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)

The term "dyspraxia" was coined by Julian de Ajuriaguerra and Mira Stambak in 1964. This clinical term was treated very differently according to which explanatory model was adopted. Nowadays, it is used to refer to developmental coordination disorder in view of its neuro-developmental origin. In any case, the actual clinical situations vary and are often complex. In our opinion, it is first necessary to examine the differential diagnosis: apraxia in children caused by lesions, dysgraphia, simply delayed motor development, non-verbal learning disability syndrome, hemispheric specialisation deficits, pervasive developmental disorders (autisms, Asperger syndrome, atypical autism and other pervasive developmental disorders), mixed specific developmental disorders, multiple developmental disorder, and children with high potential. Next we focus on co-morbidity. Firstly, we look at psychopathological disorders associated with dyspraxia: autism and pervasive developmental disorders, dyscalculia/math disability, dyslexia/reading difficulties, dysphasia accompanied by verbal dyspraxia, intelligence deficiency, anxiety disorders, and attention-deficit hyperactivity disorder (ADHD). Secondly, we examine psychopathological disorders associated with dyspraxia. Children with developmental coordination disorder are less inclined to participate in collective games. As a result, there is a greater risk of them becoming lonely and isolated. They have higher child behaviour checklist (CBCL) scores in the somatic problems scale as well as for anxiety, depression and social withdrawal. They have low self-perception in sports as well as at school, which is related to their physical appearance and their self-esteem, attention deficit and externalized behaviour. These children are often at risk of academic failure and they suffer from oppositional defiant disorder and functional disorders. And finally, we believe that it is important to touch on the impact of these disorders on the family.
 ...
PMID:[Psychopathology in children with dyspraxia]. 2061 74

Attention-deficit/hyperactivity disorder (ADHD) is a highly disruptive childhood-onset disorder that often persists into adolescence and adulthood. Comorbidity with other problems, such as autism, dyslexia and conduct disorder (CD) is very common. Although little is known about the pathophysiology of ADHD, family, twin and adoption studies have shown that it is highly heritable. Whole genome linkage studies suggest there are no common susceptibility genes of moderate effect size. Most published research has been based on functional candidate gene studies. The most consistent evidence for association with ADHD relates to a dopamine D4 receptor (DRD4) gene variable number tandem repeat (VNTR), a dopamine D5 receptor (DRD5) gene microsatellite and a dopamine transporter (DAT1) gene VNTR. In addition, the catechol-O-methyltransferase (COMT) val158/108 met variant has been shown to increase risk for associated antisocial behavior. The first genome-wide association studies (GWAS) of ADHD have been completed and although larger studies are still required to detect common risk variants, novel risk pathways are being suggested for ADHD. Further research on the contribution of rare variants, larger genome-wide association and sequencing studies and ADHD phenotype refinement is now needed.
 ...
PMID:Fitting the pieces together: current research on the genetic basis of attention-deficit/hyperactivity disorder (ADHD). 2085 18

We live in a multisensory world and one of the challenges the brain is faced with is deciding what information belongs together. Our ability to make assumptions about the relatedness of multisensory stimuli is partly based on their temporal and spatial relationships. Stimuli that are proximal in time and space are likely to be bound together by the brain and ascribed to a common external event. Using this framework we can describe multisensory processes in the context of spatial and temporal filters or windows that compute the probability of the relatedness of stimuli. Whereas numerous studies have examined the characteristics of these multisensory filters in adults and discrepancies in window size have been reported between infants and adults, virtually nothing is known about multisensory temporal processing in childhood. To examine this, we compared the ability of 10 and 11 year olds and adults to detect audiovisual temporal asynchrony. Findings revealed striking and asymmetric age-related differences. Whereas children were able to identify asynchrony as readily as adults when visual stimuli preceded auditory cues, significant group differences were identified at moderately long stimulus onset asynchronies (150-350 ms) where the auditory stimulus was first. Results suggest that changes in audiovisual temporal perception extend beyond the first decade of life. In addition to furthering our understanding of basic multisensory developmental processes, these findings have implications on disorders (e.g., autism, dyslexia) in which emerging evidence suggests alterations in multisensory temporal function.
 ...
PMID:Binding of sights and sounds: age-related changes in multisensory temporal processing. 2113 85

The ability to combine information from multiple sensory modalities into a single, unified percept is a key element in an organism's ability to interact with the external world. This process of perceptual fusion, the binding of multiple sensory inputs into a perceptual gestalt, is highly dependent on the temporal synchrony of the sensory inputs. Using fMRI, we identified two anatomically distinct brain regions in the superior temporal cortex, one involved with processing temporal-synchrony, and one with processing perceptual fusion of audiovisual speech. This dissociation suggests that the superior temporal cortex should be considered a "neuronal hub" composed of multiple discrete subregions that underlie an array of complementary low- and high-level multisensory integration processes. In this role, abnormalities in the structure and function of superior temporal cortex provide a possible common etiology for temporal-processing and perceptual-fusion deficits seen in a number of clinical populations, including individuals with autism spectrum disorder, dyslexia, and schizophrenia.
 ...
PMID:Discrete neural substrates underlie complementary audiovisual speech integration processes. 2119 98

