Manifestations Of Schizophrenia Research Articles

The Effect of a Computer-Assisted Cognitive Remediation on Improving Cognitive Functions in Patients with Schizophrenia: A Before-After Study

Background: Cognitive impairment is a chronic and disabling manifestation of schizophrenia. Objectives: This before-after study was conducted to examine the effect of a short course computer-assisted cognitive remediation on improving cognitive functions of patients with schizophrenia. Materials and Methods: Twenty patients with schizophrenia were enrolled into the study. The intervention consisted of 10 one-hour sessions held 2-3 times a week, using the Cogpack software that includes tasks to improve attention, memory, and executive function. The patients’ cognitive functioning was assessed before and after the remediation, using tests in the CANTAB battery, including stop signal task (SST) and choice reaction time (CRT) to assess attention levels, pattern recognition memory (PRM) and Paired associate learning (PAL) to examine memory, and stocking of Cambridge (SOC) and intra-extra dimensional task (IED) to evaluate executive function. Results: IED and SOC revealed a statistically significant improvement in executive function after the intervention. PAL revealed a significant improvement in memory functioning in most aspects after the intervention, while PRM did not. CRT showed a significant improvement in some aspects of attention and concentration after the intervention, while SST did not. Conclusions: This before-after study revealed that a relatively short course of a computer-assisted cognitive remediation can be applied to improve several aspects of cognitive functioning in patients with schizophrenia. A randomized controlled trial is required to establish the effectiveness of the intervention.

Decline in the severity or the incidence of schizophrenia in Japan: A survey of university students.

Clinical manifestations of schizophrenia are believed to be becoming less severe in Japan, but little evidence supports this theory. We investigated the percentages of undergraduate students attending national universities in Japan who required temporary leave and who dropped out because of schizophrenia in the academic years 1986-1987, 1994-1995, and 2013-2014. The percentages of students who required temporary leave and those who dropped out because of schizophrenia significantly decreased over time. The severity of clinical manifestations of schizophrenia may have decreased, enabling more students with schizophrenia to continue their study, or the incidence of schizophrenia might have declined.

Developmental restoration of LTP deficits in heterozygous CaMKIIα KO mice.

The Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a major mediator of long-term potentiation (LTP) and depression (LTD), two opposing forms of synaptic plasticity underlying learning, memory and cognition. The heterozygous CaMKIIα isoform KO (CaMKIIα+/-) mice have a schizophrenia-related phenotype, including impaired working memory. Here, we examined synaptic strength and plasticity in two brain areas implicated in working memory, hippocampus CA1 and medial prefrontal cortex (mPFC). Young CaMKIIα+/- mice (postnatal days 12-16; corresponding to a developmental stage well before schizophrenia manifestation in humans) showed impaired hippocampal CA1 LTP. However, this LTP impairment normalized over development and was no longer detected in older CaMKIIα+/- mice (postnatal weeks 9-11; corresponding to young adults). By contrast, the CaMKIIα+/- mice failed to show the developmental increase of basal synaptic transmission in the CA1 seen in wild-type (WT) mice, resulting in impaired basal synaptic transmission in the older CaMKIIα+/- mice. Other electrophysiological parameters were normal, including mPFC basal transmission, LTP, and paired-pulse facilitation, as well as CA1 LTD, depotentiation, and paired-pulse facilitation at either age tested. Hippocampal CaMKIIα levels were ∼60% of WT in both the older CaMKIIα+/- mice and in the younger WT mice, resulting in ∼30% of adult WT expression in the younger CaMKIIα+/- mice; levels in frontal cortex were the same as in hippocampus. Thus, in young mice, ∼30% of adult CaMKIIα expression is sufficient for normal LTD and depotentiation, while normal LTP requires higher levels, with ∼60% of CaMKIIα expression sufficient for normal LTP in adult mice.

