midbrain dopaminergic nuclei was assessed in the same subjects. Positive and negative symptoms were measured by a clinical psychologist. We did not observe group level differences in KOR expression, neuromelanin accumulation or relationships of these to positive symptoms. Unexpectedly, we did observe strong positive associations between KOR expression and symptoms of anhedonia in the patients (Pearson r > 0.7, uncorrected p < 0.01 in 8 cortical brain regions). We also observed moderate associations between KOR expression and neuromelanin levels in patients. In conclusion, we did not observe a relationship between kappa and symptoms of psychosis but the observed relationship to the negative symptom of anhedonia is in line with recent work testing kappa antagonism as a therapy for anhedonia in depression.

Investigating changes in the premotor cortex-derived frontal-striatal-thalamic subcircuit in attenuated psychosis syndrome

Frontal-striatal-thalamic circuit impairment is presumed to underlie schizophrenia. Individuals with attenuated psychosis syndrome (APS) show longitudinal volume reduction of the putamen in the striatum, which has a neural connection with the premotor cortex through the frontal-striatal-thalamic subcircuit. However, comprehensive investigations into the biological changes in the frontal-striatal-thalamic subcircuit originating from the premotor cortex in APS are lacking. We investigated differences in fractional anisotropy (FA) values between the striatum and premotor cortex (ST-PREM) and between the thalamus and premotor cortex (T-PREM) in individuals with APS and healthy controls, using a novel method TractSeg. Our study comprised 36 individuals with APS and 38 healthy controls. There was a significant difference between the control and APS groups in the right T-PREM (odds ratio = 1.76, p = 0.02). Other factors, such as age, sex, other values of FA, and antipsychotic medication, were not associated with differences between groups. However, while FA value reduction of ST-PREM and T-PREM in schizophrenia has been previously reported, in the present study on APS, the alteration of the FA value was limited to T-PREM in APS. This finding suggests that ST-PREM impairment is not predominant in APS but emerges in schizophrenia. Impairment of the neural network originating from the premotor cortex can lead to catatonia and aberrant mirror neuron networks that are presumed to provoke various psychotic symptoms of schizophrenia. Our findings highlight the potential role of changes in a segment of the frontal-thalamic pathway derived from the premotor cortex as a biological basis of APS.

Sex differences in patient-reported outcome measure of psychotic symptoms in schizophrenia.

to study sex differences in self-reported symptoms measured with the Scale of Patient-Reported Impact of Symptoms in Schizophrenia (PRISS), to investigated sex differences in the degree of agreements between self-reported symptoms and clinical symptoms assessed by professionals, and to identify which clinical and sociodemographic variables predicted a greater presence of self-reported symptoms split by sex. 161 patients (37 females; 124 males), aged between 18 and 65 years, with a diagnosis of schizophrenia assisted in non-acute mental health services at four mental health catchment areas in Andalucia and Catalonia were included. The PRISS scale was administered to asses self-reported symptoms. males reported higher presence of excitement, grandiosity, motor retardation and poor attention) than women. There was less agreement in the presence of psychotic symptoms in men than in women when comparing self-reported symptoms and clinical symptoms assessed by professionals. Finally, in men the predictors variables for the greater presence of self-perceived symptoms were greater psychotic symptomatology and more disability, while in women were greater presence of alogia and higher doses of chlorpromazine. Assessing and being aware of the self-perceived symptoms of patients with schizophrenia should be considered in the clinic, especially in men, as there appears to be a lack of agreement on certain items. This would allow treatments to be more focused on patients' need by sex, and would make them feel part of the therapeutic process, improving their therapeutic adherence, evolution and quality of life.

