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Query: UMLS:C0004352 (autism)
32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In children a "normal" aggressiveness should be distinguished from "hostile" and "inhibited" aggression; the latter usually become apparent as heteroaggressive or autoaggressive behaviour. Autoaggression is more common with younger children. Different hypotheses about the origin of aggressiveness are discussed. In the younger child nail biting, trichotillomania, rocking, an intensified phase of contrariness and enkopresis may have components of aggressiveness. In older children and adolescents dissocial forms of development, drug taking, attempted suicid, and anorexia nervosa may be parts of aggressive behaviour. Minimal brain dysfunction, autism, and postencephalitic syndromes predominate amongst organic alterations of the brain as causes for aggressive behaviour. Particularly the Lesch-Nyhan-syndrome, but equally the Cornelia de Lange-syndrome show autoaggressive tendencies.
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PMID:[The aggressive child (author's transl)]. 35 72

What is known of human evolution gives us little help in describing the biological nature of man: even our fossil history is obscure, and most statements on the evolution of human behaviour are guesses. The fact that primitive man was a predator on other species does not signify that man is "naturally aggressive" to his own kind. The notion of an inherent drive to aggression has no scientific foundation. Knowledge of the conduct of other species can lead to no valid conclusions about human behaviour. The same limitations apply to interpretations of modern man based on what is known of human hunter-gatherers. Ethology can contribute to human studies (1) by providing methods of observing and analysing behaviour, and (2) by providing hypotheses that can be tested. Zoologically-based hypotheses on the ill effects of crowding have been useful but have proved to be wrong. Others on the effects of stimulation in early life, and on breast-feeding and milk composition, have been more fruitful. Abnormal conduct, such as that of Kanner's syndrome, can be usefully studied by ethological methods. Man is a learner and a teacher, whose knowledge of himself increases slowly with the growth of critical research.
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PMID:Ethology and man: science or myth? 40 3

New-born cynomolgus monkeys were sucessfully reared by artificial nursing that was started just afterbirth with a 12% solution of a commercially prepared powdered-milk (Yukijirushi, P 7a) containing 13.3g of protein per 100g. Marked growth-retardation was observed in baby cynomolgus monkeys fed on a 12% solution of the modified P 7a milk containing only 6.6g of protein per 100g to which lactose was supplemented to give a baby monkey the same caloric value as that of the original P 7a milk. These artificially reared cynomolgus monkeys manifested various kinds of abnormal behavior such as self-clasping, autism-like self mouthing, huddling, stereotype rocking, head-knocking, autoerotism, fear, aggression, etc.. Generally, development of these abnormal behaviors was more noticeable in the monkeys nursed with a milk bottle fixed to the side of a cage without human contact than in the monkeys nursed by a care-taker with bodily touching. These qualitative observational results indicate that the new-born cynomolgus monkey can be used as a model of the human baby for research into the relationship between malnutrition and abnormal physical and mental growth.
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PMID:[Artificial nursing of new-born cynomolgus monkeys as a model of the human infant and development of abnormal behavior (author's transl)]. 81 6

The Lesch--Nyhan syndrome is a heritable disorder of the metabolism of uric acid in which behavioral manifestations are prominent and among the most provocative. The mutated or variant gene that determines this disorder is carried on the X chromosome. The disease is expressed exclusively in males. The molecular expression of the abnormal gene is in the completely defective activity of the enzyme hypoxanthine guanine phosphoribosyl transferase. As a result these patients overproduce uric acid and may develop early in life many of the clinical findings we associate with gout. They have in addition a variety of neurological abnormalities including mental retardation, spastic cerebral palsy, and involuntary, choreoathetoid movements. Involved patients have unusual, compulsive, aggressive behavior. Its most prominent but by no means exclusive feature is self-mutilation. The central feature in the management of this behavior is physical restraint. A number of practical procedures have been learned which facilitate the care and feeding of these patients. Promising new findings suggest that behavioral modification using extinction techniques and pharmacologic methods utilizing agents designed to increase the effective cerebral content of serotonin may each have a place in the management of behavior in this syndrome.
J Autism Child Schizophr 1976 Sep
PMID:Behavior in the Lesch--Nyhan syndrome. 108 51

The current status of pharmacological treatments of self-injurious behavior (SIB) and aggression in persons with mental retardation and autism was reviewed in the literature. Much of the existing literature is derived from anecdotal clinical experience, with a relative lack of well-controlled studies to determine the efficacy of different treatments. Although all psychotropics have been used to manage SIB and aggression, particularly promising are the data on the use of opioid antagonists like naltrexone. Beta-blockers may also have some role, but more controlled, systematic studies are needed. Use of neuroleptics is on the decline because of their adverse effects, such as tardive dyskinesia and possible impairment of cognitive functions. We assert that the behavioral problems of SIB and aggression are at times manifestations of different psychiatric syndromes. They present in a modified, atypical form in the developmentally disabled population because of cognitive limitations. Further understanding and classification of the psychopathology associated with this behavior is essential for its successful treatment.
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PMID:Self-injurious behavior in the developmentally disabled: pharmacologic treatment. 129 22

