The Israel Survey of Mental Health among Adolescents: prevalence of attention-deficit/hyperactivity disorder, comorbidity, methylphenidate use, and help-seeking patterns.

BACKGROUND: The prevalence of ADHD is controversial, with many feeling that this disorder is over- or under-diagnosed. OBJECTIVES: To study the prevalence of attention-deficit/hyperactivity disorder (ADHD) and its association with sociodemographic characteristics, comorbid mental disorders, medical services, and methylphenidate use in the Israeli adolescent population. METHODS: The Israel Survey of Mental Health among Adolescents was conducted in a representative national sample of 14-17 year olds and their mothers. The Development and Well-Being Assessment was administered to identify DSM-IV diagnoses of ADHD and comorbid mental and learning disorders, and the results were verified by senior child psychiatrists. Respondents were also asked about their use of medical services and psychotropic drug intake in the past 12 months. RESULTS: Three percent of the adolescents met the DSM-IV criteria for ADHD. ADHD was significantly associated with gender (higher prevalence in boys than girls), ethnicity (higher prevalence in Jews than Arabs/Druze), referral to a medical professional, and maternal help-seeking for the emotional or behavioral problems of the adolescent. Medication was prescribed to 2.9% of adolescents: 34.6% with a diagnosis of ADHD had not been prescribed methylphenidate in the past year, and 34.6% of the medicated subjects did not have a diagnosis of ADHD. None of the Arab/Druze adolescents was receiving stimulants compared to 3.7% of the Jewish adolescents. CONCLUSIONS: Despite advances in public awareness of mental disorders in youth, a substantial proportion of older Israeli adolescents, especially from minority groups, are under-diagnosed or untreated. At the same time, many, especially from the Jewish majority, are over-diagnosed and potentially over-treated. Ethnic disparities in rates of mental health care highlight the urgent need to identify and overcome barriers to the recognition and treatment of these conditions.

Response inhibition in preschoolers at familial risk for attention deficit hyperactivity disorder: a behavioral and electrophysiological stop-signal study.

Children participating in the Ben-Gurion Infant Development Study were assessed with a dynamic-tracking version of the stop-signal task at the age of 5 years. The sample consisted of 60 males. Stop-signal reaction time (SSRT) was correlated with concurrent ratings of the child's attention deficit hyperactivity disorder (ADHD) symptoms. Paternal symptoms measured in the child's early infancy predicted the child's performance in the stop-signal task: Paternal inattentiveness predicted SSRT, whereas hyperactivity predicted error proportion. Maternal symptoms were not correlated with the performance of the child in the task. A subsample of children, who were tested while electrophysiological brain activity was measured, showed that having higher ADHD symptomatology, especially hyperactivity, correlated with less activity in the brain areas that are usually recruited by children for successful inhibition.

Increased neural variability in adolescents with ADHD symptomatology: Evidence from a single-trial EEG study.

Increased intrasubject variability of reaction time (RT) refers to inconsistency in an individual's speed of responding to a task. This increased variability has been suggested as a fundamental feature of attention deficit hyperactivity disorder (ADHD), however, its neural sources are still unclear. In this study, we aimed to examine whether such inconsistency at the behavioral level would be accompanied by inconsistency at the neural level; and whether different types of neural and behavioral variability would be related to ADHD symptomatology. We recorded electroencephalogram (EEG) data from 62 adolescents, who were part of a prospective longitudinal study on the development of ADHD. We examined trial-by-trial neural variability in response to visual stimuli in two cognitive tasks. Adolescents with high ADHD symptomatology exhibited an increased neural variability before the presentation of the stimulus, but when presented with a visual stimulus, this variability decreased to a level that was similar to that exhibited by participants with low ADHD symptomatology. In contrast with our prediction, neural variability was unrelated to the magnitude of behavioral variability. Our findings suggest that adolescents with higher symptoms are characterized by increased neural variability before the stimulation, which might reflect a difficulty in alertness to the forthcoming stimulus; but this increased neural variability does not seem to account for their RT variability.

Neurocognitive functioning in adult and adolescent offspring of parents with schizophrenia.