An association between the PPARα-L162V polymorphism and nicotine dependency among patients with schizophrenia

ObjectivePatients with schizophrenia are more likely to be smokers than the general population, which makes them an interesting group with which to study the etiology of nicotine dependency. We studied the prevalence of a gene variant of peroxisome proliferator-activated receptor alpha (PPARα) in schizophrenia, together with nicotine dependency, to investigate whether the PPARα-L162V polymorphism (rs1800206) influences nicotine dependency in schizophrenia. Given evidence suggesting that smoking influences the severity of schizophrenia, together with our recent data linking the PPARα-L162V polymorphism to clinical manifestations of schizophrenia (in the Croatian population), we hypothesized that interactions between the two (smoking and the PPARα-L162V polymorphism) might contribute to disease onset and scores for the Positive and Negative Syndrome Scale. To the best of our knowledge, this is the first study to investigate the possible associations between the PPARα gene and nicotine dependency. Patients and methodsGenotyping was performed for 267 chronically ill schizophrenia patients (males/females: 140/127) by polymerase chain reaction. ResultsA significant excess of PPARα-L162V genotypes and PPARα-162V alleles were detected among female smokers in comparison to female nonsmokers (18.2% vs. 2.0%, and 9.1% vs. 1.0%, p<0.01, respectively). We also revealed a significant PPARα genotype–smoking interaction that predicted positive symptom severity among male patients (F=4.43, p<0.05). These data indicated that the PPARα-L162V heterozygous genotype, depending on smoking status, might be of relevance as either protective, or a risk factor, for the severity of positive symptoms. No interaction between the PPARα-L162V polymorphism and smoking for the time of onset of schizophrenia was detected (p>0.05, respectively). ConclusionWe demonstrated two significant yet weak effects. The first showed an effect of the PPARα-L162V polymorphism on the risk of nicotine dependency. The second linked the PPARα genotype–smoking interaction to positive symptoms severity among schizophrenia patients; both effects manifested in a gender-specific fashion.

Fractal Dimension Analysis of Subcortical Gray Matter Structures in Schizophrenia.

A failure of adaptive inference—misinterpreting available sensory information for appropriate perception and action—is at the heart of clinical manifestations of schizophrenia, implicating key subcortical structures in the brain including the hippocampus. We used high-resolution, three-dimensional (3D) fractal geometry analysis to study subtle and potentially biologically relevant structural alterations (in the geometry of protrusions, gyri and indentations, sulci) in subcortical gray matter (GM) in patients with schizophrenia relative to healthy individuals. In particular, we focus on utilizing Fractal Dimension (FD), a compact shape descriptor that can be computed using inputs with irregular (i.e., not necessarily smooth) surfaces in order to quantify complexity (of geometrical properties and configurations of structures across spatial scales) of subcortical GM in this disorder. Probabilistic (entropy-based) information FD was computed based on the box-counting approach for each of the seven subcortical structures, bilaterally, as well as the brainstem from high-resolution magnetic resonance (MR) images in chronic patients with schizophrenia (n = 19) and age-matched healthy controls (n = 19) (age ranges: patients, 22.7–54.3 and healthy controls, 24.9–51.6 years old). We found a significant reduction of FD in the left hippocampus (median: 2.1460, range: 2.07–2.18 vs. median: 2.1730, range: 2.15–2.23, p<0.001; Cohen’s effect size, U3 = 0.8158 (95% Confidence Intervals, CIs: 0.6316, 1.0)), the right hippocampus (median: 2.1430, range: 2.05–2.19 vs. median: 2.1760, range: 2.12–2.21, p = 0.004; U3 = 0.8421 (CIs: 0.5263, 1)), as well as left thalamus (median: 2.4230, range: 2.40–2.44, p = 0.005; U3 = 0.7895 (CIs: 0.5789, 0.9473)) in schizophrenia patients, relative to healthy individuals. Our findings provide in-vivo quantitative evidence for reduced surface complexity of hippocampus, with reduced FD indicating a less complex, less regular GM surface detected in schizophrenia.

Failure to mobilize cognitive control for challenging tasks correlates with symptom severity in schizophrenia.

