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 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Iowa record-linkage study was developed to investigate death rates in psychiatric patients, and involved computer matching of death certificates with a roster of patients. A list of all patients admitted to our hospital from 1972 through 1981 was obtained and after removing duplicate entries the list was pared to 5412 names. The record included multiple identifiers (e.g., name, gender, date-of-birth, hospital number). This information was then linked by computer with all Iowa death certificates for the same period; a total of 331 deaths were identified. Patients were assigned to a single psychiatric diagnostic category based on a computer program that reviewed each patient's clinical diagnoses and picked the one with the highest priority in a hierarchy we had created. Age and sex adjusted mortality tables were constructed, allowing us to compute expected numbers of deaths. Relative risk for premature death was greatest among women, and those under 20 years. Risk was associated with all psychiatric diagnoses and was significantly higher among patients of either gender with an organic mental disorder or schizophrenia; women with acute schizophrenia, depressive neuroses, alcoholism, drug abuse, and psychophysiological disorders; and men with neuroses. Death from natural causes, especially from heart disease, was significantly excessive among women, while death from accidents and suicides was excessive for both men and women. The overall SMR was 1.65 (P < 0.001). Most importantly, we found that the greatest excess of mortality occurred within the first 2 years following hospital discharge. Thus, we were able to demonstrate that risk of mortality in general, and of suicide specifically, differed according to age, gender, diagnosis, and portion of the follow-up. We have subsequently used this method to investigate specific risk factors associated with mortality in mood disorders, schizophrenia, and antisocial personality disorder. Findings from these studies are reported.
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PMID:Iowa record-linkage study: death rates in psychiatric patients. 985 87

Unlike disorders of other fields of medicine (eg., diabetes, heart disease), schizophrenia has been only marginally impacted by the study of animal models. This gap reflects the incomplete understanding of the causes and mechanisms of schizophrenia and the resulting lack of defined targets for model development. However, prior attempts at modeling in animals the complex symptoms of schizophrenia have given way to more promising component models. This review will address the evolving field of animal models of schizophrenia with a focus on models of errors in neurotransmission, and of psychophysiological deficits, with a concluding discussion of the present and future promise of genetic-based models. Evolving models based on the long-held conceptualization of schizophrenia as being based on errors in neurotransmission are discussed as regards the integration of newer findings implicating alterations in dopamine, glutamate and neurotensin function in the pathophysiology and pharmacotherapy of schizophrenia. The case for the more recent conceptualization of schizophrenia as a core deficit in information processing and stimulus filtering is discussed. Animal behavioral paradigms that model psychophysiologic constructs of stimulus processing deficits related to schizophrenia include prepulse inhibition (PPI), a model of sensorimotor gating, or latent inhibition (LI), a model of salience learning. These models represent both better supported associations with schizophrenia and more productive targets and are providing important new information regarding the psychopharmacology of schizophrenia. Genetic models of schizophrenia are based on the demonstrated heritability of the disorder and more recent pharmacogenetic findings for antipsychotic medications. Genetic-based animal models use behavioral or molecular genetic techniques to manipulate behaviors related to schizophrenia by altering the frequencies of related genes. The future development of increasingly informative animal models of schizophrenia will be dependent on a more complete understanding of schizophrenia, an integration of findings across animal models and refinements in the criteria used to assess model "validity" that better reflect the changing nature and roles of animal models of schizophrenia.
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PMID:The changing roles and targets for animal models of schizophrenia. 1174 40

Well-known adverse effects of amisulpride include nausea, insomnia or tiredness, gastrointestinal, extrapyramidal and endocrine symptoms. Cardiac disorders, however, appear to be an extremely rare complication of the drug. Only a few case reports on this complication have been published so far, which deal with QT prolongation, hypotension, hypertension and palpitations. Bradycardia has not yet been mentioned. Here, we will report on a case of asymptomatic bradycardia that developed subsequent to therapeutic doses of amisulpride in a 25-year-old male patient with chronic paranoid-hallucinatory schizophrenia. The patient had been rehospitalized for an acute exacerbation of the psychosis. When the patient failed to respond at the beginning of hospitalization, the treatment was changed from clozapine to amisulpride. After a complete switchover to amisulpride, the patient's ECG showed sinus bradycardia and QT prolongation. When the daily dose of amisulpride was reduced from 800 mg/d to 600 mg/d, the patient's ECG quickly normalized (including blood pressure and pulse rate) within a few days. The patient did not report any cardiovascular-related complaints. Since the cardiovascular-specific diagnostics did not yield any indicative results, bradycardia may be a rare complication of amisulpride treatment.
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PMID:Asymptomatic bradycardia associated with amisulpride. 1177 48

