What is so special about modules? Defining mechanisms of developmental change. Gaia Scerif School of Psychology University of Nottingham

Transcription

1 What is so special about modules? Defining mechanisms of developmental change Gaia Scerif School of Psychology University of Nottingham Address for correspondence: Dr. Gaia Scerif, School of Psychology, University of Nottingham, Nottingham NG7 2RD, United Kingdom. Abstract Enesco and Delval carefully evaluate the success of modular theories amongst developmental psychologists. They begin by reviewing the core characteristics of Fodorian modules with reference to language as a primary example and their more recent revisions. They then examine empirical evidence and alternative theoretical accounts that currently question massively modular interpretations of evolutionary psychology, human infant cognition and developmental disorders. The present commentary draws primarily from the latter source of evidence, developmental disorders, to complement and discuss the arguments presented by the authors. I focus particularly on the importance of understanding mechanisms of atypical developmental change and then briefly highlight some questions for both modular and non-modular theories.

2 Atypical cognition: Examining dissociations in a developmental context Dissociations of functions in patients who suffered brain damage in adulthood have been instrumental for neuropsychologists aiming to assess the independence of cognitive processes and thus characterise them as modules. On a similar vein, dissociations in developmental disorders have been used to suggest that modules can develop independently, to the extent that some develop to function unimpaired in the face of other deficits. Moreover, within this context developmental disorders of known genetic origin have been used to bolster claims of genetic specification of the impaired modules: if expression of a specific gene or set of genes is dysfunctional and is accompanied by a selective cognitive deficit, the gene is assumed to play a specific role in that cognitive process. Thus, double dissociations in genetic disorders seemingly afford a great opportunity in support of modular and nativist theories of cognition. However, as Enesco and Delval outline, a number of theoretical and empirical arguments suggest caution in drawing conclusions about modularity and innateness from dissociations in developmental disorders. Reasons for caution centre around the sensitivity of measurements of the developmental processes of interest, the importance of testing empirically developmental trajectories of adult strengths and weaknesses, and the potential for interactions across domains in determining the emerging cognitive profile of atypical adults. In what follows, I will complement the issues discussed by the authors with further theoretical points and recent findings. Dissociations and the sensitivity of measurement scales As multiple authors observe in the recent edited volume of Cortex (e.g., Dunn & Kirsner, 2003), the validity of dissociations, even in adults, depends greatly on how well the tasks employed are truly matched for their general demands and difficulty. When considering dissociations in a developmental context, the issue of the sensitivity of measurements is even more poignant (Karmiloff-Smith, Scerif, & Ansari, 2003). Indeed, one needs to first demonstrate that insensitive measures do not mask subtle impairments as intact performance. As Enesco and Delval review, experiments across a number of laboratories have questioned ostensibly intact functioning across component processes of language, an area of behavioural proficiency in adults with Williams syndrome (WS) (e.g., Thomas et al., 2001; Vicari et al., 2002; Volterra et al., 2003). Similar subtle impairments hold for another area of

3 relative proficiency in adults with WS, face processing (e.g., Karmiloff-Smith, 1997; Deruelle et al., 1999). Importantly, even when the sensitivity of the measurements used to reveal intact functioning is taken at face value, one needs to establish whether the multiple factors contributing to performance (concurrently and through development) load similarly on the processes of interest across patients and typically developing individuals. Indeed, measures of cognitive functioning across domains can vary in their contribution to processes of interest in normal development as opposed to genetic disorders. For example, in WS the normal relationships between triadic attention and vocabulary development do not hold, suggesting that apparently proficient performance is supported by atypical cognitive processes (Laing et al., 2002). WS infants fixate on adults and fail to disengage from their face when this would help learning about the referent of adults attention. Another illustration for caution in interpreting factors contributing to behavioural performance comes from numerical cognition, an area of striking impairment in WS. Ansari and colleagues (2003) showed that children with Williams syndrome achieve competence in reciting the counting sequence, but their understanding of cardinality is delayed and only reaches that of younger children with equivalent visuo-spatial skills. Critically, verbal abilities predict variability in cardinality understanding in WS, whereas visuo-spatial measures are predictive of variability in this important aspect of numerical representations in typically developing children. These results underline how both proficient and delayed functioning in WS, and more generally in developmental disorders, can be associated with concurrent predictors of variability that deviate from the normal case. This in turn suggests further caution in interpreting modularity from dissociations. Reasons for caution become more evident when disorders are investigated within a developmental context. Investigating developmental trajectories within cognitive domains Multiple studies by Karmiloff-Smith and colleagues suggest that one cannot infer early cognitive profiles of intact and impaired functioning from adult performance (e.g., Paterson et al., 1999). Most importantly, following the developmental trajectories of both functions that are most overtly affected and those that are seemingly intact in adulthood has revealed the need to put the cognitive profile of individuals with genetic disorders into a developmental context. For example, in the case of face processing, early trajectories of recognition performance reveal an

