The Nature-Nurture controversy has been with us since it was first outlined by Plato and Aristotle. Nobody likes it anymore. All reasonable scholars today agree that genes and environment interact to determine complex cognitive outcomes. So why does the controversy persist? First, it persists because it has practical implications that cannot be postponed (i.e., what can we do to avoid bad outcomes and insure better ones?), a state of emergency that sometimes tempts scholars to stake out claims they cannot defend. Second, the controversy persists because we lack a precise, testable theory of the process by which genes and environment interact. In the absence of a better theory, innateness is often confused with (1) domain specificity (Outcome X is so peculiar that it must be innate), (2) species specificity (we are the only species who do X, so X must lie in the human genome), (3) localization (Outcome X is mediated by a particular part of the brain, so X must be innate), and (4) learnability (we cannot figure out how X could be learned, so X must be innate). We believe that an explicit and plausible theory of interaction is now around the corner, and that many of the classic maneuvers to defend or attack innateness will soon disappear. In the interim, some serious errors can be avoided if we keep these confounded issues apart. That is the major goal of this paper, i.e., not to attack innateness but to clarify what

Developmental psychology and developmental neuropsychology have traditionally focused on the study of children. But these two fields are also supposed to be about the study of change, i.e. changes in behavior, changes in the neural structures that underlie behavior, and changes in the relationship between mind and brain across the course of development. Ironically, there has been relatively little interest in the mechanisms responsible for change in the last 15–20 years of developmental research. The reasons for this de-emphasis on change have a great deal to do with a metaphor for mind and brain that has influenced most of experimental psychology, cognitive science and neuropsychology for the last few decades, i.e. the metaphor of the serial digital computer. We will refer to this particu-

The term “aphasia ” refers to acute or chronic impairment of language, an acquired condition that is most often associated with damage to the left side of the brain, usually due to trauma or stroke. We have known about the link between left-hemisphere damage and language loss for more than a century (Goodglass, 1993). For almost as long, we have also known that the lesion/symptom correlations observed in adults do not appear to hold for very young children (Basser, 1962; Lenneberg, 1967). In fact, in the absence of other complications, infants with congenital damage to one side of the brain (left or right) usually go on to acquire language abilities that are well within the normal range (Eisele & Aram, 1995; Feldman, Holland, & Janosky, 1992; Vargha-Khadem, Isaacs, & Muter,

Aphasia (defined as the loss or impairment of language abilities following acquired brain injury) is strongly associated with damage to the left hemisphere in adults. This well-known finding has led to the hypothesis that the left hemisphere is innately specialized for language, and may be the site of a specific "language organ". However, for over a century we have known that young children with left-hemisphere damage (LHD) do not suffer from aphasia, and in most studies do not differ significantly from children with right-hemisphere damage (RHD). This result provides strong evidence for plasticity, i.e., brain reorganization in response to experience, and constitutes a serious challenge to the language organ hypothesis. This chapter reviews the history of research on language outcomes in children vs. adults with unilateral brain injury, addressing some discrepancies in the literature to date, including methodological confounds that may be responsible for those discrepancies. It also reviews recent prospective studies of children with unilateral injury as they pass through the first stages of language development. Prospective studies have demonstrated specific correlations between lesion site and profiles of language delay, but they look quite different from lesionsymptom correlations in adults, and gradually disappear across the course of language development. The classic pattern of brain organization for language observed in normal adults may be the product rather than the cause of language learning, emerging out of regional biases in information processing that are relevant for language, but only indirectly related to language itself. If those

We propose that connectionism and dynamic systems theory are strong contenders for a general theory of development that holds true whatever the content domain. We illustrate, through our own career narratives, the origins of these theories in motor and language development. We situate connectionism and dynamic systems among other classic and contemporary theories and conclude that, although there are meaningful differences, these differences pale in relation to the shared assumptions about the fundamental processes and mechanisms of change.

