Li, S.

Lindenberger, U.

English

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the endpoint of development are likely to be the outcome of anextended atypical developmental trajectory, determined by theinitial structural anomalies in the system and by its atypical inter-action with the environment (Karmiloff-Smith 1997; 1998). Thisis a plausible position in part because current genetic and biolog-ical understanding favors the view that in disorders of a geneticorigin, the effects will be wide spread and nonspecific, and thusresult in brain changes that are likely to affect learning and devel-opment. Developmental cognitive neuropsychology has notdrawn a sufficiently clear distinction between acquired deficitsand congenital ones, and has too often applied similar theoreticalframeworks to both, disregarding the crucial effects of develop-ment.The question that I would like to raise relates to the above po-sition. The assumption that in cases of congenital disorders of ge-netic origin the child in fact learns with a different brain, predictsthat disordered populations will more often than not exhibit an ab-normal developmental course. However, it is rather rare to en-counter reports of performance in disordered populations that isof a kind never seen in typically developing children. One typicallysees reports of delays and asynchronous development, but rarelyhave truly deviant patterns been reported. A typical example con-cerns the notion of extended optional infinitive, describing asyn-chronous development in children with Specific Language Im-pairment (SLI) (Rice et al. 1998). Reports of developmentaldelays in neurodevelopmental disorders of genetic origin are toonumerous to quote.Especially problematic in this regard are claims based on groupresults when the comparisons are drawn between group meansand prevalent tendencies. For example, consider the claim madeby Cossu Rossini and Marshall (1993) that children with Downsyndrome read without phonological awareness. This work mighthave qualified as an example of an atypical learning trajectory.However, the participants with Down syndrome did not performat zero level. Rather, in some cases they scored 13 out of 21 cor-rect, and there was just one child who scored 0 on three out of fourtasks (Bryne 1993). Hence, whereas there were statistically sig-nificant differences between children with Down syndrome andtypically developing children on phonological awareness tasks, Idoubt whether one can attribute these differences to a differentlearning trajectory.The authors cite work on face processing in Williams syndromesuggesting that, despite normal face recognition abilities, the un-derlying processes by which resolutions are arrived at is atypical(Deruelle et al. 1999). But are these processes of the kind neverencountered in children with normal brains? In a similar vein, inall of the research on language in Williams syndrome there havebeen very few reports, if any at all, of errors that are never seen innormal children (but see Capirci et al. 1996). Most of the findingsconcern delayed acquisition, higher error rates, and either less(Karmiloff-Smith et al. 1997) or more (Clahsen & Almazan 2001)control over grammatical rules relative to memorized words. Theconclusion from most of the work on Williams syndrome – and theauthors’ work is no exception – as well as from work on other de-velopmental syndromes, is that there are set paths for languagelearning even under pathology, with variation in speed and onsetof various components, yet with minimal options for deviation thatare not time-related (Levy et al. 2000).This is perhaps not surprising given the plasticity that is inher-ent in the young brain. Brain plasticity has been invoked mostly incases of focal damage (cf. Bach 1990). However, if brain plasticityis assumed in congenital disorders of genetic origin, then the ex-pectation is that despite genetic abnormalities that cause struc-tural deviations from typicality, functional normalcy may be pre-served throughout development. In fact, the question is to whatextent structure equals function in the brain and, consequently,whether structural differences, such as are seen in genetic dis-orders, predict functional differences. The fact that there arehealthy children who pursue developmental trajectories that char-acterize children with abnormal brains, suggests that these atyp-ical developmental options are not a consequence of structural abnormality, and that they may operate in normalcy too. In con-clusion, whether structure equals function in the brain is an em-pirical question that has to be addressed in reference to specificdevelopmental domains. Theoretically, however, given that thereis plasticity, the fact that there is structural abnormality does notin itself predict functional abnormality.Coconstructed functionality instead offunctional normalityShu-Chen Lia and Ulman LindenbergerbaCenter for Lifespan Psychology, Max Planck Institute for HumanDevelopment, D-14195 Berlin, Germany; bSchool of Psychology, SaarlandUniversity, D-66041 Saarbrücken, Germany. shuchen@mpib-berlin.mpg.delindenberger@mx.uni-saar land.de http: //www.mpib-berlin.mpg.dehttp: //www.uni-saarland.de /fak5 /lindenberger /members /ulman.htmAbstract: We agree with the critique of the Residual Normality assump-tion. Moreover, we challenge monolithic views of functional normality.Throughout life, development and adaptation require variations in corti-cal functional circuitry within and across individuals. We propose the prin-ciple of “coconstructed functionality” which maintains that brain-behaviorfunctional correspondences are