Deficits in the adaptive, flexible control of behavior contribute to the clinical manifestations of schizophrenia. We used functional MRI and an antisaccade paradigm to examine the neural correlates of cognitive control deficits and their relations to symptom severity. Thirty-three chronic medicated outpatients with schizophrenia and 31 healthy controls performed an antisaccade paradigm. We examined differences in recruitment of the cognitive control network and task performance for Hard (high control) versus Easy (low control) antisaccade trials within and between groups. We focused on the key regions involved in ‘top-down’ control of ocular motor structures – dorsal anterior cingulate cortex, dorsolateral and ventrolateral prefrontal cortex. In patients, we examined whether difficulty implementing cognitive control correlated with symptom severity. Patients made more errors overall, and had shorter saccadic latencies than controls on correct Hard vs. Easy trials. Unlike controls, patients failed to increase activation in the cognitive control network for Hard vs. Easy trials. Reduced activation for Hard vs. Easy trials predicted higher error rates in both groups and increased symptom severity in schizophrenia. These findings suggest that patients with schizophrenia are impaired in mobilizing cognitive control when presented with challenges and that this contributes to deficits suppressing prepotent but contextually inappropriate responses, to behavior that is stimulus-bound and error-prone rather than flexibly guided by context, and to symptom expression. Therapies aimed at increasing cognitive control may improve both cognitive flexibility and reduce the impact of symptoms.

Theory of Mind deficit in the behavioral variant of frontotemporal dementia and in amyotrophic lateral sclerosis: Why does it matter?

Theory of Mind (hereinafter referred to as ToM) is the ability to explain and predict other people’s behavior by attributing independent mental states to them. It allows us to recognize that mental states such as beliefs, intentions, and desires play a key role in driving and monitoring human behavior. Impairment in ToM ability can be highly disabling. ToM had been extensively studied in neuropsychiatric conditions such as autism and certain manifestations of schizophrenia [1], but only recently researchers and clinicians have started to investigate ToM in neurodegenerative conditions, such as the behavioral variant of frontotemporal dementia (bv-FTD) and amyotrophic lateral sclerosis (ALS).

An Overview on the Search for Schizophrenia Biomarkers.

Schizophrenia is a severe psychiatric disorder with a complex presentation comprising positive symptoms (e.g.: hallucinations and delusions), negative symptoms (e.g.: social withdrawal, blunted affect) and pervasive cognitive deficits that have been associated with functional decline. The pathophysiology of the disorder is equally complex, with abnormalities known to occur in the molecular, cellular, neurophysiological, and neuroanatomical domains. Despite significant progress in the comprehension of the various manifestations of schizophrenia, the full picture of its etiology remains unknown. As a result, currently available pharmacological treatments have limited efficacy and little has improved since the discovery of the first antipsychotics back in the 1950s. In addition, these medications have significant adverse effects. Differently from other medical areas, the diagnosis of schizophrenia is essentially clinical and dependent on subjective elements. In an attempt to change this, efforts have been directed to find biomarkers of the disorder that could improve diagnostic accuracy and validity, predict treatment response, enable the early identification of individuals at risk of developing schizophrenia and indicate new targets for the development of drugs with better selective, safety, and efficacy profiles. In this article we describe the main potential schizophrenia markers currently under study and suggest avenues for future research in the field. - No reliable markers exist for schizophrenia to date. - The identification of schizophrenia markers could increase diagnostic accuracy and treatment efficacy. - The main research lines in the current search for biomarkers are described.

Living with Mental Illness: A Cognitive Behavioural Group Psycho-education Programme with Women in Secure Settings.

The provision of psycho-educational groups for people diagnosed with schizophrenia is an important part of successful treatment. The value of such interventions is less clearly established in secure settings with no reports on women. Gender differences in the manifestation of schizophrenia highlight the importance of a gender-specific intervention. A 'Living with Mental Illness' group programme for women in a secure psychiatric setting is described and evaluated. Those who completed group treatments (n = 20; 63%) showed improved knowledge of schizophrenia, decreased fear of schizophrenia, greater insight and increased optimism and perceived control of the illness. They also showed increased hope and greater self-compassion. Pre-post group findings reflected improved ratings of compliance with drug treatments, appropriate behaviour and insight into risk. This was reflected in a decrease in risk behaviours, improved attendance at treatment sessions and a reduction in symptomatology. Group members also reported a positive group therapeutic alliance. Findings are discussed in the context of gender-specific treatment, research, methodological issues characteristic of a real-world evaluations and the need to assess the long-term benefits of such treatment. Copyright © 2015 John Wiley & Sons, Ltd. Psycho-educational groups for secure inpatients with schizophrenia need to address gender-specific differences in the manifestation of the condition. Such interventions as part of a broader treatment initiative can be associated with clinical improvement that is both illness specific and leads to improved engagement with care initiatives. The needs of patients who do not complete treatments needs to be regularly reassessed.