Antipsychotic Effects of Celecoxib Add-On Haloperidol in Schizophrenia: A Randomized Double-Blind Placebo-Controlled Clinical Trial

Background: Previous studies have indicated abnormalities in the immune system, such as central nervous system inflammation and high levels of activating cytokines in the cerebrospinal fluid of schizophrenic patients. Celecoxib, a modulator of proinflammatory cytokines, as an adjunctive therapy add-on risperidone (a well-established atypical antipsychotic) and amisulpiride (a benzamide antipsychotic), had improved these patients significantly. Objectives: A trial was conducted to evaluate the therapeutic effects of celecoxib add-on haloperidol, a classic antipsychotic that has been reported to have an immunomodulatory effect and mainly affects positive psychotic symptoms in schizophrenia. Methods: In a prospective, double-blind study, after a washout period, 49 patients with schizophrenia were randomly assigned to either 15 - 30 mg/day haloperidol plus 400 mg/day of celecoxib or the same dose of haloperidol plus placebo for 5 weeks. Psychopathology was evaluated via the Positive and Negative Symptoms Scale (PANSS). The data were reported as mean ± standard deviation and frequency. An Independent t-test was carried out when comparing the data of these two groups for each week. The proportion comparison was carried out using the chi-square test. In terms of age, gender, marital and educational state, and duration or severity of disease or psychopathology and subtypes of schizophrenia, there were no significant differences. Results: Over 5 weeks, there was significantly greater improvement in the celecoxib group in scores on the total PANSS and on positive symptoms and general psychopathology subscales ([t = 2.89, P = 0.006], [t = 2.37, P = 0.022], and [t = 3.34, P = 0.002] respectively). Conclusions: Celecoxib is an efficient adjuvant agent in the treatment of patients with schizophrenia. Significant superiority of management with a modulator of proinflammatory cytokine, which balances immune responses over haloperidol alone, reconfirms the immune dysfunction and inflammation hypothesis of schizophrenia.

From gut to brain: A network model of intestinal permeability, inflammation, and psychotic symptoms in schizophrenia.

Impaired intestinal permeability has recently been suggested as a possible source of chronic inflammation in schizophrenia, but its association with specific psychopathological features remains uncertain. This study aimed to explore the interaction between intestinal permeability, inflammation, and positive and negative symptoms in schizophrenia using a network analysis approach. The study sample comprised 281 adults with schizophrenia (age 40.29 ± 13.65 years, 63.0 % males), enrolled in a cross-sectional observational study assessing intestinal permeability. We estimated the network with a Gaussian graphical model, incorporating scores from 14 individual items of the Positive and Negative Syndrome Scale (PANSS), along with body mass index (BMI), and plasma C-reactive protein (CRP) and lipopolysaccharide-binding protein (LBP) levels. We calculated strength centrality and expected influence and used bridge centrality statistics to identify the bridge nodes. Distinct but highly interconnected clusters emerged for positive and negative symptoms. The biological variables were closely associated with each other. LBP was positively linked with CRP and BMI, but only indirectly connected to psychopathology. CRP exhibited direct positive relationships with various PANSS items and bridged LBP and BMI with psychopathology. Bridge nodes included Conceptual Disorganisation (P2), Active Social Avoidance (G16), Suspiciousness/Persecution (P6), and CRP. These findings support the role of gut-derived inflammation as a mechanism underlying greater symptom severity in schizophrenia and emphasise the importance of addressing dietary habits not only to enhance physical health but also to contribute to improving psychotic symptoms.

Association between cognitive function and IL-18 levels in schizophrenia: Dependent on IL18 − 607 A/C polymorphism

Accumulating evidence suggests that immune system dysregulation is associated with debilitating neurodevelopment in schizophrenia (SZ). Cognitive impairment is a persistent feature that occurs during the onset of SZ and persists throughout the course of the disease. Early studies have found that elevated interleukin (IL)− 18 interacts with IL18 polymorphism and is correlated with psychotic symptoms in SZ. This study aimed to investigate whether elevated IL-18 levels interacted with the -607 A/C polymorphism to determine cognitive decline in patients with chronic SZ. We recruited 693 inpatients and 422 healthy controls to measure IL-18 levels and genotype the − 607 A/C polymorphism. Further, cognitive function was measured by the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). We found that IL-18 serum levels were higher in patients than those in healthy controls, and were not associated with IL18 − 607 A/C in combined subjects or either patients or healthy controls, respectively. Moreover, − 607 A/C was correlated with the visuospatial/constructional index only in the patients. In addition, our research found that IL-18 levels were positively correlated to immediate memory only in patients with the C/C genotype, but not in patients with C/A or A/A genotype. This study suggests that the relationship of IL-18 with cognitive function depends on the IL18 − 607 A/C polymorphism of SZ patients.