INTRODUCTION: Neurocognitive deficits have been proposed as endophenotypes for schizophrenia. Although neurocognitive functioning has been studied extensively in first-degree relatives of schizophrenia patients at single time points, little is known about the change or continuity in deficits across development. METHOD: The longitudinal sample was composed of 86 nonpsychotic participants who had a parent with schizophrenia (n = 28), a parent with a nonschizophrenia mental disorder (n = 31) or parents without mental illness (n = 27). Executive functioning (EF) was assessed during adolescence (M = 18 years) and adulthood (M = 32 years); attention and memory were assessed at adulthood. RESULTS: The schizophrenia group, as adults, showed deficits in attention and memory relative to the no mental illness group. Only on one memory task did the schizophrenia group perform more poorly than the other mental illness group. Executive functioning improved with age for all three groups on Wisconsin Card Sorting Test perseverative errors; the rate of improvement was significantly slower for the schizophrenia and the other mental illness groups, compared to the no mental illness group. Stability in EF functioning over the 16-year period, measured by intraclass correlations, was low. CONCLUSIONS: Adults at familial risk for schizophrenia showed deficits in neurocognitive functioning. The similarity of performance between those whose parents had schizophrenia and those whose parents had other mental illness, in all but the measures of memory, raises the question as to whether the neurocognitive functions examined are endophenotypes of vulnerability to schizophrenia specifically. Modest stability of EF and improved performance with age may reflect cortical maturation during early adulthood.

"My Brain Can Stop": An ERP Study of Longitudinal Prediction of Inhibitory Control in Adolescence.

We examined the longitudinal predictors of electrophysiological and behavioral markers of inhibitory control in adolescence. Participants were 63 adolescent boys who have been followed since birth as part of a prospective longitudinal study on the developmental pathways to attention-deficit hyperactivity disorder (ADHD). At 17 years of age, they completed the stop-signal task (SST) while electroencephalography (EEG) was continuously recorded. Inhibitory control was evaluated by the stop-signal reaction time (SSRT) as well as by the amplitude of the event-related potential (ERP) component of N2 during successful inhibition. We found that higher inattention symptoms throughout childhood predicted reduced amplitude (i.e., less negative) of the N2 in adolescence. Furthermore, the N2 amplitude was longitudinally predicted by the early precursors of child familial risk for ADHD and early childhood temperament. Specifically, father's inattention symptoms (measured in the child's early infancy) and child's effortful control at 36 months of age directly predicted the N2 amplitude in adolescence, even beyond the consistency of inattention symptoms throughout development. The SSRT was predicted by ADHD symptoms throughout childhood but not by the early precursors. Our findings emphasize the relevance of early familial and temperamental risk for ADHD to the prediction of a later dysfunction in inhibitory control.

Sleep patterns of 7-week-old infants at familial risk for attention deficit hyperactivity disorder.

Sleep patterns of 26 seven-week-old boys at familial risk for attention deficit hyperactivity disorder (ADHD) and 18 control infants were compared by objective (actigraph) and subjective (maternal sleep diary) measures, over five consecutive 24-hr periods. Actigraph findings indicated that the groups differed on stability (SD) of quiet sleep only during the day. Reports in maternal sleep diaries indicated that they also differed on stability of waking and stability of sleep duration, again only during the day. No group differences were found in terms of average scores, whether calculated for the entire 24-hr periods, for nights, or for days. Mothers in the risk group reported that fathers were less involved in infant care than did those in the control group. These findings suggest that as early as 7 weeks of age, infants at risk for ADHD differ from controls only on stability of their sleep patterns during the day, when environmental regulatory factors are more intensive.

Parenting of 7-month-old infants at familial risk for attention deficit/hyperactivity disorder.

Patterns of interaction between parents and 7-month-old boys at familial risk for attention deficit/hyperactivity disorder (ADHD) and a comparison group were studied during a warm-up and two play episodes. The sample included 78 (47 at-risk, 31 comparison) mother-child and 45 (27 at-risk, 18 comparison) father-child dyads. A coding system developed by G. Kochanska (1997, 1998) was used. Infants in the risk group did not differ from the comparison group in the rate of emission of infant-related events. However, they received less adequate responsivity from both their fathers and their mothers to these events, and specifically to negative emotions or distress, than did the comparison group. Maternal psychopathology did not account for these findings. Mothers were more adequately responsive than were fathers, especially for physiological needs. The association between nonoptimal interaction in infancy and the development of ADHD is discussed.

Neurodevelopmental factors associated with schizotypal symptoms among adolescents at risk for schizophrenia.