BACKGROUND: This study examines the impact of mental illness on the labor market performance of family members of afflicted individuals. Numerous research projects have attempted to measure the impact of mental illness and related disorders on the ill individual, yet have traditionally neglected estimating potential costs accruing to family members of the ill. AIMS OF THE STUDY: Previous research estimating the impact of illness on the time allocation decisions of family caregivers has been limited in scope. I obtain estimates of the impact of mental illness on the probability of labor force participation and hours of work of all family members. The general analysis used in this study will pave the way for more accurate assessments of the costs of all types of illness and the estimates obtained will provide policy makers with a much more complete picture of the costs of mental illness. METHODS: The main empirical work in this study includes a probit estimation of labor force participation and a tobit regression of hours worked (including sample selection correction). The data sample, taken from the 1987 National Medical Expenditure Survey, is also partitioned by gender to clarify effects of family illness on labor supply for both females and males. RESULTS: Adult males are found to increase their probability of labor force participation in the presence of mental illness in the family (all else equal) when the mental illness is accompanied by a chronic physical illness. However, females are surprisingly found to have no significant impact on their probability of being a member of the labor market when a family member is afflicted with mental illness. On the other hand, hours of work are significantly reduced for both females and males when the mentally ill family member is afflicted with additional illnesses (physical and/or mental). DISCUSSION: Previous studies have traditionally not considered the effects of family illness on males because females are typically found to be the primary caregiver when a family member falls ill. The findings in this study indicate that men suffer reductions in their hours of work in an equivalent magnitude to females. Thus, males should not be ignored when estimating the opportunity costs of illness in families. IMPLICATIONS FOR HEALTH POLICIES: Current federal and state policies provide for some of the medical costs and replace some of the lost income of ill individuals, but generally do not support family members who are negatively affected by illness. This research provides evidence supporting the arguments of advocates for policy to ameliorate the financial burden borne by family members of the ill. IMPLICATIONS FOR FUTURE RESEARCH: The estimates obtained in this study show that women and men both need to be studied when determining the effects of family illness on labor supply, and should be studied separately to obtain clear results. Also, future research should include examining particular mental illnesses to see whether there is a higher cost of one over the other (e.g., schizophrenia versus major depression), as this may provide valuable information to policy makers. In addition, comparison of the costs of psychological disorders to chronic physical illnesses (such as cancer and heart disease) should be undertaken.
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PMID:The labor market consequences of family illness. 1196 30

The critical flicker fusion threshold (CFFT) is thought to index alertness and cortical arousal. Sedative drugs reduce CFFT while psychostimulants increase it. Procyclidine is an anticholinergic that is used to control the extrapyramidal side-effects of antipsychotics in schizophrenia. This study examined the effects of clinically relevant doses of oral procyclidine administration on CFFT and heart rate in two separate experiments (Experiment 1, drug dose: 10 mg, n = 16; Experiment 2, drug dose: 15 mg, n = 12) involving healthy subjects using a double-blind, placebo-controlled, cross-over design. 10 mg procyclidine had no significant effect on CFFT, heart rate or self-ratings of mood, but the 15 mg dose significantly lowered CFFT at 1 h and 2 h after procyclidine administration, increased drowsiness ratings and produced a drop in heart rate. The effects observed in this study may have implications for treatment compliance of schizophrenic patients, choice of antipsychotics, prescribing to patients with heart disease and monitoring of cardiac function under treatment. Further investigations are required to quantify the effects of procyclidine on CFFT and cardiac function in patients with schizophrenia.
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PMID:Effects of 10 mg and 15 mg oral procyclidine on critical flicker fusion threshold and cardiac functioning in healthy human subjects. 1209 79

In two randomly selected human genomes, 99.9% of the DNA sequence is identical. The remaining 0.1% of DNA contains sequence variations. The most common type of such variation is called a single-nucleotide polymorphism, or SNP. SNPs are highly abundant, stable, and distributed throughout the genome. These variations are associated with diversity in the population, individuality, susceptibility to diseases, and individual response to medicine. Recently, it has been suggested that SNPs can be used for homogeneity testing and pharmacogenetic studies and to identify and map complex, common diseases such as high blood pressure, diabetes, and heart disease. Consistent with this proposal is the identification of the patterns of SNPs in conditions such as diabetes, schizophrenia, and blood-pressure homeostasis. Although these studies have provided insight into the nature of human sequence variation, it is not known at present whether these variations are truly significant toxicologically and pharmacologically. Moreover, it is possible that most complex, common disorders are caused by the combined effects of multigenes and nongenetic environmental factors (multifactorial). Therefore, it is likely that sequence variation alone is not sufficient to predict the risk of disease susceptibility, particularly in homeostatic organisms like humans. Nevertheless, these variants may provide a starting point for further inquiry.
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PMID:SNP alleles in human disease and evolution. 1243 91

