THEORIES OF RETARDATION
The development debate
What of the development of intelligence in those with mental retardation? The classic debate has been framed around two views. The developmental view states that while the retarded as a group are disabled with respect to their same-age peers, they go through the same (Piagetian) stages of cognitive development (Zigler, 1969). They simply develop more slowly. The difference view, by contrast, says that there is a fundamental deficit associated with mental retardation, which means there can be no real cognitive equivalence between someone with mental retardation and a non-retarded person (Spitz, 1982). There is no point at which a person with low IQ will ‘catch up’ or reach adult levels of cognitive functioning. The majority of studies have found that participants with mental retardation perform more poorly on most cognitive tasks even when matched for mental age with the control group. This phenomenon, termed ‘mental-age lag’ by Spitz (1982), supports the difference, or deficit, positio . But a series of meta-analyses by Weiss and colleagues (1986) split the developmental view into two components: (a) cognitive stages defined within a Piagetian framework and (b) cognitive structures as defined by basic information-processing operations. This appoach implies that both the developmental and difference theorists are right. Children with mental retardation go through the same kinds of knowledge restructuring as described by Piaget, but do so more slowly than non-retarded children. But children and adults with mental retardation will always suffer a fundamental deficit in efficient (intelligent) information processing, even when compared with mental-age peers. So low IQ has a pervasive and enduring effect that is not ameliorated by progression through the stages of normal cognitive development. Testing Detterman’s theory As Detterman (1987) has pointed out, it is a curiosity that while the study of mental retardation has a long history and has contributed to an understanding of intelligence in g eneral, there have been few explanations of mental retardation in terms of contemporary theories. Those with retardation are regarded as simply deficient in whatever processes are hypothesized to contribute to intelligence. Such theories as there are – for example, that people with mental retardation are specifically deficient in attentional processes (Zeaman & House, 1963) or laying down memory traces (Ellis, 1970) or in executive processes (Belmont & Butterfield, 1971) – have, in turn, lacked any real applicability to theories of intelligence in general. So how does Detterman’s theory fare in helping us to understand mental retardation? To explain the phenomenon that individuals with mental retardation are poor on all cognitive tasks, Detterman (1987) has two theoretical options. 1. Because general intelligence is, by his definition, the average of all the independent component abilities, then chance alone would lead us to expect savants to be more common than they are. 2. But Detterman himself favours the second option, which is to suppose that some of the abilities are more commonly used than others. So while the basic abilities in Detterman’s theory are independent of each other, he supposes that one or two of these abilities are more ‘central’ for all of us – i.e. involved in most higher-level abilities – and it is these ‘central’ abilities that are deficient in people with mental retardation.
Detterman accommodates both the developmental and difference positions by claiming that Zigler’s developmental view applies to molar (or higher-level) measures. He argues that these are aggregate measures of the operation of the system as a whole. According to Detterman, Spitz’s (1982) difference view, by contrast, applies to molecular (or low-level) measures. In this context, molecular measures would be measures of the basic cognitive abilities, each of which contributes to the functioning of the system. While this neatly synthesizes the developmental and difference positions, it does prompt the question of why, on nearly all tests of basic abilities, not just a few central ones, groups with retardation perform more poorly than their mental-age-matched nonretarded peers. Indeed, it further prompts the question of how we can distinguish, in principle, between central abilities (i.e. those most deficient in people with mental retardation) and other basic abilities in a way that is not merely ad hoc. Testing Anderson’s theory In Anderson’s theory of the minimal cognitive architecture, the two causes of intelligence echo (to some extent) the pervasive view that there are two kinds of mental retardation. The primary cause of mental retardation is deemed to be a slow basic processing mechanism (Anderson, 1986). This view implies that the majority of retarded individuals represent the tail of a statistical distribution of processing speed across the general population but these individuals will not necessarily have compromised modular functioning. For example, Moore, Hobson and Anderson (1995) and Anderson and Miller (1998) have shown that those with mental retardation may be as capable as anyone of executing the module-based, complex, perceptual processes underlying person perception and some aspects of object perception. In contrast, performance on simple perceptual discrimination that is required by a standard inspection time task is impaired in the group of individuals with mental retardation. According to Anders n, a secondary hypothesized cause of mental retardation is where the absence of, or damage to, a module leads to a general cognitive deficit because of the module’s central role in cognitive functioning. If representations (e.g. linguistic representations) are missing because of damage to a module, there will be striking patterns of