Schizophrenia has come to be viewed as a neurodevelopmental disorder that is characterized by genetic vulnerability, stressors during the prenatal period that may be marked by minor physical anomalies and neurobehavioral deficits that emerge in early development. Less is known about the neurodevelopmental origins of schizotypal personality symptoms. The present study examines schizotypal symptoms in Israeli adolescents (mean age = 16.79 years) who have not yet reached the developmental period during which first schizophrenic episode is most likely to emerge: 39 adolescent offspring of parents with schizophrenia, 39 offspring of parents with other psychiatric disorders, and 36 offspring of parents with no history of mental illness. The Semi-Structured Kiddie Interview for Personality Syndromes was used to assess cognitive-perceptual, interpersonal, and disorganized schizotypal symptoms. Interpersonal schizotypal symptoms were more prevalent in the schizophrenia offspring group than in the no-mental-illness offspring group. Among the schizophrenia offspring group, interpersonal, but not cognitive-perceptual, schizotypal symptoms were associated with minor physical anomalies, fine motor dyscoordination, and deficits in executive functioning during adolescence. Among young people whose parents did not have schizophrenia, cognitive-perceptual schizotypal symptoms were correlated with deficits in executive functioning. Adolescent schizotypal symptoms were associated with neurobehavioral symptoms measured during middle childhood in a subgroup of the sample that had been assessed prospectively. Finally, young people who had genetic risk for schizophrenia, minor physical anomalies, and neurobehavioral signs together were at markedly increased risk for symptoms of interpersonal schizotypal symptoms, compared to young people with one or none of these risk factors.

Emotional and behavioral characteristics over a six-year period in youths with persistent and nonpersistent dyscalculia.

The authors examined behavior problems in a matched sample of 58 youths with persistent dyscalculia (PD) and nonpersistent dyscalculia (NPD). Participants were classified as having dyscalculia at age 10-11 years. Parents completed the Child Behavior Checklist for their children at ages 10-11, 13-14, and 16-17 years, while the youths did so at the last two age periods. Only at age 16-17 years were there significantly more problems, particularly attention problems and externalizing problems, reported by parents for PD youths compared to NPD youths. A higher percentage in the PD group than in the NPD group received scores in the clinical range for externalizing problems. However, the mean levels of behavior problems at this age and the earlier ages were within the normal range for both groups. For youth-reported problems, the only significant difference was for attention problems at 16-17 years. Therapeutic interventions should focus on the academic domain and improving and altering behavioral patterns.

Predicting ADHD Symptoms in Adolescence from Early Childhood Temperament Traits.

Extreme levels of certain temperament traits can be early markers of different developmental pathways of attention-deficit/hyperactivity disorder (ADHD). However, the long-term utility of using these traits as predictors of ADHD is not fully known. This study includes 64 male adolescents (M age = 13.5), who have been followed since birth as part of a longitudinal study. The primary aim was to test effortful control (EC), activity level, and anger, measured in early childhood - both with mother's reports and laboratory assessments -as predictors of ADHD symptoms in adolescence. Further, we investigated the specificity of this prediction to the different ADHD symptom domains. The results demonstrated that early temperament dimensions of EC and activity level were predictive of ADHD symptoms about 10 years later, when the participants reached adolescence. Moreover, activity level showed specificity only to hyperactivity-impulsivity symptoms whereas EC was a predictor of the two symptom domains. Anger had a predictive correlation with ADHD symptoms; however, it did not have a unique predictive contribution. These results emphasize the relevance of EC and activity level in the developmental course of ADHD. Identification of early risk factors can lead to more efficient design and implementation of intervention programs.

The Contribution of Maternal ADHD Symptomatology, Maternal DAT1, and Home Atmosphere to Child ADHD Symptomatology at 7 Years of Age.