4 atypical focus on the featural aspects of faces, and the absence of the typical shift to configural processing (Karmiloff-Smith et al., 2004). As Bishop (1997) discusses, the need to focus on trajectories extends to other developmental disorders. For example, Botting (2005) investigated longitudinal changes in performance in children and adolescents with Specific Language Impairment (SLI), who are initially diagnosed with the condition if they display language deficits in the absence of non-verbal impairments. She found a striking decrease in non-verbal IQ over developmental time, questioning the stability of their initial cognitive profile and stressing the longitudinal focus on both impaired and spared functions. Further developmental focus: studying interactions across domains Evidence reviewed thus far warns against interpreting performance in an individual cognitive domain or process without putting it into a developmental context. Psychologists modelling dissociations in developmental disorders need to also question what counts as intact performance across processes (Karmiloff-Smith, Scerif, & Ansari, 2003). Should performance at the level of matched control groups (matched by their functioning on either general mental age or a control ability level) be dismissed as simple delay? This carries the implicit assumption that delay at a particular time-point in development may not predict later deviance of the process of interest itself, or of others with which it may interact over developmental time. This in turn implies that the representational processes under investigation do not interact with others throughout developmental time, a conclusion that should be empirically tested, rather than assumed a priori. For example, performance on magnitude comparison tasks is generally considered to be a marker of numerical representations along a compressed number line (reviewed in Dehaene, 1997). If children with WS perform magnitude comparisons no worse than what would be expected for their (grossly delayed) visuo-spatial abilities as discussed above, the representations underlying comparisons will be available to other developing numerical abilities later than expected. This could be a potential cause of deviance on tasks that later tap processes other than magnitude comparisons (e.g., simple arithmetic). The issue of interactions is crucial in differentiating models of adult cognition based on patients who suffered brain damage in adulthood from developmental models: their temporal characteristics over development may be as important as the ontogeny of

5 each individual domain in understanding the emerging atypical cognitive profile. Scerif and Karmiloff-Smith (2005) have argued that such interactions could alter the course of development in multiple ways. First, the normal emergence of certain processes may be temporally offset. For example, longitudinal studies indicate that language development in WS follows an early atypical trajectory in comparison with other cognitive milestones, with the vocabulary spurt preceding the onset of exhaustive sorting and pointing following the onset of vocabulary. But interactions across domains can be even subtler. Williams syndrome is characterized by relative strengths in language, but weaknesses in visuo-spatial cognition and understanding spatial language is particularly challenging for adults and children with WS, a finding that is predicted by their poor visuo-spatial skills. Other relational but non-spatial aspects of language (for example, comparatives such as 'lighter than' or 'darker than') also appear more difficult than expected given their grammatical competences (Phillips et al., 2004). In the case of developmental disorders, testing cross-domain relations shifts the focus away from descriptive profiles of relative strengths and weaknesses and generates novel questions about the potential computational mechanisms that drive them to co-occur through development (Scerif & Karmiloff- Smith, 2005). Intriguingly, a recent proposal suggests that differential interactions across processes due to their ontogenetic heterochronicity may also account for the emergence of species differences in the understanding of the physical and social world across human and non-human primates (Gomez, 2005). Mechanisms for emerging atypical outcomes: A focus on computational properties The evidence presented above suggests that, while dissociations are not a priori impossible, researchers interested in modelling them should not stop at using them as a behavioural descriptor or heuristic. They should instead provide an account for why and under what conditions dissociations should occur (Thomas & Karmiloff-Smith, 2002). Are the computations involved in the processes that are being compared so different that they can be independent? What kind of evidence should be provided to test whether this is the case? These questions highlight the fact that, beyond either supporting or undermining massively modular accounts of cognition, developmental disorders provide a unique opportunity to investigate what parameters changes could alter developmental trajectories to result eventually in the measured differences across and within domains (Karmiloff-Smith & Thomas, 2003).

