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Glutamate-N-methyl-D-aspartate receptor modulation and minocycline for the treatment of patients with schizophrenia: an update
Chaves, C.;Marque, C.R.;Trzesniak, C.;Machado de Sousa, J.P.;Zuardi, A.W.;Crippa, J.A.S.;Dursun, S.M.;Hallak, J.E.;
Brazilian Journal of Medical and Biological Research , 2009, DOI: 10.1590/S0100-879X2009001100002
Abstract: growing consistent evidence indicates that hypofunction of n-methyl-d-aspartate (nmda) transmission plays a pivotal role in the neuropathophysiology of schizophrenia. hence, drugs which modulate nmda neurotransmission are promising approaches to the treatment of schizophrenia. the aim of this article is to review clinical trials with novel compounds acting on the nmda receptor (nmda-r). this review also includes a discussion and translation of neuroscience into schizophrenia therapeutics. although the precise mechanism of action of minocycline in the brain remains unclear, there is evidence that it blocks the neurotoxicity of nmda antagonists and may exert a differential effect on nmda signaling pathways. we, therefore, hypothesize that the effects of minocycline on the brain may be partially modulated by the nmda-r or related mechanisms. thus, we have included a review of minocycline neuroscience. the search was performed in the pubmed, web of science, scielo, and lilacs databases. the results of glycine and d-cycloserine trials were conflicting regarding effectiveness on the negative and cognitive symptoms of schizophrenia. d-serine and d-alanine showed a potential effect on negative symptoms and on cognitive deficits. sarcosine data indicated a considerable improvement as adjunctive therapy. finally, minocycline add-on treatment appears to be effective on a broad range of psychopathology in patients with schizophrenia. the differential modulation of nmda-r neurosystems, in particular synaptic versus extrasynaptic nmda-r activation and specific subtypes of nmda-r, may be the key mediators of neurogenesis and neuroprotection. thus, psychotropics modulating nmda-r neurotransmission may represent future monotherapy or add-on treatment strategies in the treatment of schizophrenia.
Sleep dysfunctions in schizophrenia: A practical review  [PDF]
Flavie Waters, Dara S. Manoach
Open Journal of Psychiatry (OJPsych) , 2012, DOI: 10.4236/ojpsych.2012.224054
Abstract: Objective: Sleep dysfunctions are common in schizophrenia, yet few evidence-based guidelines exist for the detection, diagnosis and management of sleep disturbances in this disorder. This critical review paper sought to increase awareness amongst mental health clinicians of sleep problems in schizophrenia, promote better identification of sleep problems, and help clinicians make more informed decisions about integrated treatment plans. Specifically, we examined the following key questions: 1) Which sleep problems occur in schizophrenia? 2) What evidence exists regarding the impact of poor sleep? 3) What are the underlying mechanisms of sleep problems in schizophrenia? 4) How can this information be used by clinicians to design a more complete treatment plan? Data Sources and study selection: We conducted a non-systematic review of studies that have shaped our current understanding of sleep in schizophrenia (n = 65). Data sources included PubMed, Medline, and cross-referencing. Results: Sleep disorders are pervasive and broad-ranging in people with schizophrenia, and are associated with substantial burden. An integrated model is proposed whereby a combination of highly interactive factors comprising genetic and neurobiological vulnerabilities, and behavioural and environmental factors, interact to cause sleep abnormalities. However, prospective and rigorous studies of sleep in schizophrenia are lacking. Conclusion: Patients often do not receive optimal care because sleep problems are rarely diagnosed, and treatments plans are incompletely formulated. A better understanding of sleep problems in schizophrenia will lead to increased treatment options, and a more positive clinical outcome.
SCHIZOPHRENIA: A REVIEW  [PDF]
Parle Milind,Sharma Kailash
International Research Journal of Pharmacy , 2013,
Abstract: Schizophrenia continues to be a mysterious disease fascinating the minds of psychiatrists, pharmacologists and neuroscientists all over the world for more than a century. The crucial welfare of the millions afflicted with schizophrenia is at stake. The cause of schizophrenia is not yet identified. However, it appears from the available reports that schizophrenia results from genetic, occupational and environmental risk factors, which act independently or combine synergistically to develop schizophrenia. In any case, schizophrenia should not be confined to split personality or multiple personality- disorder. Typically, a schizophrenic patient shows both, positive symptoms such as delusions, hallucinations or cognitive dysfunction and negative symptoms such as social withdrawal, inability to articulate or loss of emotional tone. Some psycho-active drugs such as Cocaine, Heroin, LSD, Prozac, and Ketamine produce positive symptoms of schizophrenia. Brain regions affected in schizophrenia are amygdala, ventral striatum, frontal cortex, temporal cortex, hippocampus and thalamus. The levels of neurotransmitters such as dopamine, glutamate, GABA, acetylcholine, serotonin and nor-epinephrine are significantly altered in schizophrenia. The enigma of schizophrenia has fascinated neuroscientists all over the world to develop parallel animal models in an attempt to discover new medicines for the effective management of this psychiatric disorder.