Sleep spindles across youth affected by schizophrenia or anti-N-methyl-D-aspartate-receptor encephalitis.

Sleep disturbances are intertwined with the progression and pathophysiology of psychotic symptoms in schizophrenia. Reductions in sleep spindles, a major electrophysiological oscillation during non-rapid eye movement sleep, have been identified in patients with schizophrenia as a potential biomarker representing the impaired integrity of the thalamocortical network. Altered glutamatergic neurotransmission within this network via a hypofunction of the N-methyl-D-aspartate receptor (NMDAR) is one of the hypotheses at the heart of schizophrenia. This pathomechanism and the symptomatology are shared by anti-NMDAR encephalitis (NMDARE), where antibodies specific to the NMDAR induce a reduction of functional NMDAR. However, sleep spindle parameters have yet to be investigated in NMDARE and a comparison of these rare patients with young individuals with schizophrenia and healthy controls (HC) is lacking. This study aims to assess and compare sleep spindles across young patients affected by Childhood-Onset Schizophrenia (COS), Early-Onset Schizophrenia, (EOS), or NMDARE and HC. Further, the potential relationship between sleep spindle parameters in COS and EOS and the duration of the disease is examined. Sleep EEG data of patients with COS (N = 17), EOS (N = 11), NMDARE (N = 8) aged 7-21 years old, and age- and sex-matched HC (N = 36) were assessed in 17 (COS, EOS) or 5 (NMDARE) electrodes. Sleep spindle parameters (sleep spindle density, maximum amplitude, and sigma power) were analyzed. Central sleep spindle density, maximum amplitude, and sigma power were reduced when comparing all patients with psychosis to all HC. Between patient group comparisons showed no differences in central spindle density but lower central maximum amplitude and sigma power in patients with COS compared to patients with EOS or NMDARE. Assessing the topography of spindle density, it was significantly reduced over 15/17 electrodes in COS, 3/17 in EOS, and 0/5 in NMDARE compared to HC. In the pooled sample of COS and EOS, a longer duration of illness was associated with lower central sigma power. Patients with COS demonstrated more pronounced impairments of sleep spindles compared to patients with EOS and NMDARE. In this sample, there is no strong evidence that changes in NMDAR activity are related to spindle deficits.

Proprioception and Tactile Perception in Schizophrenia

The aim of this review is to investigate the relationship between proprioceptive and tactile perceptual aberrations and the psychotic symptoms of schizophrenia, a correlation which has already been established by several studies (Lenzenweger, 2006; Postmes et al., 2014; Chang and Lenzenweger, 2005; Michael and Park, 2016; Germine et al., 2013; Kent et al., 2010). However, the direction of causality within the correlation is still unknown. Because several studies indicate an abnormal and uneven weighting of the senses in schizophrenic multisensory integration, it is possible that the psychotic symptoms of schizophrenia may be due to multisensory integration abnormalities involving proprioceptive and tactile perception. Several theories have also been proposed that schizophrenia itself is the cause of these proprioceptive and tactile perception anomalies. There could also be neuroanatomical factors that underlie both the schizophrenia psychotic symptoms and proprioceptive and tactile perception aberrations. Because of limitations in the current research, a definite causal direction is still unable to be determined. Several practices to improve the methods of analysis in this field of study include incorporating measures of schizotypy with less subjectivity and using longitudinal neurodevelopmental studies to pinpoint developmental aberrations in proprioception, tactile perception, and the correlated psychotic symptoms of schizophrenia. These methods may lead to better pre-emptive target interventions and could establish the directionality of causation between proprioception and tactile perception anomalies and positive schizophrenia symptoms.

Abnormal resting-state functional connectivity underlies cognitive and clinical symptoms in patients with schizophrenia.