6 Thinking about the computational level of descriptions draws attention to lower-level processes (rather than higher-level domain impairments) that may subtly affect some functions while more overtly disrupting the development of others. These lower-level processes need neither be domain-general, nor necessarily domain-specific. Indeed, these two terms are used in distinct and dichotomous ways, but it may be useful to think of them more flexibly. In this regard, Karmiloff-Smith (1998) suggested that a more useful term may be domain-relevant. Relevance depends on whether certain computational properties fulfil the neurocomputational demands of the task at hand and the constraints that the environment and the developing system may pose on them. The extent to which these properties are more relevant to certain domains than to others shifts the balance towards whether they can appear specific or general. Again, developmental disorders of known genetic origin offer simpler models within which to exemplify these points. Fragile X syndrome (FXS) is the most common form of inherited mental retardation and it is associated with the silencing of a single gene whose protein product, is crucial for the refinement of dendritic spine morphology (Greenough et al., 2001), in turn necessary for regulating activity-dependent synaptic changes across the brain (see O Donnell & Warren, 2002, for a review). Fragile X syndrome poses an intriguing puzzle: how can impairment of a general low-level process involved in dendritic spine morphology result in an uneven pattern of cognitive abilities and functioning? All cortical tissues sampled thus far reveal some anomalies, suggesting atypical effects throughout cortex. One therefore needs to ask why the computational properties of this ubiquitous change may be more relevant to the development of the impaired functions than to the development of the less overtly affected ones. In the case of impaired executive functions, Scerif and Karmiloff-Smith (2005) and Scerif et al. (2005) have suggested that long-range connections and recurrent excitatory integration across glutamatergic dendritic spines in pyramidal neurones may be critical to the development of at least some of the functions implemented in prefrontal and parietal circuits, to a greater degree than it is in circuits dedicated to lower level vision (preferentially modulated by lateral inhibitory connections). A similar argument might extend to the development of thalamocortical projections to the ventral and dorsal stream (Kogan et al., 2004, 2005). Beyond the specific neuroscientific details of such a proposal, a focus on understanding the lowlevel computational mechanisms resulting in both cognitive strengths and weaknesses

7 can enrich labels such as intact or impaired and puts them into a developmental context. Implications and further questions I have reviewed cautionary notes against interpreting dissociations in developmental disorders as immediate support for modular and nativist theories of cognition. As Enesco and Delval argue, the validity of dissociations depends on the sensitivity of the measurements used. Furthermore, even when taken at face value, dissociations have to be evaluated within a developmental context and integrated within a mechanistic account for why they should occur over development. The authors conclude by suggesting that evidence from developmental disorders, typical cognitive development in infancy and early childhood and comparative psychology seems to question nativist and massively modular theories of cognitive development. While agreeing strongly, I have used the case of developmental disorders to shift the focus of debate to the following questions: What are the mechanisms driving developmental changes within and across domains? In what ways are some of these mechanisms more relevant to certain domains than others? Are interactions across developing processes instrumental to ontogenetic change? If, for an individual domain, there are domain-specific processes but domain-general processes can be also isolated, what are their relative contributions to the development of the skill of interest? These questions remain open for theorists across the nativist-constructivist divide.

