UMLS:C0036341 - FACTA Search

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

Standing in the midst of this great historical change, as sometimes it is called the switch to the "post-modern", we are now confronted with the demand of paradigm change in every field of scientific knowledge. So it is the case with psychiatry. Just about 100 years ago, the trend of "social defense" (society's need to be protected from harm) was going on covering the whole civilized countries. It brought about a situation that could be generalized as "institutionalism" which made mental hospitals huge and custodial, resulting in the prevalence of nihilism with regard to treatment. It was just at this time that Dementia praecox, the preconcept of Schizophrenia, was formed by Kraepelin, E. (1896) as a mental disease resulting in peculiar dementia. After some period, Dementia praecox was transformed into Schizophrenia (Gruppe der Schizophrenien) by Bleuler, E. (1908) with a new methodology: to grasp the disease from the symptomatic viewpoint. Jaspers, K. (1912) as well as Schneider, K. (1938) followed him in the way that was psychopathologically more strict; the latter reached the formulation of the <symptoms of 1st rank>. Despite this eventful metamorphosis of the concept of Schizophrenia, its fundamental traits have remained unchanged until the late 1960's. They could be summarized as follows: 1) What patients mention is incomprehensible; 2) The prognosis leads to peculiar dementia; 3) The real cause of the disease is the brain disorder. These three are the reflection of the custodialism, curative nihilism and materialism through the institutionalized mental hospitals in those days. Now, since the 1970's, the situation has been completely changed, or at least, faced with inevitable changes. The tide of "deinstitutionalization" is covering all over the civilized countries, demanding the normalization of mentally disordered persons. Thus, deprived of its motherland (i.e. institutionalism), the concept of Schizophrenia has got into confusion or even crisis. And in order to relieve this confusion, severe attempts are internationally being made to identify the diagnostic criteria of Schizophrenia by means of what they call "operational diagnosis". I believe, however, that what is truely necessary is not such a compromising modification, but a more radical change that is: the DECONSTRUCTION OF SCHIZOPHRENIA.
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PMID:[The deconstructions of schizophrenia (I)]. 756 13

This article reviews some 50 neuroanatomical postmortem studies published in the last 20 years. The majority of these studies demonstrated various types of subtle anomalies in limbic structures, that is, the hippocampus, parahippocampal gyrus, entorhinal cortex, amygdala, cingulate gyrus, and septum of schizophrenia patients. A number of schizophrenic symptoms might be related to structural and functional disturbances of these brain regions. But these studies also reported subtle changes in parts of the basal ganglia, thalamus, cortex, corpus callosum, and brainstem neurotransmitter systems. Many of the studies, however, are based on small sample sizes and, therefore, must be regarded as preliminary. Cytoarchitectonic abnormalities and lack of gliosis in limbic structures as well as the absence of normal structural cerebral asymmetry in a substantial proportion of patients indicate that these structural anomalies may reflect a disorder of prenatal brain development and argue against the notion that schizophrenia is a progressive degenerative brain disorder.
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PMID:Recent advances in the neuropathology of schizophrenia. 832 39

Antipsychotic agents, most often used for treatment of schizophrenia, are sometimes prescribed for the agitated patient with an organic brain disorder. We report the case of a brain-injured patient who was prescribed chlorpromazine for agitation and who developed a delusional state while taking this antipsychotic agent. The emergence of this delusional state coincided with the exacerbation of certain cognitive deficits. Possible mechanisms for this phenomenon are discussed. Caution is advised when prescribing neuroleptics for patients with traumatic brain injury, especially those agents with significant cognitive side-effects or with a significant potential to precipitate seizures.
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PMID:Chlorpromazine-induced psychosis after brain injury. 842 19

Structural magnetic resonance imaging (MRI) data have provided much evidence in support of our current view that schizophrenia is a brain disorder with altered brain structure, and consequently involving more than a simple disturbance in neurotransmission. This review surveys 118 peer-reviewed studies with control group from 1987 to May 1998. Most studies (81%) do not find abnormalities of whole brain/intracranial contents, while lateral ventricle enlargement is reported in 77%, and third ventricle enlargement in 67%. The temporal lobe was the brain parenchymal region with the most consistently documented abnormalities. Volume decreases were found in 62% of 37 studies of whole temporal lobe, and in 81% of 16 studies of the superior temporal gyrus (and in 100% with gray matter separately evaluated). Fully 77% of the 30 studies of the medial temporal lobe reported volume reduction in one or more of its constituent structures (hippocampus, amygdala, parahippocampal gyrus). Despite evidence for frontal lobe functional abnormalities, structural MRI investigations less consistently found abnormalities, with 55% describing volume reduction. It may be that frontal lobe volume changes are small, and near the threshold for MRI detection. The parietal and occipital lobes were much less studied; about half of the studies showed positive findings. Most studies of cortical gray matter (86%) found volume reductions were not diffuse, but more pronounced in certain areas. About two thirds of the studies of subcortical structures of thalamus, corpus callosum and basal ganglia (which tend to increase volume with typical neuroleptics), show positive findings, as do almost all (91%) studies of cavum septi pellucidi (CSP). Most data were consistent with a developmental model, but growing evidence was compatible also with progressive, neurodegenerative features, suggesting a "two-hit" model of schizophrenia, for which a cellular hypothesis is discussed. The relationship of clinical symptoms to MRI findings is reviewed, as is the growing evidence suggesting structural abnormalities differ in affective (bipolar) psychosis and schizophrenia.
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PMID:MRI anatomy of schizophrenia. 1033 Nov 2

