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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The author fundamentally questions the traditional concept of the disease-entity (or several disease entities) of 'schizophrenia' and discusses an alternative concept, based on vulnerability and information-processing. According to this, schizophrenia-like psychotic phenomena develop in three phases. In the first, premorbid phase, combined biological (genetic and possibly other organic) and psycho-social influences lead to a premorbid 'vulnerability', characterised by a low tolerance of cognitive and emotional stress, corresponding to an insufficient capacity for the adequate processing of complex information. In the second phase, stressful life-events can lead to unique or repeated acute productive psychotic episodes. The third phase, that of long-term evolution, depends more on psycho-social influences than on biological factors. Under unfavourable conditions, it may lead to predominantly unproductive residual states of various degrees, which can largely be understood as regulatory mechanisms to restrict stressful over-stimulation. There is no clearly delimitable disease entity of schizophrenia with constant causes, psychopathological picture, or course, but rather a multi-conditioned life-process, occurring in people with a particular vulnerability, interacting with complex life-events and circumstances. This new concept has important consequences for therapy and prevention.
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PMID:Is there really a schizophrenia? The long-term course of psychotic phenomena. 621 Jan 25

Behavior during conditioned fear stress, a form of psychological stress, and the release of dopamine in the amygdala were measured over time using methamphetamine-sensitized rats, which are considered to be a model of hypersensitivity and vulnerability to emotional stress associated with stimulant-induced psychosis and schizophrenia. Dopamine release in the amygdala showed a delayed increase following completion of freezing behavior induced by conditioned fear stress regardless of the presence or absence of methamphetamine-sensitization. Since methamphetamine treatment did not lower the basal level of dopamine in the amygdala, under the conditions of this study, methamphetamine was presumed not to show neurotoxicity. On the other hand, basal dopamine levels after 15 h of repeated electric foot shock were about 40% lower than those in the control group (p<0.0002). In addition, dopamine release following conditioned fear stress in animals repeatedly treated with methamphetamine increased significantly from 40 to 100 min after conditioned fear stress while the duration of freezing behavior or latency of the appearance of grooming were not different from those in the control group. The above results suggested that delayed dopamine release in the amygdala is a phenomenon strongly associated with the emotional context of conditioned fear stress, and hypersensitivity and vulnerability to stress are at least partially involved with the overreaction to stress.
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PMID:Enhancement of delayed release of dopamine in the amygdala induced by conditioned fear stress in methamphetamine-sensitized rats. 1179 Mar 78

It is well known that environmental factors, such as early life events, perinatal damage, and urbanicity, which interact with multiple genes, induces persistent sensitization to stress possibly through an imbalance in interactions between dopaminergic and glutamatergic systems. This stress sensitization may be critical in the development or relapse of schizophrenia. The neural correlates of a negative mood might be impaired, resulting in stress sensitization and difficulties in social adjustment (Dr. Habel). Urbanicity is associated with later schizophrenia. Metabolic stress induces stress sensitization via dysregulation of dopaminergic and/or noradrenergic systems in activated HVA and cortical response (Dr. Marcelis). The glutamatergic regulation activates HPA axis in stress response (Dr. Zelena). Ameloblast activity in human molar's enamel slowed by exposure to stress, and the segment of enamel rods is smaller, making a particular dark line. Stress sensitization may be induced at the age of 10.5 to 11.5 years resulting from severe emotional stress at the age of 10.5 to 11.5 years (Dr. Yui). It has been reported that volume reductions in the amygdala, hippocampus, superior temporal gyrus, and anterior parietal cortex common to both patient groups may represent the vulnerability to schizophrenia, while volume loss of the prefrontal cortex, posterior parietal cortex, cingulate, insula, and fusiform cortex preferentially observed in schizophrenia may be critical for overt manifestation of psychosis (Dr. Suzuki).
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PMID:Stress sensitization in schizophrenia. 1758 79

