Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “developmental disorders”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMed2005

Supportive neurodevelopmental evidence for ADHD as a developmental disorder.

A baby is dependent on its primary caregiver (hereafter referred to as 'mother') for its emotional regulation. The development of emotional self-regulation is dependent on the growth and myelinisation of connections between cortical (control) and limbic (emotion) structures in the infant brain. The subcortical sympathetic limbic system is dominant from birth, and it is only at 14-18 months of age that the parasympathetic cortical inhibitory part develops. The maturation of specifically the right orbitofrontal cortex, which dominates both the sympathetic and parasympathetic limbic systems, is essential for the regulation of emotion for the rest of an individual's life. Behavioral hyperactivity, impulsivity and inattention are considered normal for children in the early practising phase (10-14 months). This stage is characterised by sympathetic dominance stimulated by the ventral tegmental limbic circuit. We hypothesise that children with Attention Deficit Hyperactivity Disorder remain stuck in this phase, and accordingly do not enter the next stage of emotional development, i.e., the late practising period, in which the lateral tegmental limbic circuit, which stimulates the parasympathetic system develops. Parental reactions, which may contribute to this block in emotional development, include: largely ignoring their child, until the child does something the parent disapproves of, then scolding the child, without consoling the child again afterwards. This leads susceptible children to develop defensive hyperactivity and inattention in order to avoid a shame state they are unable to cope with. Implications for therapy are that caregivers should be taught firstly to give lots of positive attention to their child, and if necessary to scold, to console the child immediately afterwards. If this can be achieved consistently, the child will have the chance to develop their parasympathetic lateral limbic circuit, and eventually right orbitofrontal dominance over both limbic circuits, which translates into the ability to self-regulate their emotional states.

Attention Deficit Disorder with Hyperactivity↗
PubMed2004

Autism and pervasive developmental disorders.

The quantity and quality of research into autism and related conditions have increased dramatically in recent years. Consequently we selectively review key accomplishments and highlight directions for future research. More consistent approaches to diagnosis and more rigorous assessment methods have significantly advanced research, although the boundaries of the 'broader phenotype' remain to be defined and the validity of Asperger's disorder as a discrete syndrome remains controversial. Recent epidemiological studies have shown that Autism Spectrum Disorders are common, but there continues to be debate about the causes of the increase in the frequency with which autism is diagnosed. Psychological research has helped to develop new developmental models for the disorder and there have also been significant advances in the molecular genetics of autism and understanding of the underlying neurobiological processes. Areas important for future research include the study of autism as it first develops, i.e., in infants and very young children, and of specific processes (psychological and neurobiological) which underlie the disorder. Significant challenges lie ahead in evaluating the growing number of treatments for autism and in integrating the results of research into treatment and educational settings.

Autistic Disorder↗
PubMed2001

Developmental disorders of activity dependent neuronal plasticity.

A number of neurodevelopmental disorders are caused by defects in activity dependent neuronal plasticity, the process by which neuronal activity shapes developing neuronal circuits. These disorders are caused by genetic mutations or other factors that disrupt intracellular signaling pathways that link the cell surface with the nuclear machinery for gene expression. The signaling pathways disrupted by these disorders are involved in learning, memory and behavior as well as in the synaptic proliferation and pruning that occurs during normal development. Examples of neurodevelopmental disorders that target plasticity include X-linked disorders such as Rett, Fragile-X and Coffin-Lowry Syndromes as well as acquired disorders such as cretinism. Several other X-linked mental retardation syndromes as well as autosomal disorders including neurofibromatosis type 1 and tuberous sclerosis also involve signaling pathways involved in neuronal plasticity. Disruption of neuronal plasticity is a mechanism that may underlie a diverse group of neurodevelopmental disorders.

Brain Diseases↗
PubMed1992

[Developmental disorders of man. Part 2].

At the beginning of this century genetics arose out of developmental history (Entwicklungsgeschichte) as the science of the causal understanding of development. After Spemann's epochal discovery (justifiably rewarded with the Nobel Prize in 1935) of the organizer and the beginning of the experimental analysis of developmental fields, little or no progress was made until the last few years when a virtual revolution occurred in developmental biology. If nothing else, this revolution has re-inspired in medicine an enormous respect for developmental animal models which are homologous to the human condition in the strict sense of the term, both in formal (formalgenetischer) and causal (kausalgenetischer) respects. Thus, the earliest stages of development in the primary field (during gastrulation) and in the later mosaic of secondary, epimorphic fields, represents the harmonically coordinated and epigenetically regulated effects of many genes which (with of without imprinting) code for cellular adhesion molecules, the peptide regulatory factors, homeobox genes, retinoic acid receptors and many other genes. Some of these genes act as regulators of DNA transcription, and, until recently no clinically identifiable developmental attribute to their function was known in humans. However, just in the last few weeks we have witnessed the identification of a gene on 11p13 in humans which is a paired box- and homeobox-containing gene as the cause of human aniridia, with the identical (homologous) mutation in the mouse Pax-6 gene producing the Sey phenotype (small eye).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