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

Around the year 1950, we observed five cases of infantile schizophrenia; these patients were personally re-examined in 1956 and 1977. Another patient, under the care of the psychiatrists of the Public Health Department was included at a later date. One case of periodic catatonia is distinguished from other cases by a normal development up to puberty. The other five cases suffer from a "systematic" catatonia with characteristic syndromes and a slowly progressing course. As early as at the age of two or five years, they were noticeable for autism and psychomotor syndromes. The diagnosis of the catatonic subform was confirmed after 25 years. Although originally able children their intellectual development came to a standstill during the progressing process as did the maturing of the personality. A causative factor of the early development can be seen in the lack of stimulation to which four only children and one child brought up in a home were exposed.
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PMID:[Follow up of early childhood schizophrenics. Progress of 6 cases over 25 years]. 738 97

An effort was made to formalize the critical clinical, demographic and historical features of schizophrenia through the development of a reliable assessment questionnaire. The criterion diagnosis was established via traditional hospital procedures and was substantiated by psychometric measures. Raters with comparable diagnostic experience were familiarized with each of the clinical, demographic and historical features before evaluating the presence or absence in a sample of both psychiatric in-patients and out-patients. A structured, standardized interview was used to reduce inconsistency and oversight due to variability in interviewing techniques and coverage of psychopathology. Using the coefficients of the discriminative functions of five major symptoms (loose associations, autism, loss of ego boundaries, emotional blunting, delusions) and two demographic and historical features (family history of mental illness, poor social relations) correctly classified 98 per cent of the total sample of 253 patients. A subsequent investigation demonstrated the utility and generalizability of the proposed system. The assets and liabilities of using such an approach are discussed.
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PMID:Using discriminant function analysis with clinical, demographic and historical variables to diagnose schizophrenia. 743 57

Recently a new form of human mutation-expansion of trinucleotide repeats-has been found to cause the diseases of fragile X syndrome, spinal and bulbar muscular atrophy, myotonic dystrophy and, most recently, Huntington's disease. We review the emerging data on the genetics and neurobiology of these disorders. Three are characterized by unusual patterns of inheritance, in particular, genetic 'anticipation', in which the severity of the disorder increases and the age of onset decreases in successive generations of a pedigree. Several idiopathic neuropsychiatric disorders have features of inheritance consistent with anticipation. In bipolar affective disorder, there is evidence for both earlier age of onset and more severe illness in the second generation of a subset of unilineal pedigrees. There is also the suggestion of anticipation in some forms of schizophrenia, spinocerebellar atrophy and autism. Triplet repeats are present in additional known genes, both in coding regions and untranslated regions. Furthermore, many novel genes with triplet repeats are expressed in the human brain, and these are candidates to cause some forms of these neuropsychiatric disorders.
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PMID:Genes with triplet repeats: candidate mediators of neuropsychiatric disorders. 768 67

Descriptions of various psychotic symptoms in children began to appear in the psychiatric literature at about the same time as descriptions of psychotic symptoms in adults. For example, Kraepelin estimated that at least 3.5 percent of his cases of dementia praecox had onsets before age 10. The construct of "childhood schizophrenia" initially emerged from attempts to classify a broad range of psychotic children. By the late 1940s and 1950s, the diagnosis of "childhood schizophrenia" was given to many disturbed children who today would be considered to have infantile autism and other developmental disabilities. In the early 1970s infantile autism and its variants was differentiated from schizophrenia of childhood onset. These changes were incorporated in DSM-III, which returned to the practice before 1930 of diagnosing schizophrenia in children using the same criteria as for adults, with minor allowances for differences in the manifestations of these symptoms during childhood. The studies presented in this issue of Schizophrenia Bulletin use DSM-III, DSM-III-R, or ICD-9 criteria for schizophrenia.
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PMID:Childhood-onset schizophrenia: editors' introduction. 770 Dec 70

An ongoing study of the phenomenology, genetics, neuropsychology, physiology (eye tracking, autonomic responsivity), neuroimaging, biochemistry, and pharmacology of childhood-onset schizophrenia is described, and pilot data are presented for the first 22 subjects. Differentiation from autism "spectrum" disorders and other poorly defined, severe neurodevelopmental disorders is needed. Eye tracking and autonomic results are similar to patterns seen in later-onset schizophrenia and possibly more striking. Magnetic resonance imaging showed larger left frontal ventricular horn area for the schizophrenia subjects, larger left caudate, and lack of normal caudate asymmetry. Fluorodeoxyglucose positron emission tomography during an auditory continuous performance task revealed decreased right parietal/occipital glucose metabolic rate in the schizophrenia subjects, which may be secondary to poor attentional performance, and increased glucose metabolic rate in three left frontal regions, a left parietal region, and the right putamen. Clozapine has been effective and well tolerated in an open trial with 12 adolescents who responded poorly to typical neuroleptics; 16 subjects have been enrolled in a double-blind comparison of haloperidol and clozapine. Longitudinal study of this narrowly defined and possibly more homogeneous group of very early-onset schizophrenia subjects will be relevant to current neurodevelopmental theories addressing the role of puberty, progression of pathology, and continuity or discontinuity with later-onset schizophrenia.
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PMID:Childhood-onset schizophrenia: an NIMH study in progress. 770 Dec 77

