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

As many as two million people in the United Kingdom repeatedly see people, animals, and objects that have no objective reality. Hallucinations on the border of sleep, dementing illnesses, delirium, eye disease, and schizophrenia account for 90% of these. The remainder have rarer disorders. We review existing models of recurrent complex visual hallucinations (RCVH) in the awake person, including cortical irritation, cortical hyperexcitability and cortical release, top-down activation, misperception, dream intrusion, and interactive models. We provide evidence that these can neither fully account for the phenomenology of RCVH, nor for variations in the frequency of RCVH in different disorders. We propose a novel Perception and Attention Deficit (PAD) model for RCVH. A combination of impaired attentional binding and poor sensory activation of a correct proto-object, in conjunction with a relatively intact scene representation, bias perception to allow the intrusion of a hallucinatory proto-object into a scene perception. Incorporation of this image into a context-specific hallucinatory scene representation accounts for repetitive hallucinations. We suggest that these impairments are underpinned by disturbances in a lateral frontal cortex-ventral visual stream system. We show how the frequency of RCVH in different diseases is related to the coexistence of attentional and visual perceptual impairments; how attentional and perceptual processes can account for their phenomenology; and that diseases and other states with high rates of RCVH have cholinergic dysfunction in both frontal cortex and the ventral visual stream. Several tests of the model are indicated, together with a number of treatment options that it generates.
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PMID:Why people see things that are not there: a novel Perception and Attention Deficit model for recurrent complex visual hallucinations. 1637 31

The overall prevalence rates of general and specific child psychiatric disorders in Danish children are unknown. In this study, which aimed to estimate prevalence rates, a multi-method strategy using a two-step design was employed. The first step involved assessment with the Child Behaviour Checklist (CBCL). The second step consisted of assessment using the Schedule for Affective Disorders and Schizophrenia for School-Aged Children; Present and Lifetime version (K-SADS-PL), The Children's Global Assessment Scale (C-GAS), The Wechsler Intelligence Scale for Children (WISCIII), The Autism Spectrum Disorder Screening Questionnaire (ASSQ), and a checklist containing the diagnostic criteria for Pervasive Developmental Disorders (PDD). Non-respondents were assessed through teachers using a modified brief version of the K-SADS-PL. A total of 751 children were targeted. The overall estimated prevalence rate of child psychopathology was 11.8 % [95% confidence interval (CI): 8.8, 14.8]. Attention Deficit/ Hyperactivity Disorder (ADHD) was found to be the most common specific child psychiatric disorder. There was no difference in prevalence rates between respondents and non-respondents. The estimated prevalence rates were broadly comparable to prevalence rates found in other epidemiological studies. The teacher-based interview proved to be a valid instrument for the assessment of non-respondents.
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PMID:The population prevalence of child psychiatric disorders in Danish 8- to 9-year-old children. 1647 77

Schizophrenia is associated with a broad range of neurodevelopmental, structural and behavioral abnormalities that often progress with or without treatment. Evidence indicates that such neurodevelopmental abnormalities may result from defective genes and/or non-genetic factors such as pre-natal and neonatal infections, birth complications, famines, maternal malnutrition, drug and alcohol abuse, season of birth, sex, birth order and life style. Experimentally, these factors have been found to cause the cellular metabolic stress that often results in oxidative stress, such as increased cellular levels of reactive oxygen species (ROS) over the antioxidant capacity. This can trigger the oxidative cell damage (i.e., DNA breaks, protein inactivation, altered gene expression, loss of membrane lipid-bound essential polyunsaturated fatty acids [EPUFAs] and often apoptosis) contributing to abnormal neural growth and differentiation. The brain is preferentially susceptible to oxidative damage since it is under very high oxygen tension and highly enriched in ROS susceptible proteins, lipids and poor DNA repair. Evidence is increasing for increased oxidative stress and cell damage in schizophrenia. Furthermore, treatments with some anti-psychotics together with the lifestyle and dietary patterns, that are pro-oxidant, can exacerbate the oxidative cell damage and trigger progression of neuropathology. Therefore, adjunctive use of dietary antioxidants and EPUFAs, which are known to regulate the growth factors and neuroplasticity, can effectively improve the clinical outcome. The dietary supplementation of either antioxidants or EPUFAs, particularly omega-3 has already been found to improve some psychopathologies. However, a combination of antioxidants and omega-3 EPUFAs, particularly in the early stages of illness, when brain has high degree of neuroplasticity, potentially may be even more effective for long-term improved clinical outcome of schizophrenia.
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PMID:Prevention of oxidative stress-mediated neuropathology and improved clinical outcome by adjunctive use of a combination of antioxidants and omega-3 fatty acids in schizophrenia. 1677 66

