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

In the context of a Finnish birth cohort, we tested the hypothesis that viral infection during the latter two thirds of fetal development would increase the risk of adult schizophrenic outcome. Psychiatric hospital diagnoses were recorded for all individuals in greater Helsinki who were fetuses during the 1957 type A2 influenza epidemic. Those exposed to the viral epidemic during their second trimester of fetal development were at elevated risk of being admitted to a psychiatric hospital with a diagnosis of schizophrenia. This was true for both males and females and independently in several psychiatric hospitals. The second-trimester effect was seen in the elevated proportion of schizophrenics among those admitted to a psychiatric hospital and also in higher rates of schizophrenia per 1000 live births in the city of Helsinki. The study has several limitations: (1) We have no direct evidence that the subjects actually suffered a viral infection. (2) The psychiatric data were obtained only for subjects up to the age of 26 years, 56 days. (3) The findings are based on hospital diagnoses. (4) The determination of stage of gestation at time of exposure to the epidemic is based on date of birth. The viral infection might have occurred outside the official epidemic window; the infant may have had a preterm or postterm delivery. These sources of error, however, should not serve to enhance the findings. The observed viral effect is interpreted as being one of many potential perturbations of gestation. We suggest that it is less the type than the timing of the disturbance during fetal neural development that is critical in determining risk for schizophrenia.
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PMID:Adult schizophrenia following prenatal exposure to an influenza epidemic. 333 16

Epidemiological, viral, behavioral and neuropathological evidence suggests that some influenza epidemics were neurovirulent. Re-examination of the data from the lethal 1918 pandemic armed with recent observations about the influenza virus implicates a neurovirulent influenza virus in manic-depressive disease, schizophrenia and Parkinson's disease. The neurovirulence seems to have been related to the species of neuraminidase.
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PMID:Why was the 1918 influenza pandemic so lethal? The possible role of a neurovirulent neuraminidase. 399 96

The neurovirulent influenza virus of the 1918 pandemic induced clinical schizophrenia. The biochemistry, the neurovascular anatomy, the afferent connections, and the efferent connections of the substantia nigra suggest that a (Na+K)-ATPase injury could be a cause of some positive schizophrenias. The genetic trait in schizophrenia may be an inheritable susceptibility to an infectious agent.
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PMID:Influenza and schizophrenia: a possible connection with the substantia nigra. 609 82

Previous research has indicated that schizophrenics are particularly likely to have been born during the winter months. In the present investigation, we studied the relationships of this birth-seasonality effect to year-to-year variations in the incidences of eight seasonal diseases and climatological temperature extremes in 3,246 schizophrenics. The winter birth-seasonality effect was greater in the years directly following those marked by high levels of infectious disorders than in years directly following those with low incidences of these diseases. Winter diseases (particularly diphtheria, pneumonia, and influenza) appeared to be more involved than others. These effects appeared among unmarried (presumably severe) schizophrenics but not among married patients, suggesting that the relationship is specific to process schizophrenia. The fact that most of the significant and near-significant relationships paired strength of birth seasonality to previous-year disease incidences suggested a prenatal rather than postnatal effect. Birth seasonality did not vary with winter or summer temperature extremes.
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PMID:Schizophrenic birth seasonality in relation to the incidence of infectious diseases and temperature extremes. 669 87

Epidemiological studies point to an association between prenatal exposure to influenza and later schizophrenia. Such studies are consistent with neuropathologic reports demonstrating cytoarchitectural abnormalities in the hippocampus and parahippocampal gyrus suggestive of second trimester developmental anomalies. The hypothesis that prenatal exposure to influenza in the second trimester may induce hippocampal pyramidal cell disarray in mice was investigated. Between days 9-16 of pregnancy, 35 Balb/c mice were intranasally inoculated with either a mouse-adapted or non mouse-adapted pool of Influenza A/Singapore/1/57 (H2N2), and 10 controls were inoculated with normal saline. Offspring were sacrificed on day 21 postpartum. Microscopic examination of the CA1-CA2 junctional areas in the offspring of mice exposed to influenza failed to demonstrate excess pyramidal cell disarray when compared with influenza-free, age matched controls. There was evidence that disarray was greater among those exposed on day 13 of pregnancy. Analyses of the data by sex and severity of maternal infection failed to reveal any significant effects.
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PMID:Does prenatal exposure to influenza in mice induce pyramidal cell disarray in the dorsal hippocampus? 899 77

