H. Hill Goldsmith

Gaze fixation and the neural circuitry of face processing in autism

Diminished gaze fixation is one of the core features of autism and has been proposed to be associated with abnormalities in the neural circuitry of affect. We tested this hypothesis in two separate studies using eye tracking while measuring functional brain activity during facial discrimination tasks in individuals with autism and in typically developing individuals. Activation in the fusiform gyrus and amygdala was strongly and positively correlated with the time spent fixating the eyes in the autistic group in both studies, suggesting that diminished gaze fixation may account for the fusiform hypoactivation to faces commonly reported in autism. In addition, variation in eye fixation within autistic individuals was strongly and positively associated with amygdala activation across both studies, suggesting a heightened emotional response associated with gaze fixation in autism.

Development and natural history of mood disorders

To expand and accelerate research on mood disorders, the National Institute of Mental Health (NIMH) developed a project to formulate a strategic research plan for mood disorder research. One of the areas selected for review concerns the development and natural history of these disorders. The NIMH convened a multidisciplinary Workgroup of scientists to review the field and the NIMH portfolio and to generate specific recommendations. To encourage a balanced and creative set of proposals, experts were included within and outside this area of research, as well as public stakeholders. The Workgroup identified the need for expanded knowledge of mood disorders in children and adolescents, noting important gaps in understanding the onset, course, and recurrence of early-onset unipolar and bipolar disorder. Recommendations included the need for a multidisciplinary research initiative on the pathogenesis of unipolar depression encompassing genetic and environmental risk and protective factors. Specifically, we encourage the NIMH to convene a panel of experts and advocates to review the findings concerning children at high risk for unipolar depression. Joint analyses of existing data sets should examine specific risk factors to refine models of pathogenesis in preparation for the next era of multidisciplinary research. Other priority areas include the need to assess the long-term impact of successful treatment of juvenile depression and known precursors of depression, in particular, childhood anxiety disorders. Expanded knowledge of pediatric-onset bipolar disorder was identified as a particularly pressing issue because of the severity of the disorder, the controversies surrounding its diagnosis and treatment, and the possibility that widespread use of psychotropic medications in vulnerable children may precipitate the condition. The Workgroup recommends that the NIMH establish a collaborative multisite multidisciplinary Network of Research Programs on Pediatric-Onset Bipolar Disorder to achieve a better understanding of its causes, course, treatment, and prevention. The NIMH should develop a capacity-building plan to ensure the availability of trained investigators in the child and adolescent field. Mood disorders are among the most prevalent, recurrent, and disabling of all illnesses. They are often disorders of early onset. Although the NIMH has made important strides in mood disorders research, more data, beginning with at-risk infants, children, and adolescents, are needed concerning the etiology and developmental course of these disorders. A diverse program of multidisciplinary research is recommended to reduce the burden on children and families affected with these conditions.

Temperament and attention deficit hyperactivity disorder: the development of a multiple pathway model.

This article outlines the parallels between major theories of attention deficit hyperactivity disorder (ADHD) and relevant temperament domains, summarizing recent research from our laboratories on (a) child temperament and (b) adult personality traits related to ADHD symptoms. These data are convergent in suggesting a role of effortful control and regulation in the core symptoms of ADHD. Negative approach and anger is also associated with ADHD, but this may be due to the overlap of ADHD and antisocial behavior. Positive approach may be involved in an alternate pathway to ADHD. The involvement of effortful control is congruent with experimental findings of executive functioning deficits in children with ADHD. We hypothesize that, whereas regulation problems may occur in most children with ADHD, a subgroup also may be characterized by positive approach problems and another subgroup by negative approach problems. We conclude with a theorized multiple process developmental model outlining alternate pathways to ADHD that warrant empirical investigation to better resolve etiological heterogeneity in ADHD.

Toward a Theory of Infant Temperament

Why do we have a chapter on temperament in a volume primarily devoted to the concepts of attachment and affiliation? Years ago, such a chapter would have been unthinkable because attachment and temperament appeared to refer to different phenomena. Classic theories of mother-infant relations such as those of Spitz (1965) and Bowlby (1951) leaned in the direction of a “tabula rasa” model of the human infant by proposing that emotional and drive-regulating experiences provided by the mother were crucial for the formation and maintenance of ego functions. The individual differences these theorists were interested in were those resulting from successes and failures of maternal interaction, although on occasion they did invoke genetic and constitutional factors to account for unusual tolerances or susceptibilities to the ill effects of maternal separation. Individual differences in temperament, then, were relegated to a shorthand description of the susceptibility of the “tabula rasa” to experience—how hard or soft the tablet was, so to speak. Little speculation took place about how such differences in the infant could be assessed or whether they played a role in attachment.

Contemporary Instruments for Assessing Early Temperament by Questionnaire and in the Laboratory

Research in behavioral science often succeeds or fails depending on the quality of its assessment instruments. Recognizing this, many temperament researchers have proposed questionnaires, interview schedules, home observation coding systems, and laboratory methods for assessing early temperament. These assessment instruments have been reviewed and evaluated from several perspectives (e. g., Bornstein, Gaughran, & Homel, 1986; Crockenberg & Acredolo, 1983; Goldsmith & Rieser-Danner, 1990; Hubert, Wachs, Peters-Martin, & Gandour, 1982; Neale & Stevenson, 1989; Rothbart & Goldsmith, 1985; Seifer & Sameroff, 1986; Slabach, Morrow, & Wachs, this volume). In this chapter, we preview some new instruments and review recent data on an established questionnaire, all developed in our laboratories. These instruments include the Infant Behavior Questionnaire, the Toddler Behavior Assessment Questionnaire, and the Children’s Behavior Questionnaire, as well as a battery of laboratory temperament assessment techniques.