The cognitive and psychotic symptoms in patients with schizophrenia (SZ) are thought to result from disrupted brain network connectivity. We capitalize on the high spatiotemporal resolution of magnetoencephalography imaging (MEG) to record spontaneous neuronal activity in resting state networks in 21 SZ compared with 21 healthy controls (HC). We found that SZ showed significant global disrupted functional connectivity in delta-theta (2-8 Hz), alpha (8-12 Hz), and beta (12-30 Hz) frequencies, compared to HC. Disrupted global connectivity in alpha frequencies with bilateral frontal cortices was associated with more severe clinical psychopathology (i.e., positive psychotic symptoms). Specifically, aberrant connectivity in beta frequencies between the left primary auditory cortex and cerebellum, was linked to greater hallucination severity in SZ. Disrupted connectivity in delta-theta frequencies between the medial frontal and left inferior frontal cortex was associated with impaired cognition. The multivariate techniques employed in the present study highlight the importance of applying our source reconstruction techniques which leverage the high spatial localization abilities of MEG for estimating neural source activity using beamforming methods such as SAM (synthetic aperture morphometry) to reconstruct the source of brain activity, together with functional connectivity assessments, assayed with imaginary coherence metrics, to delineate how neurophysiological dysconnectivity in specific oscillatory frequencies between distinct regions underlie the cognitive and psychotic symptoms in SZ. The present findings employ powerful techniques in spatial and time-frequency domains to provide potential neural biomarkers underlying neuronal network dysconnectivity in SZ that will inform the development of innovations in future neuromodulation treatment development.

Prospects for Neurotrophic Factor-Based Early Intervention in Schizophrenia: Lessons Learned from the Effects of Antipsychotic Drugs on Cognition, Neurogenesis, and Neurotrophic Factors.

Although reducing psychotic symptoms in schizophrenia has been a major focus of therapeutic interventions for decades, improving cognition is considered a better predictor of functional outcomes. However, the most commonly prescribed antipsychotic drugs (APDs) show only marginal beneficial effects on cognition in patients with schizophrenia. The neural mechanisms underlying cognitive disturbances in schizophrenia remain unknown that making drug development efforts very challenging. Since neurotrophic factors are the primary architects of neurogenesis, synaptic plasticity, learning, and memory, the findings from preclinical and clinical studies that assess changes in neurogenesis and neurotrophic factors and their relationship to cognitive performance in schizophrenia, and how these mechanisms might be impacted by APD treatment, may provide valuable clues in developing therapies to combat cognitive deficit in schizophrenia. Numerous evidence produced over the years suggests a deficit in a wide spectrum of neurotrophic factors in schizophrenia. Since schizophrenia is considered a neurodevelopmental disorder, early intervention with neurotrophic factors may be more effective in ameliorating the cognitive deficits and psychopathological symptoms associated with this pathology. In this context, results from initial clinical trials with neurotrophic factors and their future potential to improve cognition and psychosocial functioning in schizophrenia are discussed.

Schizophrenia plus - comorbidity of schizophrenia and personality disorders. Clinician's reflections.

The diagnostic criteria for schizophrenia and the diagnostic criteria for personality disorders refer to the same dimensions of mental functioning, except for the presence of typical psychotic symptoms in schizophrenia (hallucinations, delusions and catatonic behaviours). Since schizophrenia is a psychosis with a predominantly chronic course, with exacerbations and steady course periods, a simultaneous diagnosis of personality disorders, which are also "permanent" in nature, and a significant part of which affect the same areas of mental functioning, in the same patient is at least controversial. Although therapeutic interventions in patients with schizophrenia are mainly based on pharmacotherapy, psychotherapy and work with the patient's family are also important. Since pharmacotherapy is virtually ineffective for personality disorders, psychotherapy is the main form of management. This however does not constitute a justification for a simultaneous use of these two diagnoses in the same patient.

Abnormal Information Flow in Schizophrenia Is Linked to Psychosis.