The granins (secretogranins/chromogranins) are a family of soluble proteins stored and released from the secretory large dense-core vesicles of the synapse. Schizophrenia is a common and devastating brain disorder. Although the aetiology of schizophrenia is unknown, data are accumulating that synaptic disturbance or damage may be of importance. The objective of this study was to compare the levels of chromogranin A, B and C in the cerebrospinal fluid (CSF) of patients with schizophrenia and healthy controls. CSF chromogranin levels were measured by RIA in 33 subsequent admissions of patients with psychotic disorder and in 31 healthy controls. The levels of CSF chromogranin A (11.8+/-3.0 vs 14.8+/-4.8 nmol/l, P=0.004), chromogranin B (3.4+/-0.49 vs 3.7+/-0.58 nmol/l, P=0.02), but not chromogranin C (70.2+/-15.7 vs 65.3+/-20.4 pmol/l, P=0.29) were lower in the schizophrenic patients than in the healthy controls. These data indicate that two widespread constituents of large dense-core vesicles, i.e. chromogranin A and chromogranin B, are altered in chronic schizophrenic patients.
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PMID:Reduction of chromogranin A and B but not C in the cerebrospinal fluid in subjects with schizophrenia. 1042 91

There has been controversy about the role of family in the etiology and course of schizophrenia for almost 70 years. Psychoanalysts and family therapists have proposed theories about the development of schizophrenia that overtly blamed parents, and recently, expressed emotion (EE) research has been criticized as implicating families once again. However, the study of schizophrenia as a brain disorder has resulted in new understandings of the influence of the family. This article reviews recent research revealing a unique vulnerability to stress in persons with schizophrenia and suggesting that communication difficulties may be due to a shared genetic heritage. Advanced practice mental health nurses who have a solid foundation in neurobiology are ideally suited to help the person with schizophrenia and his or her family. Knowledge about the neurobiological basis of schizophrenia has become very sophisticated and complex, but that knowledge is nevertheless essential to understand the otherwise puzzling patterns of behavior shown by persons with schizophrenia.
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PMID:The family and schizophrenia. 1083 56

This is a critical review of the literature related to the neurodevelopmental hypothesis of schizophrenia which posits that the illness is related to abnormal brain development. The review focuses on data deriving from clinical studies, and it is organized according to the life phase from which the data were collected: conception and birth, infancy and childhood up to the onset of the illness, after illness onset, and postmortem. The neurodevelopmental hypothesis is supported by several pieces of evidence, including increased frequency of obstetric complications in patients with schizophrenia: the presence of minor physical anomalies; the presence of neurological, cognitive, and behavioral dysfunction long before illness onset; a course and outcome of the illness itself that is incompatible in most cases with a degenerative illness; the stability of brain structural measures over time; and the absence of postmortem evidence of neurodegeneration. A historical perspective on how this research accumulated and a section addressing important areas of future investigation are also provided. We conclude that schizophrenia is certainly not a degenerative brain disorder, and that it is likely that a brain insult in utero or at birth plays a role in its expression. Current evidence cannot completely exclude the role of environmental variables after birth. In addition, it is possible that other psychiatric disorders may also have a neurodevelopmental component.
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PMID:The neurodevelopmental hypothesis of schizophrenia: following a trail of evidence from cradle to grave. 1101 50

