Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

US Army veterans taken prisoner (POW's) in World War II and in the Korean War are compared with controls as to hospital admissions from 1946 to 1965 (1954-1965 for Korean War POW's), and as to symptoms, disability, and maladjustments in 1966-1967. Sequelae of the POW experience are both somatic and psychiatric, and are of greatest extent and severity among Pacific World War II POW's. Among European World War II POW's only psychiatric sequelae are apparent. Somatic sequelae were most prevalent in the early years after liberation, but for Pacific World War II POW's they persist in the form of higher hospital admission rates for many specific causes in the most recent period. Nevertheless, persistent psychiatric sequelae (especially psychoneurosis but also schizophrenia) are the more notable and pervasive for both Pacific World War II POW's and Korean War POW's as seen not only in elevated hospital admission rates but also in VA disability awards and in symptoms reported on the cornell Medical Index Health Questionnaire. The excess morbidity appears to correlate well with retrospective accounts of weight-loss and nutritional deficiency diseases and symptoms during the POW period.
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PMID:Follow-up studies of World War II and Korean war prisoners. II. Morbidity, disability, and maladjustments. 12 31

The nature of psychiatric disorders in tropical regions is affected much more by the effect on the patient of certain environmental and cultural factors than by any specific features of tropical diseases. In places where the standards of health care and health education are not yet fully developed, abnormalities of physical development, particularly those affecting the development of the cerebral cortex, are of great importance. For example, protein-energy malnutrition may result in deficits in cerebral maturation and efficiency that reduce the capacity of the brain to manage its behavioural functions and may give rise to impaired capacities for concentration, foresight, and judgement and impairment of inhibitory control over intensely experienced emotions. In addition, certain cultural attitudes that are widespread in pre-literate societies influence the type of secondary reaction to disease: for example, acute symptoms tend to be florid and uninhibited, and violently experienced and externalized emotions such as hilarity, terror, anger, and grief are the rule rather than the exception.Certain tropical diseases are, however, the direct cause of severe disturbance of cerebral functioning, while others affect only the finer cerebral controls so that normally controlled fears, anxieties, and other personality traits emerge. These specific brain syndromes may be acute or chronic and may be triggered by an apparently trivial physical cause. Acute brain syndromes appear to be more common in tropical countries perhaps because in the adult the cerebral cortical reserve is less than it ought to be because of the prevalence of earlier minimal brain damage. Formal psychiatric reactions are, of course, also seen in tropical countries, but the expression of, for example, schizophrenia, hypomanic and manic states, and depression is coloured by the underlying personality and the cultural background of the patient. Perhaps in no other setting is the intimate relationship between behaviour and the physical body seen more clearly than in populations living in the tropics and it is important that health workers in these regions should be aware of the role played by earlier or concurrent physical disease in behavioural disturbance.
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PMID:The psychiatric aspects of tropical disorders. 31 50

To compare methods of measuring negative symptoms, eight rating scales were employed to retrospectively assess and subtype 187 patients with schizophrenia from the Chestnut Lodge Follow-up Study. These included Andreasen's Schedule for Assessment of Negative Symptoms, Carpenter's Criteria for the Deficit Syndrome, Kay and Opler's Positive and Negative Symptom Scale, the scales developed by Krawiecka et al and Crow's modification of them, the Negative Symptom Scale developed by Lewine et al, Pogue-Geile and Harrow's Negative Symptom Scale, and Abrams and Taylor's Emotional Blunting Scale. The overlap and concordance, temporal stability, and predictive validity of these instruments are described. When rated from detailed medical records, the reliability of all scales was fair to good. Despite their inclusion of different items, there were high positive correlations between the scales when used to rate negative symptoms dimensionally. When used to classify individual patients as having the negative or deficit syndrome, however, concordance among criteria was low. Using the broadest criteria (Pogue-Geile and Harrow), 75 (40%) patients were diagnosed as having negative syndrome; the narrowest criteria (Andreasen and Olsen) yielded 11 (6%) diagnoses of negative syndrome. Narrower definitions tended to be subsets of broader ones. Carpenter's Criteria for the Deficit Syndrome focus on primary enduring negative symptoms and show the greatest temporal stability. Broader criteria, which diagnose the deficit or negative syndrome independent of severity of positive symptoms, had the greatest predictive validity.
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PMID:Testing systems for assessment of negative symptoms in schizophrenia. 156 76

The authors propose using primary and enduring negative or deficit symptoms for dichotomizing schizophrenic patients into two groups, deficit and nondeficit. The validity of this approach was examined by comparing 17 deficit and 17 nondeficit patients for differences in premorbid adjustment and degree of neurological impairment. Deficit patients were characterized by poorer premorbid adjustment and greater neurological impairment. Neurological impairment was not related to premorbid adjustment in either group or in the total patient population. These findings support the utility of deficit symptoms for defining a more homogeneous subgroup of schizophrenia.
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PMID:Clinical correlates of the deficit syndrome of schizophrenia. 230 43

The systematic assessment of subjective experience independently from its impact on schizophrenic's behavior is neglected in most structured interviews and symptoms rating scales. However, subjective complaints may predict outcome functioning, medication compliance, and future psychotic episodes and better reflects patients' well-being than does behavioral assessment. We demonstrate the reliability of the Subjective Deficit Syndrome Scale and the considerable prevalence of subjective complaints in 166 acute and chronic inpatients and outpatients. Complaints were correlated with global measures of psychopathology in acute but not chronic patients. They were not correlated with negative symptoms or neurological side effects. Some overlap was observed with measures of depression, although most patients denied depressed mood. We conclude that subjective deficits are prevalent in schizophrenia, that they can be reliably assessed, and that they constitute an independent, clinically important dimension of the disease.
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PMID:The measurement of subjective experience in schizophrenia: the Subjective Deficit Syndrome Scale. 234 Jul 16