Temporal perception deficits in schizophrenia: integration is the problem, not deployment of attentions

Patients with schizophrenia are known to have impairments in sensory processing. In order to understand the specific temporal perception deficits of schizophrenia, we investigated and determined to what extent impairments in temporal integration can be dissociated from attention deployment using Attentional Blink (AB). Our findings showed that there was no evident deficit in the deployment of attention in patients with schizophrenia. However, patients showed an increased temporal integration deficit within a hundred-millisecond timescale. The degree of such integration dysfunction was correlated with the clinical manifestations of schizophrenia. There was no difference between individuals with/without schizotypal personality disorder in temporal integration. Differently from previous studies using the AB, we did not find a significant impairment in deployment of attention in schizophrenia. Instead, we used both theoretical and empirical approaches to show that previous findings (using the suppression ratio to correct for the baseline difference) produced a systematic exaggeration of the attention deficits. Instead, we modulated the perceptual difficulty of the task to bring the baseline levels of target detection between the groups into closer alignment. We found that the integration dysfunction rather than deployment of attention is clinically relevant, and thus should be an additional focus of research in schizophrenia.

Neurodevelopmental Animal Models Reveal the Convergent Role of Neurotransmitter Systems, Inflammation, and Oxidative Stress as Biomarkers of Schizophrenia: Implications for Novel Drug Development.

Schizophrenia is a life altering disease with a complex etiology and pathophysiology, and although antipsychotics are valuable in treating the disorder, certain symptoms and/or sufferers remain resistant to treatment. Our poor understanding of the underlying neuropathological mechanisms of schizophrenia hinders the discovery and development of improved pharmacological treatment, so that filling these gaps is of utmost importance for an improved outcome. A vast amount of clinical data has strongly implicated the role of inflammation and oxidative insults in the pathophysiology of schizophrenia. Preclinical studies using animal models are fundamental in our understanding of disease development and pathology as well as the discovery and development of novel treatment options. In particular, social isolation rearing (SIR) and pre- or postnatal inflammation (PPNI) have shown great promise in mimicking the biobehavioral manifestations of schizophrenia. Furthermore, the "dual-hit" hypothesis of schizophrenia states that a first adverse event such as genetic predisposition or a prenatal insult renders an individual susceptible to develop the disease, while a second insult (e.g., postnatal inflammation, environmental adversity, or drug abuse) may be necessary to precipitate the full-blown syndrome. Animal models that emphasize the "dual-hit" hypothesis therefore provide valuable insight into understanding disease progression. In this Review, we will discuss SIR, PPNI, as well as possible "dual-hit" animal models within the context of the redox-immune-inflammatory hypothesis of schizophrenia, correlating such changes with the recognized monoamine and behavioral alterations of schizophrenia. Finally, based on these models, we will review new therapeutic options, especially those targeting immune-inflammatory and redox pathways.

Gender Dysphoria as a Clinical Manifestation of Schizophrenia – Case Series

Comorbidity of schizophrenia and transsexualism is still controversial. Some authors exclude diagnosis of transsexualism in patients with psychosis others report this coexistence as very rare. Delusions of sex change have been described by some authors in about 20-25% of schizophrenic patients. Patient's “pseudotranssexual” beliefs are usually bizarre and do not cause diagnostic doubts. In some cases complaints of gender dysphoria are predominant and psychotic symptoms can be underestimated or even unnoticed before sex reassignment procedure. Presentation of various clinical manifestation of gender dysphoria in patients with schizophrenia. Three clinical cases are described. Two patients have developed “pseudotranssexual” beliefs during course of psychosis. The first of them is an example of gender identity disorders related to psychotic process. The second patient presented complex psychopathology of schizophrenia and somatic symptoms which can hinder the diagnosis. The third patient has been diagnosed as a transsexual woman after diagnosis of severe schizophrenia and has undergone sex reassignment. Next she was hospitalized several times because relapses of psychosis but also because of alcohol withdrawal. Currently this patient has symptoms of dementia and a few severe somatic diagnoses. The experiences of practitioners indicate that coincidence of schizophrenia and gender identity disorder is possible. Nevertheless, the consequence of misdiagnosis and sex reassignment can be serious and unconvertible. That is why the diagnosis of transsexualism in patients with psychosis should not be made hastily. It needs time, careful observation, examination and cooperation of psychiatrist and sexologist.

