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

Negative symptoms of schizophrenia have generally been found in association with ventricular enlargement and prefrontal abnormalities. These relationships, however, have not been observed consistently, most probably because negative symptoms are heterogeneous and result from different pathophysiological mechanisms. The concept of deficit schizophrenia (DS) was introduced by Carpenter et al to identify a clinically homogeneous subgroup of patients characterized by the presence of primary and enduring negative symptoms. Findings of brain structural abnormalities reported by magnetic resonance imaging (MRI) studies focusing on DS have been mixed. The present study included 34 patients with DS, 32 with nondeficit schizophrenia (NDS), and 31 healthy comparison subjects, providing the largest set of MRI findings in DS published so far. The Schedule for the Deficit Syndrome was used to categorize patients as DS or NDS patients. The 2 patient groups were matched on age and gender and did not differ on clinical variables, except for higher scores on the negative dimension and more impaired interpersonal relationships in DS than in NDS subjects. Lateral ventricles were larger in NDS than in control subjects but were not enlarged in patients with DS. The cingulate gyri volume was smaller in NDS but not in DS patients as compared with healthy subjects. Both groups had smaller dorsolateral prefrontal cortex and temporal lobes than healthy subjects, but DS patients had significantly less right temporal lobe volume as compared with NDS patients. These findings do not support the hypothesis that DS is the extreme end of a severity continuum within schizophrenia.
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PMID:Patterns of structural MRI abnormalities in deficit and nondeficit schizophrenia. 1772 66

This double-blind study examined efficacy and safety of atomoxetine (ATX; < or =1.8mg/kg per day) in adolescents aged 12-18 with Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) diagnoses of both attention-deficit/hyperactivity disorder (ADHD) and co-morbid major depressive disorder (MDD). Diagnoses were confirmed by the Kiddie Schedule for Affective Disorders and Schizophrenia for School Age Children-Present and Lifetime Version and persistently elevated scores on the Attention-Deficit/Hyperactivity Disorder Rating Scale-IV, Parent version, Investigator-administered and -scored (ADHDRS-IV-Parent:Inv, > or =1.5 standard deviations above age and gender norms) and Children's Depression Rating Scale-Revised (CDRS-R, > or = 40). Patients were treated for approximately 9 weeks with ATX (n = 72) or placebo (n = 70). Mean decrease in ADHDRS-IV-Parent:Inv total score was significantly greater in the ATX group (-13.3 +/- 10.0) compared with the placebo group (-5.1 +/- 9.9; p < 0.001). Mean CDRS-R score improvement was not significantly different between groups (ATX, -14.8 +/- 13.3; placebo, -12.8 +/- 10.4). Rates of treatment-emergent mania did not differ between groups (ATX, 0.0%; placebo, 1.5%). ATX treatment was associated with significantly more nausea and decreased appetite (p = 0.002; p = 0.003). No spontaneously reported adverse events involving suicidal ideation or suicidal behavior occurred in either group. ATX was an effective and safe treatment for ADHD in adolescents with ADHD and MDD. However, this trial showed no evidence for ATX of efficacy in treating MDD.
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PMID:Efficacy and safety of atomoxetine in adolescents with attention-deficit/hyperactivity disorder and major depression. 1782 37

Exposure to prenatal undernutrition or malnutrition increases the risk of schizophrenia, although little is known about the mechanism. Pro-inflammatory factors are critical in brain development, and are believed to play an important role in neurodevelopmental disorders associated with prenatal exposure to infection, including schizophrenia. However it is not known whether pro-inflammatory factors also mediate the effects on the fetus of prenatal malnutrition or undernutrition. In this study, we established a new prenatal undernourished rat model induced by maternal exposure to a diet restricted to 50% of the low (6%) protein diet (RLP50). We observed the disappearance of maternal nest-building behavior in the RLP50 dams, increased levels of TNFA and IL6 in the placentas (P<0.001; P=0.879, respectively) and fetal livers (P<0.001; P<0.05, respectively), and a decrease in the fetal brains (P<0.05; P<0.01, respectively). Our results are similar to previous studies of maternal infection, which implies that a common pathway mediated by pro-inflammatory factors may contribute to the brain development, consequently increasing the risk of schizophrenia and other psychiatric diseases programmed by varied maternal adversities. We also provide a new prenatal undernourished model for researching prenatal problems, which differs from previous malnourished model in terms of the maternal behavior of dams and of observed pro-inflammatory factor levels in fetal tissues.
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PMID:The role of pro-inflammatory factors in mediating the effects on the fetus of prenatal undernutrition: implications for schizophrenia. 1806 7