8 References Ansari, D., et al. (2003). What makes counting count? Verbal and visuo-spatial contributions to typical and atypical number development. Journal of Experimental Child Psychology, 85, Bishop, D.V. (1997). Cognitive neuropsychology and developmental disorders: uncomfortable bedfellows. Quarterly Journal of Experimental Psychology A, 50, Botting, N. (2005). Non-verbal cognitive development and language impairment. Journal of Child Psychology and Psychiatry, 46, Dehaene, S. (1997). The number sense. Oxford: Oxford University Press. Deruelle, C., Mancini, J., Livet, M. O., Cassé-Perrot, C. & de Schonen, S. (1999). Configural and local processing of faces in children with Williams syndrome. Brain and Cognition, 41, Dunn, J. & Kirsner, K. (2003). What can we infer from double dissociations? Cortex, 39, 1-7. Gomez, J. C. (2005). TiCS. Greenough, W.T., Klintsova, A.Y., Irwin, S.A., Galvez, R., Bates, K.E., & Weiler, I.J. (2001). Synaptic regulation of protein synthesis and the fragile X protein. Proceedings of the National Academy of Sciences, 98, Karmiloff-Smith, A. (1997). Karmiloff-Smith, A. (1998) Development itself is the key to understanding developmental disorders. Trends in Cognitive Sciences, 2, 10, Karmiloff-Smith, A. & Thomas, M.S.C. (2003). What can developmental disorders tell us about the neurocomputational constraints that shape development? The case of Williams syndrome. Development and Psychopathology, 15, Karmiloff-Smith, A., Scerif, G., & Ansari, D. (2003). Double dissociations in developmental disorders: Theoretically misconceived, empirically dubious. Cortex, 39, Karmiloff-Smith, A. et al. (2004) Exploring the Williams syndrome face processing debate: The importance of building developmental trajectories. Journal of Child Psychology and Psychiatry, 45, Kogan, C.S. et al. (2004) Differential impact of the FMR1 gene on visual processing in fragile X syndrome. Brain, 127,

9 Kogan, C.S. et al. (2005) Integrative cortical dysfunction and pervasive motion perception deficit in fragile X syndrome. Neurology, 63, Laing, E., Butterworth, G., Ansari, D., Gsoedl, M., Longhi, E., Panagiotaki, G., Paterson, S., & Karmiloff-Smith, A. (2002). Atypical development of language and social communication in toddlers with Williams syndrome. Developmental Science, 5, O Donnell, W. T., & Warren, S. T. (2002). A decade of molecular studies of fragile X syndrome. Annual Review of Neuroscience, 25, Paterson, S.J., Brown, J. H., Gsödl, M. K., Johnson, M. H. & Karmiloff-Smith, A. (1999). Cognitive modularity and genetic disorders. Science, 286, 5448: Phillips, C.E. et al. (2004) Comprehension of spatial language terms in Williams syndrome: evidence for an interaction between domains of strength and weakness. Cortex, 40, Scerif, G., & Karmiloff-Smith, A. (2005). The dawn of cognitive genetics? Crucial developmental caveats. Trends in Cognitive Sciences. Scerif, G., Karmiloff-Smith, A., Campos, R., Elsabbagh, M., Driver, J., & Cornish, K. (2005). To look or not to look? Typical and atypical development of oculomotor control. Journal of Cognitive Neuroscience. Thomas, M. S. C., Grant, J., Barham, Z., Gsödl, M., Laing, E., Lakusta, L., Tyler, L. K., Grice, S., Paterson, S. & Karmiloff-Smith, A. (2001). Past tense formation in Williams syndrome. Language and Cognitive Processes, 16, Thomas, M.S.C. & Karmiloff-Smith, A. (2002). Are developmental disorders like cases of adult brain damage? Implications from connectionist modelling. Behavioral and Brain Sciences 25, Vicari, S. et al. (2002) Language acquisition in special populations: a comparison between Down and Williams syndromes. Neuropsychologia, 40, Volterra, V. et al. (2003) Early linguistic abilities of Italian children with Williams syndrome. Developmental Neuropsychology, 23,