Clinically, we most often associate Wernicke's encephalopathy (WE) with an alcohol abusing population. However, it is important to consider other causes of malnutrition and vitamin deficiency as risk factors for the development of this disorder. We present a case of a 51-year-old man with schizophrenia and malnutrition who presented with delirium, ophthalmoplegia, and seizures. He responded rapidly to the administration of IV thiamine. Because of the high rate of mortality and morbidity, WE should be high on the differential of any patient at risk for malnutrition or with ophthalmoplegia, regardless of alcohol history. This is particularly important in psychiatric patients where the syndrome may be masked and thus treatment delayed.
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PMID:Wernicke's encephalopathy in a patient with schizophrenia. 1692 99

Although classically considered to be involved only in motor coordination, the cerebellum has more recently been implicated also in cognitive control. Anatomical studies have shown the cerebellum to be linked to pre-frontal, occipito-parietal and temporal cortical associative areas, as well as to the limbic system, in a closed loop circuit. Functional studies revealed activation of the cerebellum during performance on cognitive tasks not related to movement. Pathological, morphological and functional imaging studies have shown the cerebellum to be one of the cerebral structures affected in some of the cognitive and behavioural developmental disorders, like Attention Deficit with Hyperactivity Disorder, Autism and Schizophrenia. Neuropsychological studies in patients with degenerative cerebellar ataxia also showed cognitive dysfunction, mainly of the executive type. Investigation performed with child and adult patients with focal lesions of the cerebellum has helped to better discriminate the cognitive role of specific areas on the cerebellum, revealing a characteristic constellation of cognitive deficits, affecting executive, visual-spatial, linguistic and behavioural functions. However, much remains to be explained on the precise nature of cerebellar contributions to cognition, in part because of the difficulty in finding adequate investigation models. Studies performed on primates have contributed to better delineate the connections between the cerebellum and cortical cognitive domains, but is always uncertain to transfer this kind of data to the human brain. Functional imaging studies although useful to investigate directly in the human model and in real time, are not yet able to completely isolate cerebellar cognitive and behavioural functions. Degenerative and developmental disorders are not the most adequate model for studying cerebellar influence on higher mental functions, as they affect other regions besides the cerebellum. Young patients with isolated cerebellar stroke provide a useful clinical model for investigating cerebellar cognitive functions, because they permit to isolate in space and time the specific contribution of the cerebellum to the cognitive deficits.
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PMID:[Role of the cerebellum in cognitive and behavioural control: scientific basis and investigation models]. 1723 89

