Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
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

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.
 ...
PMID:Dietary influences on neurotransmission. 302 51

Deficit in social interaction is a primary component of infantile autism. However, in the majority of drug studies, social interaction has not been measured consistently over time. Therefore, we examined, in a crossover design, the effect of fenfluramine on the social interactions of seven autistic children. Social interaction was measured one to three times per week, while the children were in open placebo, placebo, or drug phases of the study. The results demonstrated that the effect of fenfluramine on social interaction was inconsistent across children, with two children possibly demonstrating a tolerance to the behavioral effects of the drug. The results are discussed with respect to genetic and pharmacologic factors.
J Autism Dev Disord 1988 Dec
PMID:Effects of fenfluramine on social behavior in autistic children. 321 87

Autism is a developmental disorder characterized by impaired social and communicative development, and restricted interests and activities. This article will argue that we can discover more about developmental disorders such as autism through demonstrations of task success than through examples of task failure. Even in exploring and explaining what people with autism find difficult, such as social interaction, demonstration of competence on contrasting tasks has been crucial to defining the nature of the specific deficit. Deficit accounts of autism cannot explain, however, the assets seen in this disorder; for example, savant skills in maths, music and drawing, and islets of ability in visuospatial tests and rote memory. An alternative account, reviewed here, suggests that autism is characterized by a cognitive style biased towards local rather than global information processing - termed 'weak central coherence'. Evidence that weak coherence might also characterize the relatives of people with autism, and form part of the extended phenotype of this largely genetic disorder, is discussed. This review concludes by considering some outstanding questions concerning the specific cognitive mechanism for coherence and the neural basis of individual differences in this aspect of information processing.
 ...
PMID:Autism: cognitive deficit or cognitive style? 1035 74

We tested whether dimensional measures of empathic ability, theory of mind, and intelligence would differentiate autism spectrum disorders from each other and from non-spectrum disorders. Tests were administered to children with a diagnosis of Autistic Disorder (AutD; n = 20), Asperger's Disorder (AspD; n = 28), Attention Deficit/Hyperactivity Disorder (Inattentive Type) (ADHD; n = 35), Mental Retardation (Mild) (MR; n = 34), Anxiety Disorder (AnxD; n = 14), or No Psychological Disorder (NPD; n = 36). Results showed that empathic ability discriminated among groups on the autism spectrum (AutD < AspD < NPD). Because empathic ability is not independent of intelligence (AutD < AspD < NPD on intelligence; MR < ADHD < NPD on empathic ability), both dimensions are necessary to discriminate autism spectrum from non-spectrum disorders. When intelligence is covaried, empathic ability discriminated AutD, but not AspD, from other disorders (AutD < MR < ADHD < NPD = AnxD = AspD).
 ...
PMID:Do autism spectrum disorders differ from each other and from non-spectrum disorders on emotion recognition tests? 1146 82

In assessing and assimilating the neurodevelopmental basis of the so-called movement disorders it is probably useful to establish certain concepts that will modulate both the variation and selection of affliction, mechanisms-processes and diversity of disease states. Both genetic, developmental and degenerative aberrations are to be encompassed within such an approach, as well as all deviations from the necessary components of behaviour that are generally understood to incorporate "normal" functioning. In the present treatise, both conditions of hyperactivity/hypoactivity, akinesia and bradykinesia together with a constellation of other symptoms and syndromes are considered in conjunction with the neuropharmacological and brain morphological alterations that may or may not accompany them, e.g. following neonatal denervation. As a case in point, the neuroanatomical and neurochemical points of interaction in Attention Deficit and Hyperactivity disorder (ADHD) are examined with reference to both the perinatal metallic and organic environment and genetic backgrounds. The role of apoptosis, as opposed to necrosis, in cell death during brain development necessitates careful considerations of the current explosion of evidence for brain nerve growth factors, neurotrophins and cytokines, and the processes regulating their appearance, release and fate. Some of these processes may possess putative inherited characteristics, like alpha-synuclein, others may to greater or lesser extents be endogenous or semi-endogenous (in food), like the tetrahydroisoquinolines, others exogenous until inhaled or injested through environmental accident, like heavy metals, e.g. mercury. Another central concept of neurodevelopment is cellular plasticity, thereby underlining the essential involvement of glutamate systems and N-methyl-D-aspartate receptor configurations. Finally, an essential assimilation of brain development in disease must delineate the relative merits of inherited as opposed to environmental risks not only for the commonly-regarded movement disorders, like Parkinson's disease, Huntington's disease and epilepsy, but also for afflictions bearing strong elements of psychosocial tragedy, like ADHD, autism and Savantism.
 ...
PMID:Brain sites of movement disorder: genetic and environmental agents in neurodevelopmental perturbations. 1283 21

