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

"Nurturing the Brain" is a new research field aiming at facilitating development and maintenance of healthy brains and keeping their learning capabilities at full display throughout life. It is based on recent remarkable progress in developmental neuroscience and non-invasive technologies for visualizing brain activities in humans, even infants and children. "Nurturing the Brain" research will help us to cure or prevent various types of developmental disorders such as ADHD and autism. It will also help us in choosing an appropriate timing for child care and education on the basis of new knowledge of the critical period of development for various brain functions.
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PMID:[Why "nurturing the brain" now?]. 1266 Oct 92

Attention-deficit/hyperactivity disorder (ADHD [MIM 143465]) is a common, highly heritable neurobehavioral disorder of childhood onset, characterized by hyperactivity, impulsivity, and/or inattention. As part of an ongoing study of the genetic etiology of ADHD, we have performed a genomewide linkage scan in 204 nuclear families comprising 853 individuals and 270 affected sibling pairs (ASPs). Previously, we reported genomewide linkage analysis of a "first wave" of these families composed of 126 ASPs. A follow-up investigation of one region on 16p yielded significant linkage in an extended sample. The current study extends the original sample of 126 ASPs to 270 ASPs and provides linkage analyses of the entire sample, using polymorphic microsatellite markers that define an approximately 10-cM map across the genome. Maximum LOD score (MLS) analysis identified suggestive linkage for 17p11 (MLS=2.98) and four nominal regions with MLS values >1.0, including 5p13, 6q14, 11q25, and 20q13. These data, taken together with the fine mapping on 16p13, suggest two regions as highly likely to harbor risk genes for ADHD: 16p13 and 17p11. Interestingly, both regions, as well as 5p13, have been highlighted in genomewide scans for autism.
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PMID:A genomewide scan for attention-deficit/hyperactivity disorder in an extended sample: suggestive linkage on 17p11. 1268

This study examined changes in the diagnostic patterns among children and adolescents treated for mental health problems between the years 1995 and 2000. Using a large database (MarketScan) which compiles claims information from private health insurance plans nationwide, our sample consisted of 100,716 children (under the age of 18) who submitted claims for outpatient mental health services, out of a total of 1,723,681 covered children. Over the five years period, there was a dramatic increase in the proportion of children diagnosed with both Autism and Bipolar disorders. An increase was also observed in Anxiety, ADHD and Depressive disorders. A decrease was observed in diagnostic prevalence of Oppositional, Adjustment and Substance Abuse disorders.
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PMID:Changes in outpatient psychiatric diagnosis in privately insured children and adolescents from 1995 to 2000. 1503 5

This study analyses the prevalence of ASD, comorbidity, educational provision and ability in autistic children in a single health district, born between 1983 and 1996. The number of recorded diagnoses doubled over a 4 year period. This appeared to be due to greater recognition of ASD in more able children, in children initially presenting with ADHD, and possibly in females. ADHD accounted for a substantial proportion of comorbidity. Age at diagnosis appeared to be related to school placement. Cognitive ability levels ranging from more than three standard deviations below the mean to more than one standard deviation above the mean were found in the moderate and severe learning difficulty school population as well as in the mainstream population. Exceptionally low levels of verbal ability were present in a high proportion of mainstream pupils. Measured levels of cognitive function show poor relationship with actual educational placement.
Autism 2004 Mar
PMID:Autistic spectrum disorder: a child population profile. 1507 May 46

The highly evolutionarily conserved serotonin transporter (SERT) regulates the entire serotoninergic system and its receptors via modulation of extracellular fluid serotonin concentrations. Differences in SERT expression and function produced by three SERT genes and their variants show associations with multiple human disorders. Screens of DNA from patients with autism, ADHD, bipolar disorder, and Tourette's syndrome have detected signals in the chromosome 17q region where SERT is located. Parallel investigations of SERT knockout mice have uncovered multiple phenotypes that identify SERT as a candidate gene for additional human disorders ranging from irritable bowel syndrome to obesity. Replicated studies have demonstrated that the SERT 5'-flanking region polymorphism SS genotype is associated with poorer therapeutic responses and more frequent serious side effects during treatment with antidepressant SERT antagonists, namely, the serotonin reuptake inhibitors (SRIs).
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PMID:Serotonin transporter: gene, genetic disorders, and pharmacogenetics. 1508 84