After more than 100 years of research, the neuropathology of schizophrenia remains unknown and this is despite the fact that both Kraepelin (1919/1971: Kraepelin, E., 1919/1971. Dementia praecox. Churchill Livingston Inc., New York) and Bleuler (1911/1950: Bleuler, E., 1911/1950. Dementia praecox or the group of schizophrenias. International Universities Press, New York), who first described 'dementia praecox' and the 'schizophrenias', were convinced that schizophrenia would ultimately be linked to an organic brain disorder. Alzheimer (1897: Alzheimer, A., 1897. Beitrage zur pathologischen anatomie der hirnrinde und zur anatomischen grundlage einiger psychosen. Monatsschrift fur Psychiarie und Neurologie. 2, 82-120) was the first to investigate the neuropathology of schizophrenia, though he went on to study more tractable brain diseases. The results of subsequent neuropathological studies were disappointing because of conflicting findings. Research interest thus waned and did not flourish again until 1976, following the pivotal computer assisted tomography (CT) finding of lateral ventricular enlargement in schizophrenia by Johnstone and colleagues. Since that time significant progress has been made in brain imaging, particularly with the advent of magnetic resonance imaging (MRI), beginning with the first MRI study of schizophrenia by Smith and coworkers in 1984 (Smith, R.C., Calderon, M., Ravichandran, G.K., et al. (1984). Nuclear magnetic resonance in schizophrenia: A preliminary study. Psychiatry Res. 12, 137-147). MR in vivo imaging of the brain now confirms brain abnormalities in schizophrenia. The 193 peer reviewed MRI studies reported in the current review span the period from 1988 to August, 2000. This 12 year period has witnessed a burgeoning of MRI studies and has led to more definitive findings of brain abnormalities in schizophrenia than any other time period in the history of schizophrenia research. Such progress in defining the neuropathology of schizophrenia is largely due to advances in in vivo MRI techniques. These advances have now led to the identification of a number of brain abnormalities in schizophrenia. Some of these abnormalities confirm earlier post-mortem findings, and most are small and subtle, rather than large, thus necessitating more advanced and accurate measurement tools. These findings include ventricular enlargement (80% of studies reviewed) and third ventricle enlargement (73% of studies reviewed). There is also preferential involvement of medial temporal lobe structures (74% of studies reviewed), which include the amygdala, hippocampus, and parahippocampal gyrus, and neocortical temporal lobe regions (superior temporal gyrus) (100% of studies reviewed). When gray and white matter of superior temporal gyrus was combined, 67% of studies reported abnormalities. There was also moderate evidence for frontal lobe abnormalities (59% of studies reviewed), particularly prefrontal gray matter and orbitofrontal regions. Similarly, there was moderate evidence for parietal lobe abnormalities (60% of studies reviewed), particularly of the inferior parietal lobule which includes both supramarginal and angular gyri. Additionally, there was strong to moderate evidence for subcortical abnormalities (i.e. cavum septi pellucidi-92% of studies reviewed, basal ganglia-68% of studies reviewed, corpus callosum-63% of studies reviewed, and thalamus-42% of studies reviewed), but more equivocal evidence for cerebellar abnormalities (31% of studies reviewed). The timing of such abnormalities has not yet been determined, although many are evident when a patient first becomes symptomatic. There is, however, also evidence that a subset of brain abnormalities may change over the course of the illness. The most parsimonious explanation is that some brain abnormalities are neurodevelopmental in origin but unfold later in development, thus setting the stage for the development of the symptoms of schizophrenia. Or there may be additional factors, such as stress or neurotoxicity, that occur during adolescence or early adulthood and are necessary for the development of schizophrenia, and may be associated with neurodegenerative changes. Importantly, as several different brain regions are involved in the neuropathology of schizophrenia, new models need to be developed and tested that explain neural circuitry abnormalities effecting brain regions not necessarily structurally proximal to each other but nonetheless functionally interrelated. (ABSTRACT TRUNCATED)
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PMID:A review of MRI findings in schizophrenia. 1134 62

Schizophrenia is a brain disorder characterized by a heterogeneous clinical symptomatology. Accordingly, many structural brain changes are not associated directly with clinical symptoms. These structural changes can be detected in the frontotemporal cortex and may correlate with the course of the disease. The most important etiological concept is the neurodevelopmental hypothesis according to which developmental, morphologically detectable changes predispose for the acquisition of schizophrenia. The relevance of neurodegenerative components also remains to be determined. However, it is becoming increasingly clear that schizophrenia is not associated with pathological changes in a circumscribed brain region but with widely distributed morphological changes. Presently, the leading hypothesis for explaining these changes is a frontotemporolimbic network disturbance with cytoarchitectural changes in the heteromodal association cortex. Present research therefore focuses on testing this theory using functional imaging on a macroscopic level and examination of the neuronal cytoarchitecture on a microscopic level.
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PMID:[Structural brain changes in patients with schizophrenic psychoses. From focal pathology to network disorder]. 1138 43

Schizophrenia is a devastating psychiatric disorder with a high prevalence worldwide. There is therefore a need for animal models allowing the development of new therapeutic interventions and reliable diagnostic tests. In the temporal domain, cannabinoid receptor gene (CB1) knockout mice exhibit behavioural alterations, which parallel symptoms in schizophrenia, cannabis intoxication and dopamine D2 activation. While a specific nucleotide homology between CB1 and D2 accounts for the pathophysiology, pre-inserted spirochaetal DNA on the polyadenylation signal of CB1 reveals the aetiology of schizophrenia. If, in analogy to thalassaemia, mutations occur within this 3' regulatory domain, the genetic expression of CB1 is disrupted and sequential information lost in time. CB1, previously unrecognized as a candidate gene, thus unifies the different aspects of schizophrenic psychosis: cannabis-induced model psychosis, disrupted information processing, spatio-temporal distortions and other psychotic symptoms, disturbed neuronal migration, schizophrenic brain disorder, familial transmission, and prenatal infection by Borrelia burgdorferi.
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PMID:Are cannabinoid receptor knockout mice animal models for schizophrenia? 1139 12

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