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

Infantile autism and schizophrenia have been regarded as unrelated and distinct disorders. There is, however, some evidence in the literature that supports a relationship between the two disorders in that there may be a subgroup of autistic children in whom schizophrenia develops. The diagnostic criteria used in the literature to describe infantile autism and schizophrenia in childhood has not been uniform. The three cases in this report, diagnosed on the basis of current criteria and detailed clinical descriptions, clearly point to an initial diagnosis of infantile autism followed by the development of schizophrenia.
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PMID:Autistic children who become schizophrenic. 669 93

102 children whose histories included a diagnosis of infantile autism or childhood schizophrenia were followed longitudinally to assess cognitive developmental trends. Despite some sample attrition, administration of a test battery of 5 language skill measures and 2 perception skill measures during 5 test periods over 4 years yielded 336 usable test batteries. After all tests had been administered, diagnosis of subjects for autism and schizophrenia using developmental histories and behavioral observations drawn at the time of first test-battery administration showed 111 test batteries on 33 children diagnosed as autistic, and 100 test batteries on 27 children diagnosed as schizophrenic. Comparisons of age and test score correlations, comparisons of cross-sequential means, and trends for means for diagnostic subgroups and normal controls suggest developmental delay for all skills at all ages for both autistic and schizophrenic children. Findings also suggest a trend for steady prepubertal cognitive skill development, followed by a postpubertal decline in skills for both diagnostic groups.
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PMID:Developmental trends in cognitive skills for children diagnosed as autistic and schizophrenic. 670 25

What we have tried to do in this paper is to question the universality of Infantile Autism as implied by the various definitions which have been provided. Our research of the literature has convinced us that infantile autism appears to be an illness of Western Civilization, and appears in countries of high technology, where the nuclear family dominates. We indicated that no research studies were located in the U.S.A. on Hispanics, in spite of their large number. Furthermore, it was found to be quite rare among Black families. We also saw that the illness seems to be quite infrequent in Latin American countries, Africa, and India, while the rate is high in Japan, but only in westernized families. Tinbergen (1974) likewise feels that infantile autism is "actually on the increase in a number of Western and westernized societies". Two major variables which are interconnected seem to be responsible for the confusion in the findings. One of them is the problem of diagnosis. It would seem that many researchers have extended the definition of infantile autism to include other seriously afflicted children, including those who are brain-damaged. This is no surprise, since such conflicts exist as Ritvo (1981) estimating that there are 300,000 autistic children in the U.S., while a report by the National Institute for Handicapped Research estimates the number of autistic children to be 71,000 (1981). Another aspect of the findings which has been contradictory is that some investigators have found that parents of autistic children tend to be of higher S.E.S., particularly in European studies, while some studies in the U.S.A. did not find such a difference among the parents of autistic and non-autistic children. We have provided some illustrations to indicate that studies which have found no differences were not dealing exclusively with autistic children as defined by Kanner, and often used childhood schizophrenia and autism interchangeably. Cantwell, Baker, and Rutter (1978) have pointed out that this persistent difference of superior S.E.S. of parents of autistic children is an embarrassing finding which is very hard to explain if one holds that the disease is organically determined. In conclusion to his review of the literature on the universality of adult schizophrenia, Torrey (1973) wrote the following: "Studies must be done soon or it will be too late to do them at all. But, until the universal prevalence of schizophrenia becomes an open question, this task is unlikely to be undertaken". The writer of this paper is of the same opinion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Is infantile autism a universal phenomenon? An open question. 674 21

Abnormalities of functional connection between specialized areas in the human brain may underlie the symptoms which constitute the schizophrenia syndrome. Callosal and intrahemispheric fibres may be equally involved. The clinical emergence of symptoms in the later stages of brain maturation may be dependent on myelination of these fibre groups, both of which have extended myelination cycles. Ontogenetically earlier variants of the same mechanism could theoretically result in dyslexia and the syndromes of Kanner and Gilles de la Tourette. As new and unique extensions of specialized function emerge within the evolving brain, biological trial and error of connection both within and between them may produce individuals possessing phylogenetically advanced abilities, or equally, others possessing a wide range of abnormalities including those which comprise the schizophrenia syndrome. A dormant phenotypic potential for schizophrenia may exist in individuals who never develop symptoms during the course of a lifetime though some of these may become clinically apparent under the influence of various precipitating factors. It is concluded that abnormal functional connection and its normal and "supernormal" counterparts may be natural, essential, and inevitable consequences of brain evolution, and that this may have been so throughout the history of vertebrate brain evolution.
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PMID:Schizophrenia, abnormal connection, and brain evolution. 687 13