Children of mothers with attention-deficit/hyperactivity disorder (ADHD) have an increased genetic and environmental risk for ADHD. The unique and interactive contributions of a maternal dopamine receptor gene (DAT1), maternal ADHD symptoms (hyperactive- impulsive, inattentive), and home atmosphere to the prediction of ADHD symptoms (hyperactive- impulsive, inattentive) in 7- year-old boys (N = 96) were examined using data from a longitudinal study of familial risk for ADHD. During the first 6 months of the study, mothers and their spouses completed a questionnaire about the mother's ADHD symptoms. Home atmosphere questionnaire data were collected 4 years later. At the 7-year assessment, mothers reported on their child's ADHD symptoms. Negative home atmosphere was significantly associated with child hyperactive-impulsive and inattentive symptoms. Maternal inattentive symptoms were significantly correlated with both child symptom dimensions. Regression models, with child genotype and maternal education controlled, showed main effects for maternal inattentive symptoms, maternal DAT1 10/10 genotype, and home atmosphere in the prediction of child inattentive symptoms. Only home atmosphere predicted child hyperactive-impulsive symptoms. There was a significant home atmosphere x maternal hyperactive-impulsive symptoms interaction in the prediction of child hyperactive-impulsive symptoms. Boys with higher levels of symptoms came from homes characterized by higher levels of negative atmosphere and had mothers with higher levels of hyperactive-impulsive symptoms. There was also a trend (p = 0.075) for a maternal DAT1 x home atmosphere interaction. Boys with higher levels of inattentive symptoms came from homes with higher levels of negative atmosphere and had mothers with the homozygous 10/10 genotype. The maternal heterozygous 9/10 genotype did not predict child symptoms.

Response variability in Attention-Deficit/Hyperactivity Disorder: a neuronal and glial energetics hypothesis.

BACKGROUND: Current concepts of Attention-Deficit/Hyperactivity Disorder (ADHD) emphasize the role of higher-order cognitive functions and reinforcement processes attributed to structural and biochemical anomalies in cortical and limbic neural networks innervated by the monoamines, dopamine, noradrenaline and serotonin. However, these explanations do not account for the ubiquitous findings in ADHD of intra-individual performance variability, particularly on tasks that require continual responses to rapid, externally-paced stimuli. Nor do they consider attention as a temporal process dependent upon a continuous energy supply for efficient and consistent function. A consideration of this feature of intra-individual response variability, which is not unique to ADHD but is also found in other disorders, leads to a new perspective on the causes and potential remedies of specific aspects of ADHD. THE HYPOTHESIS: We propose that in ADHD, astrocyte function is insufficient, particularly in terms of its formation and supply of lactate. This insufficiency has implications both for performance and development: H1) In rapidly firing neurons there is deficient ATP production, slow restoration of ionic gradients across neuronal membranes and delayed neuronal firing; H2) In oligodendrocytes insufficient lactate supply impairs fatty acid synthesis and myelination of axons during development. These effects occur over vastly different time scales: those due to deficient ATP (H1) occur over milliseconds, whereas those due to deficient myelination (H2) occur over months and years. Collectively the neural outcomes of impaired astrocytic release of lactate manifest behaviourally as inefficient and inconsistent performance (variable response times across the lifespan, especially during activities that require sustained speeded responses and complex information processing). TESTING THE HYPOTHESIS: Multi-level and multi-method approaches are required. These include: 1) Use of dynamic strategies to evaluate cognitive performance under conditions that vary in duration, complexity, speed, and reinforcement; 2) Use of sensitive neuroimaging techniques such as diffusion tensor imaging, magnetic resonance spectroscopy, electroencephalography or magnetoencephalopathy to quantify developmental changes in myelination in ADHD as a potential basis for the delayed maturation of brain function and coordination, and 3) Investigation of the prevalence of genetic markers for factors that regulate energy metabolism (lactate, glutamate, glucose transporters, glycogen synthase, glycogen phosphorylase, glycolytic enzymes), release of glutamate from synaptic terminals and glutamate-stimulated lactate production (SNAP25, glutamate receptors, adenosine receptors, neurexins, intracellular Ca2+), as well as astrocyte function (alpha1, alpha2 and beta-adrenoceptors, dopamine D1 receptors) and myelin synthesis (lactate transporter, Lingo-1, Quaking homolog, leukemia inhibitory factor, and Transferrin). IMPLICATIONS OF THE HYPOTHESIS: The hypothesis extends existing theories of ADHD by proposing a physiological basis for specific aspects of the ADHD phenotype - namely frequent, transient and impairing fluctuations in functioning, particularly during performance of speeded, effortful tasks. The immediate effects of deficient ATP production and slow restoration of ionic gradients across membranes of rapidly firing neurons have implications for daily functioning: For individuals with ADHD, performance efficacy would be enhanced if repetitive and lengthy effortful tasks were segmented to reduce concurrent demands for speed and accuracy of response (introduction of breaks into lengthy/effortful activities such as examinations, motorway driving, assembly-line production). Also, variations in task or modality and the use of self- rather than system-paced schedules would be helpful. This would enable energetic demands to be distributed to alternate neural resources, and energy reserves to be re-established. Longer-term effects may manifest as reduction in regional brain volumes since brain areas with the highest energy demand will be most affected by a restricted energy supply and may be reduced in size. Novel forms of therapeutic agent and delivery system could be based on factors that regulate energy production and myelin synthesis. Since the phenomena and our proposed basis for it are not unique to ADHD but also manifests in other disorders, the implications of our hypotheses may be relevant to understanding and remediating these other conditions as well.