It is well recognized that investigation into the relationship between early life programming and subsequent neurological disorders may have powerful implications for understanding the human vulnerability to psychopathology. The present article will propose that schizophrenia may be adaptively programmed by early environmental adversity permitting physiological and behavioral characteristics that would have created a fitness advantage in the ancestral environment under conditions of nutritional scarcity and severe environmental stress. This proposition will be analyzed in terms of phenotypic plasticity theory which explains how and why specific environmental stressors can alter normal gene expression resulting in an alternative phenotype that is better suited for an adverse environment. The primary neurophysiological symptoms of schizophrenia can be induced in animals through exposure to prenatal and postnatal stressors, and that schizophrenia itself is known to be associated with exposure to stress during development, supports the view that the "disorder" may represent a predictive, adaptive response to adversity. In fact, maternal malnutrition, maternal stress, multiparity, short birth interval and stress provoking postnatal events are well recognized epidemiological risk factors for schizophrenia that may represent cues for the initiation of epigenetic programming. Behavioral and physiological characteristics of schizophrenia will be analyzed and interpreted as protective in the context of environmental hardship. For instance, the hypometabolic areas of the schizophrenic brain--the hippocampus and the frontal lobes--are the same areas that are known to become adaptively hypometabolic in response to starvation, stress and variations in ecological rigor in birds and mammals. Individuals with schizophrenia are also highly genetically inclined to develop the metabolic syndrome, which is widely thought to allow developmentally deprived mammals to conserve energy under poor circumstances. It is well known that schizophrenia features an up-regulated hypothalamic-pituitary-adrenal axis and an exaggerated stress response--both alterations thought to represent predictive, adaptive responses to stress in mammals--which may have increased attentiveness to the environment and created a defensive, vigilance-based behavioral strategy. The habituation deficits characteristic of schizophrenia--which can be induced in other mammals through stress--may represent a cognitive strategy that alerts the organism to salient, potentially informative stimuli and that permits it to be more impulsive and vigilant. Inability to calm instinctual drives, ignore arousing stimuli, and inhibit transient desires are all core characteristics of the disorder, which predict social and vocational disabilities in modern times, but may have amounted to a robust, selfish strategy in prehistoric times.
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PMID:Schizophrenia and phenotypic plasticity: schizophrenia may represent a predictive, adaptive response to severe environmental adversity that allows both bioenergetic thrift and a defensive behavioral strategy. 1732 Oct 61

Prenatal protein malnutrition continues to be a significant problem in the world today. Exposure to prenatal protein malnutrition increases the risk of a number of neuropsychiatric disorders in adulthood including depression, schizophrenia and attentional deficit disorder. In the present experiment, we have examined the effects of stress on extracellular serotonin (5-HT) and dopamine in the medial prefrontal cortex and dorsal hippocampus of rats exposed in utero to protein malnutrition. The medial prefrontal cortex and dorsal hippocampus were chosen as two limbic forebrain regions involved in learning and memory, attention and the stress response. Extracellular 5-HT and dopamine were determined in the medial prefrontal cortex and dorsal hippocampus of adult male Sprague-Dawley rats using dual probe in vivo microdialysis. Basal extracellular 5-HT did not differ between malnourished and well-nourished controls in either the medial prefrontal cortex or the dorsal hippocampus. Basal extracellular dopamine was significantly decreased in the medial prefrontal cortex of malnourished animals. Restraint stress (20 m) produced a significant rise in extracellular dopamine in the medial prefrontal cortex of well-nourished rats but did not alter release in malnourished rats. In malnourished rats, stress produced an increase in 5-HT in the hippocampus, whereas stress produced a decrease in 5-HT in the hippocampus of well-nourished rats. These data demonstrate that prenatal protein malnutrition alters dopaminergic neurotransmission in the medial prefrontal cortex as well as alters the dopaminergic and serotonergic response to stress. These changes may provide part of the bases for alterations in malnourished animals' response to stress.
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PMID:Stress-induced changes in extracellular dopamine and serotonin in the medial prefrontal cortex and dorsal hippocampus of prenatally malnourished rats. 1736 32

