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In the past decades, there has been an overemphasis of a descriptive/behavioral approach to study conduct disorder. In an equifinal perspective, we aimed to examine the developmental multitrajectory groups of psychological features (irritability, interpersonal callousness, hyperactivity/impulsivity, and depressive–anxiety symptoms) and their associations with conduct problems. In a population-based cohort (n = 1,309 participants followed from 5 months to 17 years old), latent-class growth analysis was performed for each psychological feature to identify a two-trajectory model (from ages 6 to 12 years). Based on parameter estimates of the two-trajectory models for each of the four psychological features, a parallel process growth mixture model identified eight significant developmental patterns that were subsequently compared with typically developing children. Furthermore, we observed that while interpersonal callousness conferred an increased risk for childhood and adolescence conduct problems, its co-occurrence with hyperactivity/impulsivity, irritability, and/or depressive–anxiety symptoms heightened the general risk, but also predicted distinct subtypes of conduct problems (i.e., aggressive and rule-breaking behaviors). Thus, by studying complex developmental combinations of psychological features, we observed qualitatively distinct pathways towards conduct problems. A multitrajectory framework of psychological features should be considered as a significant step towards unveiling the multiple etiological pathways leading to conduct disorder and its substantial clinical heterogeneity.
Symptoms of attention deficit hyperactivity disorder (ADHD) and trait impulsivity have been associated with disordered eating but are seldom assessed in community studies, or longitudinally and little is known about the mediating mechanisms.
We tested associations between ADHD symptoms and disordered eating cross-sectionally and between trait impulsivity and disordered eating longitudinally. We utilised data from a normative cohort of young adults (642 participants: 65% female, Mage = 23 years). Participants were classified as high risk or low risk for disordered eating using the SCOFF instrument. In the first two steps of both cross-sectional and longitudinal hierarchical logistic regression models, demographics and covariates were entered. For the cross-sectional regression, Adult ADHD self-report scale (ASRS) scores, separated into inattentive and hyperactive/impulsive symptoms, were entered in the third step. In a separate longitudinal model, Barratt impulsivity scale subscales (attentional, motor and non-planning impulsivity) were entered in the third step. Depression, as assessed by the moods and feelings questionnaire (MFQ), was examined as a mediator.
Cross-sectionally, sex, MFQ score and inattentive symptoms predicted disordered eating risk (model R2 = 20%). Longitudinally, sex, MFQ score and attentional impulsivity predicted disordered eating risk (model R2 = 16%). The relationship between inattentive symptoms and the disordered eating risk was partially mediated by MFQ score, whereas the relationship between attentional impulsivity and the disordered eating risk was fully mediated by MFQ scores.
These data highlight (1) a specific role for inattentive symptoms of ADHD and (2) the importance of both depression and impulsivity in predicting eating disorder risk.
A growing body of evidence suggests that child aggression is likely to be driven by multiple developmental pathways. However, little is known about the complex interactions between developmental trajectories of child psychological factors (such as anxiety, irritability, and hyperactivity/impulsivity dimensions) and their associations with aggression from childhood to adolescence. Therefore, the current study aimed to identify clusters of individuals with different developmental multi-trajectory, investigate their early risk factors, and describe their longitudinal associations with physical aggression.
The sample comprised 4898 children derived from the Fragile Families and Child Wellbeing Study. A parallel process growth mixture model was used to identify developmental multi-trajectory groups at 5, 9 and 15 years old. Associations between multi-trajectory group membership and physical aggression were examined with Generalized Estimating Equations models. Finally, multinomial logistic regression was performed to assess perinatal and early risk factors for multi-trajectory groups.
Multi-trajectory groups differed in the magnitude of risk for exhibiting physical aggression, compared to typically developing children. The risk for physical aggression was the most prominent in children who were hyperactive/impulsive and irritable [odds ratio (OR) 6.47; 95% confidence interval (CI) 5.44–7.70] and hyperactive/impulsive, irritable, and anxious (OR 7.68; CI 6.62–8.91). Furthermore, maternal cigarette and alcohol use during pregnancy and maternal depression consistently predicted multi-trajectory groups characterized by problematic levels of at least two co-occurrent psychological symptoms.
