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

Two institutionalized children who exhibited high rates of severely self-injurious behaviors were punished with aromatic ammonia inhalation on a response-contingent basis. This contingency was applied throughout all aspects of each child's institutional program which focused on teaching of self-help skills. Suppression of the self-injurious responses was both rapid and general. The contingency was maintained for 2 months, although there was no responding after the first 5 days. Follow-up sessions, conducted 4 months after the punishment contingency was removed, revealed that suppression effects were highly durable. Aromatic ammonia inhalation appears to be an effective alternative for decelerating extremely maladaptive behaviors that do not yield to more conventional nonaversive forms of therapy. However, the procedure should be used with great caution, for it may involve risk to the subject.
J Autism Child Schizophr 1978 Mar
PMID:Suppression of repetitive self-injurious behavior by contingent inhalation of aromatic ammonia. 64 Oct 2

The course of treatment for hair pulling in a moderately retarded, visually impaired 9-year-old male is described along with the effectiveness of an ammonia inhalation procedure to eliminate this behavior. However, before discovering this successful procedure, other well-known techniques such as DRO, TO, overcorrection, and shaping all failed. Since rapid treatment effectiveness could be assumed to be the norm, given the operant literature, the extensive course of treatment reported here serves to document that perseverance may also be a necessary component of successful behavior management strategies.
J Autism Dev Disord 1980 Sep
PMID:Treatment of assaultive hair pulling in a multihandicapped youth. 692 59

This paper describes the use of a GABA-transaminase agonist for the treatment of infantile autism. An approximate one third reduction of GABA and ammonia levels for an autistic patient with noticeable improvement of verbal/language skills and a reduction of repetitious ritualistic self-stimulatory behavior (stimming) was observed. A reduction of the plasma GABA (by administrating a GABA-T agonist, Imipramine) probably results in more axon(s)-to-oligodendrocyte signaling in the corpus callosum and it is postulated that this could result in a reduction of the autistic features for the patient.
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PMID:Use of a GABA-transaminase agonist for treatment of infantile autism. 1216 Jun 95

Cohen has illustrated that extremely high Gamma-aminobutyric acid (GABA) levels in the urine and blood and high plasma ammonia were observed for an autistic male child diagnosed with infantile autism. GABA is a major inhibitory neurotransmitter of the mammalian brain and the enzyme responsible for catabolism is GABA-Transaminase (GABA-T). Elevated levels of ammonia in the plasma results in a decrease in the efficiency for the GABA-T enzyme and this results in higher GABA concentrations after regulation in the liver. It is postulated that a link between plasma ammonia and plasma GABA exists where the concentration of GABA in the plasma is directly related to the ammonia plasma concentration. A ratio of approximately 0.30 (plasma ammonia/GABA) is a consistent finding for normal subjects and for subjects with infantile autism and liver diseases such as hepatic encephalopathy.
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PMID:The significance of ammonia/gamma-aminobutyric acid (GABA) ratio for normality and liver disorders. 1244 21

Long chain acyl-CoA dehydrogenase (LCAD) has recently been shown to be the mitochondrial enzyme responsible for the beta-oxidation of branched chain and unsaturated fatty acids [Biochim. Biophys. Acta 1393 (1998) 35; Biochim. Biophys. Acta 1485 (2000) 121]. Whilst disorders of short, medium and very long chain acyl dehydrogenases are known, there is no known disorder of LCAD deficiency in humans. Experimental LCAD deficiency in mice shows an acyl-carnitine profile with prominent elevations of unsaturated fatty acid metabolites C14:1 and C14:2 [Hum. Mol. Genet. 10 (2001) 2069]. A child with autism whose acyl-carnitine profile also shows these abnormalities is presented, and it is hypothesized that the child may have LCAD deficiency. Additional metabolic abnormalities seen in this patient include alterations of TCA energy production, ammonia detoxification, reduced synthesis of omega-3 DHA, and abnormal cholesterol metabolism. These metabolic changes are also seen as secondary abnormalities in dysfunction of fatty acid beta-oxidation, and have also been reported in autism. It is hypothesized that LCAD deficiency may be a cause of autism. Similarities between metabolic disturbances in autism, and those of disorders of fatty acid beta-oxidation are discussed.
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PMID:Is autism a disorder of fatty acid metabolism? Possible dysfunction of mitochondrial beta-oxidation by long chain acyl-CoA dehydrogenase. 1514 59

Autism is an ever increasing problem in the United States. Characterized by multiple deficits in the areas of communication, development, and behavior; autistic children are found in every community in this country and abroad. Recent findings point to a significant increase in autism which can not be accounted for by means such as misclassification. The state of California recently reported a 273% increase in the number of cases between 1987 and 1998. Many possible causes have been proposed which range from genetics to environment, with a combination of the two most likely. Since the introduction of clavulanate/amoxicillin in the 1980s there has been the increase in numbers of cases of autism. In this study 206 children under the age of three years with autism were screened by means of a detailed case history. A significant commonality was discerned and that being the level of chronic otitis media. These children were found to have a mean number 9.96 bouts of otitis media (with a standard error of the mean of +/-1.83). This represents a sum total for all 206 children of 2052 bouts of otitis media. These children received a mean number of 12.04 courses of antibiotics (standard error of the mean of +/-.125). The sum total number of courses of antibiotics given to all 206 children was 2480. Of those 893 courses were Augmentin. with 362 of these Augmentin courses administered under the age of one year. A proposed mechanism whereby the production of clavulanate may yield high levels of urea/ammonia in the child is presented. Further an examination of this mechanism needs to be undertaken to determine if a subset of children are at risk for neurotoxicity from the use of clavulanic acid in pharmaceutical preparations.
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PMID:Could one of the most widely prescribed antibiotics amoxicillin/clavulanate "augmentin" be a risk factor for autism? 1627 50

