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

There are some evidences to propose blood platelets as a model of bioaminergic neurons. Similarities between platelets and neurons are particularly important with respect to serotonin metabolism but now it is possible to extend this model to other neurotransmitters such as dopamine, GABA, glutamate... The reason for these similarities may be due to the common embryonic origin of these two very different cell types. Some changes of platelet functions are observed in psychiatric syndromes. For example: serotonin uptake, bioamine storage, enzymatic activities are modified in different types of depression and schizophrenia, infantile autism, neurologic diseases (migraine, chorea, Down syndrom). Furthermore, psychotropic drugs also alter the platelet functions. Recently, the discovery of neuro-endocrine disorders in psychiatric diseases has led to the proposal of platelets as a model in neuro-endocrinology. Some arguments can be developed to support this hypothesis. In biological psychiatry, the platelet model seems actually useful essentially in the classification of psychiatric diseases, the management of treatments and the study of new psychotropic drugs. However methodologic difficulties still presently limit the development of this model.
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PMID:[Blood platelets: neuronal model in psychiatric disorders]. 286 6

By keeping in mind that not a psychosis is schizophrenia, the primary care physician can often avoid misdiagnosis in behaviorally disturbed patients. Abnormal behavior may result from mood disorders, drug-induced psychosis and other organic disorders, personality disorders, delusional disorders, autism, or mental retardation. A long-term history is essential for correct diagnosis and treatment.
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PMID:Differential diagnosis of psychosis. A brief guide for the primary care physician. 292 77

During the 1970s, vitamins and vitamin therapy became household words. Vitamin therapy, better known as "orthomolecular psychiatry," is both appealing and very popular. The question that must be asked is: Does this popularity and appeal validate this form of therapy? This paper presents findings from various sources that give results of research in megavitamin nutritional therapy. The following categories are examined: learning disabilities in general, schizophrenia, autism, mental retardation and Down's syndrome, and hyperkinesis.
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PMID:Behavioral disorders, learning disabilities and megavitamin therapy. 296 2

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

[3H]Imipramine binding to platelet membranes was evaluated in ten autistics, eight schizophrenics and seven normal controls. The schizophrenics and eight out of the ten autistics were maintained on chronic neuroleptic treatment. Diagnosis of autism and schizophrenia was established according to the DSM-III criteria. No significant difference in the maximal binding capacity of [3H]imipramine (Bmax) and Kd values could be found among the three groups. It seems that the imipramine binding site is intact both in autism and schizophrenia.
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PMID:Platelet [3H]imipramine binding in autism and schizophrenia. 310 51

Symptom development from birth to 12 years of age was examined in 18 children who met DSM-III criteria for schizophrenia with onset before 10 years of age. Using a follow-back design, symptom development was rated at each of four age levels using a DSM-III Symptom Rating Scale and the Achenbach Child Behavior Checklist. Results revealed a gradual developmental unfolding of a broad spectrum of symptoms affecting social, cognitive, sensory and motor functioning and beginning many years before the appearance of schizophrenic symptoms--usually in early infancy. Prior to 6 years of age, severe language deficits and motor development problems were each found in 72% of the sample and symptoms of infantile autism were found in 39% of the sample. Onset of schizophrenia occurred at an earlier age for children with a history of autistic symptoms during infancy than for other children in the sample. Schizophrenia as defined by DSM-III was entirely absent before 6 years of age.
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PMID:Symptom development in childhood onset schizophrenia. 323 94

The authors have studied 30 patients with torpid schizophrenia associated with unfavourable changes of the 'verschroben' type. Only those cases are considered in which manifestations of this defect almost completely determined the clinical picture of the disease. A detailed psychopathological analysis has demonstrated that in patients presenting unfavourable changes of the 'verschroben' type all features characteristic of a mild typical schizophrenic defect or a defect of schizoid structure (autism, emotional changes, bizarre behaviour, paradoxic features in thinking and behaviour, motor peculiarities, disturbances in the sphere of instincts and inclinations) become most expressed. It has also been established that a 'verschroben' type defect forms at later stages of the disease taking a form of evolutional schizophrenia.
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PMID:[The verschroben-type defect in torpid schizophrenia]. 342 82

It is argued that further research to achieve more detailed diagnostic systems in many psychiatric disorders is unlikely to be productive without taking genetic effects into account. Even when this is done, for example when carrying out segregation analysis to determine a mode of genetic transmission, mental illnesses often pose specific problems that preclude accurate analysis. Because techniques in molecular biology and genetics have made it possible to study gene effects in human disease systematically it should now be possible to specify the genes that are involved. When this has been achieved then a diagnostic system based on genetic causation can develop. This will have the advantage of helping to pinpoint environmental factors more accurately. Specific strategies will need to be adopted to overcome uncertain modes of inheritance, incomplete or non-penetrance of disease alleles and disease heterogeneity. Highly speculative hypotheses can be put forward for a locus causing Alzheimer's disease on a portion of the long arm of chromosome 21. For autism it is plausible that there is a disease locus at or near the fragile X site on the X chromosome. A locus for manic depression has been very tentatively mapped using DNA markers to chromosome 11 and in a small proportion of families DNA markers have also shown some evidence for X linkage. Schizophrenia does not seem to be associated with any favoured loci. Candidate genes for schizophrenia include those encoding dopamine, other neurotransmitter receptors or enzymes and various neuropeptides such as enkephalin and beta endorphin.
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PMID:Candidate genes and favoured loci: strategies for molecular genetic research into schizophrenia, manic depression, autism, alcoholism and Alzheimer's disease. 355 29

The role of cognition in child development is reviewed with respect to the role of cognitive processing and cognitive deficits. Cognitive processing is discussed with respect to the self-system; the effects of psychosocial experiences; risk, vulnerability and protective mechanisms; vulnerability to depression; aetiology and treatment of depression. Cognitive deficits are discussed with respect to the socio-emotional consequences of language delay and reading difficulties; hyperkinetic/attentional deficit syndromes; schizophrenia; and autism. It is concluded that the ways in which we appraise our life circumstances and the ways in which we react to experiences of all kinds are greatly influenced by how we think about ourselves and our environment. Biases and distortions in such cognitive processing may be associated with social and emotional malfunction. These biases may derive from earlier experiences, from intensive temperamental styles, or from deficits in the ability to process incoming information. The further study of cognitive processing and cognitive deficits is likely to be rewarding and helpful for clinical practice.
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PMID:The role of cognition in child development and disorder. 356 6

The performance of children meeting DSM-III criteria for schizophrenic disorder and infantile autism and of normal children (ages 7 years 10 months to 14 years 4 months) was compared on the Wisconsin Card Sorting Test, Rey's Tangled Line Test, Benton Judgment of Line Orientation, Digit Symbol Substitution Test, and Peabody Picture Vocabulary Test. The mean performance IQ of the schizophrenic and autistic children was equal and in the normal range. The normal children were of average intelligence as estimated by the PPVT. As compared to normal children, both autistic and schizophrenic children were impaired on the DSST and RTLT. The autistic children had significantly lower scores on the PPVT than schizophrenic and normal children. The schizophrenic children made significantly more perseverative responses on the WCST than did normal children. They significantly increased their nonperseverative errors on the second half of the WCST, after having been taught the correct sorting principles. It is argued that in schizophrenia a core deficit in momentary processing capacity underlies the above performance pattern. In contrast, in autism the core cognitive deficit involves an inability to use language to regulate and control ongoing behavior.
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PMID:A comparison of cognitive/neuropsychological impairments of nonretarded autistic and schizophrenic children. 357 38


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