Identified combinations of developmental trajectories of psychological characteristics were associated with different magnitude in risk for exhibiting physical aggression. These results may highlight the heterogeneity of developmental trajectories associated with childhood aggression.
Replicated evidence indicates that children with attention-deficit/hyperactivity disorder (ADHD) show disproportionate increases in hyperactivity/physical movement when their underdeveloped executive functions are taxed. However, our understanding of hyperactivity’s relation with set shifting is limited, which is surprising given set shifting’s importance as the third core executive function alongside working memory and inhibition. The aim of this study was to experimentally examine the effect of imposing set shifting and inhibition demands on objectively measured activity level in children with and without ADHD.
The current study used a validated experimental manipulation to differentially evoke set shifting, inhibition, and general cognitive demands in a carefully phenotyped sample of children aged 8–13 years with ADHD (n = 43) and without ADHD (n = 34). Activity level was sampled during each task using multiple, high-precision actigraphs; total hyperactivity scores (THS) were calculated.
Results of the 2 × 5 Bayesian ANOVA for hyperactivity revealed strong support for a main effect of task (BF10 = 1.79 × 1018, p < .001, ω2 = .20), such that children upregulated their physical movement in response to general cognitive demands and set shifting demands specifically, but not in response to increased inhibition demands. Importantly, however, this manipulation did not disproportionally increase hyperactivity in ADHD as demonstrated by significant evidence against the task × group interaction (BF01 = 18.21, p = .48, ω2 = .002).
Inhibition demands do not cause children to upregulate their physical activity. Set shifting produces reliable increases in children’s physical movement/hyperactivity over and above the effects of general cognitive demands but cannot specifically explain hyperactivity in children with ADHD.
Attention-Deficit/Hyperactivity Disorder is a very prevalent disorder in children and adolescents determining important impairments in those affected. This review aims to discuss some clinical and therapeutic dilemmas found by clinical psychiatrists in the treatment of the disorder.
This is a comprehensive, non-systematic review of the literature addressing the following issues:
a) differentiation normality/presence of the disorder;
b) clinical relevance of the age-of-onset of impairment criterion;
c) frontiers with Bipolar Disorders (BD);
d) guidelines for treatment when the disorder is associated with comorbidities.
Clinical tips are presented to make the diagnosis without significantly increasing the proportion of false positives, as well as to help in both the differential diagnosis with BD and the pharmacological management of the disorder associated to comorbidities.
The precise diagnosis, avoiding very flexible criteria, is crucial in a disorder with a dimensional construct in the population, as well as the adequate use of medication for a highly comorbid disorder.
Internet gaming disorder (IGD) has been included in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Currently, associations between IGD in early adolescence and mental health are largely unexplained. In the present study, the relation of IGD with adolescent and parental mental health was investigated for the first time.
We surveyed 1095 family dyads (an adolescent aged 12–14 years and a related parent) with a standardized questionnaire for IGD as well as for adolescent and parental mental health. We conducted linear (dimensional approach) and logistic (categorical approach) regression analyses.
Both with dimensional and categorical approaches, we observed statistically significant associations between IGD and male gender, a higher degree of adolescent antisocial behavior, anger control problems, emotional distress, self-esteem problems, hyperactivity/inattention and parental anxiety (linear regression model: corrected R2 = 0.41, logistic regression model: Nagelkerke's R2 = 0.41).
IGD appears to be associated with internalizing and externalizing problems in adolescents. Moreover, the findings of the present study provide first evidence that not only adolescent but also parental mental health is relevant to IGD in early adolescence. Adolescent and parental mental health should be considered in prevention and intervention programs for IGD in adolescence.
Childhood disruptive behaviors are highly prevalent and associated with adverse long-term social and economic outcomes. Trajectories of welfare receipt in early adulthood and the association of childhood behaviors with high welfare receipt trajectories have not been examined.