Synaptic proteins in the hippocampus indicative of increased neuronal activity in CA3 in schizophrenia.

In schizophrenia, hippocampal perfusion is increased and declarative memory function is degraded. Based on an a priori model of hippocampal dysfunction in schizophrenic psychosis, the authors postulated molecular and cellular changes in CA3 consistent with increased NMDA receptor signaling. Postmortem hippocampal subfield tissue (CA3, CA1) from subjects with schizophrenia and nonpsychiatric comparison subjects was analyzed using Western blotting and Golgi histochemistry to examine the hypothesized outcomes. The GluN2B-containing NMDA receptors (GluN2B/GluN1) and their associated postsynaptic membrane protein PSD95 were both increased in schizophrenia in CA3 tissue, but not in CA1 tissue. Quantitative analyses of Golgi-stained hippocampal neurons showed an increase in spine density on CA3 pyramidal cell apical dendrites (stratum radiatum) and an increase in the number of thorny excrescences. The hippocampal data are consistent with increased excitatory signaling in CA3 and/or with an elevation in silent synapses in CA3, a state that may contribute to an increase in long-term potentiation in CA3 with subsequent stimulation and "unsilencing." These changes are plausibly associated with increased associational activity in CA3, with degraded declarative memory function, and with formation of false memories with psychotic content. The influence of these hyperactive hippocampal projections on targets in the limbic neocortex could contribute to components of schizophrenia manifestations in other cerebral regions.

Исследования речевых нарушений при шизофрении. История и современное состояние проблемы

The article reviews studies of speech disorders in schizophrenia. The authors paid attention to a historical course and characterization of studies of areas: the actual psychopathological (speech disorders as a psychopathological symptoms, their description and taxonomy), psychological (isolated neurons and pathopsychological perspective analysis) separately analyzed some modern foreign works, covering a variety of approaches to the study of speech disorders in the endogenous mental disorders. Disorders and features of speech are among the most striking manifestations of schizophrenia along with impaired thinking (Savitskaya A. V., Mikirtumov B. E.). With all the variety of symptoms, speech disorders in schizophrenia could be classified and organized. The few clinical psychological studies of speech activity in schizophrenia presented work on the study of generation and standard speech utterance; features verbal associative process, speed parameters of speech utterances. Special attention is given to integrated research in the mainstream of biological psychiatry and genetic trends. It is shown that the topic for more than a half-century history of originality of speech pathology in schizophrenia has received some coverage in the psychiatric and psychological literature and continues to generate interest in the modern integrated multidisciplinary approach.

Positive and negative symptoms of schizophrenia as correlates of help-seeking behaviour and the duration of untreated psychosis in south-east Nigeria

&lt;p&gt;&lt;strong&gt;Background.&lt;/strong&gt; Duration of untreated psychosis (DUP) has been widely recognised in recent years as a potentially important predictor of illness outcome, and the manifestations of schizophrenia have been known to influence its early recognition as a mental illness. &lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objective.&lt;/strong&gt; To assess the association between the positive and negative symptoms of schizophrenia, help-seeking and DUP. &lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods.&lt;/strong&gt; We performed a cross-sectional study of 360 patients with schizophrenia, who had had no previous contact with Western mental health services. The Sociodemographic Questionnaire, World Health Organization Pathway Encounter Form and a questionnaire to establish DUP were used. The positive and negative syndrome scale and Composite International Diagnostic Interview were used for the assessment of mental disorders and to diagnose.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results.&lt;/strong&gt; Respondents who had predominant positive symptoms and who had a median DUP of 8 weeks or 24 weeks, tended to use psychiatric hospitals and other Western medical facilities, respectively, as their first treatment options. However, those who had predominant negative symptoms and who had a median DUP of 144 weeks or 310 weeks, tended to use faith healers and traditional healers, respectively, as first treatment options.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion.&lt;/strong&gt; The predominance of negative symptoms could militate against early presentation among people with schizophrenia, probably because negative symptoms are poorly recognised as indicating mental illness in Nigeria, as they could be interpreted as deviant behaviour or spiritual problems that would require spiritual solutions.&lt;/p&gt;