cognitive breakdown in specific areas. But these deficits are not confined only to those areas where modules ‘feed in’ to a range of other cognitive skills. The clearest example of this is the association between mental retardation and autism (Anderson, 1998; Frith, 2003; Frith & Happé, 1998). It has been suggested that modular damage, specifically to the ‘theory of mind’ module (see chapter 9), may underlie specific cognitive deficits in autism (Baron-Cohen, Leslie & Frith, 1985; Frith, 1989; 2003; Leslie & Thais, 1992). A ‘theory of mind’ module would normally include representations like ‘she wants’ or ‘he wishes’, which are used to make inferences (i.e. to think) about social interactions. The absence of these kinds of representations not only makes any reasoning about human behaviour strikingly difficult, but, interestingly, it also seems to spill over to make most everyday problem solving extremely difficult and computationally expensive. It certainly results in low IQ scores. Equally, Anderson’s theory of the minimal cognitive architecture predicts that the normal apparatus underlying thoughtful processing might be spared in those with ‘modular’ deficits, in which case these individuals should show normal levels of speed of processing. This has recently been confirmed for performance on an inspection time task, where autistic participants were shown to have, if anything, superior levels of speed of processing (Scheuffgen et al., 2000). As for the developmental versus difference views, Anderson argues that cognitive development is determined primarily by the acquisition of modules and that this accumulation will change the (Piagetian) cognitive stage of the child. Anderson sugge sts that modular functions are independent of IQ, so modules should be acquired according to the same developmental sequence in children with retardation as in other children. This could explain the finding from Weisz and colleagues that, in terms of Piagetian development, there is no deficit associated with mental retardation. But Anderson’s theory of the mimimal cognitive architecture also accommodates the difference position. If the majority of children with mental retardation have slow speed of processing, this explains why they are still deficient in on-line processing (as measured, for example, by inspection time) compared with their non-retarded peers, even when matched for mental age.
The development debate
What of the development of intelligence in those with mental retardation? The classic debate has been framed around two views. The developmental view states that while the retarded as a group are disabled with respect to their same-age peers, they go through the same (Piagetian) stages of cognitive development (Zigler, 1969). They simply develop more slowly. The difference view, by contrast, says that there is a fundamental deficit associated with mental retardation, which means there can be no real cognitive equivalence between someone with mental retardation and a non-retarded person (Spitz, 1982). There is no point at which a person with low IQ will ‘catch up’ or reach adult levels of cognitive functioning. The majority of studies have found that participants with mental retardation perform more poorly on most cognitive tasks even when matched for mental age with the control group. This phenomenon, termed ‘mental-age lag’ by Spitz (1982), supports the difference, or deficit, positio . But a series of meta-analyses by Weiss and colleagues (1986) split the developmental view into two components: (a) cognitive stages defined within a Piagetian framework and (b) cognitive structures as defined by basic information-processing operations. This appoach implies that both the developmental and difference theorists are right. Children with mental retardation go through the same kinds of knowledge restructuring as described by Piaget, but do so more slowly than non-retarded children. But children and adults with mental retardation will always suffer a fundamental deficit in efficient (intelligent) information processing, even when compared with mental-age peers. So low IQ has a pervasive and enduring effect that is not ameliorated by progression through the stages of normal cognitive development. Testing Detterman’s theory As Detterman (1987) has pointed out, it is a curiosity that while the study of mental retardation has a long history and has contributed to an understanding of intelligence in g eneral, there have been few explanations of mental retardation in terms of contemporary theories. Those with retardation are regarded as simply deficient in whatever processes are hypothesized to contribute to intelligence. Such theories as there are – for example, that people with mental retardation are specifically deficient in attentional processes (Zeaman & House, 1963) or laying down memory traces (Ellis, 1970) or in executive processes (Belmont & Butterfield, 1971) – have, in turn, lacked any real applicability to theories of intelligence in general. So how does Detterman’s theory fare in helping us to understand mental retardation? To explain the phenomenon that individuals with mental retardation are poor on all cognitive tasks, Detterman (1987) has two theoretical options. 1. Because general intelligence is, by his definition, the average of all the independent component abilities, then chance alone would lead us to expect savants to be more common than they are. 2. But Detterman himself favours the second option, which is to suppose that some of the abilities are more commonly used than others. So while the basic abilities in Detterman’s theory are independent of each other, he supposes that one or two of these abilities are more ‘central’ for all of us – i.e. involved in most higher-level abilities – and it is these ‘central’ abilities that are deficient in people with mental retardation.