Stigma can be a major stressor for people with schizophrenia and other mental illnesses, leading to emotional stress reactions and cognitive coping responses. Stigma is appraised as a stressor if perceived stigma-related harm exceeds an individual's perceived coping resources. It is unclear, however, how people with mental illness react to stigma stress and how that affects outcomes such as self-esteem, hopelessness and social performance. The cognitive appraisal of stigma stress as well as emotional stress reactions (social anxiety, shame) and cognitive coping responses were assessed by self-report among 85 people with schizophrenia, schizoaffective or affective disorders. In addition to self-directed outcomes (self-esteem, hopelessness), social interaction with majority outgroup members was assessed by a standardized role-play test and a seating distance measure. High stigma stress was associated with increased social anxiety and shame, but not with cognitive coping responses. Social anxiety and shame predicted lower self-esteem and more hopelessness, but not social performance or seating distance. Hopelessness was associated with the coping mechanisms of devaluing work/education and of blaming discrimination for failures. The coping mechanism of ingroup comparisons predicted poorer social performance and increased seating distance. The cognitive appraisal of stigma-related stress, emotional stress reactions and coping responses may add to our understanding of how stigma affects people with mental illness. Trade-offs between different stress reactions can explain why stress reactions predicted largely negative outcomes. Emotional stress reactions and dysfunctional coping could be useful targets for interventions aiming to reduce the negative impact of stigma on people with mental illness.
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PMID:A stress-coping model of mental illness stigma: II. Emotional stress responses, coping behavior and outcome. 1923 66

Although emotional dysfunction in patients with schizophrenia is thought to be associated with poorer outcomes in terms of overall quality of well-being, only a few basic studies have been done on the biochemical effect of antipsychotics on the fear response of a neurotransmitter (i.e. dopamine). To examine the reaction to emotional stress, conditioned fear stress has been developed as a form of psychological stress based on classical conditioning theory. Using this model, the amygdala was found to be one of the most potent modulators of the mechanisms responsible for the emotional memory system. Methamphetamine-induced sensitization (reverse tolerance phenomenon) in rats has been widely and successfully used as an animal model of stimulant-induced psychosis and schizophrenia in terms of the paranoid psychotic state and its vulnerability to relapse. Methamphetamine-sensitized animals show significantly higher extracellular dopamine release in the amygdala than unsensitized rats after exposure to a conditioned stimulus. This hypersensitivity of dopamine release is considered to be a biochemical marker of hypersensitivity and vulnerability to stress in psychosis. Aripiprazole and haloperidol equally suppressed the marked increase in extracellular dopamine levels in fear-conditioned rats, whereas haloperidol increased and aripiprazole decreased basal dopamine levels. The effect of antipsychotics attenuates the dopamine fear response in the amygdala, modulating basal dopamine level.
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PMID:[Action of amygdala dopamine and effect of antipsychotics]. 2049 Dec 83

The purpose of this study was to explore ways of coping and its association with specific stress responses in adolescents with schizophrenia. Additionally, subjects and healthy controls were compared to identify stress responses. Forty subjects were drawn from a self-management therapy study for youth with schizophrenia. Thirty community-dwelling controls were selected. A revised Ways of Coping scale and the Symptom of Stress at baseline, 6, 30 and 54 weeks measured coping and stress response. Descriptive statistics, cluster analysis and Pearson correlation provided data analysis. Thirty-two subjects were male, and eight were female. Average age was 17.25 (SD=1.37) years. Twenty-two (55%) were Caucasian; 18 (45%) were non-Caucasian. Seventeen (57%) of the 30 controls were female. The mean age was 17.10 years old (SD=1.16). Adolescents with schizophrenia used emotion-focused coping more than problem-focused coping at baseline and 6 weeks (P<0.01). Subjects reported higher stress than controls (t=4.73, P<0.01) and used emotion-focused coping with emotional stress responses (r=0.34, P=0.05). Adolescent coping strategies may persist into adulthood unless new skills are introduced. Developing effective coping skills for adolescents with schizophrenia is important for practice and future studies.
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PMID:Ways of coping in adolescents with schizophrenia. 2129 28