With the present review, we intend to highlight the importance of considering the age- and development-dependent occurrence of comorbidity in ADHD and to outline distinct trajectories of symptom progression with possible impact on course and outcome of ADHD. The review will focus on introducing the concepts of "developmental epidemiology" and "developmental comorbidity". Psychiatric and non-psychiatric age-dependent comorbidity can be seen in the majority of children, adolescents and adults with ADHD, resulting in a severe impairment of everyday life with considerable functional and psychosocial problems. Concerning the temporal order of occurrence, psychiatric conditions may be present before the appearance of first definite ADHD symptoms ("pre-comorbidity", such as temperament factors, sleep disturbance, autism spectrum disorders and atopic eczema). They may coincide with the time when ADHD symptoms reach a clinically significant level ("simultaneous comorbidity": enuresis, encopresis, developmental dyslexia). The majority of comorbidity, however, appears after the onset of ADHD in the course of disease ("post-comorbidity": tic disorder, depression and suicidality, anxiety disorders, obsessive compulsive disorder, bipolar disorder, conduct and substance use disorders, obesity and personality disorders). The aetio-pathophysiology of ADHD and its comorbid disorders and also the nature of comorbidity itself being highly heterogeneous, we additionally discuss possible models of comorbidity. In the future, longitudinal data on distinct patterns of symptom and comorbidity progression would help to refine disease classification systems, strengthen the power of future genetic studies and finally allow for more specific treatment strategies.
 ...
PMID:Developmental comorbidity in attention-deficit/hyperactivity disorder. 2143 12

The aim of the current study was to document the peer interaction patterns of students with autistic spectrum disorders in mainstream settings. Structured observations of a group of 38 adolescents with ASD drawn from 12 mainstream secondary schools were conducted over a two-day period and data compared with those of school, age, and gender matched comparison groups of 35 adolescents with dyslexia and 38 with no identified special educational needs (the ASD and dyslexia groups were also matched on SEN provision). Frequency and duration of peer interaction behaviours were coded. In terms of duration, multivariate analyses of variance (MANOVAs) indicated that participants with ASD spent more time engaged in solitary behaviours, less time engaged in co-operative interaction with peers, and more time engaging in reactive aggression towards peers than either comparison group. In terms of frequency, similar patterns emerged, but additionally participants with ASD engaged in fewer instances of rough/vigorous play, and were subject to more instances of social initiation and instrumental verbal aggression by peers than either comparison group. The findings of the current study support the authors' theoretical model of peer group interaction processes for individuals with ASD, and have implications for both social skills training and the development of peer awareness and sensitivity. Limitations are noted.
Autism 2011 Jul
PMID:Peer interaction patterns among adolescents with autistic spectrum disorders (ASDs) in mainstream school settings. 2145 85

This review provides an overview of the involvement of the corpus callosum (CC) in a variety of developmental disorders that are currently defined exclusively by genetics, developmental insult, and/or behavior. I begin with a general review of CC development, connectivity, and function, followed by discussion of the research methods typically utilized to study the callosum. The bulk of the review concentrates on specific developmental disorders, beginning with agenesis of the corpus callosum (AgCC)-the only condition diagnosed exclusively by callosal anatomy. This is followed by a review of several genetic disorders that commonly result in social impairments and/or psychopathology similar to AgCC (neurofibromatosis-1, Turner syndrome, 22q11.2 deletion syndrome, Williams yndrome, and fragile X) and two forms of prenatal injury (premature birth, fetal alcohol syndrome) known to impact callosal development. Finally, I examine callosal involvement in several common developmental disorders defined exclusively by behavioral patterns (developmental language delay, dyslexia, attention-deficit hyperactive disorder, autism spectrum disorders, and Tourette syndrome).
 ...
PMID:Developmental malformation of the corpus callosum: a review of typical callosal development and examples of developmental disorders with callosal involvement. 2148 94

Although best known for work with children and adults with intellectual disabilities and autism spectrum disorders, training in speech pathology and a doctorate in clinical psychology and neuropsychology was the foundation for Sara Sparrow's long-term interest in reading disabilities. Her first papers were on dyslexia and laterality, and the maturational lag theory of developmental dyslexia proposed with Paul Satz, her mentor. The research program that emerged from this work had a wide impact on early neuropsychological models of reading disabilities. Although Sara went on to research focused on children with other developmental disabilities after she moved to Yale University, this initial research influenced her career- long interests in assessment, developmental models of disabilities, and early screening methods.
J Autism Dev Disord 2014 Feb
PMID:Reading, laterality, and the brain: early contributions on reading disabilities by Sara S. Sparrow. 2159 45

The white matter is the main connection between different regions of the brain and helps them to work in a unified, coordinated way. Diffusion tensor imaging is an ideal technique with which to study it in order to detect the degree of integrity of these fibres. Nowadays, they are considered to play a significant role in the development and pathophysiology of different developmental disorders, and the aim of this study was to examine this role. On reviewing disorders such as autism, dyslexia or attention deficit hyperactivity disorder, certain fibres were found to be clearly involved. This was especially the case of the (arcuate) superior longitudinal fasciculus and the temporal-parietal network (related with the regulation of motor and attentional behaviour), the corpus callosum (which ensures the efficient and swift exchange of information between the hemispheres of the brain) and cingulate regions (which would be related with social cognition and self-consciousness).
 ...
PMID:[White matter in developmental disorders]. 2189 7

The importance of genetic influences on cognitive disability has been recognized for a long time, but molecular analysis has only recently begun to yield insights into the pathogenesis of this common and disabling condition. The availability of genome sequences has enabled the characterization of the chromosomal deletions and trisomies that result in cognitive disability, and mutations in rare single-gene conditions are being discovered. The molecular pathology of cognitive disability is turning out to be as heterogeneous as the condition itself, with unexpected complexities even in apparently simple gene-deletion syndromes. One remarkable finding from studies on X-linked mental retardation is that mutations in different small guanosine triphosphate (GTP)-binding proteins result in cognitive disability without other somatic features. Advances are also being made in cognitive disability with polygenic origins, such as dyslexia and autism. However, the genetic basis of mild intellectual disability has yet to be satisfactorily explained.
 ...
PMID:Genetic basis of cognitive disability. 2203 45


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