Boys (n = 1000) from low socioeconomic backgrounds were assessed by kindergarten teachers for inattention, hyperactivity, aggression, opposition, and prosociality, and prospectively followed up for 30 years. We used group-base trajectory modeling to estimate trajectories of welfare receipt from age 19–36 years using government tax return records, then examined the association between teacher-rated behaviors and trajectory group membership using mixed effects multinomial regression models.
Three trajectories of welfare receipt were identified: low (70.8%), declining (19.9%), and chronic (9.3%). The mean annual personal employment earnings (US$) for the three groups at age 35/36 years was $36 500 (s.d. = $24 000), $15 600 (s.d. = $16 275), and $1700 (s.d. = $4800), respectively. Relative to the low welfare receipt group, a unit increase in inattention (mean = 2.64; s.d. = 2.32, range = 0–8) at age 6 was associated with an increased risk of being in the chronic group (relative risk ratio; RRR = 1.16, 95% CI 1.03–1.31) and in the declining group (RRR = 1.13, 95% CI 1.03–1.23), after adjustment for child IQ and family adversity, and independent of other behaviors. Family adversity was more strongly associated with trajectories of welfare receipt than any behavior.
Boys from disadvantaged backgrounds exhibiting high inattention in kindergarten are at elevated risk of chronic welfare receipt during adulthood. Screening and support for inattentive behaviors beginning in kindergarten could have long-term social and economic benefits for individuals and society.
In 2013, Internet gaming disorder (IGD) was incorporated in the current version of the DSM-5. IGD refers to a problematic use of video games. Longitudinal studies on the etiology of IGD are lacking. Furthermore, it is currently unclear to which extent associated psychopathological problems are causes or consequences of IGD. In the present survey, longitudinal associations between IGD and adolescent and parental mental health were investigated for the first time, as well as the temporal stability of IGD.
In a cross-lagged panel design study, family dyads (adolescent with a parent each) were examined in 2016 (t1) and again 1 year later (2017, t2). Overall, 1095 family dyads were assessed at t1 and 985 dyads were re-assessed at t2 with standardized measures of IGD and several aspects of adolescent and parental mental health. Data were analyzed with structural equation modeling (SEM).
Male gender, a higher level of hyperactivity/inattention, self-esteem problems and IGD at t1 were predictors of IGD at t2. IGD at t1 was a predictor for adolescent emotional distress at t2. Overall, 357 out of the 985 adolescents received a diagnosis of IGD at t1 or t2: 142 (14.4%) at t1 and t2, 100 (10.2%) only at t1, and 115 (11.7%) only at t2.
Hyperactivity/inattention and self-esteem problems seem to be important for the development of IGD. We found first empirical evidence that IGD could prospectively contribute to a deterioration of adolescent mental health. Only a subgroup of affected adolescents showed IGD consistently over 1 year.
Prenatal maternal obesity has been linked to adverse childhood neuropsychiatric outcomes, including increased symptoms of attention deficit hyperactivity disorder (ADHD), internalizing and externalizing problems, affective disorders and neurodevelopmental problems but few studies have studied neuropsychiatric outcomes among offspring born to very severely obese women or assessed potential familial confounding by maternal psychological distress.
We evaluated neuropsychiatric symptoms in 112 children aged 3–5 years whose mothers had participated in a longitudinal study of obesity in pregnancy (50 very severe obesity, BMI ⩾40 kg/m2, obese class III and 62 lean, BMI 18.5–25 kg/m2). The mothers completed the Conners’ Hyperactivity Scale, Early Symptomatic Syndrome Eliciting Neurodevelopmental Clinical Examination Questionnaire (ESSENCE-Q), Child's Sleep Habits Questionnaire (CSHQ), Strengths and Difficulties Questionnaire (SDQ), and Child Behavior Checklist (CBCL) to assess child neuropsychiatric symptoms. Covariates included child's sex, age, birthweight, gestational age, socioeconomic deprivation levels, maternal age, parity, smoking status during pregnancy, gestational diabetes and maternal concurrent symptoms of anxiety and depression assessed using State Anxiety of Spielberger State-Trait Anxiety Index (STAI) and General Health Questionnaire (GHQ), respectively.
