Faculty Bibliography

Intra-individual variability in behavior and functioning is ubiquitous among children with attention-deficit/hyperactivity disorder (ADHD), but it has not been systematically examined or integrated within causal models. This article seeks to provide a conceptual, methodologic, and analytic framework as a foundation for future research. We first identify five key research questions and methodologic issues. For illustration, we examine the periodic structure of Eriksen Flanker task reaction time (RT) data obtained from 24 boys with ADHD and 18 age-matched comparison boys. Reaction time variability in ADHD differed quantitatively from control subjects, particularly at a modal frequency around .05 Hz (cycle length approximately 20 sec). These oscillations in RT were unaffected by double-blind placebo and were suppressed by double-blind methylphenidate. Together with converging lines of basic and clinical evidence, these secondary data analyses support the speculative hypothesis that the increased power of multisecond oscillations in ADHD RT data, and by inference, in attentional performance, represents a catecholaminergic deficit in the ability to appropriately modulate such oscillations in neuronal activity. These results highlight the importance of retaining time-series data and quantitatively examining intra-subject measures of variability as a putative endophenotype for ADHD

Until recently, causal models of attention-deficit/hyperactivity disorder (ADHD) have tended to focus on the role of common, simple, core deficits. One such model highlights the role of executive dysfunction due to deficient inhibitory control resulting from disturbances in the frontodorsal striatal circuit and associated mesocortical dopaminergic branches. An alternative model presents ADHD as resulting from impaired signaling of delayed rewards arising from disturbances in motivational processes, involving frontoventral striatal reward circuits and mesolimbic branches terminating in the ventral striatum, particularly the nucleus accumbens. In the present article, these models are elaborated in two ways. First, they are each placed within their developmental context by consideration of the role of person x environment correlation and interaction and individual adaptation to developmental constraint. Second, their relationship to one another is reviewed in the light of recent data suggesting that delay aversion and executive functions might each make distinctive contributions to the development of the disorder. This provides an impetus for theoretical models built around the idea of multiple neurodevelopmental pathways. The possibility of neuropathologic heterogeneity in ADHD is likely to have important implications for the clinical management of the condition, potentially impacting on both diagnostic strategies and treatment options

Before assigning full etiologic validity to a psycopathologic disorder, disease theory suggests that a causal dysfunction in a mechanism within the affect individuals must be identified. Existing theories on attention-deficit/hyperactivity disorder (ADHD) suggest such dysfunctions in cognitive, neuropsychological, or motivational processes in the child. To date, researchers have tested these theories by comparing groups with DSM-defined ADHD to children without ADHD. Using executive functioning as an illustration of an issue that exists across all such theories, this article describes substantial overlaps in the group performance data. Thus only a subgroup may have executive deficits. Noted are other supportive data suggesting multiple pathways to ADHD. The article explores implications and recommends that future theory and research give more consideration to the probability that only a subset of behaviorally defined children will have a deficit in a given neurocognitive mechanism believed to contribute to the disorder. Creation of a provisional set of criteria in DSM-V for defining an 'executive deficit type' could stimulate research to validate the first etiologic subtype of ADHD and spur the development of more sophisticated causal models, which in the longer term may give clinicians ways to target and tailor treatments

OBJECTIVE: The prevalence and workplace consequences of adult attention deficit/hyperactivity disorder (ADHD) are unknown. METHODS: An ADHD screen was included in a national household survey (n = 3198, ages 18-44). Clinical re-interviews calibrated the screen to diagnoses of Diagnostic and Statistical Manual of Mental Disorders, 4th edition ADHD. Diagnoses among workers were compared with responses to the WHO Health and Work Performance Questionnaire (HPQ). RESULTS: A total of 4.2% of workers had ADHD. ADHD was associated with 35.0 days of annual lost work performance, with higher associations among blue collar (55.8 days) than professional (12.2 days), technical (19.8 days), or service (32.6 days) workers. These associations represent 120 million days of annual lost work in the U.S. labor force, equivalent to dollar 19.5 billion lost human capital. CONCLUSIONS: ADHD is a common and costly workplace condition. Effectiveness trials are needed to estimate the region of interest of workplace ADHD screening and treatment programs

OBJECTIVE: The aim of this study was to examine the characteristics and outcome of adolescents with psychotic disorder not otherwise specified (PsyNOS) and brief psychotic disorder (BrPsy), two neglected subsyndromal diagnostic entities. METHODS: As part of an ongoing, naturalistic study investigating adolescents considered to be prodromal for schizophrenia, 29 youngsters (mean age, 16.2 +/- 2.7 years) with PsyNOS or BrPsy were identified as theoretically at highest risk for schizophrenia and followed for over 6 (mean, 22.8 +/- 19.4) months. RESULTS: Contrary to our expectations, only 7 of the 26 individuals (27.0%) with follow-up data developed schizophrenia or schizoaffective disorder, and only 2 subjects (7.7%) retained their diagnosis of BrPsy/PsyNOS. The most frequent other diagnoses at follow-up were mood disorders (34.6%), personality disorders (11.5%), and obsessive-compulsive disorder (7.7%). Regarding severity of outcome, 38.5% of the patients progressed to a syndromal psychotic disorder, 23.1% continued to have attenuated positive symptoms, and 38.4% improved to having attenuated negative symptoms only, or no positive or negative symptoms. BrPsy was associated with lower maximum levels of negative symptoms (p = 0.02) and higher likelihood of symptom remission (p = 0.02). CONCLUSIONS: This study indicates that psychotic symptoms not fulfilling criteria for schizophrenia or a psychotic mood disorder are unreliable predictors of a syndromal psychotic disorder outcome at 2 years. Long-term studies of PsyNOS and BrPsy are needed to clarify where these disorders fall in the developmental course of schizophrenia.