dynamically coproduced by neurobiolog-ical, experiential, and contextual processes.Thomas & Karmiloff-Smith (T&K-S) argue against a canonical hy-pothesis of developmental cognitive neuropsychology. Accordingto this hypothesis, similarities between domain-specific cognitiveimpairments observed after damage to the adult brain, on the onehand, and developmental disorders, on the other, point to simi-larities in underlying causes, thereby lending support to a modu-lar organization of normal adult cognition. They challenge the va-lidity of this inference by demonstrating that its underlyingassumption (the “Residual Normality assumption”) is untenable,primarily because developing systems generally compensate forselective deficits by modifying other parts of the system. We agreewith this critique and would like to take it a step further. We callinto question the notion of functional normality and advocate theprinciple of “coconstructed functionality” for investigating indi-vidual and life-span differences in brain-behavior mappings.Coconstructed functionality . A monolithic divide betweennormality and abnormality is unproductive and misleading, if“normal” signifies invariance of functional correspondences be-tween brain and behavior. Variations within and between individ-uals are fundamental to living organisms (Ford 1987; Mayr 1998).Rather than being one-to-one, functional mappings of brain struc-tures and processes to behaviors tend to be many-to-many. At thebehavioral level, research on the organization of intellectual abil-ities has long since identified substantial individual differenceswithin the normal range of functioning (e.g., Deary 2001; Spear-man 1904). Similarly, life-span intellectual development is con-ceptualized as dynamic, multifunctional, and multidirectional(e.g., Baltes et al. 1998; Cattell 1971; Engle 2002; Horn 1968).Among others (e.g., Siegler 1994), Francophone scholars em-phasize the importance and ubiquity of multiple developmentalpathways with vicariance (i.e., alternation among several pro-cesses fulfilling similar functions) being a source of within- and between-individual variations and development (Lautrey, in press;Reuchlin 1978; de Ribaupierre 1993). At the neurobiologicallevel, intra-individual (e.g., Makeig et al. 2002), interindividual(e.g., Toga 2002), and life-span (e.g., Cabeza 2002; Johnson 2001;Raz 2000) differences in brain functioning are large and wide-spread in the absence of pathology (e.g., within the “normal range”of functioning). Cognition and behavior reflect the reciprocal in-teractions between neurobiological and experiential contexts oflife that vary both within and across individuals. Therefore, in-stead of reaffirming the orthodox dichotomy between the normalCommentary/Thomas & Karmiloff-Smith: Are developmental disorders like cases of adult brain damage?BEHAVIORAL AND BRAIN SCIENCES (2002) 25:6 761and the abnormal, “normality” is better viewed as the potential ofindividuals (and environments) to produce an adaptive range ofbehaviors in a variety of ways. Specifically, any attempt to definenormality in terms of invariant brain-behavior mappings neglectsthe pivotal role of variation at all level and timescales of biological(Mayr 1998) and biocultural organization (Baltes & Singer 2001;Li 2003).Life-span dif ferences in brain-behavior mappings. In arguingagainst biological determinism, recent coconstructive theories(e.g., Baltes & Singer 2001; Cole 1999, Elman et al. 1996; Li 2003;Nelson 1996) have stressed the importance of interactive pro-cesses and developmental plasticity occurring across differenttimescales and levels in shaping brain-behavior relations. For ex-ample, face processing is less localized or specialized in infantsthan in adults. In infants, face processing involves both left andright ventral visual pathways; in adults, face processing primarilyinvolves the right ventral visual pathway (de Haan et al. 2002).During senescence, cortical information processing in differentbrain areas becomes less specific or more integrated (see Cabeza2002; Logan et al. 2002; Reuter-Lorenz 2002 for reviews). A re-cent cross-level neurocomputational theory suggests that senes-cent decrements in neuromodulation, which affect the distinc-tiveness of neuronal representations of environment-experienceinteractions, may account for some of the observed losses in cor-tical specialization (e.g., Li et al. 2001). It is unclear to what extentcortical reorganization in late adulthood directly reflects senes-cent changes in structural and neurochemical integrity, or com-pensatory adaptations to such changes. In either case, evidencefrom both child development and aging indicates that the modalfunctional circuitries brought to bear upon “nominal cognitivetasks” differ widely by age.At the behavioral level, life-span changes in the structure of in-telligence support our critical appraisal of functional normality.The differentiation-dedifferentiation hypothesis (e.g., Baltes et al.1980) postulates that intellectual abilities are rather undiffer-entiated in childhood, undergo differentiation during maturation,leading to a multifaceted ability structure that stays largely invari-ant during adulthood, and again become more homogeneous(dedifferentiated) during aging. A recent study with a wide rangeof ages (6 to 89 years) and a comprehensive battery of intelligencetests and standard reaction-time tasks revealed that correlationsamong different aspects of intelligence and information-process-ing parameters are indeed higher at both ends of the life span (Liet al., in press). Again, such life-span transformations call for dy-namic views