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INTRODUCTION

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Mental retardation or cognitive disability occurring in childhood is a condition with enormous public health implications for at least four reasons. One is its relative frequency; with prevalence as high as 1% or greater in most populations, mental retardation is among the most common childhood disability.1,2,3 Another is its early onset and frequent life-long duration. A third is its socioeconomic impacts, which include adverse impacts on productivity and quality of life of affected individuals and caregivers as well as increased expenditures for medical care and residential services. A fourth reason is that prevention, whether primary, secondary, or tertiary, is attainable via public health interventions for nearly all forms of mental retardation. Examples of primary prevention include nutritional interventions such as iodine and folic acid supplementation and food fortification, immunization programs, and removal of environmental sources of lead exposure. Early identification followed by therapeutic interventions, for conditions such as Down syndrome and phenylketonuria (PKU), are examples of secondary prevention of mental retardation. Examples of tertiary prevention include early cognitive stimulation, special education, and habilitation to enhance functioning.

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One of the challenges mental retardation poses to public health is that certain prevention strategies, highly effective in one respect, have had the paradoxical side effect of increasing the occurrence of mental retardation in the population in terms of either incidence (new cases) or prevalence (by means of improved survival). Examples of this paradox include mental retardation associated with inborn errors of metabolism, Down syndrome, and premature birth. These and other specific topics in mental retardation are discussed below, following an overview of definitions and prevalence.

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DEFINITION AND CLASSIFICATION

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Mental retardation implies significant deficits, with onset early in life, in intelligence (as measured by standardized intelligence tests) and in adaptive behavior (e.g., communication, self-care, social interaction, school, and/or work).4 The deficits are recognized in the performance of social roles and age-appropriate tasks. The infant and preschool child may fail to achieve developmental milestones of sitting, responding to familiar faces, walking, talking, and sphincter control at expected ages. The schoolchild falls short of social expectations for classroom behavior and for reading, writing, and arithmetic. The adult may have difficulty in performing work within and outside the home, communicating, or understanding money, transport, and locality.

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Functional limitations in mental retardation can potentially be identified at three levels: impairment (altered brain structure and/or function), disability (deficits in intellectual function and adaptive behavior), and social participation (limitations in social roles and opportunities experienced by persons with disabilities due to environmental conditions).5,6 One-to-one correlations between currently understood causes, identifiable impairments, and levels of disability and participation appear to be the exception rather than the rule. For example, in people with mental retardation, identifiable neuropathological lesions often correlate weakly or not at all with specific causes and/or clinical/functional attributes.7,8

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The dominant approach to defining ...

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