The plasma amino acid profiles of 36 children with autism spectrum disorders were reviewed to determine the impact of diet on amino acid patterns. Ten of the children were on gluten and casein restricted diets administered by parents, while the other 26 consumed unrestricted diets. No amino acid profile specific to autism was identified. However, children with autism had more essential amino acid deficiencies consistent with poor protein nutrition than an age/gender matched control group. There was a trend for children with autism who were on restricted diets to have an increased prevalence of essential amino acid deficiencies and lower plasma levels of essential acids including the neurotransmitter precursors tyrosine and tryptophan than both controls and children with autism on unrestricted diets. These data indicate that larger, more focused studies of protein nutrition in children with autism are needed in order to determine the extent to which restricted diets might place the developing brains of children with autism at risk from protein malnutrition. The high rate of tryptophan and tyrosine deficiency in this group is also of concern given their role as neurotransmitter precursors.
J Autism Dev Disord 2003 Aug
PMID:Plasma amino acids profiles in children with autism: potential risk of nutritional deficiencies. 1295 24

The author addresses issues interfacing neuropsychiatry and psychoanalysis. He recommends psychoanalysis for children with Attention Deficit, Hyperactivity Disorder (ADHD) and Dysfunction in Attention and activity control, Motility control and Perception (DAMP). He attributes its low status in neuropsychiatric treatment recommendations partly to the fact that psychoanalysts do not always declare their specific field of investigation. The scientific community then assumes that psychoanalysis aims to comment on issues outside its field of investigation, e.g. on neurobiological aetiology. The community therefore fails to discern the psychoanalyst's specific task, to help the child express and work through his conscious and unconscious experiences. Clarity on the analyst's part will improve relations with the scientific community and facilitate a relevant comparison of treatment methods. Another reason for neuropsychiatry's negative attitude towards analysis is its unwillingness to accept that unconscious conflict influences behaviour. With theoretical and clinical arguments, the author argues that unconscious factors must be taken in to understand and to treat the child. Countertransference, often cumbersome with neuropsychiatric children, becomes easier to handle if the analyst is clear about his field of investigation. If he sees through simplistic formulations on aetiology, countertransference gets even more manageable. Psychoanalysis can result in considerable intellectual and emotional development, as illustrated by work with a latency boy with DAMP, autism and slight mental retardation. In his psychoanalytic theoretical framework of the case, the author unites ego-psychological formulations with a Bionian conceptualisation of the thought disturbance.
 ...
PMID:Some psychoanalytic viewpoints on neuropsychiatric disorders in children. 1500 97