For some time it has been known through the results of family, twin, and adoption studies that heredity appears to play a significant causal role in many mental disorders, including schizophrenia, bipolar disorder, and other mood disorders, Alzheimer's Disease, panic disorder, obsessive compulsive disorder, autism, dyslexia, and Tourette's Syndrome. The precise patterns of inheritance of these complex disorders have not been determined, nor have the relevant genes been localized or cloned. Because the genetics are complex and because there is also clearly an environmental contribution to behavior, we expect the analysis of the genetics of mental illness to be arduous, and not quickly resolved. There are several compelling reasons to continue to focus our attention on uncovering the genetic factors for severe mental illness. Prominent among these are the implications for better treatment of mental disorders. The National Institute of Mental Health supports a wide range of studies on psychiatric genetic research.
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PMID:Psychiatric genetic research at the National Institute of Mental Health. 772 97

Bufotenine (BUTN) is a hallucinogen with psychotropic effects. High levels of BUTN and its precursor, N-methylserotonin are shown for the first time to occur and to accumulate mainly in the brain during the degradation of serotonin in the central nervous system of the toad, Bufo bufo japonicus. These compounds are concentrated in the hindbrain, which includes the cerebellum and medulla oblongata. BUTN can also be detected in blood and urine specimens from the toad. In humans, autism is a subtype of schizophrenia that appears to be a functional disease of the brain. BUTN can be detected in urine specimens from infant autistic patients. Analysis by three-dimensional HPLC suggests that the presence and levels of BUTN may be important markers for the diagnosis of autism. It appears, therefore, that some aspects of the central nervous system of Bufo may provide useful pharmacological clues to the etiology of human psychiatric diseases, such as autism, that are known to be linked to the methylation of serotonin.
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PMID:Serotonin-degradative pathways in the toad (Bufo bufo japonicus) brain: clues to the pharmacological analysis of human psychiatric disorders. 774 94

Research findings on continuities and discontinuities in psychopathology between childhood and adult life are reviewed with respect to major depressive disorders, anxiety states, obsessional conditions, anorexia nervosa, conduct disorders, hyperkinetic disorders, autism, specific developmental disorders of language and schizophrenia. The findings are used to consider both the conceptual issues and possible mediating mechanisms.
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PMID:Relationships between mental disorders in childhood and adulthood. 777 74

To limit genetic heterogeneity, this study focused on the widely extended pedigrees of Ashkenazi Jewish schizophrenic and autistic probands, to determine if similar causal mechanisms might obtain for both conditions. At least two previous epidemiological studies have demonstrated increased risk for schizophrenia in Ashkenazi Jews. The hypothesis posed is that increased prevalence of various rare autosomal recessive diseases among the Ashkenazim might contribute to the increased vulnerability to schizophrenia and to autism in this large genetic isolate. Rates of amyotrophic lateral sclerosis (ALS) and bleeding disorders were significantly increased among relatives of schizophrenic and autistic probands, compared to relatives of normal probands. These results suggest new candidate loci in schizophrenia and autism, particularly the chromosome 15q23-24 locus of the hexosaminidase A gene, causing various GM2 gangliosidoses, and the 21q22.1-q22.2 loci of the antioxidant, superoxide dismutase gene, and a cytokine receptor gene.
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PMID:A family history study of schizophrenia spectrum disorders suggests new candidate genes in schizophrenia and autism. 783 15

Many forms of psychopathology in higher animals and humans include the production of maladaptive, repetitive behaviour. Behaviour which is both repetitive and excessive in amount can be described as stereotyped whereas behaviour which represents a restriction of behavioural possibilities without excessive production can be described as perseverative. Both types of repetition can result from pathology in the neural mechanisms which control either the production of motor output or the organisation of behaviour at a higher level. A number of forms of repetitive behaviour can be induced environmentally. Confinement in adulthood results in a functional disorder which rapidly dissipates when normal conditions are restored but confinement in infancy may have a permanent effect on the organism's ability to interact in a flexible and creative way with its environment. The permanence of these disorders suggests that the environment can affect the way in which the nervous system develops. Repetitive behaviour is also a feature of mental illness including schizophrenia, autism, OCD, addiction and some neurological disorders including frontal lobe lesions, Tourette's syndrome and PD. In experimental studies in animals, stereotyped behaviour seems to be related mainly to excess dopaminergic activity in the basal ganglia while perserverative behaviour can be produced by lesions of the frontal lobes. It is supposed that the level of dopamine activity in the basal ganglia affects the baseline level of behavioural activation such that excess activation results in the excessive execution of the most probable response to the environment to the exclusion of other possibilities (i.e. stereotypy) while deficient activation results in the production of only a few responses which can exceed the necessary activation level (i.e. perseveration). In either case behaviour is 'stimulus-bound', being driven by only the most salient feature of the environment. The symptoms of PD result from inadequate levels of dopamine in the basal ganglia while the stimulant psychoses result from excessive availability of dopamine. The frontal lobes have a modulating effect on (i) the activation of motor activity by the basal ganglia, (ii) in the generation of self-initiated behaviour, i.e. volition, and (iii) in the neural mechanisms which permit different modes of neural function (e.g. perceiving, remembering or thinking) to be identified. Failures in these three functions could result in excessive and repetitive motor activity, stimulus-bound behaviour, the paucity of volitional and creative behaviour, and the perceptual and experiential symptoms of psychosis.
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PMID:The psychology of perserverative and stereotyped behaviour. 783 78


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