The pharmacotherapy of schizophrenia remains an ongoing challenge for researchers and clinicians alike. Current medications remain suboptimal to effectively treat this illness despite the recent surge of what are considered to be better antipsychotics: the atypicals. The atypicals cause fewer extrapyramidal symptoms and tardive dyskinesia, but there is growing concern regarding the significant long-term metabolic and cardiac adverse effects of these novel antipsychotics. There are differences among the atypicals in their propensity to produce these adverse effects, and clinicians should weigh the risk-benefit ratio for each drug with each individual patient. Diabetes, heart disease, obesity, and unhealthy lifestyle choices are on the rise in the general population, and individuals with chronic schizophrenia are even more at risk. The dilemma clinicians face in trying to avoid the neurological morbidity of the typicals (extrapyramidal side effects and tardive dyskinesia) is the risk of consequently exposing patients to both the morbidity and potential mortality of the atypicals (cardiovascular, endocrine, and metabolic adverse effects). The importance of baseline investigations and monitoring at regular intervals as well as identification of patients at risk for obesity, diabetes, and cardiovascular morbidity has become crucial. Informed decision making is essential for successful antipsychotic pharmacotherapy. For a condition, which often necessitates long-term pharmacotherapy, the importance of prevention and (or) minimization of morbidity and mortality related to adverse effects of such pharmacotherapy cannot be understated.
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PMID:From chlorpromazine to clozapine--antipsychotic adverse effects and the clinician's dilemma. 1563 57

A hemizygous deletion of the q11 band on chromosome 22 occurs in 1 of every 5,950 live births (0.017%). The deletion is mediated by low copy repeats (LCRs) flanking this locus. Presence of the deletion is associated with variable phenotypic expression, which can include distinctive facial dysmorphologies, congenital heart disease and learning disabilities. An unusually high percentage of individuals with this deletion (25-30%) have been described to develop schizophrenia or schizoaffective disorder. In previous studies, the prevalence of the 22q11 deletion in patients with schizophrenia was found to be approximately 2% in Caucasian adults and 6% in childhood-onset cases. Both these frequencies represent a dramatic increase from the prevalence of the deletion in the general population. In this study, we investigate the occurrence of the 22q11 deletion in an independent sample of schizophrenic patients of Afrikaner origin. We first ascertained a sample of 85 patients who meet full diagnostic criteria for schizophrenia for presence of two or more of the clinical features associated with presence of the 22q11 deletion. A group of six patients (7%) met these criteria. This group was subjected to fluorescent in situ hybridization (FISH) and presence of the 22q11 deletion was confirmed for two subjects. Our study therefore confirms the previously reported rate of 2% frequency of the 22q11 deletion in adult schizophrenic patients and provides a two-stage screening protocol to identify these patients.
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PMID:Assessment of the frequency of the 22q11 deletion in Afrikaner schizophrenic patients. 1527 32

This study investigated the relationship of executive impairment and heart disease burden to remission of major depression among elderly patients. A total of 112 elderly subjects suffering from major depression received treatment with citalopram at a target daily dose of 40 mg for 8 weeks. Diagnosis was assigned using the Research Diagnostic Criteria and the DSM-IV Criteria after an interview with the Schedule for Affective Disorders and Schizophrenia. Executive dysfunction was assessed with the Initiation/Perseveration subscale of the Dementia Rating Scale (DRS) and the Color-Word Stroop test. Medical burden, including heart disease burden, was rated with the Cumulative Illness Rating Scale, and disability with Philadelphia Multilevel Instrument. Both abnormal initiation/perseveration and abnormal Stroop scores were associated with low remission rates of geriatric depression. Similarly, heart disease burden and baseline severity of depression also predicted low remission rates. The relationship of heart disease burden to remission was not mediated by executive dysfunction. Impairment in other DRS cognitive domains, disability, medical burden unrelated to heart disease did not significantly influence the outcome of depression in this sample. Executive dysfunction and heart disease burden constitute independent vulnerability factors that increase the risk for chronicity of geriatric depression. The findings of this study provide the rationale for investigation of the role of specific frontostriatal-limbic pathways in predisposing to geriatric depression or worsening its course.
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PMID:Executive dysfunction, heart disease burden, and remission of geriatric depression. 1534 Mar 93

The hypothesis that there is a developmental component to subsequent adult disease initially arose from epidemiological findings relating birth size to either indices of disease risk or actual disease prevalence in later life. While components of the epidemiological analyses have been challenged, there is strong evidence that developmental factors contribute to the later risk of metabolic disease--including insulin resistance, obesity, and heart disease--as well as have a broader impact on osteoporosis, depression and schizophrenia. We suggest that disease risk is greater when there is a mismatch between the early developmental environment (i.e., the phase of developmental plasticity) versus that experienced in mature life (i.e., adulthood), and that nutritional influences are particularly important. It is also critical to distinguish between those factors acting during the developmental phase that disrupt development from those influences that are less extreme and act through regulated processes of epigenetic change. A model of the relationship between the developmental and mature environment is proposed and suggests interventional strategies that will vary in different population settings.
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PMID:Life-long echoes--a critical analysis of the developmental origins of adult disease model. 1556 79


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