Children exposed to prenatal maternal very severe obesity had significantly higher scores in the Conners’ Hyperactivity Scale; ESSENCE-Q; total sleep problems in CSHQ; hyperactivity, conduct problems and total difficulties scales of the SDQ; higher externalizing and total problems, anxious/depressed, aggressive behaviour and other problem syndrome scores and higher DSM-oriented affective, anxiety and ADHD problems in CBCL. Prenatal maternal very severe obesity remained a significant predictor of child neuropsychiatric problems across multiple scales independent of demographic factors, prenatal factors and maternal concurrent symptoms of anxiety and depression.
Prenatal maternal very severe obesity is a strong predictor of increased neuropsychiatric problems in early childhood.
Recently, there has been increased research into the etiology of the comorbidity between hyperactivity/inattention problems (HIP) and conduct problems (CP). However, the nature of the etiology of the comorbidity has remained unclear. Mothers of 507 pairs of twins, comprised of 221 monozygotic (MZ) and 286 dizygotic (DZ) twin pairs aged from 6 to 13 years (mean = 9.6 years; SD = 2.0 years), completed the HIP and the CP scale of the Strengths and Difficulties Questionnaire (SDQ) via a telephone interview. The phenotypic correlation between HIP and CP was 0.43 (p < .01). MZ and DZ twin correlations were, respectively, 0.48 (95%CI: 0.37–0.58) and 0.06 (95%CI: -0.06–0.19) for HIP and 0.38 (95%CI: 0.26–0.49) and 0.35 (95%CI: 0.25–0.45) for CP. The bivariate model-fitting results revealed additive genetic correlation of 1.0 (95% CI: 0.72–1.00), a complete overlap of additive genetic variance component between HIP and CP, supporting the importance of correlated additive genetic risk factors for the comorbid condition of HIP and CP. HIP was additionally influenced by non-additive genetic factors that did not contribute to the relationship between HIP and CP. There was a significant but moderate child-specific environmental correlation (re = 0.37) between HIP and CP. CP was additionally influenced by shared family environmental influences. While the results of the present study are generally consistent with the findings from Western twin studies of the relationship between HIP and CP, they add a new finding to the extant literature by showing that it is additive rather than non-additive genetic factors that are responsible for the co-occurrence of HIP and CP.
Course and predictors of persistence of attention deficit hyperactivity disorder (ADHD) in adults are still largely unknown. Neurobiological and clinical differences between child and adult ADHD raise the need for follow-up studies of patients diagnosed during adulthood. This study investigates predictors of ADHD persistence and the possibility of full remission 7 years after baseline assessment.
A 7-year follow-up study of adults with ADHD (n = 344, mean age 34.1 years, 49.9% males) was conducted. Variables from different domains (social demographics, co-morbidities, temperament, medication status, ADHD measures) were explored with the aim of finding potential predictors of ADHD persistence.
Retention rate was 66% (n = 227). Approximately a third of the sample (n = 70, 30.2%) did not maintain ADHD criteria and 28 (12.4%) presented full remission (<4 symptoms), independently of changes in co-morbidity or cognitive demand profiles. Baseline predictors of diagnostic persistence were higher number of inattention symptoms [odds ratio (OR) 8.05, 95% confidence interval (CI) 2.54–25.45, p < 0.001], number of hyperactivity/impulsivity symptoms (OR 1.18, 95% CI 1.04–1.34, p = 0.01), oppositional defiant disorder (OR 3.12, 95% CI 1.20–8.11, p = 0.02), and social phobia (OR 3.59, 95% CI 1.12–11.47, p = 0.03).