A viral hypothesis for the pathogenesis of schizophrenia has been under serious consideration for more than 70 years. To date, attempts have failed to identify a specific virus which contributes to the aetiology of the disorder. There has, however, been a recent resurgence of interest in a possible relationship between viral illness and schizophrenia. This renewed attention is the result of epidemiological evidence suggesting an excess of winter births in patients with schizophrenia, indications of foetal insults in persons who develop schizophrenia and an association between foetal exposure to the influenza virus and the subsequent development of schizophrenia. Advances in our understanding of the pathophysiology of viral diseases and the development of sophisticated techniques to study them have resulted in more complex viral hypotheses of schizophrenic aetiology, such as viral disruption of normal neurodevelopment, viral induced autoimmunity and retroviral integration. These hypotheses are now beginning to be tested experimentally.
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PMID:Viruses and schizophrenia. 752 32

This article reviews evidence for morphological abnormalities in schizophrenia as assessed by brain imaging and neurohistochemical techniques including immunohistochemistry and in situ hybridization. Localized deficits in schizophrenic brain appear in many regions including frontal and temporal lobes, anterior cingulate, mediodorsal thalamic nucleus, and corpus callosum. These areas are interconnected and may provide the basis for a "psychosis circuitry." Neuronal disruption of elements in this circuitry may result in a hypothesized dysconnection syndrome. Evidence suggests an alteration in neuronal development related to either genetic and/or environmental factors. Primary and secondary anterograde and retrograde effects may accompany this neurodevelopmental defect and may further alter intrinsic and extrinsic neuronal communications. A number of studies are consistent with the second trimester of gestation being a critical period for fetal brain development, especially for neuronal migration. Fetal trauma due to environmental insults (e.g., influenza) during this trimester may increase the incidence of schizophrenia. Recent advances in the identification of factors that modulate neuronal development including axon guidance molecules, neurotrophins, and programmed cell death genes provide intriguing new areas for potential investigation. Future research may focus on the factors controlling neuronal migration and programmed cell death in the schizophrenic brain.
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PMID:New morphological and neuropathological findings in schizophrenia: a neurodevelopmental perspective. 758 23

Over the last five years a body of literature has been generated concerning whether or not prenatal exposure to influenza results in an increased risk of developing schizophrenia in the exposed offspring. The studies are reviewed with respect to the traditional epidemiological criteria that help to define causality. There is a modest degree of consistency in support of an association between the 1957 influenza epidemic--and less so, for influenza epidemics in general--and later schizophrenia. Two cohort studies examining the 1957 epidemic do not support an association. The strength and specificity of the association remain weak. The proposed association draws coherence from the neurodevelopmental hypothesis of schizophrenia. Suggestions are made for future research that could add to our understanding of the putative association between influenza and schizophrenia.
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PMID:Does influenza cause schizophrenia? A five year review. 762 72

The hypothesis that viruses or other infectious agents may cause schizophrenia or bipolar disorder dates to the 19th century but has recently been revived. It could explain many clinical, genetic, and epidemiologic aspects of these diseases, including the winter-spring birth seasonality, regional differences, urban birth, household crowding, having an older sibling, and prenatal exposure to influenza as risk factors. It could also explain observed immunological changes such as abnormalities of lymphocytes, proteins, autoantibodies, and cytokines. However, direct studies of viral infections in individuals with these psychiatric diseases have been predominantly negative. Most studies have examined antibodies in blood or cerebrospinal fluid, and relatively few studies have been done on viral antigens, genomes, cytopathic effect on cell culture, and animal transmission experiments. Viral research on schizophrenia and bipolar disorder is thus comparable to viral research on multiple sclerosis and Parkinson's disease: an attractive hypothesis with scattered interesting findings but no clear proof. The application of molecular biological techniques may allow the identification of novel infectious agents and the associations of these novel agents with serious mental diseases.
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PMID:Viruses, schizophrenia, and bipolar disorder. 770 91

Compared with their male counterparts, females with schizophrenia, on average, show better premorbid functioning, later onset, and a more benign course of illness. They are also more likely to have a family history of schizophrenia and/or affective illness, to exhibit "atypical" and affective features, and to show a seasonal pattern of hospital admission that mimics that of patients with mania. However, there exists a paradox. Although schizophrenia in females has much in common with affective disorder, the "schizophrenogenic" effect of maternal influenza also appears to be more significant in female than in male schizophrenia. Perhaps females with a predisposition to affective psychosis who have also been subject to the effects of maternal viral infection during gestation develop some subtle neurodevelopmental damage that renders their psychosis schizophrenia-like.
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PMID:Gender differences in schizophrenia: hormonal effect or subtypes? 777 Jul 31


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