Intellectual Disability

Author(s):  
Rejani Thudalikunnil Gopalan

Intellectual Disability (ID, also known as mental retardation) is a condition of arrested or incomplete development of the mind. ID is especially characterized by impairment of skills manifested during the developmental period, which contribute to the overall level of intelligence, i.e. cognitive, language, motor, and social abilities. This chapter focused to give an overall view about its history, changes in terminology, classification, epidemiology, etiology, comorbidities and management. Current understanding and latest trends and issues were highlighted.

Author(s):  
Rejani Thudalikunnil Gopalan

Intellectual disability (ID, also known as mental retardation) is a condition of arrested or incomplete development of the mind. ID is especially characterized by impairment of skills manifested during the developmental period, which contribute to the overall level of intelligence (i.e., cognitive, language, motor, and social abilities). The understanding about intellectual disability, mainly its features, causes and intervention has a long history. Researches on causes of intellectual disability lead to finding of multiple etiological factors which reflected well on its improved management techniques. The changes in terminology used describe intellectual disability also reflected our understanding about it different dimensions including social stigma. This chapter focused to give an overall view about its history, changes in terminology, classification, epidemiology, etiology, comorbidities, and management. Over the years, there are many changes and findings that have happened, yet many questions are unanswered related to this condition.


2022 ◽  
pp. 1-12
Author(s):  
Rejani Thudalikunnil Gopalan

Intellectual disability (ID, also known as mental retardation) is a condition of arrested or incomplete development of the mind. ID is especially characterized by impairment of skills manifested during the developmental period, which contribute to the overall level of intelligence (i.e., cognitive, language, motor, and social abilities). The understanding about intellectual disability, mainly its features, causes and intervention has a long history. Researches on causes of intellectual disability lead to finding of multiple etiological factors which reflected well on its improved management techniques. The changes in terminology used describe intellectual disability also reflected our understanding about it different dimensions including social stigma. This chapter focused to give an overall view about its history, changes in terminology, classification, epidemiology, etiology, comorbidities, and management. Over the years, there are many changes and findings that have happened, yet many questions are unanswered related to this condition.


2013 ◽  
Vol 51 (2) ◽  
pp. 113-116 ◽  
Author(s):  
Marc J. Tassé

Abstract The World Health Organization (WHO) is in the process of developing the 11th edition of the International Classification of Diseases (ICD–11). Part of this process includes replacing mental retardation with a more acceptable term to identify the condition. The current international consensus appears to be replacing mental retardation with intellectual disability. This article briefly presents some of the issues involved in changing terminology and the constraints and conventions that are specific to the ICD.


2020 ◽  
Vol 9 (2) ◽  
pp. 213-228
Author(s):  
A.M. Shcherbakova ◽  
N.S. Lykova

The article focuses on the problem of development of moral sphere of personality of children with intellectual disability (mild mental retardation) in the context of development of their life competence. Personal outcomes are considered as one of the most important indicators of the formation of life competence. Particular attention is paid to the moral development of children with intellectual disability. The results of an experimental study of the characteristics of moral perceptions and behavior of younger students with mental retardation of 9-10 years old brought up in different conditions - family and institutional are presented. Students of a comprehensive school with a normotypic development were also involved. The sample was 76 people. A study was made of the moral position, and on this basis the prediction of one's own behavior and the behavior of others in solving moral dilemmas, as well as the actual behavior of the child in a situation of moral choice.


Diagnostics ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1780
Author(s):  
Mark Roth ◽  
Lucienne Ronco ◽  
Diego Cadavid ◽  
Blythe Durbin-Johnson ◽  
Randi J. Hagerman ◽  
...  

Fragile X syndrome (FXS) is the most common form of inherited intellectual disability. FXS is an X-linked, neurodevelopmental disorder caused by a CGG trinucleotide repeat expansion in the 5′ untranslated region (UTR) of the Fragile X Mental Retardation gene, FMR1. Greater than 200 CGG repeats results in epigenetic silencing of the gene leading to the deficiency or absence of Fragile X mental retardation protein (FMRP). The loss of FMRP is considered the root cause of FXS. The relationship between neurological function and FMRP expression in peripheral blood mononuclear cells (PBMCs) has not been well established. Assays to detect and measure FMR1 and FMRP have been described; however, none are sufficiently sensitive, precise, or quantitative to properly characterize the relationships between cognitive ability and CGG repeat number, FMR1 mRNA expression, or FMRP expression measured in PBMCs. To address these limitations, two novel immunoassays were developed and optimized, an electro-chemiluminescence immunoassay and a multiparameter flow cytometry assay. Both assays were performed on PMBCs isolated from 27 study participants with FMR1 CGG repeats ranging from normal to full mutation. After correcting for methylation, a significant positive correlation between CGG repeat number and FMR1 mRNA expression levels and a significant negative correlation between FMRP levels and CGG repeat expansion was observed. Importantly, a high positive correlation was observed between intellectual quotient (IQ) and FMRP expression measured in PBMCs.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Gin S. Malhi ◽  
Pritha Das ◽  
Erica Bell ◽  
Greg Mattingly ◽  
Zola Mannie

AbstractRecent conceptualisations of resilience have advanced the notion that it is a dynamic and multifaceted construct. However, its adaptive components, especially those forged by adversity, have not been fully realised, and its neurobiological and psychosocial underpinnings are yet to be meaningfully integrated. In part, this is because a developmental perspective is often neglected in the formulation of resilience. In this review, we consider the findings of resilience research, with a specific emphasis on the developmental period of adolescence. To bridge the gaps in our current understanding, we propose a model of resilience that is predicated on experiencing adversity. Specifically, our model provides a sophisticated insight into the components of resilience, which, together with intrinsic features, involves facilitation of, and skill acquisition via strengthening processes we term tempering and fortification. The model also points to the potential trajectories of adversity-driven resilience and forms the basis of a framework that allows for individual variance in resilience, and the identification of both neurobiological and psychosocial targets for prevention and therapeutic interventions.


2019 ◽  
Vol 9 (1) ◽  
pp. 13 ◽  
Author(s):  
Rachel Saré ◽  
Christopher Figueroa ◽  
Abigail Lemons ◽  
Inna Loutaev ◽  
Carolyn Beebe Smith

Fragile X syndrome (FXS) is caused by silencing of the FMR1 gene leading to loss of the protein product fragile X mental retardation protein (FMRP). FXS is the most common monogenic cause of intellectual disability. There are two known mammalian paralogs of FMRP, FXR1P, and FXR2P. The functions of FXR1P and FXR2P and their possible roles in producing or modulating the phenotype observed in FXS are yet to be identified. Previous studies have revealed that mice lacking Fxr2 display similar behavioral abnormalities as Fmr1 knockout (KO) mice. In this study, we expand upon the behavioral phenotypes of Fmr1 KO and Fxr2+/− (Het) mice and compare them with Fmr1 KO/Fxr2 Het mice. We find that Fmr1 KO and Fmr1 KO/Fxr2 Het mice are similarly hyperactive compared to WT and Fxr2 Het mice. Fmr1 KO/Fxr2 Het mice have more severe learning and memory impairments than Fmr1 KO mice. Fmr1 KO mice display significantly impaired social behaviors compared to WT mice, which are paradoxically reversed in Fmr1 KO/Fxr2 Het mice. These results highlight the important functional consequences of loss or reduction of FMRP and FXR2P.


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