Categorical induction abilities are robust in typically developing (TD) preschoolers, while children with Autism Spectrum Disorders (ASD) frequently perform inconsistently on tasks asking for the transference of traits from a known category member to a new example based on shared category membership. Here, TD five-year-olds and six-year-olds with ASD participated in a categorical induction task; the TD children performed significantly better and more consistently than the children with ASD. Concurrent verbal and nonverbal tests were not significant correlates; however, the TD children's shape bias performance at two years of age was significantly positively predictive of categorical induction performance at age five. The shape bias, the tendency to extend a novel label to other objects of the same shape during word learning, appears linked with categorical induction ability in TD children, suggesting a common underlying skill and consistent developmental trajectory. Word learning and categorical induction appear uncoupled in children with ASD.

Although deficits in cognitive empathy are well established in individuals with autism spectrum disorder (ASD), the literature on emotional empathy, or emotional contagion, in individuals with ASD is sparse and contradictory. The authors tested susceptibility to contagious yawning and laughter in children with ASD (n = 60) and typically developing (TD) children (n = 60), ages 5–17 years, under various conditions, to elucidate factors that may affect emotional contagion in these populations. Although TD children showed equal amounts of emotional contagion across conditions, children with ASD were highly influenced by the familiarity of the target stimulus, as well as task instructions that encourage eye gaze to target. More specifically, children with ASD exhibited less contagious yawning and laughter than their TD peers except when their attention was explicitly directed to the eyes or (and even more so) when their parents served as the stimulus targets. The authors explore the implications of these findings for theories about the mechanisms underlying empathic deficits in ASD as well as the clinical implications of having parents involved in treatment.

Early autism research focused on behavior and cognition. In recent decades, the pace of research has accelerated, and advances in imaging and genetics have allowed the accumulation of biological data. Nevertheless, a coherent picture of the syndrome at either phenotypic or biological level has not emerged. We see two fundamental obstacles to progress in basic understanding of autism. First, the two defining features (impairment in social interactions and communication, and restricted, repetitive behaviors and interests) are historically seen as integrally related. Others hold that these two major traits are fractionable and must be studied independently, casting doubt on autism as a coherent syndrome. Second, despite much recent research on brain structure and function, environmental factors, and genetics/genomics, findings on the biological level have not generally aligned well with those on the phenotypic level. In the first two sections, we explore these challenges, and in the third section, we review approaches that may facilitate progress, such as (1) including in studies all individuals defined by social impairment without regard to repetitive behaviors, (2) forming narrowly defined subtypes by thorough characterization on specific features, both diagnostic and non-diagnostic, (3) focusing on characteristics that may be relatively robust to environmental influence, (4) studying children as early as possible, minimizing environmental influence, and including longitudinal course as an important part of the phenotype, (5) subtyping by environmental risk factors, (6) distinguishing between what participants can do and what they typically do, and (7) aggregating large data sets across sites. (JINS, 2017, 23, 903–915)

Social deficits have been implicated in the language delays and deficits of children with autism (ASD); thus, the extent to which these children use language input in social contexts similarly to typically developing (TD) children is unknown. The current study investigated how caregiver input influenced the development of wh-question comprehension in TD children and language-matched preschoolers with ASD. Children were visited at four-month intervals over 1.5 years; mother–child play sessions at visits 1–2 were coded for maternal wh-question use. At visits 3–5 children watched videos in the Intermodal Preferential Looking paradigm, to assess their comprehension of subject and object wh-questions. Mothers' use of wh-questions with verbs and complex wh-questions positively predicted wh-question comprehension in the TD group; in contrast, mothers' use of wh-questions with ‘be’ as the main verb negatively predicted wh-question comprehension in the ASD group. Thus, TD children and children with ASD appear to use their linguistic input differently.

Comprehension of six syntactic structures was tested across four age groups. Each structure was presented with both plausible and implausible content. The contribution of cognitive nonlinguistic factors important for comprehension (attention, short-term memory, and mental control) was tested via standard neuropsychological tasks. Sixty-six women aged 30–79 were tested. Both errors and reaction times increased with age, especially for more complex syntactic types and implausible sentences. The neuropsychological factors tested contributed minimally to an age-related decline in comprehension, suggesting that the subtle breakdown seen in syntactic processing may be a language-specific impairment.

