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

Comparison of the properties of blood platelets and serotonergic synaptosomes suggests that the human platelet can serve as an appropriate model for the transport, metabolism, and release of serotonin (5-HT) by CNS serotonergic neurons. The study of blood 5-HT levels and platelet 5-HT pharmacodynamics in patients with a variety of psychiatric and neurologic disorders has generated interesting leads into possible abnormalities of CNS 5-HT neurons in these patients. This article reviews the experimental evidence, which uses the human platelet model to investigate neurotransmitter-related abnormalities in Down syndrome, mental retardation, infantile autism, hyperactivity syndromes (minimal brain dysfunction), schizophrenia, affective disorders, Duchenne muscular dystrophy, Parkinson disease, Huntington chorea, and migraine headaches.
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PMID:The human platelet. A diagnostic and research tool for the study of biogenic amines in psychiatric and neurologic disorders. 14 Jun 32

The diagnosis of "autism" has been used to encompass a heterogeneous group of children who may differ in etiology, clinical manifestations, prognosis, and needed treatment. This paper presents the results of a comprehensive evaluation, using strict diagnostic criteria, of 33 children comprising the entire population of a self-contained unit for "autistic" children in the public school system of Hillsborough County, Florida. Only five of the children fit the criteria for early infantile autism. Six were diagnosed as suffering from schizophrenia, two as atypical developmental disorders. Twelve of the 33 showed evidence of neurological or recognized genetic abnormality, five had specific developmental language disorders, and three were severely retarded, cause unknown. Of the 12 children with evidence of neurological disease, five had chromosome abnormalities evident on cytogenetic study, two had high serum Cux++, one had histidinemia, one had maternal rubella, and three had dyskinesis of unknown origin. The heterogeneous nature of this group underlines the need for comprehensive evaluation of the autistic syndrome.
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PMID:Children with autistic behavior in a self-contained unit in the public schools. 242 17

Childhood autism is not usually considered as a neurological disease although frequent antecedents of ante, peri and postnatal injuries are found in its antecedents. Several symptoms of autism particularly in the early development, resemble the signs observed in frontal, temporal, striatal and brainstem dysfunctioning. These cerebral structures are connected with the central dopaminergic system which may be disturbed in autistic children. Such hypotheses suggest the necessary elaboration of an infant and child "behavioral neurology".
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PMID:[Neurological aspects of infantile autism]. 352 86

To investigate pediatric brain impairment, beta-endorphin levels, one of the opioid peptides that modulate human high cortical functions, were measured in cerebrospinal fluid (CSF). The study included 19 patients with infantile autism, 3 patients with Rett syndrome, 6 patients with infantile spasms, 16 patients with aseptic meningitis, and 23 age-matched controls. In the control group, the CSF beta-endorphin concentrations were negatively correlated with increasing age. There was no correlation between body temperature and the levels, and no significant difference in the levels according to sex. In infantile autism, the CSF level was not significantly different from that in controls. In Rett syndrome, it was significantly higher, while in infantile spasms it was lower than in controls. In aseptic meningitis, the CSF beta-endorphin level was significantly higher than in controls. The alterations in CSF beta-endorphin levels may play a role in these neurologic disorders and/or in central nervous system (CNS) infections.
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PMID:CSF beta-endorphin levels in pediatric neurologic disorders. 800 32

A possible role of the immune system in the pathogenesis of some neurologic disorders, including infantile autism, was recently postulated. This observation prompted the authors to investigate some immunologic aspects in a group of patients with Rett syndrome, a disorder still not completely clarified but with some points of commonality with infantile autism. Humoral and cell-mediated immunity were investigated in 20 females with Rett syndrome. Peripheral lymphocyte subsets revealed a reduced percentage of CD8+ suppressor-cytotoxic cells in all of the patients with Rett syndrome, resulting in an increased CD4+/CD8+ ratio. In addition, 15 (75%) of the 20 patients had low levels of natural killer cells. Soluble interleukin-2 receptor was elevated in the youngest patients. Antineuronal and antimyelin ganglioside antibodies were absent, as were antinuclear antibodies, antistriated muscle antibodies, and antismooth muscle antibodies. Immunoglobulin fractions and complement were normal for age in all of the patients.
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PMID:Peripheral lymphocyte subsets and other immune aspects in Rett syndrome. 1051 87

Conventional medical treatment for neurologic disorders such as epilepsy, migraine, and autism focuses on the brain. Although standard medical treatment is often helpful, the underlying causes of these disorders are not well understood. Furthermore, some individuals respond poorly or not at all to regular medicine. Evidence is accumulating in the medical literature that the enteric nervous system (ENS)-that part of the nervous system associated with the alimentary canal-also plays a role in these disorders. Historically, the concept of an autonomous abdominal nervous system was advocated by Byron Robinson, Johannis Langley, and Edgar Cayce. The work of these three prominent historical figures is considered along with modem view-points on the abdominal nervous system. Complementary therapies that address the nervous system of the abdomen have potential as useful adjuncts to conventional treatment for certain neurologic disorders.
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PMID:The abdominal brain and enteric nervous system. 1063 Mar 51