Right Frontal Brain Activity, Cortisol, and Withdrawal Behavior in 6-Month-Old Infants

Although several studies have examined anterior asymmetric brain electrical activity and cortisol in infants, children, and adults, the direct association between asymmetry and cortisol has not systematically been reported. In nonhuman primates, greater relative right anterior activation has been associated with higher cortisol levels. The current study examines the relation between frontal electroencephalographic (EEG) asymmetry and cortisol (basal and reactive) and withdrawal-related behaviors (fear and sadness) in 6-month-old infants. As predicted, the authors found that higher basal and reactive cortisol levels were associated with extreme right EEG asymmetry. EEG during the withdrawal-negative affect task was associated with fear and sadness behaviors. Results are interpreted in the context of the previous primate work, and some putative mechanisms are discussed.

Three Reasons Not to Believe in an Autism Epidemic

According to some lay groups, the nation is experiencing an autism epidemic—a rapid escalation in the prevalence of autism for unknown reasons. However, no sound scientific evidence indicates that the increasing number of diagnosed cases of autism arises from anything other than purposely broadened diagnostic criteria, coupled with deliberately greater public awareness and intentionally improved case finding. Why is the public perception so disconnected from the scientific evidence? In this article we review three primary sources of misunderstanding: lack of awareness about the changing diagnostic criteria, uncritical acceptance of a conclusion illogically drawn in a California-based study, and inattention to a crucial feature of the “child count” data reported annually by the U.S. Department of Education.

Developmental Models of Infant and Childhood Temperament.

The developmental courses of specific temperamental constructs were explored by using structural equation model fitting. Maternal ratings were obtained from either 2 or 3 different temperament questionnaires for 180 children at 3, 6, 12, 18, 24, 36, and 48 months of age. Several formal structural models were fit in infancy (3-18 months), in the toddler-preschooler period (24-48 months), and across all measurement occasions. In infancy, the autoregressive simplex model fit well for all 4 composites considered: Positive Emotionality, Distress-Anger, Fear, and Activity Level. In contrast to the considerable change in temperament during infancy, temperament appears to be very stable from 24 to 48 months of age, and a common factor model fits well with these data. Across all measurement occasions, models that allowed for stability in temperament to be at least partially mediated through intermediate forms of the trait fit best.

Linking temperamental fearfulness and anxiety symptoms: a behavior–genetic perspective

Research on mood and anxiety disorders has historically proceeded without sufficient reference to the growing body of work on the nature of typical emotional development and temperament. Reviewing data from several studies, we consider experiential, biological, and genetic factors as providing causal input to typical developmental variation in fearfulness and anxiety during infancy and early childhood. Longitudinal behavioral methods, psychophysiologic measures, and a behavior-genetic framework are used to approach these issues. Results from twin studies implicate moderately strong genetic influences on different facets of temperamental fearfulness, as well as childhood anxiety symptoms. Then, we consider the distinction between normal range temperament and overt anxiety symptoms from a quantitative genetic perspective. Biological correlates (cortisol, asymmetric frontal EEG activation, cardiac reactivity) of inhibited behavior are considered as related endophenotypes for anxiety. In a nongenetic analysis, we report the prediction of internalizing problems during kindergarten from earlier temperament and earlier basal cortisol measures. Our review highlights connections between behavioral indicators and various putative endophenotypes and the fuzzy boundary between normal-range temperament and anxiety disorders.

Early Risk Factors and Developmental Pathways to Chronic High Inhibition and Social Anxiety Disorder in Adolescence

OBJECTIVE Evidence suggests that chronic high levels of behavioral inhibition are a precursor of social anxiety disorder. The authors sought to identify early risk factors for, and developmental pathways to, chronic high inhibition among school-age children and the association of chronic high inhibition with social anxiety disorder by adolescence. METHOD A community sample of 238 children was followed from birth to grade 9. Mothers, teachers, and children reported on the childrens behavioral inhibition from grades 1 to 9. Lifetime history of psychiatric disorders was available for the subset of 60 (25%) children who participated in an intensive laboratory assessment at grade 9. Four early risk factors were assessed: female gender; exposure to maternal stress during infancy and the preschool period; and at age 4.5 years, early manifestation of behavioral inhibition and elevated afternoon salivary cortisol levels. RESULTS All four risk factors predicted greater and more chronic inhibition from grades 1 to 9, and together they defined two developmental pathways. The first pathway, in girls, was partially mediated by early evidence of behavioral inhibition and elevated cortisol levels at age 4.5 years. The second pathway began with exposure to early maternal stress and was also partially mediated by childhood cortisol levels. By grade 9, chronic high inhibition was associated with a lifetime history of social anxiety disorder. CONCLUSIONS Chronic high levels of behavioral inhibition are associated with social anxiety disorder by adolescence. The identification of two developmental pathways suggests the potential importance of considering both sets of risk factors in developing preventive interventions for social anxiety disorder.