Social Neuroscience: People Thinking About Thinking People. John T. Cacioppo, Penny S. Visser, and Cynthia L. Pickett (Eds.). 2006. Cambridge, MA: The MIT Press, 328 pp., $45.00 (HB)

Perhaps not since the flowering of clinical neuropsychology thirty years ago have we seen this sense of exhilaration about the emergence of a new field through the integration of existing disciplines. Clearly, these authors and thinkers feel the same excitement that could be felt when new collaborations were being forged among neurologists, psychiatrists, psychologists, and communication specialists in earlier decades. For the emerging field of social neuroscience, the parent fields include social psychology (see, for example, chapters on Race and Emotion, The Social Neuroscience of Stereotyping and Prejudice, Social and Physical Pain, and Animal Models of Human Attitudes), clinical neuropsychology (Neurological Substrates of Emotional and Social Intelligence: Evidence from Patients with Focal Brain Lesions), social cognition (Neural Substrates of Self Awareness, and three chapters bearing directly on Theory of Mind) and, of course, cognitive and basic neuroscience. Each chapter includes theoretical perspectives from multiple fields and reviews studies that use diverse techniques (including functional imaging, ERP, behavioral scales, lesion studies, developmental studies, and animal studies), although the book is very heavy on functional imaging data. As the editors acknowledge, animal and patient data are not represented in a thorough way.

The aims of this book are grand indeed. Rolls addresses such questions as, What are emotions? Why do we have emotions? What are the rules by which emotion operates? What are the brain mechanisms of emotion, and how can disorders of emotion be understood? Why does it feel like something to have an emotion? Why is the brain built to have reward, and punishment, systems? How does the brain produce behavior by using reward, and punishment, mechanisms? And in fact he does succeed remarkably well in presenting a synthesis of experimental data to elucidate many of these questions.

Executive functioning was investigated in 34 children (24 boys and 10 girls) with developmental language disorder (DLD) and 21 children (18 boys and 3 girls) with high-functioning autistic disorder (HAD) matched on Full Scale IQ, Nonverbal IQ, age (mean age 9 year, 1 month), and SES. The DLD group had a Verbal IQ that was 10 points higher than the HAD group. These children were given the Wisconsin Card Sorting Test (WCST), the Mazes subtest from the WISC-R, the Underlining test, and the Rapid Automatized Naming test. In addition, these children were given the Vineland Scales of Adaptive Functioning and the Wing Diagnostic Symptom Checklist in order to assess severity of autistic symptomatology. Results indicated that the only significant difference between the two groups on the cognitive tasks was perseverative errors on the WCST; there was no significant difference on total number of categories achieved or total number of errors on the WCST or on the other executive function measures. There was also significant overlap in the scores between the two groups and the difference in perseverative errors was no longer significant when Verbal IQ was partialled out. Executive functioning was strongly related to all IQ variables in the DLD group and particularly related to Verbal IQ in the HAD group. Although there was a relationship in the HAD group between executive functioning and adaptive functioning, as well as between executive functioning and autistic symptomatology, these relationships were generally no longer significant in the HAD group after the variance due to Verbal IQ was accounted for. The results are interpreted to indicate that although impaired executive functioning is a commonly associated feature of autism, it is not universal in autism and is unlikely to cause autistic behaviors or deficits in adaptive function.

Although roles have been proposed for both graphomotor speed and learning in the execution of Digit Symbol, few data have been available concerning performance across the adult lifespan on the Symbol Copy, paired associates, or free recall measures derived from Digit Symbol and recommended in the WAIS–R–NI. We report findings on 177 healthy older adults (ages 50–90), providing normative data by age group, education level, and gender. As previously reported, Digit Symbol scores decline steeply with age (r = −.64). Symbol Copy speed declines almost as steeply (r = −.58). Incidental learning, however, declines only modestly (r = −.26 on both measures). Symbol Copy is a far stronger correlate of Digit Symbol (r = .72) than are paired associates or free recall (r = .26 and r = .28, respectively). The 2 incidental learning measures do, however, offer valuable supplementary information as part of a comprehensive individual assessment. When low Digit Symbol scores are produced by slowing on Symbol Copy, further evaluation of perceptual and motor speed and dexterity are indicated. When low incidental learning scores are obtained, further evaluation of memory is warranted. Qualitative analysis of errors (e.g., rotations) made on the incidental learning procedures may also be valuable. (JINS, 2000, 6, 770–780.)