The deficit subtype is hypothesized to constitute a homogeneous subgroup of schizophrenia patients. The Schedule for the Deficit Syndrome (SDS) was developed to categorize schizophrenia patients into deficit and non-deficit subtypes. Only one report, however, has suggested the use of a two-factor SDS. The present study used a two-factor SDS and examined the relationships between the factors and the demographic and clinical variables in deficit-type schizophrenia patients. Principal component analysis was performed on data obtained from 70 schizophrenia patients with the deficit syndrome. The two-factor SDS was replicated. Factor 1, avolition, was significantly correlated only with the relational disorder domain, which consisted of two negative items from the Positive and Negative Syndrome Scale. Factor 2, poor emotional expression, was significantly correlated with both the negative symptom domain, which consisted of three negative items, and the relational disorder domain. Since the SDS has two factors, there appear to be different underlying processes for these two factors.
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PMID:A two-factor structure for the Schedule for the Deficit Syndrome in schizophrenia. 1820 48

Deficit schizophrenia is a relatively homogeneous subtype of patients which is considered helpful to explore the pathogenesis of schizophrenia. The aim of the present study was to reexamine the clinical characteristics of deficit (n=30) and nondeficit schizophrenia (n=93) in a Chinese sample and investigate the differences of neurocognitive function among the two subtypes of schizophrenia and the normal controls (n=103). Schizophrenia patients completed the Brief Psychiatric Rating Scale (BPRS), Scale for the Assessment of Negative Symptoms (SANS) and Scale for the Assessment of Positive Symptoms (SAPS). Additionally, all participants completed an abbreviated version of the Wechsler Adult Intelligence Scale (WAIS-RC) and a neuropsychological test battery examining the executive functions, visuospatial abilities and explicit memory related to the frontal, parietal, and temporal lobe functions. The deficit group received higher scores than the nondeficit group on the BPRS anergia factor and SANS affective flattening, alogia, avolition-apathy, anhedonia-asociality subscales, but not on the SAPS. Both two schizophrenia subgroups performed more poorly on the WAIS-RC and neuropsychological tests than the normal controls. Moreover, deficit patients performed worse than nondeficit patients on the prorated IQ, the Trail Making Test, Wisconsin Card Sorting test and Block Design test. The present study replicated symptom profiles in deficit vs. nondeficit schizophrenia in the Chinese sample. Furthermore, this study suggested that deficit schizophrenia is associated with frontal and parietal lobe impairment, and that temporal lobe dysfunction may be a common basis for cognitive impairment in schizophrenia as a whole.
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PMID:Psychopathology and neuropsychological impairments in deficit and nondeficit schizophrenia of Chinese origin. 1824 36

Affective impairments were examined in patients with and without deficit syndrome schizophrenia. Two Emotional Stroop tasks designed to measure automatic processing of emotional information were administered to deficit (n=15) and non-deficit syndrome (n=26) schizophrenia patients classified according to the Schedule for the Deficit Syndrome, and matched non-patient control subjects (n=22). In comparison to non-deficit patients and controls, deficit syndrome patients demonstrated a lack of attention bias for positive information, and an elevated attentional lingering effect for negative information. These findings suggest that positive information fails to automatically capture attention of deficit syndrome patients, and that when negative information captures attention, it produces difficulty in disengagement Attentional abnormalities were significantly correlated with negative symptoms, such that more severe symptoms were associated with less attention bias for positive emotion and a greater lingering effect for negative information. Results are generally consistent with a mood-congruent processing abnormality and suggest that impaired automatic processing may be core to diminished emotional experience symptoms exhibited in deficit syndrome patients.
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PMID:Automatic affective processing impairments in patients with deficit syndrome schizophrenia. 1831 70