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.
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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.
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PMID:From superior adaptation and function to brain dysfunction--the neglect of epigenetic factors. 1561 23

Our study supports the reliability and validity of profile analysis in children with neurobiological disorders. Three mutually exclusive WISC-III profiles were identified that characterized the majority of children with autism (low coding or Freedom from Distractibility Index with low Comprehension), attention deficit hyperactivity disorder and learning disability (low Coding or FDI without low comprehension), and brain injury (low Performance without low Coding or FDI). The profiles suggest attention, writing, and performance speed deficits in autism, ADHD, and LD; global visual-motor problems in brain injury; and specific difficulty with language comprehension and social reasoning in autism. Children with anxiety, depression, and behavior disorders did not exhibit distinct profiles. Our profile analysis is based on the simple rank ordering of standard scores. The profiles are clinically useful because they may alert clinicians to certain diagnostic possibilities, they reveal characteristic strengths and weaknesses that have implications for educational intervention, and they are consistent with preliminary WISC-IV data.
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PMID:Similarities and differences in Wechsler Intelligence Scale for Children--Third Edition (WISC-III) profiles: support for subtest analysis in clinical referrals. 1584 57

Tuberous Sclerosis (TSC) is a genetic disorder characterised by abnormal growths in a wide range of organs. In the brain, abnormalities of differentiation, proliferation and migration can produce a range of neuropsychiatric features such as mental retardation, autism and ADHD. Although these manifestations are not diagnostic of the disorder, cognitive and behavioural features are often of greatest concern to families yet limited clinical assessment and interventions are currently offered. A consensus panel at a TSC Brain/Behaviour workshop recommended that the cognitive and behavioural profiles of individuals with TSC should be assessed at regular intervals in a planned fashion in accordance with the difficulties associated with the disorder. Evaluations should include the use of standardised neuropsychological and behavioural tools as appropriate to the age and developmental level of the individual assessed. These cognitive and behavioural profiles should be incorporated in the overall formulation of the needs of the person with TSC to plan educational, social and clinical management strategies. Assessments should be documented so that individual longitudinal progress can be monitored. The paper outlines the problems associated with TSC, the purpose of recommended assessments, developmentally appropriate stages for assessment, and identifies specific areas that should be targeted for assessment.
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PMID:Consensus clinical guidelines for the assessment of cognitive and behavioural problems in Tuberous Sclerosis. 1598 Nov 29

This study compares DSM-IV symptoms in children (ages 6 to 12 years) with pervasive developmental disorder (PDD), clinic controls, and community-based samples. Parents/teachers completed the Child Symptom Inventory-4 for four samples: PDD (N = 284/284) and non-PDD psychiatric clinic referrals (N = 189/181) and pupils in regular (N = 385/404) and special (N = 61/60) education classes. The PDD group received higher symptom severity ratings than the regular education group, but was similar to the non-PDD clinic sample. Screening prevalence rates were highest for ADHD, ODD, and generalized anxiety disorder. PDD subtypes exhibited differentially higher rates of psychiatric symptoms. The magnitude of rater and gender differences in symptom severity ratings was modest. Clinic-referred children with PDD exhibit a pattern of psychiatric symptoms highly similar to nonPDD clinic referrals. Although much additional research is needed on comorbidity, these symptoms have important treatment implications.
Autism 2005 Oct
PMID:Comparison of DSM-IV symptoms in elementary school-age children with PDD versus clinic and community samples. 1615 56


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