Psicopatología y delimitación clínica de la esquizofrenia

La demencia precoz o esquizofrenia, psicosis frecuente en la edad juvenil y condicionada fundamentalmente por factores hereditarios, se distingue por aparecer sin causa exterior notoria y manifestar un conjunto especial de síntomas orgánicos y mentales. Entre los últimos se encuentran algunos característicos. De ahí el interés del estudio psicopatológico de esta psicosis. Las manifestaciones psicopatológicas más importantes de la esquizofrenia Son las siguientes: 1° En el campo de la actividad perceptiva: la impresión de extrañeza del mundo, las pseudopercepciones de la sensibilidad corporal, las alucinaciones o pseudoalucinaciones verbales y verbomotrices, sobre todo el pensamiento que se hace sonoro, el eco del pensamiento, las voces dialogantes y las de comentario de la propia acción. En general, las pseudopercepciones genuinamente esquizofrénicas se distinguen por ser experiencias que el sujeto vive sin asimilarlas en su existir autónomo. 2° En materia de pensamiento: la disgregación, la forma precategorial (simbolismo arcaico, autismo, participación en el ser ajeno), los pensamientos hechos, la substracción, la publicación y el bloqueo del pensamiento y las delusiones o delirios primarios (por falla directa del juicio, estableciendo relaciones sin motivo). En conjunto, el pensamiento esquizofrénico se puede caracterizar así: descabal el contenido concreto, frustráneo el aliento de la función activa, impersonal y mediata la substancia primaria. 3° El sentimiento se apaga hasta el vacío afectivo con alguna frecuencia y manifiesta anormalidades cualitativas como las siguientes: ambivalencia, sentimientos de (falsa) anafectividad, de imposición, de privación etc. 4° En materia de instinto, lo más significativo es la emergencia de obscuras fuerzas titánicas a la vez que la reanimación desconcertada de actitudes afectivas y valorativas del pasado personal, manifestándose las infantiles no como infantiles e inocentes sino, adulteradas, como actuales y perversas, a causa de que la conciencia del adulto enfermo reacciona con una mezcla de malicia y grosería, mezcla anexa al espíritu conmovido y violentado en su inserción existencial por la sexualidad desatada. 5° La acción en la esquizofrenia tiene como desviaciones relevantes: actos impulsivos, estereotipias, amaneramiento, estupor, ambitendencia, negativismo, ecopraxia, fenómenos catatónicos etc. 6° La conciencia del yo muestra una alienación del albedrío casi específica de la esquizofrenia, que puede llegar a la completa despersonalización y a la parálisis del yo. 7° La personalidad pierde su unidad y su perspectiva de valores, de motivos eficaces y evidentes: la objetividad espiritual perenne es sustituida por el capricho subjetivo que cambia con el instante y no se funda en nada. Los desórdenes de la memoria, de la atención, de la conciencia, salvo la impotencia del acto intencional, son raros y poco característicos; los de la conciencia del tiempo son mal conocidos todavía. La esquizofrenia no es una entidad nosológica sino un tipo clínico, con varias formas, susceptible de convertirse en un grupo de psicosis semejantes. Su diagnóstico diferencial tiene tres frentes: 1° el de la psicosis orgánicas de origen conocido, en que pueden presentarse cuadros clínicos con síntomas esquizofrénicos y aún "pseudoesquizofrenias" o "esquizofrenias sintomáticas"; 2° el de las psicosis de origen desconocido, sobre todo la psicosis maníaco-represiva; 3° las neurosis o reacciones pseudoesquizofrénicas, que aparecen en personalidades anormales o predispuestas. De las primeras difiere por la carencia de etiología manifiesta, de las segundas por la diversidad del cuadro de conjunto y la evolución, de las últimas en que no es comprensible en relación con las vicisitudes exteriores y la personalidad premórbida.