At the present time, neuroleptics are indicated for the treatment of acute psychotic states as well as Tourette's syndrome in children and adults. Neuroleptics may have a useful role in the attenuation of problem behaviors, such as stereotypies, hyperactivity, self-injury, and aggressive outbursts in infantile autism, pervasive developmental disorder NOS, and mental retardation, but they do not improve the underlying condition. Neuroleptics are not the agents of first choice for treatment of hyperactivity or aggression in children who do not have major developmental handicaps. Common and troublesome side effects associated with neuroleptic use in children and adolescents include sedation, extrapyramidal symptoms, and withdrawal dyskinesias; therefore, close monitoring is required. Neuroleptics should be used cautiously and only as an adjunct to other nonpharmacologic interventions.
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PMID:Neuroleptics in pediatric psychiatry. 134 40

Fifty habitually aggressive men were assessed for self-directed aggressive behavior (SDAB) and other-directed aggressive behavior (QDAB). Subjects displaying SDAB were compared with subjects exhibiting exclusively ODAB. The former were found to engage in more frequent acts of verbal aggression, physical aggression against objects, and physical aggression against others, as well as in more severe acts of verbal aggression and physical aggression against others. They were also more likely to receive diagnoses of mental retardation, organic personality disorder, intermittent explosive disorder, or autism. Findings are consistent with the presence of a neurologically based behavioral dyscontrol in the SDAB subjects.
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PMID:Self-directed and other-directed aggressive behavior in a forensic sample. 144 Jul 47

The behaviour profiles of 176 mentally retarded individuals from two reception centres and nine group homes were assessed. The correlations between behaviour and age, sex, degree of mental retardation, etiology of mental retardation and medical diagnosis were assessed using the Revised Child Behaviour Profile. The severity of behaviour disturbance did not vary with age or medical diagnosis. The moderately retarded subjects presented with more severe behaviour problems, such as aggression, than the severely mentally retarded subjects. The variable most predictive of behavioural problems was etiology of the disorder. Individuals with Down's syndrome had significantly fewer behaviour disturbances and those with autism and pervasive developmental disorder had significantly more behaviour disturbances than other subjects. A psychiatric disorder was found in 10.2% of the sample. The implications of these findings are discussed with respect to public policy.
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PMID:Behaviour problems of the mentally retarded. 179 May 15

This study assessed the impact of choice making on the serious problem behaviors of 3 students with severe autism and/or mental retardation. In the context of within-subject reversal designs, the results showed consistently reduced levels of problem behaviors (e.g., aggression) when the students were given opportunities to make choices among instructional tasks and reinforcers. Additional data showed no systematic differences in the rate of correct responding between the two conditions. The results are discussed in relation to the continuing search for effective, nonintrusive solutions to the occurrence of serious problem behavior.
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PMID:Effects of choice making on the serious problem behaviors of students with severe handicaps. 207 40

Many conditions in clinical neurology may be responsive to pyridoxine as a therapeutic agent. The current difficulty is in trying to isolate the conditions that are most likely to respond. Treating seizures is a major part of a neurologic practice. Our current therapeutic agents are only partially successful and limited by multiple side effects. One problem is that patients often have to take these agents for an entire lifetime, further raising the risk of toxicity. If pyridoxine supplementation can improve the efficacy of currently used medications, it will be gladly accepted into our therapeutic arsenal. Headache, chronic pain, and depression all appear to run together in many of our patients. The observations that serotonin deficiency is a common thread between them and that pyridoxine can raise serotonin levels open a wide range of therapeutic options. Small studies have been carried out with mixed success. Comparison with amitriptyline in the treatment of headache appears to show about equal efficacy, although side effects would be expected to be more of a problem with the amitriptyline. Behavioral disorders are relatively common and continue to be a major problem, disrupting the lives of the patients and their families. Current treatments are not acceptable to most people because of the risk of side effects with long-term usage. If, as Dr. Feingold suggests, many of these problems are caused by "toxic" exposures to chemicals that are pyridoxine antagonists, supplementation at early ages may reduce the incidence of hyperactivity and aggressive behavior. This raises the question of safety. Is pyridoxine safe for long-term use in large segments of the population, including children? The studies on children with Down's syndrome and autism, utilizing much higher doses than are used for other therapeutic purposes, seem to indicate relative safety if carefully monitored. Studies involving large population groups with carpal tunnel syndrome, all adults, using 100-150 mg/day have shown minimal or no toxicity in five- to 10-year studies. Women self-medicating for PMS taking 500 to 5000 mg/day have shown peripheral neuropathy within one to three years. It would appear from this retrospective analysis that pyridoxine is safe at doses of 100 mg/day or less in adults. In children there is not enough data to make any sort of suggestion. Because the major neurologic complication is a peripheral neuropathy and the causes of this condition are myriad, pyridoxine may cause neuropathy only in patients with a pre-existing susceptibility to this condition.
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PMID:Vitamin B6 in clinical neurology. 216 44


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