A random retrospective chart review was conducted to document serum carnitine levels on 100 children with autism. Concurrently drawn serum pyruvate, lactate, ammonia, and alanine levels were also available in many of these children. Values of free and total carnitine (p < 0.001), and pyruvate (p = 0.006) were significantly reduced while ammonia and alanine levels were considerably elevated (p < 0.001) in our autistic subjects. The relative carnitine deficiency in these patients, accompanied by slight elevations in lactate and significant elevations in alanine and ammonia levels, is suggestive of mild mitochondrial dysfunction. It is hypothesized that a mitochondrial defect may be the origin of the carnitine deficiency in these autistic children.
J Autism Dev Disord 2004 Dec
PMID:Relative carnitine deficiency in autism. 1567 82

Because boys are four times more likely than girls to develop autism, the role of male hormones (androgens) has received considerable scrutiny. Some researchers implicate arginine vasopressin, an androgen-dependent hormone from the pituitary gland that elicits male behavior. Elevated vasopressin is also the most common cause of low blood sodium (hyponatremia)--most serious in the brains of children. Hyponatremia causes astrocytes to swell, then release the amino acids taurine and glutamine and their water to compensate. Taurin--the brain osmolyte/inhibitory neurotransmitter that suppresses vasopressin--was the amino acid most wasted or depleted in urine of autistic children. Glutamine is a critical metabolic fuel in brain neurons, astrocytes, endothelial cells, and the intestines, especially during hypoglycemia. Because glutamine is not thought to cross the blood-brain barrier significantly, the implications of low blood glutamine in these children are not recognized. Yet children with high brain glutamine from urea cycle disorders are rarely diagnosed with autistic disorders. Other common events in autistic children that release vasopressin are gastrointestinal inflammation, hypoglycemia, and stress. Signs of hyponatremia in these children are salt cravings reported online and anecdotally, deep yellow urine revealing concentration, and relief of autistic behavior by fluid/salt diets. Several interventions offer promise: (a) taurine to suppress vasopressin and replenish astrocytes; (b) glutamine as fuel for intestines and brain; (c) arginine to spare glutamine, detoxify ammonia, and increase brain blood flow; and (d) oral rehydration salts to compensate dilutional hyponatremia. This hypothesis appears eminently testable: Does your child crave salt? Is his urine deep yellow?
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PMID:Do salt cravings in children with autistic disorders reveal low blood sodium depleting brain taurine and glutamine? 2192 97

A novel explanation is proposed for the metabolic differences underlying two distinct rat urinary compositional phenotypes i.e. that these may arise from differences in the gut microbially-mediated metabolism of phenylalanine. As part of this hypothesis, it is further suggested that elements of the mammalian gut microbiota may convert phenylalanine to cinnamic acid, either by means of an ammonia lyase-type reaction or by means of a three step route via phenylpyruvate and phenyllactate. The wider significance of such conversions is discussed with similar metabolism of tryptophan and subsequent glycine conjugation potentially explaining the origin of trans-indolylacryloylglycine, a postulated marker for autism.
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PMID:Metabolic differences underlying two distinct rat urinary phenotypes, a suggested role for gut microbial metabolism of phenylalanine and a possible connection to autism. 2230 94

Autism is a disorder characterized by difficulty with social interactions, difficulty expressing empathy and intimacy and, in many cases, mild to severe language and learning deficits. Current estimates suggest autism now affects approximately one in 88 children, with rates increasing rapidly, making autism one of the most common and devastating developmental disorders. This trend is especially alarming considering that a cause for this disorder has yet to be discovered, nor are there successful biological treatments. Here a possible biochemical etiology is proposed for a certain spectrum of autism based on a reaction between propionic acid and ammonia released by Candida albicans in the gastrointestinal tract. A reaction between ammonia and propionic acid should result in the production of beta-alanine, a chemical similar in composition to gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter which has been shown to be present in higher quantities in autistic patients. Assuming beta-alanine is able to cross the blood-brain barrier, beta-alanine would be used in the brain as a partial antagonist, blocking the receptor sites for GABA, thus facilitating the production of more GABA to achieve equilibrium. An excess of GABA has been proposed as a possible contributor to autism. Further research should be conducted with this hypothesis to determine whether the chemical reaction in the human body between propionic acid and ammonia does in fact produce a chemical structurally and functionally similar to beta-alanine, as well as how this product affects the brain. Positive conclusions from this follow-on research could result in a preventative screening test for sensitivity to propionic acid and gastrointestinal yeast, thus slowing the progression of this type of autism. A more targeted treatment for children already diagnosed with autism could also result.
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PMID:A biochemical rationale for the interaction between gastrointestinal yeast and autism. 2302 72


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