Detterman accommodates both the developmental and difference positions by claiming that Zigler’s developmental view applies to molar (or higher-level) measures. He argues that these are aggregate measures of the operation of the system as a whole. According to Detterman, Spitz’s (1982) difference view, by contrast, applies to molecular (or low-level) measures. In this context, molecular measures would be measures of the basic cognitive abilities, each of which contributes to the functioning of the system. While this neatly synthesizes the developmental and difference positions, it does prompt the question of why, on nearly all tests of basic abilities, not just a few central ones, groups with retardation perform more poorly than their mental-age-matched nonretarded peers. Indeed, it further prompts the question of how we can distinguish, in principle, between central abilities (i.e. those most deficient in people with mental retardation) and other basic abilities in a way that is not merely ad hoc. Testing Anderson’s theory In Anderson’s theory of the minimal cognitive architecture, the two causes of intelligence echo (to some extent) the pervasive view that there are two kinds of mental retardation. The primary cause of mental retardation is deemed to be a slow basic processing mechanism (Anderson, 1986). This view implies that the majority of retarded individuals represent the tail of a statistical distribution of processing speed across the general population but these individuals will not necessarily have compromised modular functioning. For example, Moore, Hobson and Anderson (1995) and Anderson and Miller (1998) have shown that those with mental retardation may be as capable as anyone of executing the module-based, complex, perceptual processes underlying person perception and some aspects of object perception. In contrast, performance on simple perceptual discrimination that is required by a standard inspection time task is impaired in the group of individuals with mental retardation. According to Anders n, a secondary hypothesized cause of mental retardation is where the absence of, or damage to, a module leads to a general cognitive deficit because of the module’s central role in cognitive functioning. If representations (e.g. linguistic representations) are missing because of damage to a module, there will be striking patterns of cognitive breakdown in specific areas. But these deficits are not confined only to those areas where modules ‘feed in’ to a range of other cognitive skills. The clearest example of this is the association between mental retardation and autism (Anderson, 1998; Frith, 2003; Frith & Happé, 1998). It has been suggested that modular damage, specifically to the ‘theory of mind’ module (see chapter 9), may underlie specific cognitive deficits in autism (Baron-Cohen, Leslie & Frith, 1985; Frith, 1989; 2003; Leslie & Thais, 1992). A ‘theory of mind’ module would normally include representations like ‘she wants’ or ‘he wishes’, which are used to make inferences (i.e. to think) about social interactions. The absence of these kinds of representations not only makes any reasoning about human behaviour strikingly difficult, but, interestingly, it also seems to spill over to make most everyday problem solving extremely difficult and computationally expensive. It certainly results in low IQ scores. Equally, Anderson’s theory of the minimal cognitive architecture predicts that the normal apparatus underlying thoughtful processing might be spared in those with ‘modular’ deficits, in which case these individuals should show normal levels of speed of processing. This has recently been confirmed for performance on an inspection time task, where autistic participants were shown to have, if anything, superior levels of speed of processing (Scheuffgen et al., 2000). As for the developmental versus difference views, Anderson argues that cognitive development is determined primarily by the acquisition of modules and that this accumulation will change the (Piagetian) cognitive stage of the child. Anderson sugge sts that modular functions are independent of IQ, so modules should be acquired according to the same developmental sequence in children with retardation as in other children. This could explain the finding from Weisz and colleagues that, in terms of Piagetian development, there is no deficit associated with mental retardation. But Anderson’s theory of the mimimal cognitive architecture also accommodates the difference position. If the majority of children with mental retardation have slow speed of processing, this explains why they are still deficient in on-line processing (as measured, for example, by inspection time) compared with their non-retarded peers, even when matched for mental age.
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