Positive and negative symptoms of schizophrenia as correlates of help-seeking behaviour and the duration of untreated psychosis in south-east Nigeria

Background. Duration of untreated psychosis (DUP) has been widely recognised in recent years as a potentially important predictor of illness outcome, and the manifestations of schizophrenia have been known to influence its early recognition as a mental illness. Objective. To assess the association between the positive and negative symptoms of schizophrenia, help-seeking and DUP. Methods. We performed a cross-sectional study of 360 patients with schizophrenia, who had had no previous contact with Western mental health services. The Sociodemographic Questionnaire, World Health Organization Pathway Encounter Form and a questionnaire to establish DUP were used. The positive and negative syndrome scale and Composite International Diagnostic Interview were used for the assessment of mental disorders and to diagnose. Results. Respondents who had predominant positive symptoms and who had a median DUP of 8 weeks or 24 weeks, tended to use psychiatric hospitals and other Western medical facilities, respectively, as their first treatment options. However, those who had predominant negative symptoms and who had a median DUP of 144 weeks or 310 weeks, tended to use faith healers and traditional healers, respectively, as first treatment options. Conclusion. The predominance of negative symptoms could militate against early presentation among people with schizophrenia, probably because negative symptoms are poorly recognised as indicating mental illness in Nigeria, as they could be interpreted as deviant behaviour or spiritual problems that would require spiritual solutions.

Serum levels of BDNF, folate and homocysteine: In relation to hippocampal volume and psychopathology in drug naïve, first episode schizophrenia

ObjectiveThe present study was to examine serum levels of brain-derived neurotrophic factor (BDNF), folate, homocysteine (Hcy), and their relationships with hippocampal volume and psychopathology in drug naïve, first episode schizophrenia. MethodDrug naïve, first episode schizophrenia patients and healthy controls were enrolled in the study. Serum levels of BDNF, folate and Hcy were measured using enzyme-linked immunosorbent assay (ELISA), electrochemiluminescence immunoassay (ECLIA), and enzymatic cycling method respectively. Hippocampus was parcellated and bilateral hippocampal volumes were measured using FreeSurfer. ResultsForty-six patients with drug naïve, first episode schizophrenia (SZ group) and 30 healthy controls (control group) were enrolled. The SZ group had significantly lower serum levels of BDNF and folate, and significantly higher serum levels of Hcy compared with the control group (p=0.013, p<0.001, p=0.003 respectively). There were no significant differences in hippocampal volumes between the two groups (ps>0.2). Within the SZ group, there were significant positive relationships between serum levels of BDNF and both left and right hippocampal volumes (r=0.327, p=0.026; r=0.338, p=0.022 respectively). In contrast, such relationships did not exist in the control group. Within the SZ group, there were significant negative relationships between serum levels of folate and PANSS-total scores and PANSS-negative symptom scores (r=0.319, p=0.031; r=0.321, p=0.030 respectively); and there was a positive relationship between serum levels of Hcy and PANSS-total scores (r=0.312, p=0.035). Controlling for potential confounding variables resulted in similar findings. ConclusionsDrug naïve, first episode schizophrenia presents decreased serum levels of BDNF, folate and increased serum levels of Hcy, which may play an important role in the neurodevelopmental process and clinical manifestation of schizophrenia.

Прогнозирование эффективности экзистенциально-личностной реабилитации у больных с манифестным приступом шизофрении

Прогнозирование эффективности экзистенциально-личностной реабилитации у больных с манифестным приступом шизофрении

Meaning of life and value orientation in patients with manifestation of schizophrenia

Емоційний дистрес, душевне страждання і соціальна стигма, які супроводжують хворих на шизофренію, часто призводять до втрати сенсу подальшої діяльності, а іноді й усього життя, що пов’язане із втратою значущих цілей і духовних ціннісних орієнтирів. З метою аналізу ефективності екзистенційно-особистісної реабілітації у 237 хворих, які перенесли маніфестний напад шизофренії, вивчили показники життєвих сенсів і ціннісних орієнтацій за допомогою методики сенсожиттєвих орієнтацій (Д.А. Леонтьєв, 2000). Встановили, що у хворих на шизофренію, які пройшли курс реабілітації, показники методики поліпшувались (p<0,05) протягом 2 наступних років і були вище (p<0,05), ніж у пацієнтів, які отримували тільки фармакотерапію. Це свідчило про ефективність екзистенційно-особистісної реабілітації щодо формування цілей, цінностей і сенсів, підвищуючи якість життя хворих на шизофренію і будучи профілактикою суїцидальної поведінки.