I agree with Thomas & Karmiloff-Smith (T&K-S) in their critique of Residual Normality. However, first-person data must be integrated into their account of neurobiological development of disabilities. Furthermore, psychological development itself is not only about an individual’ brain and how it interacts with the world; rather, development depends crucially on the sociocultural context in which (normal and abnormal) children develop.

Evidence from various subtypes of Specific Language Impairment and developmental peripheral dyslexias is presented to support the idea that even developmental disorders can be modular. However, in developmental letter position dyslexia and neglect dyslexia we show that additional errors can occur because of insufficient orthographic-lexical knowledge.

Either genetically specified modular cognitive architecture for syntactic processing does not exist (neuroconstructivism), or there is a module but its development is so abnormal in Williams syndrome (WS) that no conclusion can be drawn about its normal architecture (moderate nativism). Radical nativism, which holds that WS is a case of intact syntax, is untenable. Specific Language Impairment and WS create a dilemma that radical nativism cannot accommodate.

Thomas & Karmiloff-Smith (T&K-S) raise the excellent and, in retrospect, obvious point that in a dynamic learning environment where feedback is possible, we should expect networks to adapt to damage by altering details of their behavior. We should therefore not expect that developmental disorders should result in “normal” modules. The implications of this point go much further, since interprocess dependency in the brain does not rely only on learned neural connections. This argues strongly against behavioral and process-related definitions, as opposed to structural and architecture-related definitions, of mental modularity.

Models of the architecture of mature cognitive systems can inform the study of normal and disordered cognitive development, if one distinguishes between proximal and distal causes of performance. The assumption of residual normality need not be made in order to apply adult models to performance early in development, because these models can be modified to reflect the results of compensatory processing.

Thomas & Karmiloff-Smith (T&K-S) show that the assumption of residual normality (RN) does not hold in connectionist simulations, and argue that RN has been inappropriately applied to childhood disorders. We agree. However, we suggest that the RN hypothesis may never have been fully viable, either empirically or computationally.

This commentary questions the authors’claim that cognitive neuropsychology is defined by modularity and that other theoretical frames, that is, connectionism, are a priori rejected. It also points to the fact that whereas in genetic disorders there are developmental delay and asynchrony, there are few reports of deviant developmental trajectories that are never seen in typical development. It is suggested that the possibility that structure does not equal function in the developing brain, may be a viable option.

We agree with the critique of the Residual Normality assumption. Moreover, we challenge monolithic views of functional normality. Throughout life, development and adaptation require variations in cortical functional circuitry within and across individuals. We propose the principle of “coconstructed functionality” which maintains that brain-behavior functional correspondences are dynamically coproduced by neurobiological, experiential, and contextual processes.

This commentary discusses the logic of inferring modularity or the lack of modularity from observed patterns of developmental disorders.

Different developmental anomalies produce contrasting deficits in a single, integrated system. In a network that inflects regular and exception verbs correctly, a disproportionate deficit with exceptions occurs if connections are deleted, whereas a disproportionate deficit with regulars occurs when an auditory deficit impairs perception of the regular inflection. In general, contrasting deficits do not license the inference of underlying modularity.

Thomas & Karmiloff-Smith (T&K-S) provide evidence from computational modeling against modular assumptions of “Residual Normality” (RN) in developmental disorders. Even though I agree with their criticism, I find their choice of empirical evidence disappointing. Cognitive neuroscience cannot as yet provide a complete understanding of most developmental disorders, but what is known is more than enough to debunk the idea of RN.

The developmental modeling approach to investigating developmental disorders appears highly promising. In this commentary, we question the untapped potential of this approach for supporting insights into particular developmental disorders, developmental processes across the life span, and the viability of traditional theories of developmental disorders.

One of the debated issues regarding Residual Normality (RN) is frequency sensitivity in Williams syndrome (WS). We present some data on frequency sensitivity in Hungarian WS subjects. Based on vocabulary measures, we suggest that instead of the across-the-board frequency insensitivity proposed by some, a higher frequency threshold characterizes these subjects’performance. Results from a category fluency task show that whereas frequency sensitivity in WS is in line with controls, error patterns imply a qualitatively distinct, looser categorical organization. Regarding the much-debated issue of morphological overgeneralizations, our data suggest that frequency sensitivity cuts across the divisions proposed by dual-process theories. In general, some of the frequency effects are the same as in typically developing populations, but with a delayed pattern. Frequency may be interpreted as supporting RN, but in WS it operates with higher thresholds that might be a general processing feature of WS individuals.

Thomas & Karmiloff-Smith (T&K-S) claim that “Residual Normality” is a priori unlikely, that is, that specific cognitive deficits should not exist in developmental disorders. Here I review evidence that a specific cognitive deficit is at the core of developmental dyslexia and I provide a possible neurological account thereof.

Thomas & Karmiloff-Smith (T&K-S) raise an issue of considerable theoretical importance: Are developmental disorders like cases of adult brain damage? However, a related question: Are developmental disabilities the same in children and adults? is rarely addressed. Failure to consider the cumulative and differing effects of aberrant development across the life span confounds the current literature on both developmental dyslexia and Specific Language Impairment.

Using connectionist modelling, Thomas & Karmiloff-Smith (T&K-S) claim that developmental disorders in children are characterised by atypical trajectories and an ultimate functional architecture that is fundamentally different from normal. We argue that there is no empirical evidence for these claims in any developmental disorder and that the available evidence provides support for Residual Normality in both developmental and acquired disorders. We also refute the claim that modular accounts cannot encompass developmental trajectories in children with developmental disorders.

Functional magnetic resonance imaging studies of developmental disorders and normal cognition that include children are becoming increasingly common and represent part of a newly expanding field of developmental cognitive neuroscience. These studies have illustrated the importance of the process of development in understanding brain mechanisms underlying cognition and including children in the study of the etiology of developmental disorders.

Connectionist models aiming to reveal the mechanisms of atypical development must in their undamaged form constitute plausible models of normal development and follow a developmental trajectory that matches empirical data. Constructivist models that adapt their structure to the learning task satisfy this demand. They are therefore more informative in the study of atypical development than the static models employed by Thomas & Karmiloff-Smith (T&K-S).

In response to our target article, many of the commentators concentrated on our notion of Residual Normality. In our response, we focus on the questions raised by this idea. However, we also examine broader issues concerning the importance of incorporating a realistic theory of the process of development into explanations of developmental deficits.