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

The article outlines the relationships that obtain among schizophrenia, smoking, and smog. An overview of known scientific facts concerning the pathogenesis of schizophrenia is first provided. The relationship this has with nicotine addiction is discussed next, and finally the notion is introduced that heterocyclic amines found in cigarette smoke and petroleum fumes serve as a potent environmental neurotoxin that seriously compromises mental health in biologically susceptible individuals. It is argued that such biologic susceptibility takes the form of cerebral diabetes, which accounts for the serious impairment of glucose metabolism as demonstrated by positron emission tomography. Central to this argument is the view that diabetes can be peripheral, without affecting the central nervous system, or central, without affecting the peripheral system.
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PMID:Schizophrenia, smoking, and smog. 783 84

While one of the original underpinnings of the dopamine theory of schizophrenia was the paranoid psychosis which often develops during the binges or speed runs of chronic amphetamine addicts (and, more recently, in cocaine addicts), neurochemical studies of such drug abusers or from animals given continuous stimulants in an effort to model stimulant psychoses have not played a major role in the further evolution of this theory. One clear persisting alteration produced by continuous amphetamine is a neurotoxicity to dopaminergic innervations in caudate. Yet continuous cocaine administration apparently does not induce a similar neurotoxicity and this makes this effect a poor candidate for an underpinning of stimulant psychoses. However, it has recently been found that both continuous amphetamine and cocaine induce a strong pattern of degeneration which is highly confined to the lateral habenula and its principal output pathway, fasciculus retroflexus. This finding has led to a reconsideration of the role of these structures in psychoses. The habenula, as the chief relay nucleus of the descending dorsal diencephalic system (consisting of stria medullaris, habenula and fasciculus retroflexus), is an important link between limbic and striatal forebrain and lower diencephalic and mesencephalic centers. Studies of glucose utilization have consistently shown the habenula to be highly sensitive to dopamine agonists and antagonists. Lesions of habenula produce a wide variety of behavioral alterations. The dorsal diencephalic system has major and predominantly inhibitory connections onto dopamine-containing cells and it mediates part of the negative feedback from dopamine receptors onto dopamine cell bodies. It represents one of the major inputs in brain to the raphe nuclei and has anatomical and functional connections to modulate important functions such as sensory gating through thalamus, pain gating through central gray and raphe and motor stereotypies and reward mechanisms through substantia nigra and the ventral tegmental area. It is argued that alterations in these pathways are ideal candidates for producing the behaviors which occur during psychosis and that future considerations of the circuitry underlying psychoses need to include this highly important but relatively neglected system.
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PMID:Stimulant-induced psychosis, the dopamine theory of schizophrenia, and the habenula. 791 93

Schizophrenia has become an elusive medical conundrum since it was first described at the turn of the 19th century. Over time, a variety of causal hypotheses have been advanced to explain the spectrum of schizophreniform disorders. This etiological explanation outlines the relationship that obtains between smoking, schizophrenia, and impaired glycometabolism which also includes disruption to the dopaminergic and serotinergic pathways. A possible genetic explanation for this disruption will be identified which links mental illness to a locus of genes contained on the short arm of chromosome 11. These genes are all essential to normal glucose transport which positron emission tomography (PET) scans show is seriously abnormal in schizophrenia. Thus, a redefinition of schizophrenia as 'cerebral diabetes' will be proposed since this term implies a diabetic brain state consistent with PET scans of schizophrenic patients.
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PMID:Schizophrenia: an extended etiological explanation. 802 29

A brain imaging study was conducted in the case of a catatonic type of schizophrenia (DSM-IIIR) by applying (i) positron emission tomography (PET) and (ii) single photon emission computed tomography (SPECT). A PET study using [18F]-2-fluoro-2-deoxy-D-glucose revealed a lower glucose utilization in the dorsal frontal and parietal lobes of both cerebral hemispheres. Correlative SPECT studies using [123I]-iodoamphetamine showed a diminished regional cerebral blood flow in similar regions of the cerebral hemisphere. A three-dimensional volume rendering method of the SPECT images (TITAN) identified the dorsal region of the fronto-parietal lobe as the most severely affected region. These patterns of deficits implicated the role of the dorsal frontal and parietal lobes in the pathogenesis of catatonic syndromes.
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PMID:Functional brain imaging of a catatonic type of schizophrenia: PET and SPECT studies. 820 98

Phencyclidine (PCP), a psychotomimetic drug of abuse, produces mental changes and manifestations in humans which are reminiscent of schizophrenia, though the mechanism of these actions remains unknown. We report here a biphasic time course of PCP action on regional cerebral glucose metabolism extending over 48 h. A single dose of PCP (8.6 mg/kg) produces an initial increase in glucose metabolism (at 3 h) and a later decrease in glucose metabolism (at 24 h) without a return to baseline until 48 h. A single lower dose of PCP (0.86 mg/kg), a dose which is considered selective for action at the NMDA-PCP receptor, produces no early metabolic change (at 3 h), but replicates the regional hypometabolism albeit less intense at 24 h. The delayed cerebral hypometabolism does not appear to be related to PCP-induced intracellular vacuolization, seen in the retrosplenial cortex. These metabolic changes may be associated with the psychotomimetic effects of PCP and thus may be relevant to psychosis in humans.
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PMID:Delayed regional metabolic actions of phencyclidine. 822 27