Despite the stage of brain maturation in adults suggests stability, approximately one third of the sample did not keep full DSM-IV diagnosis at follow-up, regardless if at early, middle or older adulthood. Although full remission is less common than in childhood, it should be considered as a possible outcome among adults.
A twin design was used to examine the developmental nature of genetic, environmental, and phenotypic variations in hyperactivity and inattention problems (HIP). Mothers of 662 complete pairs of twins (273 monozygotic [MZ] pairs and 389 dizygotic [DZ] pairs) aged from 3 to 13 years (mean [SD] age = 8.3 [2.9] years) responded to the items of the HIP scale of the Strengths and Difficulties questionnaire via a telephone interview. Maximum likelihood MZ and DZ twin correlations in the total sample were 0.47 (95% CI: 0.37–0.55) and −0.01 (95% CI: −0.11–0.09). A standard univariate model incorporating age as a modifier was applied to the raw data. Results of model-fitting analyses showed that the phenotypic variation of HIP monotonically increased from age 3 to age 12 and that this increase was completely due to an increase in genetic variance, suggesting that it is genes that expand individual difference in ADHD symptoms with age during childhood. Child-specific environmental variance was constant during this age period. In terms of relative influences, total genetic factors increased from 33% (95% CI: 27–44%) at age 3 to 51% (95% CI: 28–71%) at age 13 and this increase was accompanied by a decrease in relative influences of child-specific environmental factors from 67% (95% CI: 56–73%) at age 3 to 49% (95% CI: 29–72%) at age 13. These estimates of genetic influences were somewhat lower than those found in most twin studies of ADHD symptoms. However, the increasing trend of genetic influences with age during childhood was consistent with the results of a recent meta-analysis of ADHD symptoms.
Taxometric and behavioral genetic studies suggest that attention deficit hyperactivity disorder (ADHD) is best modeled as a dimension rather than a category. We extended these analyses by testing for the existence of putative ADHD-related deficits in basic information processing (BIP) and inhibitory-based executive function (IB-EF) in individuals in the subclinical and full clinical ranges. Consistent with the dimensional model, we predicted that ADHD-related deficits would be expressed across the full spectrum, with the degree of deficit linearly related to the severity of the clinical presentation.
A total of 1547 children (aged 6–12 years) participated in the study. The Development and Well-Being Assessment (DAWBA) was used to classify children into groups according to levels of inattention and hyperactivity independently: (1) asymptomatic, (2) subthreshold minimal, (3) subthreshold moderate and (4) clinical ADHD. Neurocognitive performance was evaluated using a two-choice reaction time task (2C-RT) and a conflict control task (CCT). BIP and IB-EF measures were derived using a diffusion model (DM) for decomposition of reaction time (RT) and error data.
Deficient BIP was found in subjects with minimal, moderate and full ADHD defined in terms of inattention (in both tasks) and hyperactivity/impulsivity dimensions (in the 2C-RT). The size of the deficit increased in a linear manner across increasingly severe presentations of ADHD. IB-EF was unrelated to ADHD.
Deficits in BIP operate at subclinical and clinical levels of ADHD. The linear nature of this relationship provides support for a dimensional model of ADHD in which diagnostic thresholds are defined in terms of clinical and societal burden rather than representing discrete pathophysiological states.
The relationship between prenatal tobacco exposure and hyperactivity remains controversial. To mitigate limitations of prior studies, we used a strategy involving comparison of maternal and paternal smoking reports in a historical sample where smoking during pregnancy was common.
Data were drawn from a longitudinally followed subsample of the Child Health and Development Study (n = 1752), a population-based pregnancy cohort ascertained in 1961–1963 in California. Maternal prenatal smoking was common (33.4%). Maternal and paternal smoking patterns were assessed at three time points by mother report. Hyperactivity was assessed at the mean of age of 10 years based on mother report to a personality inventory.