Development from birth to adolescence of children at-risk for schizophrenia.

OBJECTIVE: Offspring of patients with schizophrenia are at-risk for developing schizophrenia in adult life. The aim of this paper is to describe the development from infancy through adolescence of a sample of Israeli young people at-risk for schizophrenia. METHODS: The Jerusalem Infant Development Study (JIDS) has followed prospectively from birth through adolescence 15 young people who have a parent with schizophrenia. Neurobehavioral data were gathered at infancy, middle childhood, and adolescence. Mental disorder was assessed at adolescence. RESULTS: Data suggest that some children whose parents have schizophrenia are at increased risk for a variety of neuromotor, cognitive, and attentional problems during infancy and childhood, compared to children whose parents had no mental disorder or nonschizophrenia mental disorder. Those high-risk children with neurobehavioral signs are also more likely to have poorer social adjustment, greater social withdrawal, and more symptoms within the schizophrenia spectrum. Case studies are presented of two children with early neurobehavioral impairment who, as adolescents, developed disorders within the schizophrenia spectrum. CONCLUSION: Because neurobehavioral impairment may be marking genetic vulnerability to schizophrenia spectrum disorders, clinicians treating children whose parents have schizophrenia need to thoroughly evaluate symptoms of mental disorder--but also neuromotor and neuropsychological functioning.

Offspring of parents with schizophrenia: mental disorders during childhood and adolescence.

Although offspring of parents with schizophrenia are at risk for schizophrenic illness as adults, little is known about their pattern of symptoms as children and adolescents. Lifetime Axis I and II DSM-III-R diagnoses were made for 116 young people (ages 12-22). Forty-one subjects had a parent with schizophrenia, 39 had a parent with a nonschizophrenic mental disorder, and 36 had parents with no mental illness. Schizophrenia spectrum disorders occurred at higher rates among young people with a parent with schizophrenia (17.1%) than in other young people (5.3%), even after controlling for mental disorder in the nonproband parent. Schizophrenia and schizotypal personality disorder occurred exclusively in offspring of parents with schizophrenia. Offspring of parents with schizophrenia were also at increased risk for avoidant personality disorder but not paranoid personality disorder. Although lifetime anxiety disorders were common in all young people regardless of parent diagnosis, current anxiety disorders were more prevalent for the adolescent offspring of parents with schizophrenia. These data strongly suggest familial vulnerability to schizophrenia spectrum disorder that is observable before adulthood, particularly for males.

Speed of performance of children with developmental right hemisphere syndrome and with attention-deficit hyperactivity disorder.

Slowness is a common complaint in children with attention-deficit hyperactivity disorder (ADHD) and with developmental right hemisphere syndrome. However, it was our clinical impression that slowness in developmental right hemisphere syndrome was more prominent than in ADHD. Our objective was to assess slowness as operationalized by speed of performance in children with developmental right hemisphere syndrome, children with ADHD, and controls. The research sample comprised 19 children in each group, matched for age, gender, socioeconomic status, IQ, and handedness. The subjects were administered a reaction time battery assessing speed of performance. Overall, the average performance differed among the three study groups (F(2,53) = 2.40, P < .01). Children with developmental right hemisphere syndrome were slower than their peers with ADHD (t(35) = 1.99, P < .05) and slower than controls (t(35) = 4.55, P < .001). Children with ADHD performed more slowly than controls, although for the majority of tasks, this was nonsignificant. We conclude that slowness is an integral and consistent component of developmental right hemisphere syndrome and cannot be attributed only to the ADHD symptomatology.

Prediction of preschool aggression from DRD4 risk, parental ADHD symptoms, and home chaos.

