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4 - The similar-structure hypothesis and differential rate of development in mental retardation

from Part 1 - Developmental theory

Published online by Cambridge University Press:  07 September 2010

Robert M. Hodapp
Affiliation:
University of California, Los Angeles
Jacob A. Burack
Affiliation:
Yale University, Connecticut
Edward Zigler
Affiliation:
McGill University, Montréal
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Summary

The formulation or recognition of contrasting models is an essential process in any scientific enterprise. Just as the juxtaposition of color and line may intensify the perception of elements in a painting, so the contrast of models in science brings the fundamental principles and questions of a field of inquiry into clearer focus. Within the field of mental retardation the debate over the developmental and difference models has exemplified this process (Baumeister, 1987).

Two fundamental questions are commonly associated with this debate. The first concerns the etiology of mental retardation. Advocates of difference theories of mental retardation often maintain that mental retardation is the result of a distinct organic disturbance that leads to deficits in intellectual development. For example, Ellis and Cavalier (1982) have argued that mental retardation is presumptive evidence of organic pathology.

Alternatively, the developmental model suggests that there are two groups of mentally retarded individuals – one resulting from a distinct disturbance of physiology (e.g., Down syndrome or hydrocephaly), the other with an unknown etiology. It is assumed that for a significant number of individuals in this latter group, mental retardation results not from a distinct disturbance of organic process, but rather from natural, genetic variation in processes associated with intellectual development (Zigler, 1967; Zigler, 1982; Zigler & Hodapp, 1986).

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Publisher: Cambridge University Press
Print publication year: 1990

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