Prior research has shown that patients with schizophrenia (SZ) show disruption in brain network connectivity that is thought to underlie their cognitive and psychotic symptoms. However, most studies examining functional network disruption in schizophrenia have focused on the temporally correlated coupling of the strength of network connections. Here, we move beyond correlative metrics to assay causal computations of connectivity changes in directed neural information flow, assayed from a neural source to a target in SZ. This study describes a whole-brain magnetoencephalography-imaging approach to examine causal computations of connectivity changes in directed neural information flow between brain regions during resting states, quantified by phase-transfer entropy (PTE) metrics, assayed from a neural source to an endpoint, in 21 SZ compared with 21 healthy controls (HC), and associations with cognitive and clinical psychotic symptoms in SZ. We found that SZ showed significant disruption in information flow in alpha (8-12 Hz) and beta (12-30 Hz) frequencies, compared to HC. Reduced information flow in alpha frequencies from the precuneus to the medio-ventral occipital cortex was associated with more severe clinical psychopathology (ie, positive psychotic symptoms), while reduced information flow between insula and middle temporal gyrus was associated with worsening cognitive symptoms. The present findings highlight the importance of delineating dysfunction in neural information flow in specific oscillatory frequencies between distinct regions that underlie the cognitive and psychotic symptoms in SZ, and provide potential neural biomarkers that could lead to innovations in future neuromodulation treatment development.

Aberrant salience correlates with psychotic dimensions in outpatients with schizophrenia spectrum disorders

BackgroundAberrant salience is a well-known construct associated with the development and maintenance of psychotic symptoms in schizophrenia. However, only a few studies have investigated aberrance salience as a trait, with no study investigating the association between the five aberrant salience domains and psychotic symptoms. We aimed to explore the role of aberrant salience and its domains on psychotic dimensions in both clinically remitted and non-remitted patients.MethodsA sample of 102 patients diagnosed with schizophrenia spectrum disorders was divided according to the Positive and Negative Syndrome Scale (PANSS) remission criteria into two groups: remitted and non-remitted. Differences regarding psychotic symptomatology assessed by the PANSS and aberrant salience measured by the Aberrant Salience Inventory (ASI) were explored. Finally, a correlation analysis between the PANSS and the ASI was run.ResultsSignificantly higher ASI scores were evident among non-remitted patients. Positive symptoms (i.e. delusions, conceptual disorganization, and hallucinatory behaviour) and general psychopathology (i.e. postural mannerisms, unusual thought content) were correlated to the aberrant salience subscales ‘sharpening of senses’, ‘heightened emotionality’ and ‘heightened cognition’ and with the ASI total score. Significant correlations emerged between negative symptoms (blunted affect and social withdrawal) and ‘heightened cognition'. Finally, lack of spontaneity of conversation was related to the subscales ‘heightened emotionality’ and ‘heightened cognition’, as well as to the ASI total score.ConclusionsThese preliminary results support the hypothesis of an association between aberrant salience and psychotic symptoms in schizophrenia. Further research is needed, especially into the mechanisms underlying salience processing, in addition to social and environmental factors and cognitive variables.

Progressive Changes in Brain Regional Homogeneity Induced by Electroconvulsive Therapy Among Patients With Schizophrenia.

Electroconvulsive therapy (ECT) has significant effects on improving psychotic symptoms in schizophrenia (SZ), but the changes of brain function induced by it are unclear. The purpose of the study was to explore progressive ECT-induced changes in regional homogeneity (ReHo) at multiple time points before, during, and after a course of ECT. The 27 in-patients with SZ (SZ group) who met the recruitment criteria accepted clinical evaluations and resting-state functional magnetic resonance imaging scans before the first ECT (pre-ECT), after the first ECT (ECT1), and after the eighth ECT (ECT8), all conducted within 10 to 12 hours. Forty-three healthy controls (HCs; HC group) who matched well with the patients for age, sex, and years of education were recruited. For Positive and Negative Syndrome Scale (PANSS) and ReHo, progressive changes were examined. Pair-wise comparisons of patient pre-ECT, ECT1, and ECT8 ReHo values with HC ReHo values revealed that ECT normalized the ReHo values in bilateral superior occipital gyrus (SOG), right lingual gyrus (LG), left medial prefrontal cortex. Furthermore, improved ReHo in bilateral SOG and right LG appeared after the first ECT application. The ReHo values in right middle occipital gyrus, right middle temporal gyrus, and right inferior parietal lobule were not significantly altered by ECT. The total PANSS score was lower even after the first ECT application (mean ΔPANSSECT1, 11.7%; range, 2%-32.8%) and markedly reduced after the eighth application (mean ΔPANSSECT8, 86.3%; range, 72.5%-97.9%). The antipsychotic effects of ECT may be achieved through regulating synchronization of some regions such as bilateral SOG, right LG, and left medial prefrontal cortex. Furthermore, the enhanced synchronizations also take place in other regions.