While Wernicke's encephalopathy (WE) is a well-characterized syndrome in alcoholism and malnutrition, little is written of its prevalence or presentation in patients with psychiatric illness. We present a case of a 37-year-old Nigerian male with schizophrenia and malnutrition who presented with delirium and ophthalmoplegia. The clinical diagnosis was supported by dramatic reversal of the symptoms and signs following the administration of intravenous thiamine. Owing to the high rate of mortality and morbidity, WE should be considered in the evaluation of any patient with unexplained nystagmus, gaze palsies, gait ataxia, or confusion, especially if a condition associated with malnutrition is present. This is particularly important in psychiatric patients where the clinical history and syndrome may be obscured and treatment delayed.
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PMID:Wernicke's encephalopathy in a Nigerian with schizophrenia. 1835 48

Cognitive impairments in schizophrenia are well documented and correlated with functional disability. Although some patients demonstrate normal neuropsychological (NP) functioning, little is known about their functional disability. We examined the cross-sectional functional implications of NP normality and symptomatic remission in older outpatients diagnosed with schizophrenia or schizoaffective disorder, who were administered a NP battery and performance-based measures of functional and social competence, with their real-world functioning rated by case managers. NP status was classified by the General Deficit Score (GDS) and remission status was based on the Positive and Negative Syndrome Scale (PANSS), yielding four subsamples of patients: NP normal-remitted (n = 21), NP normal-symptomatic (n = 22), NP impaired-remitted (n = 90), and NP impaired-symptomatic (n = 97). NP normal patients demonstrated better functional and social competence and better ratings of real world functioning, after controlling for premorbid abilities. However, compared to normative date, NP normal patients manifested disability in several real-world domains, including residential status. These results suggest that NP status is a better predictor of functional outcome then symptom status or the interaction of the two factors. The disability seen in NP normal cases indicates that factors other than cognitive impairments may determine aspects of everyday outcomes in schizophrenia.
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PMID:Functional implications of neuropsychological normality and symptom remission in older outpatients diagnosed with schizophrenia: A cross-sectional study. 1841 46

Although we have studied schizophrenia as a major disease entity over the past century, its causes and pathogenesis remain obscure. In this article, we critically review genetic and other epidemiological findings and discuss the insights they provide into the causes of schizophrenia. The annual incidence of schizophrenia averages 15 per 100,000, the point prevalence averages approximately 4.5 per population of 1000, and the risk of developing the illness over one's lifetime averages 0.7%. Schizophrenia runs in families and there are significant variations in the incidence of schizophrenia, with urbanicity, male gender, and a history of migration being associated with a higher risk for developing the illness. Genetic factors and gene-environment interactions together contribute over 80% of the liability for developing schizophrenia and a number of chromosomal regions and genes have been "linked" to the risk for developing the disease. Despite intensive research and spectacular advances in molecular biology, however, no single gene variation has been consistently associated with a greater likelihood of developing the illness and the precise nature of the genetic contribution remains obscure at this time. Environmental factors linked to a higher likelihood of developing schizophrenia include cannabis use, prenatal infection or malnutrition, perinatal complications, and a history of winter birth; the exact relevance or nature of these contributions is, however, unclear. How various genetic and environmental factors interact to cause schizophrenia and via which precise neurobiological mechanisms they mediate this effect is not understood. Etiological heterogeneity, complex patterns of gene-gene and gene-environment interaction, and inadequately elucidated schizophrenia pathophysiology are among the explanations invoked to explain our inadequate understanding of the etio-pathogenesis of schizophrenia. The ability to question some of our basic assumptions about the etiology and nature of schizophrenia and greater rigor in its study appear critical to improving our understanding about its causation.
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PMID:Schizophrenia, "just the facts" what we know in 2008. 2. Epidemiology and etiology. 2145 40

It is well established that malnutrition in children has adverse effects on development. Only recently, however, has it become possible to examine the full scope of adverse effects of malnutrition across the life course, which would include latent effects of fetal or childhood malnutrition on health and disease in adult life. We review here a series of studies which have linked early prenatal famine to the risk of schizophrenia in the offspring. Thus we aim to draw attention to the need to look beyond the concurrent effects of malnutrition and consider also the effects that may become apparent decades later.
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PMID:Latent effects of prenatal malnutrition on adult health: the example of schizophrenia. 1857 82


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