Critical appraisal of lurasidone in the management of schizophrenia
Caccia S, Pasina L, Nobili A
Neuropsychiatric Disease and Treatment , 2012, DOI: http://dx.doi.org/10.2147/NDT.S18059
Abstract: itical appraisal of lurasidone in the management of schizophrenia Review (3720) Total Article Views Authors: Caccia S, Pasina L, Nobili A Published Date April 2012 Volume 2012:8 Pages 155 - 168 DOI: http://dx.doi.org/10.2147/NDT.S18059 Received: 04 February 2012 Accepted: 02 March 2012 Published: 17 April 2012 Silvio Caccia, Luca Pasina, Alessandro Nobili Istituto di Ricerche Farmacologiche, “Mario Negri”, Milan, Italy Abstract: Lurasidone is a new atypical antipsychotic in the benzoisothiazoles class of chemicals. Like most second-generation antipsychotics it is a full antagonist at dopamine D2 and serotonin 5-HT2A receptors, and is a partial agonist at 5-HT1A receptors, a property shared by some but not all older agents. It has much greater affinity for 5-HT7 subtype receptors than other atypical antipsychotics. Pharmacokinetic studies showed that lurasidone is reasonably rapidly absorbed, with bioavailability appearing to be increased by food. Lurasidone undergoes extensive metabolism to a number of metabolites, some of which retain pharmacological activities. Metabolism is mainly by CYP3A4, resulting in steady-state concentrations that vary between individuals and are potentially affected by strong inducers and inhibitors of this enzyme. Short-term clinical trials have demonstrated the efficacy of lurasidone in acute schizophrenia, with doses of 40 and 80 mg/day giving significant improvements from baseline in the PANSS and BPRS scores. The most common adverse events are nausea, vomiting, akathisia, dizziness, and sedation, with minimal increases in the risk of developing metabolic syndrome. Lurasidone did not raise the risk of QTc interval prolongation, although additional studies are required. Long-term trials are also needed to assess the risk of new-onset diabetes. Ongoing trials in patients with bipolar disorder are being completed but, again, efficacy and safety have been investigated only in a few short-term clinical trials.
A Systematic Review of the Prevalence of Schizophrenia  [PDF]
Sukanta Saha,David Chant,Joy Welham,John McGrath
PLOS Medicine , 2005, DOI: 10.1371/journal.pmed.0020141
Abstract: Background Understanding the prevalence of schizophrenia has important implications for both health service planning and risk factor epidemiology. The aims of this review are to systematically identify and collate studies describing the prevalence of schizophrenia, to summarize the findings of these studies, and to explore selected factors that may influence prevalence estimates. Methods and Findings Studies with original data related to the prevalence of schizophrenia (published 1965–2002) were identified via searching electronic databases, reviewing citations, and writing to authors. These studies were divided into “core” studies, “migrant” studies, and studies based on “other special groups.” Between- and within-study filters were applied in order to identify discrete prevalence estimates. Cumulative plots of prevalence estimates were made and the distributions described when the underlying estimates were sorted according to prevalence type (point, period, lifetime, and lifetime morbid risk). Based on combined prevalence estimates, the influence of selected key variables was examined (sex, urbanicity, migrant status, country economic index, and study quality). A total of 1,721 prevalence estimates from 188 studies were identified. These estimates were drawn from 46 countries, and were based on an estimated 154,140 potentially overlapping prevalent cases. We identified 132 core studies, 15 migrant studies, and 41 studies based on other special groups. The median values per 1,000 persons (10%–90% quantiles) for the distributions for point, period, lifetime, and lifetime morbid risk were 4.6 (1.9–10.0), 3.3 (1.3–8.2), 4.0 (1.6–12.1), and 7.2 (3.1–27.1), respectively. Based on combined prevalence estimates, we found no significant difference (a) between males and females, or (b) between urban, rural, and mixed sites. The prevalence of schizophrenia in migrants was higher compared to native-born individuals: the migrant-to-native-born ratio median (10%–90% quantile) was 1.8 (0.9–6.4). When sites were grouped by economic status, prevalence estimates from “least developed” countries were significantly lower than those from both “emerging” and “developed” sites (p = 0.04). Studies that scored higher on a quality score had significantly higher prevalence estimates (p = 0.02). Conclusions There is a wealth of data about the prevalence of schizophrenia. These gradients, and the variability found in prevalence estimate distributions, can provide direction for future hypothesis-driven research.