The Comparison Between Positive and Negative Symptoms Severity in Prolonged Methamphetamine-induced Psychotic Disorder and Schizophrenia.

This study aims to compare the positive and negative symptoms of schizophrenia in patients who had psychotic symptoms more than one month after discontinuation of methamphetamine abuse. These factors were analyzed by the positive and negative syndrome scale (PANSS) questionnaire. Sixty participants were selected from patients referred to Iran Psychiatric Hospital with psychotic symptoms (delusions or hallucinations, disorganized behavior, and speech). The control group was 30 patients with schizophrenia based on a semi-structured interview according to DSMIV-TR (SCID). Thirty patients with a prolonged methamphetamine-induced psychotic disorder were also placed in the case group. For both groups of patients, questionnaires of PANSS, Brief Psychiatric Rating Scale (BPRS), and Global Assessment Of Functioning (GAF) were filled out after obtaining the companions' consent. The scale scores were compared between groups. We used the Mann-Whitney and the Chi-square test to evaluate the mean values of PANSS, BPRS, and GAF scores between the two groups. here was an insignificant difference in positive and general pathology scores between the two groups, but the total score of negative symptoms in the schizophrenia group was significantly higher than in the group of prolonged methamphetamine psychotic disorders (P=0.034). Average scores of uncooperativeness (0.008), difficulty in abstract thinking (0.004), motor retardation (0.002), unusual thought content (0.001), and hostility (0.011) in the schizophrenia group were significantly higher than those in the prolonged methamphetamine psychosis. The results showed that most of the disturbances in patients with schizophrenia might be more influenced by the expression of cognitive disabilities than those with methamphetamine psychosis. The difference in negative symptom scores suggests that schizophrenia and prolonged methamphetamine psychotic disorder can be two different disorders. General and positive symptoms scores don't have significant differences.Negative symptoms are much more in schizophrenia.Uncooperativeness, unusual thought content and, motor retardation have more scores in schizophrenia. In clinical practice, Schizophrenia and prolonged methamphetamine-induced psychotic disorder have some similar mental presentations. Additionally, in scientific literature, there is scarce evidence about these similarities. In this regard, this research was designed to investigate the aforementioned obscurity. Determination of similarities and differences between them helps us to address these disorders in terms of treatment and follow-up and awareness of their prognosis of them. This research is a case-control study in which we examine positive and negative psychotic symptoms in schizophrenia and prolonged methamphetamine-induced psychotic disorder. Researchers investigated psychotic symptoms with positive and negative syndrome scale (PANSS), brief psychiatric rating scale (BPRS), and global assessment of functioning (GAF) questionnaires. Moreover, results demonstrate general and positive symptoms scores don't have many differences but negative symptoms are much more in patients with schizophrenia than in patients with a prolonged methamphetamine-induced psychotic disorder. Also, other features like uncooperativeness, unusual thought content, motor retardation, difficulty in abstract thinking, and hostility have higher scores in schizophrenia than the others. In conclusion, this research showed that these disorders are two distinct disorders with some similarities in positive symptoms but not in all features. So, some studies can be designed about why there are similarities between them?

Differential effects of chronic adolescent glucocorticoid or methamphetamine on drug-induced locomotor hyperactivity and disruption of prepulse inhibition in adulthood in mice