The Nature-Nurture controversy has been with us since it was first outlined by Plato and Aristotle. Nobody likes it anymore. All reasonable scholars today agree that genes and environment interact to determine complex cognitive outcomes. So why does the controversy persist? First, it persists because it has practical implications that cannot be postponed (i.e., what can we do to avoid bad outcomes and insure better ones?), a state of emergency that sometimes tempts scholars to stake out claims they cannot defend. Second, the controversy persists because we lack a precise, testable theory of the process by which genes and environment interact. In the absence of a better theory, innateness is often confused with (1) domain specificity (Outcome X is so peculiar that it must be

ural defects would follow. Instead, this knockout caused cardiovascular defects; neural development appears to be affected only when ephrinB2 is knocked out in tandem with other ephrinB oncogenes, suggesting substantial redundancy for neural development but (in this case) not for the cardiovascular system. In the same vein, Hoxa1 knockout mice lack part of the hindbrain, while Hoxb1 mice lack certain hindbrain nuclei; neither gene by itself causes large changes outside the nervous system, but their combined knockout causes defective hindbrain development plus almost complete agenesis of the lungs and thymus. It is now clear that genes provide context for each other, in redundant and plastic relationships. Furthermore, many genes respond to the outside environment throughout the animal's lifetime (including genes involved in neurogenesis that are "turned on" when adult animals are placed in a rich environment---Kempermann et al., 1998). The resulting picture is one of exquisitely comple

Three exploratory studies were carried out to determine if there was continuity in the development of language in young children at the upper and lower extremes of the normal continuum, and if it was possible to use variables from an early assessment to predict their language status at a later date. Studies 1 and 2 examined continuity over 6-month period (from approximately 20 to 26 and 13 to 20 months of age, respectively); Study 3 examined continuity from 8 to 30 months of age. Results provided solid evidence for continuity at the group level but no evidence of ability to predict outcome for individual children using the vocabulary production, vocabulary comprehension, and gesture production variables included in this study. 2 Many parents wonder whether their child is normal. They wonder whether he or she is abnormally slow to develop, or so precocious that early celebration is warranted. During their child's first year of life, most parents worry about issues like sleeping, eating, and attainment of motor milestones (especially crawling and walking). During the second year, the focus switches to communication and language. This is true for physicians and other health care professionals

This paper attempts to identify certain neurobiological constraints of natural language processing and exam- ines the behavior of recurrent networks for the task of classifying aphasic subjects. The specific question posed here is: Can we train a neural network to distinguish between Broca aphasics, Wernicke aphasics and a control group of normal subjects on the basis of syntactic knowledge? This approach could aid dia- gnosis/classification of potential language disorders in the brain and it also addresses computational modeling of language acquisition.

We present the first direct comparison of language production in brain-injured children and adults, using agecorrected z scores for multiple lexical and grammatical measures. Spontaneous speech samples were elicited in a structured biographical interview from 38 children (5-8 years of age), 24 with congenital left-hemisphere damage (LHD) and 14 with congenital right-hemisphere damage (RHD), compared with 38 age- and gender-matched controls, 21 adults with unilateral injuries (14 LHD, 7 RHD), and 12 adult controls. Adults with LHD showed severe and contrasting profiles of impairment across all measures (including classic differences between fluent and nonfluent aphasia). Adults with RHD (and three nonaphasic adults with LHD) showed fluent but disinhibited and sometimes empty speech. None of these qualitative or quantitative deviations were observed in children with unilateral brain injury, who were in the normal range for their age on all measures. There were no significant differences between children with LHD and RHD on any measure. When LHD children were compared directly with LHD adults using age-corrected z scores, the children scored far better than their adult counterparts on structural measures. These results provide the first systematic confirmation of differential free-speech outcomes in children and adults, and offer strong evidence for neural and behavioral plasticity following early brain damage. For more than 3000 years, we have known that