Although the DSM-IV diagnostic criteria for Attention Deficit/Hyperactivity Disorder (AD/HD) exclude Pervasive Developmental Disorder (PDD), some clinicians find that the two disorders can be comorbid and, in fact, make a dual diagnosis. Nevertheless, few empirical studies have investigated the clinical necessity for this practice. In the first of our two studies, children with high-functioning PDD were selected from among 520 outpatients. Of these, children also meeting the DSM-IV criteria for AD/HD were identified through a psychologist's observation, the completion of the ADHD-Rating Scale by parents and/or teachers, and a child psychiatrist's examination. We then examined the impact of PDD subtype and age on the co-occurrence rate. Study 2 analyzed comorbidity in two cases taken from Study 1. Of the 53 subjects in Study 1, 36 children also met the DSM-IV criteria for AD/HD. The co-occurrence rate for Asperger's Disorder (AS)/Pervasive Developmental Disorder, Not Otherwise Specified (PDDNOS) (85%) was significantly higher than for Autistic Disorder (57.6 %), and AD/HD symptoms were more common in younger children. Study 2 demonstrated the existence of comorbidity of PDD and AD/HD as separate disorders. We conclude not only that AD/HD symptoms occur frequently in children with PDD, but also that in some cases a dual diagnosis is essential to the implementation of effective treatment.
 ...
PMID:The clinical necessity for assessing Attention Deficit/Hyperactivity Disorder (AD/HD) symptoms in children with high-functioning Pervasive Developmental Disorder (PDD). 1549 Feb 78

With optimal pregnancy conditions (natural, enriched diet which includes fish) African (Digo) infants are 3-4 weeks ahead of European/American infants in sensorimotor terms at birth, and during the first year. Infants of semi-aquatic sea-gypsies swim before they walk, and have superior visual acuity compared with us. With adverse pregnancy behaviour (fear of fat, a trend to dieting), neglecting the need for brain fat to secure normal brain development and function, we run a risk of dysfunction--death. Sudden Infant Death Syndrome victims have depressed birth weight, lower levels of marine fat in brainstem than controls, and >80 suffer multiple hypoxic episodes prior to death. Depressed birth weight (more than 10% below mean) is seen in learning and behaviour disorders, and a trend towards weights of less than 3kg is increasing, which supports a rise in antenatal sub optimality. Given marine fat deficiency in pregnancy and infancy, neurons starved for fuel could delay myelination and maturation in the latest developed Frontal Lobes. The phylogenetic oldest Lateral Frontal Lobe System (feed-back mechanism etc.) derived from olfactory bulb-amygdala, which crosses in Anterior Commisure is probably spared, while the Medial Frontal Lobe System derived from Hippocampus-Cingulum and crosses in Corpus Callosum (delayed response task) is most likely affected. The rise in infantile autism (intact vision and hearing) with deficit in delayed response task only, could suggest a deficit in the Medial Frontal Lobe System. The human species is unique; 70% of total energy to the foetus goes to development of the brain, which mainly consists of marine fat. It undergoes pervasive regressive events, before birth, in infancy and at puberty. Minimal retraction of neuronal arborisation is advantageous. Attributable to adverse pregnancy childrearing practice, excessive retraction is likely prenatally and in infancy. Pubertal age affects the fundamental property of nervous tissue, excitability: excessive excitatory drive is seen in early, and a deficiency in late puberty. It is postulated that with adequate marine fat, there is probably no risk of psychopathology at the extremes, whereas a deficiency could lead to paroxysmal (subcortical) dysfunction in early puberty, and breakdown of cortical circuitry and cognitive dysfunctions in late puberty. The post-pubertal psychoses, schizophrenia and manic-depressive psychosis at the extremes of the pubertal age continuum, with contrasting excitability and biological treatment, are probably the result of continuous dietary deficiency, which has inactivated the expression of genes for myelin development and oligodendrocyte-related genes in their production of myelin. The beneficial effect of marine fat in both disorders, in other CNS disorders as well as in developmental dyslexia (DD) and ADHD among others, supports our usual diet is persistently deficient. We have neglected the similarity of our great brain to other mammals, and our marine heritage. Given the amount of marine fat needed to secure normal brain development and function is not known, nor the present dietary level, it seems unduly conjectural to postulate that a dietary deficiency in marine fat is causing brain dysfunction and death. However, all observations point in the same direction: our diet focusing on protein mainly, is deficient, the deficiency is most pronounced in maternal nutrition and in infancy.
 ...
PMID:From superior adaptation and function to brain dysfunction--the neglect of epigenetic factors. 1561 23


1 2 3 4 5 6 7 8 9 10 Next >>