Unadjusted, maternal smoking during pregnancy was associated with offspring hyperactivity [β = 0.22, 95% confidence interval (CI) 0.11–0.33] and, to a similar degree, when the father smoked (β = 0.18, 95% CI 0.07–0.30). After adjustment, maternal smoking remained robustly predictive of offspring hyperactivity (β = 0.25, 95% CI 0.09–0.40) but father smoking was not (β = 0.02, 95% CI −0.20 to 0.24). When examined among the pairs matched on propensity score, mother smoking was robustly related to offspring hyperactivity whether the father smoked (β = 0.26, 95% CI 0.03–0.49) or did not smoke (β = 0.30, 95% CI 0.04–0.57). By number of cigarettes, associations with hyperactivity were present for 10–19 and 20+ cigarettes per day among mothers.
In a pregnancy cohort recruited in a time period in which smoking during pregnancy was common, we document associations between prenatal smoking exposure and offspring hyperactivity. Novel approaches to inferring causality continue to be necessary in describing the potential adverse consequences of prenatal smoking exposure later in life.
Attention deficit hyperactivity disorder (ADHD) is common in children, adolescents, and adults, with extensive research establishing it as a valid neurobiological disorder. Without intervention, ADHD can result in significant impairment throughout the lifespan for the individuals it afflicts. Fortunately, multiple evidence-based options are available for the treatment of ADHD, including several efficacious pharmacotherapies. The role of medication, including stimulants as well as non-stimulants, is well-documented by an extensive body of literature. Although there may be less enthusiasm for behavioural and other psychosocial interventions as stand-alone treatments for moderate to severe ADHD, they are recommended as first-line treatment for ADHD management in preschool-aged children, for those patients with mild symptoms, and as an adjunct to medication in patients with comorbid disorders or suboptimal responses to pharmacotherapy. When planning treatment for individuals with ADHD, the potential risks associated with the available interventions must be carefully balanced against the risks of not treating, or not treating adequately. The treatment plan must also include ongoing re-assessment of the effectiveness of and the need for continued therapy. Recent practice parameters provide further specific guidance for the evidence-based assessment and treatment of children and adolescents with ADHD.
There is a growing body of evidence suggesting that animal models can be developed to probe the specific domains of bipolar disorder (BD) using the endophenotype approach. Here we tested clinically active antimanic drugs to validate amphetamine-induced hyperactivity in Black Swiss mice as a putative model of the manic phase of BD. We also co-administered a mood stabilizer and an atypical antipsychotic drug in a manner akin to the clinical treatment regimens. Since lithium has been shown to potentially act through glycogen synthase kinase-3 (GSK3) inhibition, we evaluated the efficacy of selective GSK3 inhibitors in this model. Habituated animals were pretreated with a compound of interest before being challenged with amphetamine (2.0 mg/kg) and returned to activity cages for an additional 1.5 h. We tested lithium, sodium valproate, carbamazepine, olanzapine, ziprasidone as well as co-administered lithium and olanzapine at sub-efficacious doses. The GSK3 inhibitors tested included indirubin, alsterpaullone, TDZD-8, AR-A014418, SB-216763, and SB-627772. All mood stabilizers and antipsychotic drugs reduced hyperactivity without affecting spontaneous locomotion. While subactive doses of lithium and olanzapine were without effect, their co-administration produced robust reductions in hyperactivity. All GSK3 inhibitors were active in the model, producing selective inhibition of rearing hyperactivity. These data support the predictive validity of the model for the acute manic phase of BD and may have utility as an in-vivo model for identifying novel antimanic therapeutics.
This chapter concerns emotional, behavioural and developmental disorders that arise in the first two decades of life. Few formal tests or assessments can contribute to the clinical assessment for common behavioural and emotional disorders. Clinical physiological assessments can provide helpful information for neuropsychiatric disorders. Risks for psychopathology occur from a variety of sources both internal and external to the child. Many children and adolescents demonstrate an ability to withstand exposure to risk processes and not develop psychiatric disorders. Disturbances in parent-child relationships in infancy significantly influence the development of psychopathology. Hyperactivity and impulsivity are more closely associated with each other than either is to attentional difficulties. Autistic syndromes are lifelong disorders even in those who show real improvements by young adult life. Child psychiatrists should continue to contribute to basic research aimed at understanding the causes of mental illness and behavioural syndromes.