The study sought to determine whether 100 emotionally disturbed mentally retarded subjects assigned four distinct diagnostic labels could be differentiated from each other on the basis of sex, age, degree of mental impairment, and adaptive behavior. Univariate and multivariate analyses indicated that the autism classification was distinguishable from psychosis, schizophrenia, and severe emotional disturbance in terms of degree of retardation and adaptive behavior. The primary distinguishing feature was the autistic group's low level of language development. The schizophrenics, psychotics, and severely emotionally disturbed subjects were indistinguishable from each other on the variables examined.
J Autism Dev Disord 1980 Sep
PMID:Emotional disturbance in mental retardation: an investigation of differential diagnosis. 692 62

Haloperidol is safe and effective in children for relieving psychotic symptoms associated with childhood autism, schizophrenia and mental retardation. It is the drug of choice for Tourette's syndrome, and may be useful in nonpsychotic hyperactive or aggressive children to control acute episodes, or when the stimulants normally useful in hyperactive children are ineffective. Such children taking haloperidol not only become calmer, but are often better able to respond to other modalities of therapy and to school instruction. Dosage, initially low, is increased gradually to minimize drowsiness and extrapyramidal symptoms, the most common side effects. Haloperidol in children is usually well-tolerated.
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PMID:Haloperidol -- its use in children. 693 55

It is well documented that peptides have a major role in the effective functioning of higher animals at all levels from enzyme stabilization to homeostatic mechanisms governing essential functions such as eating, sexual behavior, and temperature regulation. The effects of exogenously administered peptides on neurotransmitter release, uptake, metabolism and behavioral consequences are also well established. We have attempted to extend these findings by postulating peptidergic neurons as transducers of multisignal inputs, and that development of pathological states may be due to genetically-determined reduced levels of activity of key peptidases, leading to excretion of regulatory peptides into the circulation. We have been able to demonstrate that, in schizophrenia and autism (in well defined clinical cases), the patterns of peptides and associated proteins from urinary samples differ considerably from each other and from normal controls. In addition to this, further purification of the material obtained has led to the discovery of a number of factors capable of modulating the function of major neurotransmitters. Some of these are in the final stages of characterization as peptides, while the remainder are also probably peptides, as purification has been followed by both biological testing and chemical analysis for peptidic material. We have outlined a number of parameters which we consider relevant in any attempt to put psychiatric disorders on a biological foundation. Any new advances in the neurochemical understanding of such disorders must take into consideration the observations of several different disciplines including genetics and psychology. However, at this stage of research it is far too early to speculate on the relevance of the various biological activities to the etiology and symptomatology of schizophrenia and childhood autism.
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PMID:Biologically active peptide-containing fractions in schizophrenia and childhood autism. 701 Sep 49

The subjects of this study were 19 children and 11 adolescents who had been psychotic since childhood and who satisfied DSM-III criteria for schizophrenia except for the stipulation that a "deterioration from a previous level of functioning" must have occurred. Seven subjects had had documented signs of psychosis before the age of 30 months. The presence of thought disorder precluded giving these 7 subjects the diagnosis of early infantile autism. The authors argue that only symptoms and signs, not age at onset, can define a disorder. They also emphasize that in children and adolescents, developmental issues influence the clinical presentation.
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PMID:Childhood schizophrenia: present but not accounted for. 708 88

The authors describe 6 cases of post-traumatic schizophrenia and make a critical review of the literature concerning this unusual post-traumatic personality disturbance. Various schizophrenic manifestations are observed: they principally consist of delusion, hallucination, paranoid and mystical ideas, autism, psychomotor instability, fugues. Post-traumatic schizophrenia occurs mostly in young men, before thirty years. The severity of traumatic brain injury appears irrelevant in its genesis. Temporal lobes are more often involved (one third of the cases). Pre-traumatic personality disturbances are the main factor as demonstrated by the anamnesis and by the results of Rorschach test.
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PMID:[Post traumatic schizophrenic bouts: with regard to 6 cases of traumatic schizophrenia (author's transl)]. 709 69

Hospitalized schizophrenic (N = 15) and nonschizophrenic (N = 18) youngsters were compared on measures of verbal and imagery development as well as on four paired-associate learning tasks involving combinations of word and picture stimuli pairs. The results showed the schizophrenic group to be similar to the controls on verbal and full-scale intelligence measures but significantly inferior on performance measures. The schizophrenic group also showed a general disadvantage in paired-associate learning, with a trend toward specific differential difficulty with words as stimulus items. Results suggest the presence of nondominant hemisphere deficit in the target group and also provide weak support for theories of dominant hemisphere dysfunction in schizophrenia.
J Autism Dev Disord 1982 Sep
PMID:Schizophrenic children's utilization of images and words in performance of cognitive tasks. 715 2


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