mental retardation: timing and thresholds; (italic)b(/italic)) endocrine dysfunction and developmental disabilities: dose and target implications; (italic)c(/italic)) attention-deficit disorder-ADHD and learning disabilities; and (italic)d(/italic)) new horizons: extending the boundaries. Support for the Rochester conference came from both public and private sources. The National Institute of Environmental Health Sciences (NIEHS), the National Institute of Child Health and Human Development, and the EPA represented the federal government. The conference also received grants from several foundations: the Jennifer Altman Foundation, the Heinz Family Foundation, the National Alliance for Autism Research, the Violence Research Foundation, the Wacker Foundation, and the Winslow Foundation. The second of these conferences helped launch a new Center for Children's Health and the Environment at the Mount Sinai School of Medicine. It was held in New York City on 24-25 May 1999, and was convened specifically to consider the intersection between neurodevelopmental impairment, environmental chemicals, and prevention. Over 300 health scientists, pediatricians, and public health professionals examined the growing body of evidence linking environmental toxins to neurobehavioral disorders. The conference title was Environmental Influences on Children: Brain, Development, and Behavior. The conference began by reviewing well-known examples of deleterious effects of environmental chemicals, including lead and PCBs, on children's brains. The conferees then considered the potential impact of environmental chemicals on neurological disorders with particular focus on ADHD, autism, and Parkinson's disease. The inclusion of Parkinson's disease was intended to signal the notion that exposures in early life may have an influence on the evolution of neurological disease in later life. Support for the Mount Sinai conference came from the Superfund Basic Research Program (NIEHS); The Pew Charitable Trusts; the Institute for Health and the Environment at the University of Albany School of Public Health; the Agency for Toxic Substances and Disease Research (ATSDR); the Ambulatory Pediatric Association; Myron A. Mehlman, PhD; the National Center for Environmental Assessment (EPA); the National Center for Environmental Health (CDC); the National Institute of Child Health and Human Development; the Office of Children's Health Protection (EPA); Physicians for Social Responsibility; The New York Academy of Medicine; The New York Community Trust; and the Wallace Genetic Foundation. The impact of environmental toxins on children's health has become a topic of major concern in the federal government. Eight new research centers in children's environmental health have been established in the past 2 years with joint funding from EPA and NIEHS. Clinical units that specialize in the treatment of children with environmentally induced illness have been developed across the nation with grant support from ATSDR. The American Academy of Pediatrics has just published its (italic)Handbook of Pediatric Environmental Health (/italic)((italic)17(/italic)), the "Green Book," which is available to pediatricians throughout the Americas. Children's environmental health has climbed to a critical position as we launch the new millennium. This monograph marks a significant milestone in the evolution of this emerging discipline.
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PMID:The developing brain and the environment: an introduction. 1085 30

We report a family with a heterogeneous group of neurologic disorders associated with the mitochondrial DNA G8363A transfer ribonucleic acid (RNA)Lys mutation. The phenotype of one child in the family was consistent with autism. During his second year of life, he lost previously acquired language skills and developed marked hyperactivity with toe-walking, abnormal reciprocal social interaction, stereotyped mannerisms, restricted interests, self-injurious behavior, and seizures. Brain magnetic resonance imaging (MRI) and repeated serum lactate studies were normal. His older sister developed signs of Leigh syndrome with progressive ataxia, myoclonus, seizures, and cognitive regression. Her laboratory studies revealed increased MRI T2-weighted signal in the putamen and posterior medulla, elevated lactate in serum and cerebrospinal fluid, and absence of cytochrome c oxidase staining in muscle histochemistry. Molecular analysis in her revealed the G8363A mutation of the mitochondrial transfer RNA(Lys) gene in blood (82% mutant mitochondrial DNA) and muscle (86%). The proportions of mutant mitochondrial DNA from her brother with autism were lower (blood 60%, muscle 61%). It is likely that the origin of his autism phenotype is the pathogenic G8363A mitochondrial DNA mutation. This observation suggests that certain mitochondrial point mutations could be the basis for autism in some individuals.
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PMID:Autism associated with the mitochondrial DNA G8363A transfer RNA(Lys) mutation. 1086 77

Studies have identified structural abnormalities in areas of the autistic brain, with a pattern suggesting that a neurodevelopmental anomaly took place. Neural cell adhesion molecule (NCAM), which is involved in development of the central nervous system, was previously shown to be decreased in the serum of autistic individuals. In the present study, we measured NCAM protein in the sera from controls, patients with autism, siblings of autistic patients, and individuals with other neurologic disorders, but found no significant differences. We also measured NCAM protein in autistic postmortem brain samples and found the longest isoform, NCAM-180, to be significantly decreased. In addition, we investigated the mRNA expression of NCAM in these brain samples using cDNA microarrays and RT-PCR. Results show that NCAM mRNA levels are not altered in autism.
J Autism Dev Disord 2001 Apr
PMID:Assessment of neural cell adhesion molecule (NCAM) in autistic serum and postmortem brain. 1145 Aug 17

The growth and differentiation of the central nervous system are closely related to the presence of iodine and thyroid hormones. It has been hypothesized that neurobehavioral disabilities of childhood, such as attention deficit hyperactivity disorder (ADHD), learning disorders, and autism can be attributed to fetal thyroidal endocrine disruption in utero. To determine whether there is an association between neonatal thyroid status and a subsequent diagnosis of a neurobehavioral disability, neonatal thyroxine (T(4)) levels have been used as the indicator of the presence of intrauterine thyroidal dysfunction. Neonatal T(4) levels were obtained from the neonatal hypothyroidism screening program. All cases were diagnosed at medical school diagnostic clinics, the diagnostic categories being ADHD, autism spectrum disorder, behavioral disorder, cognitive disorder, developmental delay, emotional disorder, learning disability, and speech/language disorder. Conditional logistic regression analysis was performed for each clinical condition. Odds ratios for the conditions ranged from 0.92 to 1.13 with p values ranging between 0.19 and 0.84. No significant differences were detected between neonatal T(4) values of the cases and the controls for any of the neurobehavioral conditions. All neonatal T(4) values were within normal ranges. The data provide no evidence to suggest that intrauterine thyroid status as reflected by the neonatal T(4) values had an impact on the neurologic disorders diagnosed in childhood.
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PMID:Lack of a relation between human neonatal thyroxine and pediatric neurobehavioral disorders. 1507 8


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