Physical hyperactivity has often been described in anorexia nervosa (AN) patients but up until now in-depth research has been scarce. Experience sampling methodology (ESM), a structured diary technique assessing momentary mental state at random times during the day, may be useful in studying hyperactivity in AN.
In two single case reports, ESM was used to investigate the variation across time of the urge to move in relation to potentially relevant eliciting conditions such as positive and negative emotions, weight preoccupation and attractiveness.
Frequency distribution of the involved variables indicated substantial individual differences between patients. While both patients' tendency to be hyperactive was positively related to their weight preoccupation and negative emotions, in only one patient, the urge to move turned out to be significantly related to (the absence of) positive emotions.
ESM can be useful to test whether general theories of psychopathology apply to specific patients, and it may be conceived as an individually tailored approach to self-monitoring. As such, it may guide the clinician to devise therapeutic interventions in particular patients.
The purpose of this study was to investigate whether
inappropriate/excessive motor activity seen in children with Attention
Deficit Hyperactivity Disorder (ADHD) could be characterized as
Utilization Behavior (UB). Given evidence that the neuropathology of ADHD
may involve frontal-striatal systems, we investigated the possibility that
children with ADHD may demonstrate “utilization behavior.”
Utilization Behavior (UB) is a neurobehavioral syndrome documented in
individuals with damage or dysfunction in the frontal areas of the brain;
patients exhibiting UB are often described as reaching out and utilizing
objects in the environment in an automatic and inappropriate manner. The
sample consisted of two group of children; children with ADHD (n
= 32) and control children (n = 31). Children were assessed
individually in a testing room where various objects, selected to elicit
UB, were present. They completed cognitive tests and also were allowed to
engage in an unsupervised activity. Testing sessions were videotaped and
instances of physical activity (i.e., upper limb motor activity and
utilization of objects) were counted by two raters. Results indicated high
levels of object utilization in approximately one-half of the children
with ADHD, whereas almost no such behavior was observed in controls. This
behavior did not appear to be a result of generally heightened activity
levels or due to instruction set, but differed according to object
familiarity and object visibility. Levels of UB were statistically
associated with the severity of hyperactivity, as reported by parents, of
children with ADHD. This study suggests that inappropriate/excessive
motor activity may, at least in part, be characterized as UB in some
children with ADHD. (JINS, 2005, 11, 367–375.)
sagvolden, johansen, aase, and russell (sagvolden et al.) examine attention-deficit/hyperactivity disorder (adhd) at levels of analysis ranging from neurotransmitters to behavior. at the behavioral level they attribute aspects of adhd to anomalies of delay-of-reinforcement gradients. with a normal gradient, responses followed after a long delay by a reinforcer may share in the effects of that reinforcer; with a diminished or steepened gradient they may fail to do so. steepened gradients differentially select rapidly emitted responses (hyperactivity), and they limit the effectiveness with which extended stimuli become conditioned reinforcers, so that observing behavior is less well maintained (attention deficit). impulsiveness also follows from steepened gradients, which increase the effectiveness of smaller, more immediate consequences relative to larger, more delayed ones. individuals who vary in the degree to which their delay gradients are steepened will show different balances between hyperactivity and attention deficit. given the range of adhd phenomena addressed, it may be unnecessary to appeal to additional behavioral processes such as extinction deficit. extinction deficit is more likely a derivative of attention deficit, in that failure to attend to stimuli differentially correlated with extinction should slow its progress. the account suggests how relatively small differences in delay gradients early in development might engender behavioral interactions leading to very large differences later on. the steepened gradients presumably originate in properties of neurotransmitter function, but behavioral interventions that use consistently short delays of reinforcement to build higher-order behavioral units as a scaffolding to support complex cognitive and social skills may nonetheless be feasible.