Cognitive rehabilitation has been gradually disseminated in Japan lately. Cognitive rehabilitation is distinct from other psychosocial rehabilitation methods, which aims to enhance cognitive function per se, by various training tools, using paper and pencil tasks, computer games, etc. It stands on the hypothesis that enhancing cognitive function should lead to improvement in social functioning. However, it is becoming clear that cognitive rehabilitation on its own is not strongly effective on social functioning, but rather it appears effective when combined with other methods of rehabilitation. Moreover, it does not treat the emotional problems, which is essential considering the treatment endpoint, to enhance "subjective well-being". Emotional problems arise much often at social interaction in patients with schizophrenia, which can be amended by improving their social cognition as well as social skills. Recently, one of the social cognition training programs has been developed in USA by Penn and his colleagues, named SCIT (Social Cognition and Interaction Training) . The program treats a number of factors involved in social cognition, a) emotion perception, b) attributional style, and c) theory of mind, using various techniques such as Socrates quotes. In previous studies, SCIT showed good effectiveness in various aspects of social cognition for inpatients, whereas the finding was not as clear for outpatients. It may be assumed that integrating SCIT into a cognitive rehabilitation program should alleviate emotional stress the patients often encounter at social interaction in their daily activities. Presumably the next candidate target for psychosocial treatments coming after cognition and emotion should be "intrinsic motivation".
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PMID:[Adding the perspective of emotion on cognitive rehabilitation]. 2225 Apr 44

Oxidative stress is an imbalance between cellular production of reactive oxygen species and the counteracting antioxidant mechanisms. The brain with its high oxygen consumption and a lipid-rich environment is considered highly susceptible to oxidative stress or redox imbalances. Therefore, the fact that oxidative stress is implicated in several mental disorders including depression, anxiety disorders, schizophrenia and bipolar disorder, is not surprising. Although several elegant studies have established a link between oxidative stress and psychiatric disorders, the causal relationship between oxidative stress and psychiatric diseases is not fully determined. Another critical aspect that needs much attention and effort is our understanding of the association between cellular oxidative stress and emotional stress. This review examines some of the recent discoveries that link oxidative status with anxiety, depression, schizophrenia and bipolar disorder. A discussion of published results and questions that currently exist in the field regarding a causal relationship between oxidative and emotional stress is also provided.
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PMID:Oxidative stress and psychological disorders. 2466 8

Catalepsy is an inability to correct an externally imposed awkward posture; it is associated with schizophrenia and depression in human. We created new recombinant B6.CBA-D13Mit76C and B6.CBA-D13Mit76B mouse lines on the C57Bl/6 genome, carrying the 102.73-110.56Mbp fragment of chromosome 13 derived from the catalepsy-prone CBA strain and catalepsy-resistant C57BL/6 strain, respectively. We compared the behavior and brain morphology (11.7T BioSpec 117/16 USR tomograph, Germany) in these lines. The effects of acute emotional stress on corticosterone's level in the blood and mRNA expression of Bdnf and Arc genes in the brain were investigated. The B6.CBA-D13Mit76B mice were non-cataleptic, while about 17% of B6.CBA-D13Mit76C mice demonstrated catalepsy-like immobility. No difference between these lines was revealed in the open field and social interaction tests. In the Morris water maze test, both lines effectively found the platform on the fourth day; however B6.CBA-D13Mit76B mice achieved significantly better results than cataleptic-prone animals. B6.CBA-D13Mit76C mice were characterized by decreased volume of the total brain and reduced sizes of striatum, cerebellum and pituitary gland. The both lines showed the similar basal and stress-induced levels of corticosterone, while the brain expression of Bdnf and Arc genes was more vulnerable to stress in the catalepsy-prone B6.CBA-D13Mit76C line.
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PMID:Alteration of the brain morphology and the response to the acute stress in the recombinant mouse lines with different predisposition to catalepsy. 2788 98

The psychopathological condition of Robert Schumann has been a prominent object of study in psychiatry since his hospitalization in 1854. Renowned psychiatrists have diagnosed Schumann with syphilis, schizophrenia, and bipolar and personality disorders. Until today, these analyses of his symptomatology have led to contradictory results. Recent discussion has suggested that his hospitalization was due to professional failure and separation wishes on the part of his wife, her family, and her friends. In line with this hypothesis is the opinion that the separation insisted upon by Clara Schumann was reinforced by the economic interests of the psychiatrist who kept Schumann in custody for 2 years until his death in 1856. In this article, we trace the complex interaction of bipolar vulnerability and pathogenic life events with hypersensitive talent and "creative bipolarity," defined as the capacity, motivation, and resilience to transform emotional stress and cognitive inconsistency into coherent artistic products. Finally, we present our conclusions about comprehensive psychiatric and psychotherapeutic treatment with respect to "creative bipolarity."
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PMID:Bipolar Disorder and/or Creative Bipolarity: Robert Schumann's Exemplary Psychopathology - Combining Symptomatological and Psychosocial Perspectives with Creativity Research. 2901 53


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