OBJECTIVE: To evaluate the SAFE Homes (SH) program, a short-term group care program for children between 3 and 12 years of age who enter care for the first time. The program aims to improve case outcomes by consolidating resources to facilitate assessment and treatment planning. METHODS: The 1-year outcomes of 342 children who received SAFE Home services and 342 matched foster care (FC) control children were compared. The 684 subjects used in this report were selected from a larger pool of 909 subjects using propensity score matching to control for hidden bias in treatment group assignment. We hypothesized that SAFE Homes would result in greater continuity of care for children (e.g., fewer placements, more placements with siblings and in towns of origin), identification of more relatives for substitute care when needed, reduced use of high-cost restrictive care settings (e.g., residential, inpatient), and reduced rates of re-abuse through earlier detection and provision of services to meet child and family treatment needs. RESULTS: Prior to the initiation of the SAFE Homes program, 75% of the children who entered care in the State experienced three or more placements in the first year. The outcomes of both the SH and FC cases were significantly improved over pre-SAFE Home State statistics. The FC group, however, had comparable or better outcomes on most variables examined. In addition, the total cost for out-of-home care for the children in FC was significantly less, despite the fact that the two groups spent similar amounts of time in care (average time in care: 7 months). This finding held when the total placement cost was calculated using the State reimbursement rate of 206.00 US dollars per day for SAFE Home care (SH: 20,851 US dollars +/- 24,231 US dollars; FC: 8,441 US dollars +/- 21,126 US dollars, p < .001), and a conservative SAFE Home program fee of 85.00 US dollars per day that only considered the child care and custodial staffing costs uniquely associated with the program (SH: 13,314 US dollars +/- 21,718 US dollars; FC: 8,441 US dollars +/-21,126 US dollars, p < .001). CONCLUSION: Improvements in outcomes related to continuity of care can be attained through staff training. The SAFE Home model of care is not cost-effective for first-time placements

BACKGROUND: Few studies have compared the related diagnostic constructs of depressive personality disorder (DPD) and dysthymic disorder (DD). The authors attempted to replicate findings of Klein and Shih in longitudinally followed patients with personality disorder or major depressive disorder (MDD) in the Collaborative Longitudinal Personality Disorders Study. METHODS: Subjects (N = 665) were evaluated at baseline and over 2 years (n = 546) by reliably trained clinical interviewers using semistructured interviews and self-report personality questionnaires. RESULTS: Only 44 subjects (24.6% of 179 DPD and 49.4% of 89 early-onset dysthymic subjects) met criteria for both disorders at baseline. Depressive personality disorder was associated with increased comorbidity of some axis I anxiety disorders and other axis II diagnoses, particularly avoidant (71.5%) and borderline (55.9%) personality disorders. Depressive personality disorder was associated with low positive and high negative affectivity on dimensional measures of temperament. Depressive personality disorder subjects had lower likelihood of remission of baseline MDD at 2-year follow-up, whereas DD subjects did not. The DPD diagnosis appeared unstable over 2 years of follow-up, as only 31% (n = 47) of 154 subjects who had DPD at baseline and also had follow-up assessment met criteria on blind retesting. LIMITATIONS: Results from this sample may not generalize to other populations. CONCLUSIONS: Depressive personality disorder and dysthymic disorder appear to be related but differ in diagnostic constructs. Its moderating effect on MDD and predicted relationship to measures of temperament support the validity of DPD, but its diagnostic instability raises questions about its course, utility, and measurement

BACKGROUND: Treatment outcome and brain laterality differ between early onset (<20 years) chronically (no well-being >2 months) depressed patients with atypical features (early/chronic atypical) and those with either later onset or less chronic illness (late/nonchronic atypical). Because hypothalamic-pituitary-adrenal (HPA) axis abnormalities have been hypothesized to distinguish atypical depression from melancholia, we examined whether HPA measures would also differentiate these two groups of depressed patients with atypical features. METHODS: Three-hour afternoon cortisol levels, stimulation of cortisol by afternoon dextroamphetamine, and suppression of cortisol by dexamethasone were investigated in 85 depressed patients with atypical features. The latter group was divided into early/chronic atypical and late/nonchronic atypical based on chart review of course of illness. RESULTS: Patients with early/chronic atypical had significantly lower mean 3 h afternoon cortisol levels (N=21) and 4:00 p.m. post-dexamethasone cortisol levels (N=20) than did those with late/nonchronic atypical (N=43 with afternoon cortisol; N=26 with post-dexamethasone cortisol). Post-dextroamphetamine cortisol levels were numerically higher in the early/chronic atypical group (N=15 vs. 19), but this failed to reach conventional significance (0.05

PMID: 15935235

ISSN: 0165-0327

CID: 998342