This study investigated the influence of a child's DRD4 risk, parental levels of ADHD symptoms, and the interactive influence of these factors on the development of preschool aggression. Additionally, the study investigated the role of home chaos as a mediator between parental ADHD symptoms and child aggression. The sample consisted of 84 4.5-year-old children and their parents. Children were genotyped for the DRD4 polymorphism. ADHD symptoms were self-reported by parents when the child was 2 to 6 months old. Parental reports of home chaos and the child's aggression were collected 4 years later. Child's DRD4 risk and parental ADHD symptoms significantly contributed to the prediction of preschool aggression. However, contrary to our hypotheses, no interactions were found between the child's DRD4 risk and the levels of parental ADHD symptoms. Home chaos played a mediating role in the relation between paternal ADHD symptoms and the child's aggression. The relation between maternal ADHD symptoms and the child's aggression was not significantly mediated through the level of home chaos. The current study emphasizes the importance of longitudinally investigating the contribution of parental ADHD symptoms to child aggression, while also exploring the differential contribution of maternal/paternal inattention and hyperactivity-impulsivity symptoms. Moreover, home chaos was found to be a significant environmental mechanism through which paternal ADHD symptoms affect children's aggression in the preschool years.

Dopamine risk and paternal ADHD symptomatology associated with ADHD symptoms in four and a half-year-old boys.

OBJECTIVE: This study examined the influence of allelic variation in two dopamine genes, the dopamine receptor D4 (DRD4) gene and the dopamine transporter D1 (DAT1) gene, and paternal attention-deficit hyperactivity disorder (ADHD) symptomatology on the level of ADHD symptoms in 96 four and a half-year-old boys. METHOD: DNA was collected by means of a buccal swab and genotyped for DRD4 and DAT1. Mothers completed the Dupaul ADHD checklist on their sons. ADHD symptomatology ratings for fathers were based on a summed father self-reported and spouse-reported symptoms (Conners Adult ADHD Rating Scale). RESULTS: There were main effects for DAT1 and father symptomatology for the child Total ADHD and Hyperactivity-Impulsivity scores. The main effects for DRD4 were limited to the child Hyperactivity-Impulsivity scores. Child Inattentive scores were influenced only by father symptomatology. Interaction effects between DAT1 and DRD4 and between DAT1 and the father ADHD risk group were found for child Hyperactivity-Impulsivity scores. Boys with the highest level of symptomatology were those with the 10/10 DAT1 genotype and the DRD4-7 genotype or fathers with high symptomatology. CONCLUSION: The findings of this study indicate that the risk for ADHD, particularly hyperactivity-impulsivity, is exacerbated in the presence of dopamine risk genes and paternal ADHD symptomatology. This study adds to the growing literature on the efficacy of including multiple genetic and environmental risk factors in studies related to the development of psychopathology.

Parenting of 7-month-old infants at familial risk for ADHD during infant's free play, with restrictions on interaction.

Patterns of interaction of 34 mothers and fathers with their 7-month-old boys at familial risk for ADHD and 25 comparison families were studied during infant play with blocks. The parents were instructed to refrain from intervening as much as possible. Infants in the risk group did not differ from those in the comparison group in frequency of needing help or involving parents in play. Nonetheless, they received adequate responsivity from their mothers less often than infants in the comparison group. Mothers in the risk group were also more likely not to respond to these needs at all. Mothers in the comparison group were more physically intrusive. No group difference was found for maternal rebuilding of the infant's play. No group differences were found for any of father's behaviors. However, fathers in both groups rebuilt their infant's play more frequently than mothers, infants looked at them more often, and a larger number of infants involved the father in their play.

Emerging developmental pathways to ADHD: possible path markers in early infancy.

Sixty-six male infants participating in the Ben-Gurion Infant Development Study of familial risk for attention deficit hyperactivity disorder (ADHD) were assessed at 7 months of age using observational and mother report measures. Risk for ADHD was based on ADHD symptoms in the father. Infants whose fathers had seven or more symptoms formed the ADHD risk group; infants whose fathers had three or less symptoms formed the comparison group. The ADHD risk group significantly differed from the comparison group on measures of interest, anger, and activity level and showed less interest in block play and more anger reactivity but less directed anger in a barrier task. According to mother report, the ADHD risk group had higher levels of activity than the comparison group. Measures of neonatal immaturity and activity were related to behavior at 7 months. The findings suggest that possible developmental pathways to ADHD may be emerging in early infancy.