The Infection Hypothesis of Schizophrenia: A Systematic Review  [PDF]
Alexander M. Scharko
Journal of Behavioral and Brain Science (JBBS) , 2011, DOI: 10.4236/jbbs.2011.12007
Abstract: Objectives: The objective of this paper is to accomplish a systematic review of the infection hypothesis of schizophrenia. Methods: All English language publications from January 1989 to March 2010 as related to infection and schizophrenia were obtained. Each study selected for analysis must either deal with the direct infection of an individual and schizophrenia or maternal infection during pregnancy and the subsequent development of schizophrenia in the offspring. The primary outcome measure was the calculated odds ratio and 95% confidence interval (CI). Results: Over 300 titles and abstracts were reviewed. Eight retrospective studies regarding in utero exposure were analyzed. Five nested case-controlled studies yielded an overall odds ratio of 3.58 (95% CI: 2.71 - 4.71) with a percent attributable risk of 6.3%. Three Scandinavian populational studies yielded an overall odds ratio of 0.62 (95% CI: 0.49 - 0.79). Twenty-six papers were identified as retrospective studies focused on linking evidence of past infection in individuals with history of schizophrenia. A total of 77 microorganisms were assessed with 18 (23.4%) showing a positive association with schizophrenia. But positive associations in a given trial were negative in other trials. Conclusions: Direct infection of an individual as a cause of schizophrenia is unlikely. Results were mixed regarding maternal infection, in utero exposure, and the later development of schizophrenia in the offspring and likely accounts for a modest proportion of those with schizophrenia, possibly 6%.
Critical appraisal of lurasidone in the management of schizophrenia  [cached]
Caccia S,Pasina L,Nobili A
Neuropsychiatric Disease and Treatment , 2012,
Abstract: Silvio Caccia, Luca Pasina, Alessandro NobiliIstituto di Ricerche Farmacologiche, “Mario Negri”, Milan, ItalyAbstract: Lurasidone is a new atypical antipsychotic in the benzoisothiazoles class of chemicals. Like most second-generation antipsychotics it is a full antagonist at dopamine D2 and serotonin 5-HT2A receptors, and is a partial agonist at 5-HT1A receptors, a property shared by some but not all older agents. It has much greater affinity for 5-HT7 subtype receptors than other atypical antipsychotics. Pharmacokinetic studies showed that lurasidone is reasonably rapidly absorbed, with bioavailability appearing to be increased by food. Lurasidone undergoes extensive metabolism to a number of metabolites, some of which retain pharmacological activities. Metabolism is mainly by CYP3A4, resulting in steady-state concentrations that vary between individuals and are potentially affected by strong inducers and inhibitors of this enzyme. Short-term clinical trials have demonstrated the efficacy of lurasidone in acute schizophrenia, with doses of 40 and 80 mg/day giving significant improvements from baseline in the PANSS and BPRS scores. The most common adverse events are nausea, vomiting, akathisia, dizziness, and sedation, with minimal increases in the risk of developing metabolic syndrome. Lurasidone did not raise the risk of QTc interval prolongation, although additional studies are required. Long-term trials are also needed to assess the risk of new-onset diabetes. Ongoing trials in patients with bipolar disorder are being completed but, again, efficacy and safety have been investigated only in a few short-term clinical trials.Keywords: lurasidone, pharmacology, pharmacokinetics, efficacy, safety
Schizophrenia and Violence: Systematic Review and Meta-Analysis  [PDF]
Seena Fazel ,Gautam Gulati,Louise Linsell,John R. Geddes,Martin Grann
PLOS Medicine , 2009, DOI: 10.1371/journal.pmed.1000120
Abstract: Background Although expert opinion has asserted that there is an increased risk of violence in individuals with schizophrenia and other psychoses, there is substantial heterogeneity between studies reporting risk of violence, and uncertainty over the causes of this heterogeneity. We undertook a systematic review of studies that report on associations between violence and schizophrenia and other psychoses. In addition, we conducted a systematic review of investigations that reported on risk of homicide in individuals with schizophrenia and other psychoses. Methods and Findings Bibliographic databases and reference lists were searched from 1970 to February 2009 for studies that reported on risks of interpersonal violence and/or violent criminality in individuals with schizophrenia and other psychoses compared with general population samples. These data were meta-analysed and odds ratios (ORs) were pooled using random-effects models. Ten demographic and clinical variables were extracted from each study to test for any observed heterogeneity in the risk estimates. We identified 20 individual studies reporting data from 18,423 individuals with schizophrenia and other psychoses. In men, ORs for the comparison of violence in those with schizophrenia and other psychoses with those without mental disorders varied from 1 to 7 with substantial heterogeneity (I2 = 86%). In women, ORs ranged from 4 to 29 with substantial heterogeneity (I2 = 85%). The effect of comorbid substance abuse was marked with the random-effects ORs of 