Sensitization of dopaminergic activity has been suggested as an underlying mechanism in the psychotic symptoms of schizophrenia. Adolescent stress and chronic abuse of methamphetamine (Meth) are well-known risk factors for psychosis and schizophrenia; however it remains unknown how these factors compare in terms of dopaminergic behavioural sensitization in adulthood. In addition, while Brain-Derived Neurotrophic Factor (BDNF) has been implicated in dopaminergic activity and schizophrenia, its role in behavioural sensitization remains unclear. In this study we therefore compared the effect of chronic adolescent treatment with the stress hormone, corticosterone (Cort), or with Meth, on drug-induced locomotor hyperactivity and disruption of prepulse inhibition in adulthood in BDNF heterozygous mice and their wild-type controls, as well as on dopamine receptor gene expression. Between 6 and 9 weeks of age, the animals either received Cort in the drinking water or were treated with an escalating Meth dose protocol. In adulthood, Cort-pretreated mice showed significantly reduced Meth-induced locomotor hyperactivity compared to vehicle-pretreated mice. In contrast, Meth hyperlocomotion was significantly enhanced in animals pretreated with the drug in adolescence. There were no effects of either pretreatment on prepulse inhibition. BDNF Het mice showed greater Meth-induced hyperlocomotion and lower prepulse inhibition than WT mice. There were no effects of either pretreatment on D1 or D2 gene expression in either the dorsal or ventral striatum, while D3 mRNA was shown to be reduced in male mice only irrespective of genotype. These results suggest that in adolescence, chronically elevated glucocorticoid levels, a component of chronic stress, do not cause dopaminergic sensitization adulthood, in contrast to the effect of chronic Meth treatment in the same age period. BDNF does not appear to be involved in the effects of chronic Cort or chronic Meth.

Features of Psychotic Symptoms in Methamphetamine Use Disorder Patients and Ketamine Use Disorder Patients: A Cross-Sectional Study.

BackgroundMethamphetamine and ketamine are commonly used club drugs. Both of them have been reported to mimic psychotic symptoms of schizophrenia. However, the prevalence and detailed features of psychotic symptoms among methamphetamine use disorder (MUD) and ketamine use disorder (KUD) patients are largely unknown. This study aimed to measure psychotic symptoms among patients with MUD and KUD.MethodsA total sample of 842 patients from voluntary drug rehabilitation centers, including 462 MUD patients and 380 KUD patients, were invited to this study. The Positive and Negative Syndrome Scale (PANSS) was applied to assess psychotic symptoms in these two groups of patients.ResultsThe prevalence of psychotic symptoms was significantly higher among MUD patients than KUD patients (75.1 vs. 50.5%, 95% CI: 3.532 – 11.858, p < 0.001). Compared with KUD patients, MUD patients were more likely to experience positive symptoms (PANSS positive scores: 11.5 ± 6.07 vs. 15.1 ± 8.22, P < 0.001) and negative symptoms (PANSS negative scores: 12.4 ± 6.60 vs. 14.5 ± 8.63, P < 0.001), but not general symptoms (PANSS general scores: 31.2 ± 13.90 vs. 32.2 ± 15.13, P < 0.001).ConclusionsThe current study found that more than half of MUD and KUD patients experienced psychotic symptoms, and that patients with MUD are more likely to experience positive and negative symptoms than patients with KUD. The findings provide a new perspective for exploring the neuropathological mechanism of psychotic symptoms of schizophrenia.

Adjunctive Magnetic Seizure Therapy for Schizophrenia: A Systematic Review

Objective: The efficacy and safety of adjunctive magnetic seizure therapy (MST) for patients with schizophrenia are unclear. This systematic review was conducted to examine the efficacy and safety of adjunctive MST for schizophrenia.Methods: Chinese (WanFang and Chinese Journal Net) and English (PubMed, EMBASE, PsycINFO, and the Cochrane Library) databases were systematically searched.Results: Two open-label self-controlled studies (n = 16) were included and analyzed in this review. In these studies, the Positive and Negative Syndrome Scale (PANSS) total scores and Brief Psychiatric Rating Scale (BPRS) total scores significantly decreased from baseline to post-MST (all Ps < 0.05), without serious adverse neurocognitive effects. Mixed findings on the neurocognitive effects of adjunctive MST for schizophrenia were reported in the two studies. A discontinuation rate of treatment of up to 50% (4/8) was reported in both studies. The rate of adverse drug reactions (ADRs) was evaluated in only one study, where the most common ADRs were found to be dizziness (25%, 2/8) and subjective memory loss (12.5%, 1/8).Conclusion: There is inconsistent evidence for MST-related adverse neurocognitive effects and preliminary evidence for the alleviation of psychotic symptoms in schizophrenia.