Diet clearly influences neurotransmission. This can be important in grossly undernourished children. It can also be important in children in whom normal homeostatic mechanisms governing food intake are bypassed. Subtle differences in behavior can occur with physiologic variation in food intake. Components of foods can also be used as drugs. Starvation can impair neuronal maturation and can have lasting effects upon behavior and intellectual performance. The extent of starvation's impact upon the brain depends upon whether undernutrition occurred during a critical phase in brain development. Short-term fasting has small, but significant, effects upon intellectual performance. Even when gross malnutrition is not present, subtle changes in diet may modulate brain function. Tryptophan, tyrosine, and choline in the diet are used as precursors for neuronal synthesis of serotonin, dopamine and norepinephrine, and acetylcholine, respectively. It is likely that the brain's sensitivity to certain components of the diet exists to permit monitoring of food intake by the central nervous system. Tryptophan, tyrosine, and choline may be useful in treatment of humans with sleep disorders, pain depression, mania, hypertension, shock, or dyskinesias. Other components of the diet that may affect behavior include food additives, sugar, and caffeine. Food additives may exacerbate hyperactive symptoms in a small proportion of children with attention deficit disorder. Given that there is little potential for harm and that there is a subpopulation that may respond, a trial of a diet that contains no food additives may be a valid diagnostic approach for children with attention deficit disorder who do not respond to stimulant therapy or for children for whom stimulant therapy is not desired. Refined sugar has been blamed for many behavioral abnormalities. Subtle effects of carbohydrate upon behavior have been reported, but the existing data do not support the hypothesis that sucrose or fructose exert special effects upon neurotransmission. Caffeine is easily detected as a stimulant by humans, but it has little effect upon cognitive function. Administration of large doses of vitamins has no beneficial effect in most humans with schizophrenia, attention deficit disorder, autism, Down's syndrome, or drug addiction. Large doses of niacinamide may even be harmful, as they may cause hepatic damage.
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PMID:Dietary influences on neurotransmission. 302 51

Studies investigating the association between the risk of schizophrenia and season of birth are reviewed and the association clearly established. This association cannot be explained on the basis of age-incidence or age-prevalence artifacts. Other studies suggest there may be an association between bipolar disorder and season of birth. The leading theory in explaining the season of birth phenomenon is that a seasonal factor (such as viral infection, malnutrition, vitamin deficiency, prenatal or obstetrical complications, or ambient temperature) can damage an infant's brain and thereby predispose the child to later development of psychosis. Evidence suggests that the seasonal effect is associated with a subgroup of schizophrenics who have early onset of psychosis, less genetic loading than other schizophrenics, and better prognosis. Case-control studies are needed comparing winterborn to nonwinter-born schizophrenics.
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PMID:Season of birth: schizophrenia and bipolar disorder. 352 Aug 3

On the basis of examining 86 senile schizophrenics with defective initial conditions two groups of such conditions were specified: 1) defect conditions retaining the structure specific for schizophrenia (apathic defect, apathic mental deficiency and its variant with pseudosenile disturbances); 2) defect conditions, approaching by their manifestations to the picture of psychic disintegration associated with senile dementia. The psychopathological structure of the first group of defect conditions primarily reflects the degree of the schizophrenia progression. Their time course in old age was limited to insignificant age-related modifications and decompensation. Deficit conditions in the second group develop the more frequently, the closer to old age the period of the maximum activity of the schizophrenic process and the older the patients.
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PMID:[Status of profound deficits during the late stages of schizophrenia with a unfavorable course]. 646 90

The height and weight were measured and the total fat and fat-free mass were estimated in 1123 patients in a mental hospital. The results were compared with the reported values in healthy persons. The young patients weighed the same as young healthy persons whereas the average weight in the elderly patients was much less than healthy elderly persons. In the elderly women patients, this difference in weight was much greater in those with dementia than in those with affective disorders or schizophrenia. The difference in weight was not related to the duration of stay in hospital, and there was no evidence that it was due to malnutrition. The lower weight may therefore by a marker for those persons likely to need institutional care rather than the result of loss of weight. A minority of the elderly patients, particularly the ill and immobile, had one of the biochemical markers of malnutrition, low plasma concentrations of either albumin or vitamin C or vitamin D. On average, these patients weighed less and had less body fat than the others. These patients may be the high-risk group for nutritional deficiency but there was no evidence that any of them had a clinically significant nutritional problem.
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PMID:The body composition of the chronic mentally ill. 716 Nov 39

We will review evidence from preclinical literature that prenatal nutritional deprivation produces neurochemical, morphological, and electrophysiological effects reminiscent of those seen in clinical studies of schizophrenia. We will focus on effects of nutritional deficiency that are likely to have implications for schizophrenia. These include disruption of neurotransmitter systems such as dopamine and serotonin and dysgenesis of the hippocampal formation. Preclinical studies show enhanced release and turnover of dopamine and serotonin following prenatal and early postnatal nutritional deficiency. Morphology of the hippocampus, as well as electrophysiology and hippocampally-mediated behaviors are also altered. Although intriguing, these studies have not been conducted with schizophrenia in mind, and thus, outcome measures that may be more specifically related to schizophrenia have not been examined. We propose that further preclinical studies that examine the consequences of prenatal nutritional deficiency, which may lead to altered neuronal migration and other developmental abnormalities, may be useful in understanding the etiology of schizophrenia.
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PMID:Prenatal nutritional deprivation as a risk factor in schizophrenia: preclinical evidence. 785 97


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