The developmental cognitive neuroscience approach to the study of developmental disorders Elise Temple Department of Human Development, Cornell University, Ithaca, NY 14853. et62@cornell.edu Abstract: Functional magnetic resonance imaging studies of develop- mental disorders and normal cognition that include children are becom- ing 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 mecha- nisms underlying cognition and including children in the study of the eti- ology of developmental disorders. Our current understanding of how the brain is organized owes a great deal to the study of brain lesions in adult patients. These studies have helped scientists gain insight into the brain mecha- nisms underlying language (Broca 1861), memory (Scoville & Mil- ner 2000), attention (Posner et al. 1984), vision (Farah et al. 1989), and many other cognitive and perceptual systems. Thomas & Karmiloff-Smith (T&K-S) argue that it may not be appropriate to utilize the same adult patient model for the study of developmen- tal disorders and the development of brain mechanisms for cog- nition. They make the case that it is imperative to take into account the process of development when studying developmental disor- ders. This argument has many implications, including the primary one emphasized by T&K-S, that one cannot equate developmen- tal disorders with adult brain damage even if the symptoms are similar. Another implication of this argument is that it may be in- appropriate to study the etiology of developmental disorders by studying adults who have the disorder. Most functional brain imaging studies of the etiology of devel- opmental disorders use adult subjects. In the early days of brain imaging, when positron emission tomography (PET) was the only choice for studying functional localization in humans’ brains, this was a necessary experimental choice. PET requires the injection of radioactive isotopes and cannot be utilized in minors except in very specific circumstances. However, with the advent of func- tional magnetic resonance imaging (fMRI), a noninvasive tech- nique for studying brain function and functional localization be- came available that can be used in children – as long as they are able to keep their movement restricted. Even with the advent of fMRI, many studies on developmental disorders have continued to use adult subjects. This practice reflects an assumption that the process of development is not important, and implies that the dis- rupted brain process associated with the disorder is isolated from and does not affect the rest of the brain. fMRI studies of developmental disorders and normal cognition that include children are becoming increasingly common and rep- resent part of a newly expanding field of developmental cognitive neuroscience. These studies have already illustrated the impor- tance of studying children as opposed to adults. Some results have confirmed previous adult findings, but others have shown differ- ences between the adult and child organization. For example, a study of amygdala response to fearful faces in children (Thomas et al. 2001) showed less amygdala response in children as com- pared to adults; interestingly, this was because of an increased re- sponse in the children to the neutral faces. In a developmental study of inhibitory control (Luna et al. 2001), differences were found not only between children and adults but also in adoles- cents. Some of the brain differences shown in adolescents were different from both the children and the adults, illustrating the need to study the whole developmental trajectory (even in the rel- atively simple task of controlling eye movements). In addition, a study of cognitive control (Bunge et al. 2002) showed differences between adults and children in the brain regions associated with effective cognitive control, suggesting that the frontal network adults use to suppress interference and inhibit responses is not fully developed in children. In our own studies of developmental dyslexia, my colleagues and I have found both similarities and differences between children with dyslexia and adult studies of dyslexia. For example, we found that children with developmental dyslexia showed decreased ac- tivity in left hemisphere posterior language areas where adults with dyslexia had shown decreases in previous studies (Temple et al. 2001; 2003). This decrease in left temporo-parietal cortex has been shown in other studies of children (Shaywitz et al. 2002; Simos et al. 2002), suggesting that this disruption in temporo-parietal re- sponse seen in adults with dyslexia may be fundamental to the dis- order (Temple 2002). However, in our studies we have also seen differences in the functional brain organization of children with dyslexia. We examined the brain response to rapid auditory stimuli in adults with dyslexia (Temple et al. 2000) and found that whereas normal reading adults showed left prefrontal responsivity to rapid auditory stimuli, the dyslexic reading adults did not show left pre- frontal response to the same stimuli. In addition, two of three adult subjects who participated in a training program to improve their reading and rapid auditory processing ability showed increases in left prefrontal cortex after training. When we studied the brain response to rapid auditory process- ing in normal and dyslexic reading children (Temple 2001), we found some similarities to and differences from the adult study. In normally reading children, left prefrontal cortex was responsive to rapid auditory stimuli, but other brain regions were also involved in a network of response that was more distributed than we had seen in adults. In children with dyslexia, we saw the same lack of prefrontal responsivity to rapid auditory stimuli that we had seen in adults, but we also saw lack of response in the whole larger net- work of brain areas responsive in normally reading children. After training we saw increased activity in not only the left prefrontal cortex of the children with dyslexia but across the larger network. These results suggest to us that the neural response to rapid au- ditory stimuli undergoes developmental changes from childhood to adulthood, becoming more focused and involving an increas- ingly smaller network. In addition, this study suggests that this larger network is disrupted in developmental dyslexia and the re- sults seen in adults with dyslexia represent only one aspect of the disrupted response seen in children with dyslexia. These examples of recent studies of normal and abnormal devel- opmental cognitive neuroscience illustrate the point that the brain mechanisms involved in cognitive processes do undergo develop- mental changes. In the case of developmental disorders, it may be that entire networks are disrupted. Taking these processes of de- velopment into account may be crucial to our understanding of the etiology of developmental disorders. I would argue that, when fea- sible, studies of the neurobiology underlying developmental disor- ders as well as normal cognitive functioning should be conducted with children and taking the process of development into account. Models of atypical development must also be models of normal development Gert Westermann and Denis Mareschal Centre for Brain and Cognitive Development, School of Psychology, Birkbeck College, London WC1E 7HX, United Kingdom. {g.westermann; d.mareschal}@bbk.ac.uk http://www.cbcd.bbk.ac.uk/people/gert; denis/ Abstract: Connectionist models aiming to reveal the mechanisms of atyp- ical development must in their undamaged form constitute plausible mod- els 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 infor- mative in the study of atypical development than the static models em- ployed by Thomas & Karmiloff-Smith (T&K-S). Commentary/Thomas & Karmiloff-Smith: Are developmental disorders like cases of adult brain damage? BEHAVIORAL AND BRAIN SCIENCES (2002) 25:6 771