A number of studies of chronically ill, medicated patients have found that the clinical symptoms of schizophrenia segregate into three syndromes which can be labelled poverty, disorganization, and reality distortion. It has been previously found that each of these syndromes is associated with a specific pattern of perfusion (rCBF) in paralimbic and association cortex and in related subcortical nuclei. We replicated the symptom factors in 20 untreated subjects. Utilizing positron emission tomography with 18-F-fluorodeoxyglucose as a tracer for glucose metabolism, we reconstructed a map of the entire cortical activity from 16 to 20 tomographic slices. Each of the three syndromes was associated with a different pattern of regional glucose metabolism. Findings in common with previous studies were an association of poverty with left cortical metabolic activity in prefrontal and superior parietal areas, reality distortion with left temporal activity, and disorganization with left inferior parietal lobule. This is the first report of an association between regional metabolic activity and clinical syndromes in untreated patients, strengthening previous models of distributed neural networks in this disorder.
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PMID:Three clinical syndromes of schizophrenia in untreated subjects: relation to brain glucose activity measured by positron emission tomography (PET). 829 4

Patterns of regional cerebral glucose metabolism were examined in a group of patients with schizophrenia (n = 17) and normal controls (n = 16) to determine if different metabolic profiles were present. For the patients with schizophrenia, two profiles were found. The first was characterized by a normal "shape" but overall reductions in cerebral metabolism. The second had focal reductions in frontal metabolism. This latter group also had significantly larger frontal horns than the other schizophrenic group. The two groups with schizophrenia did not differ on other attributes or clinical variables. These results are discussed in terms of our understanding of heterogeneity in schizophrenia and etiology.
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PMID:Metabolic subtypes in patients with schizophrenia. 843 8

For some considerable time, there has been a growing awareness that defective essential fatty acid metabolism plays a causal role in the pathogenesis of both schizophrenia and non-insulin-dependent diabetes mellitus (NIDDM) but the influence of defective essential fatty acid metabolism in the pathogenesis of rheumatoid arthritis and cancer is less well appreciated. An EFA deficiency, or defective EFA metabolism, negatively influences prostaglandin synthesis and glucose regulation and transport. Moreover, defective EFA metabolism negatively influences estrogen availability which contributes to the observed gender bias some of these illnesses manifest. While fluctuations of estrogen are known to contribute to the pathogenesis of these conditions, so also do fluctuations of IGF-II and there is some suggestion that IGF-II and insulin may well be inversely regulated. In addition, insulin-dependent diabetes mellitus (IDDM), rheumatoid arthritis, and schizophrenia are thought to be autoimmune disorders, while cancer is associated with immune system failure. Consequently, this paper aims to examine the pathophysiological similarities and differences between mental illness, diabetes, rheumatoid arthritis and cancer in respect of which the causal relationship that obtains between essential fatty acids, estrogen, IGF-II, glucose regulation and autoimmunity will be addressed.
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PMID:The estrogen connection: the etiological relationship between diabetes, cancer, rheumatoid arthritis and psychiatric disorders. 853 40

Twenty-five schizophrenic patients, fourteen adults with a history of infantile autism, and twenty normal controls performed a test of sustained attention, the degraded stimulus continuous performance test (CPT), during the 35 minute 18-fluoro-2-deoxyglucose uptake period preceding positron emission tomographic (PET) scan acquisition. This is the first analysis comparing correlations between glucose metabolic rate (GMR) for selected regions and CPT performance. CPT performance differed in controls and schizophrenics, but autistics did not differ from either group. In controls and schizophrenic patients, task performance correlated with GMR in medial superior frontal gyrus and lateral inferior temporal gyrus, suggesting that activation of those regions is important in the normal performance of the task and that damage to those regions, which also showed low GMR in schizophrenics, contributes to the attentional dysfunction in schizophrenia. Also, schizophrenics showed negative correlations of task performance with anterior cingulate activity suggesting that overactivity of that region, which is involved in mental effort and whose GMR was low in our larger study of schizophrenia, impairs task performance in schizophrenics. Autistic patients showed negative correlations of medial frontal cortical GMR with attentional performance, suggesting that neuronal inefficiency in that region may contribute to poor performance.
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PMID:Glucose metabolic correlates of continuous performance test performance in adults with a history of infantile autism, schizophrenics, and controls. 854 Dec 54

Positron emission tomography with [18F]-fluoro-2-deoxy-D-glucose as tracer was used to investigate frontal glucose metabolism in 15 unmedicated schizophrenic patients and 15 healthy subjects under resting conditions. Although no difference in absolute frontal cerebral metabolic rates of glucose (CMRglu) were found between schizophrenic patients and control subjects, relative measures significantly differentiated the two groups. Whole frontal metabolism and frontocaudate ratio were significantly decreased in both hemispheres in the patients. The results confirm the existence of hypofrontality in unmedicated schizophrenia and indicate disturbances in metabolic relationships between the frontal cortex and the striatum in this disorder.
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PMID:Altered frontostriatal relationship in unmedicated schizophrenic patients. 854


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