2.1 (95% confidence interval [CI] 1.7–2.7) without comorbidity, and an OR of 8.9 (95% CI 5.4–14.7) with comorbidity (p<0.001 on metaregression). Risk estimates of violence in individuals with substance abuse (but without psychosis) were similar to those in individuals with psychosis with substance abuse comorbidity, and higher than all studies with psychosis irrespective of comorbidity. Choice of outcome measure, whether the sample was diagnosed with schizophrenia or with nonschizophrenic psychoses, study location, or study period were not significantly associated with risk estimates on subgroup or metaregression analysis. Further research is necessary to establish whether longitudinal designs were associated with lower risk estimates. The risk for homicide was increased in individuals with psychosis (with and without comorbid substance abuse) compared with general population controls (random-effects OR = 19.5, 95% CI 14.7–25.8). Conclusions Schizophrenia and other psychoses are associated with violence and violent offending, particularly
Social Cognition in Schizophrenia: A Review Study  [PDF]
Neama Kamel, Fryial AlQahtani
Open Journal of Psychiatry (OJPsych) , 2019, DOI: 10.4236/ojpsych.2019.92007
Abstract: Social cognition includes all operations encountered in the process of perceiving, understanding & production of appropriate reactions while confronting with others. These include: social awareness, theory of mind, attributive style, and emotion processing. Social cognition skills have been recognized as a vital component in the rehabilitation process for schizophrenic persons, its strong contributors in social function among individual suffering from schizophrenia. The purpose of this review is to appraise various researches about social cognition and its correlates in addition to evaluating various cognitive interventions targeted toward improving social cognition function among patients group and to find the best techniques to ameliorate social cognitive deficits in schizophrenia. Databases were searched from the period from the year 2000 to October 2018. The search terms used were “Social cognition”, emotional management program, schizophrenia. A total of 85 articles were identified and those who meet inclusion criteria including 27 articles. Finding indicates the efficacy of social intervention that targets cognitive aspect in functional abilities of schizophrenic patients and also emotion processing which are significant mediators of social performance aptitudes in patients group.
Prolactin and Psychopathology in Schizophrenia: A Literature Review and Reappraisal  [PDF]
Ravi Philip Rajkumar
Schizophrenia Research and Treatment , 2014, DOI: 10.1155/2014/175360
Abstract: Secretion of the anterior pituitary hormone prolactin can be significantly increased by antipsychotic drugs, leading to a range of adverse effects in patients with schizophrenia. However, there is evidence from a variety of studies that prolactin may also be related to symptom profile and treatment response in these patients, and recent work has identified variations in prolactin secretion even in drug-free patients. In this paper, a selective review of all relevant studies pertaining to prolactin and schizophrenia, including challenge and provocation studies, is presented. The implications of this work are discussed critically. A tentative model, which synthesizes these findings and argues for a significant role for prolactin in the development of schizophrenia, is outlined. 1. Introduction Prolactin is a polypeptide hormone secreted by the anterior pituitary gland. Prolactin has multiple functions, including lactation and maternal-infant bonding, in mammals. Recent work has found it to be relevant to parental and sexual behaviour in humans [1, 2] as well. Various factors, including gender, sexual activity, childbirth, stress, smoking, and drugs, can affect the release of prolactin [3, 4]. The production of prolactin is inhibited by dopamine release in the hypothalamo-pituitary circuit and can be increased by blocking type 2 (D2) dopamine receptors. Most available antipsychotic drugs can therefore cause elevations in prolactin secretion. This increase is associated with a variety of adverse effects: lack of libido and erectile dysfunction in men [5], amenorrhoea and galactorrhoea in women [6], acceleration of osteoporosis in women [7], weight gain [8], and—potentially—an increased risk of cancer, particularly breast cancer in women [9]. The association of prolactin with male sexual dysfunction is complex and has been challenged by some authors [10] but is supported by research showing that antipsychotics which cause greater elevations in prolactin also have more marked sexual adverse effects [11]. Besides this, a variety of studies over the past four decades have examined other facets of the relationship between prolactin and schizophrenia and call for a reappraisal of this relationship. In this paper, the author highlights the important findings pertaining to prolactin and schizophrenia, excluding the literature on drug-induced hyperprolactinemia which has been extensively reviewed elsewhere. The author also proposes a model that may explain these findings. In the discussion that follows, the term “prolactin levels” refers to plasma prolactin, unless
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