on brain-behavior mappings.Individual dif ferences in brain-behavior mappings. Variabilityand plasticity of functional circuitry are not confined to the ex-treme ends of the life span; rather, they are general prerequisitesfor cumulative experiential tunings reflecting the provisions, de-mands, and constraints of specific sociocultural contexts. For ex-ample, posterior regions of the hippocampi, involved in process-ing spatial representation of the environment, have been reportedto be significantly larger in London taxi drivers than in age-matchedcontrols (Maguire et al. 2000). Similarly, there are marked differ-ences between native speakers of English and Italian with respectto the brain areas involved in reading (Paulesu et al. 2000): En-glish readers show greater activations in the left posterior inferiortemporal gyrus and the anterior frontal gyrus, areas associatedwith word retrieval. Presumably, these differences reflect lan-guage-specific adaptations in the functional circuitry supportinggrapheme-to-phoneme translation.Conclusion. Life-span changes, interindividual differences,and intra-individual variability in brain-behavior mappings are notadequately described or explained in relation to a “gold standard”of normality. The principle of coconstructed functionality, with itsemphasis on socioculturally embedded experiential tuning, seemsmore productive than the normal/abnormal dichotomy. To cap-ture the dynamic and multivariate picture of brain-behavior rela-tions, we need systematically to investigate biocultural cocon-structive processes that lead to individual and life-span differencesin cortical functioning. Undoubtedly, invariant properties of cor-tical organization will also emerge from such an approach, butthey will be located at higher levels of abstraction, be it coherentpatterns of neural assembly (e.g., Singer 1995), or general princi-ples of human behavior (e.g., Nesselroade 1991).ACKNOWLEDGMENTWe thank Paul B. Baltes for his comments on an early draft of the com-mentary.What can developmental disorders tell usabout modularity?Gary F. MarcusPsychology Department, New York University, New York, NY 10012.gary.marcusl@nyu.edu http: //www.psych.nyu.edu /gary /Abstract: This commentary discusses the logic of inferring modularity orthe lack of modularity from observed patterns of developmental disorders.Developmental disorders are, as Thomas & Karmiloff-Smith(T&K-S) observe, not necessarily like cases of adult brain damage.Their simulations well illustrate why one cannot directly infer un-derlying mental organization from surface behavior, a problemthat has long made the discipline of psychology challenging(Chomsky 1959; McClelland 1979). And T&K-S are quite right tohighlight the perils of inferring modularity from a pairing of ap-parently normal behavior in some domains with impaired behav-iors in other domains; seemingly normal behavior could always bethe product of compensatory mechanisms. (Exactly the sameworry hampers the study of second-language acquisition – whena nonnative speaker succeeds, it is difficult to know in advancewhether she is relying on remnants of universal grammar or somekind of domain-general cognitive substitute.)But the naive inference from impairment in multiple domainsto a lack of modularity is equally riddled with danger. Althoughcognitive systems are often caricatured as being the product of ei-ther entirely modular or entirely shared resources, the reality isthat every complex neural system – even ones that are modular inthe sense of performing computations that are informationally en-capsulated – probably relies on a mixture of domain-specific anddomain-general resources. A system for language understanding,for example, probably relies on both shared resources like mem-ory and symbol-manipulation machinery (Marcus 2001) and non-shared machinery that is specialized for linguistic representation(Hauser et al. 2002). A disorder that impaired the neural under-pinnings of memory might well then impair both linguistic andnonlinguistic systems, even if the linguistic system included somespecialized resources. Disorders that affect multiple domainshence may tell us little about questions about underlying modu-larity.What is true at the psychological level is perhaps even more trueat the genetic level. Even where two organs are specialized andphysical distinct, they often depend in large part on overlappingsets of genes. A chicken’s wing and its leg, for example, are for the most part built under the direction of the same set of genes.Out of the hundreds or thousands of genes involved in limb for-mation, only a handful style59color:black9.(Margulies et al.2001), black9.. In a similar way, it is possible, perhaps even likely,that separate style59color:black9.on common sets of genes, justas separate limbs the case of the specialization of limbs, the spe-cialization of neural function might rely on a handful of novelgenes specific to that domain interacting with a larger number ofconserved (shared) genes.It follows that we must be extremely careful about inferring alack of modularity from the distribution of disorders. We shouldexpect that many disorders will affect multiple subsystems, yetkeep our eyes open for deficits that are more focused. Even if, forCommentary/Thomas & Karmiloff-Smith: Are developmental disorders like cases of adult brain damage?762 BEHAVIORAL AND BRAIN SCIENCES (2002) 25:6

Coconstructed functionality instead of functional normality

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Coconstructed functionality instead of functional normality

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