Schizophrenia patients with the deficit syndrome (DS) may represent a homogeneous subgroup. To increase the practicability of diagnosing the DS, Kirkpatrick et al. [Kirkpatrick, B., Buchanan, RW., Breier, A. Carpenter, WT., 1993. Case identification and stability of the deficit syndrome of schizophrenia. Psychiatry Res. 47, 47-56.] proposed the use of a 'proxy' case identification tool using standardized symptom ratings instead of the Schedule for the Deficit Syndrome (SDS) which requires an independent clinical assessment. The Proxy for the Deficit Syndrome (PDS) is based on the extraction of symptoms that are essentially equivalent or overlap substantially with the restricted affect and diminished emotional range on the SDS. Kirkpatrick et al. [Kirkpatrick, B., Buchanan, RW., Breier, A. Carpenter, WT., 1993. Case identification and stability of the deficit syndrome of schizophrenia. Psychiatry Res. 47, 47-56.] reported good sensitivity and specificity in a comparison of SDS and PDS assessments among 100 chronic schizophrenia outpatients. The present investigation involves the comparison of the deficit syndrome as assessed by the "gold standard" Schedule for the Deficit Syndrome with the ratings of the same symptoms embodied in the "proxy instrument" the PANSS, within the same group of 156 inpatients. Forty-four patients were assessed by the SDS to have the deficit syndrome. Patients with and without the DS, as defined by the SDS, did not differ for age, education, age at illness onset and duration of illness. The two main 'proxy' measures PDS1 and PDS2 discriminated across the SDS groups. The direct dichotomous comparison of the actual SDS and the 'proxy' derived PDS groups demonstrated good specificity (78.6% and 79.5%) and moderate to very good sensitivity (61.4% and 86.4%) and there was a moderately low rate of false positive cases (21.4% and 20.5%). For the two main 'proxy' measures (PDS1 and PDS2) kappas were .38 and .59, representing poor to good agreement. In our sample of rigorously diagnosed schizophrenia inpatients, the use of a 'proxy' case identification tool for the deficit syndrome would appear to be a viable alternative in identifying a subgroup of schizophrenia patients with the deficit syndrome when the use of the actual SDS is not feasible. Further study is indicated before the PDS as extracted from the PANSS can be used in lieu of the SDS for identifying patients with this syndrome.
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PMID:Validity of a 'proxy' for the deficit syndrome derived from the Positive And Negative Syndrome Scale (PANSS). 1743 29

Poor insight into illness is a characteristic and common phenomenon in schizophrenic disorders. Lack of insight may lead to poor clinical outcome, thus, research focused on this phenomenon could help develop effective treatment strategies. The relationship between compliance with treatment and insight is complex and it may be influenced mostly by specific components of insight. The aim of the present study was to review the current definitions of insight, the tools and questionnaires used for its measurement, as well as the relationship between insight and psychopathological symptoms. Three theoretical models developed for the explanation of impaired insight are described; the Psychological Defence Model, the Cognitive Deficit Model, and the Neuropsychological Deficit Model. The neurocognitive bases of impaired insight is given special attention in this article. Administration of second generation antipsychotics and psychosocial interventions (psychoeducation with problem solving procedures and motivating techniques) can improve insight, and enhance compliance with treatment, thus, optimizing long-term therapeutic outcome for schizophrenia patients.
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PMID:[Insight into illness and compliance in schizophrenic disorders]. 1743 58

Cardiovascular disease (CVD), which includes coronary heart, cerebrovascular, and peripheral vascular disease, is the leading cause of death in the United States and most developed countries, accounting for about 50% of all deaths. The major risk factors include obesity and its consequences, dyslipidemia, hypertension, insulin resistance leading to diabetes, and cigarette smoking. In developing countries, CVD will become the leading cause of death due to alarming increases in obesity, sedentary lifestyles, cigarette smoking, and improvements in prevention and treatment of malnutrition and infection. Compared with nonschizophrenics, patients with schizophrenia have a 20% shorter life expectancy (i.e., from 76 to 61 years). In general populations, about 1% die from suicide compared with about 10% among patients with schizophrenia (relative risk = 10). For CVD, the corresponding figures are 50% and about 75% (relative risk = 1.5). In patients with schizophrenia, however, CVD occurs more frequently and accounts for more premature deaths than suicide. Patients with schizophrenia have alarmingly higher rates of obesity, dyslipidemia, hypertension, diabetes, and cigarette smoking than nonschizophrenic individuals in the general population. Compounding these data, patients with schizophrenia have less access to medical care, consume less medical care, and are less compliant. Primary prevention strategies should include the choice of antipsychotic drug regimens that do not adversely affect the major risk factors for CVD.
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PMID:Increasing global burden of cardiovascular disease in general populations and patients with schizophrenia. 1753 93


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