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Advances in the field of child psychiatric genetics since the drafting of the human genome are described. Research on the genetics of developmental psychopathology has grown exponentially during this period.

The use of the quantitative trait locus approach identifies the genetic basis for autism spectrum disorder symptoms in children with attention-deficit/hyperactivity disorder. The findings support the hypothesis that differential genetic factors causes the three autistic spectrum disorder.

The links of chromosomes 1p21, 6p21, and 8q21 to the Child Behavior Checklist Juvenile Bipolar Disorder (CBCL-JBD) are examined. Findings indicate an increased probability that genes in these regions affect variation on the CBCL-JBD and emotional and behavioral dysregulation associated with psychopathology.

The prediction of prodromal psychosis in adolescents with velocardiofacial syndrome is investigated. The best predictors of adolescent prodromal psychotic symptoms are parent ratings of childhood odd/eccentric symptoms and performance on the Wisconsin Card Sorting Test.

The growth of children who were treated with lisdexamfetamine dimesylate (LDX) for attention deficit hyperactivity disorder was compared with norms from the Centers for Disease Control and it is found that there are growth delays in this group in terms of weight and body mass index. The growth of children being treated with LDX should be monitored and growth delays should be corrected.

A meta-analysis of 16 subjective and objective sleep studies with a sample of 722 children with attention deficit hyperactivity disorder (ADHD) versus a control that numbers 638 shows that the children with ADHD are significantly more impaired in most of the subjective and some of the objective sleep measures than their counterpart.

Four hundred forty-four subjects aged 6-55 years were evaluated to examine the role of COMT and SLC6A4 genes in the risk for conduct disorder and its symptomatic subtypes in the context of attention deficit hyperactivity disorder. No significant association is found between these genes and the risk for conduct disorder.

Analysis of the data from a genetics study of children with Attention-deficit/hyperactivity disorder (ADHD) and their affected or unaffected siblings finds that ADHD-affected children had significantly more motor problems than their unaffected siblings. It is concluded that there is a common basis between ADHD and motor problems that may be due to genetic factors.

The article reviews existing literature on the effects of stimulant medications on the growth of children with attention-deficit/hyperactivity disorder. It concludes that treatment with stimulants in childhood results in moderate growth deficit in height and weight.

A study was conducted to establish the relationship between Attention-Deficit/Hyperactivity (ADHD) disorder and high-IQ children and whether ADHD has a high predictive value among youths with high-IQ. Results further supported the hypothesis for the predictive validity of ADHD in high-IQ youths.

The association between attention-deficit/hyperactivity disorder (ADHD) and major depression (MD) in adolescent and young adult females is evaluated. Findings indicate that MD emerging in the context of ADHD is an impairing and severe comorbidity which needs to be considered further clinically and scientifically.

Ongoing debate over the validity of the attention-deficit/hyperactivity disorder (ADHD) construct in adulthood is fueled in part by uncertainty regarding implications of potentially extensive yet incompletely described comorbid Axis I and II psychopathology. Three hundred sixty-three adults ages 18 to 37 completed semistructured clinical interviews; informants were also interviewed, and best estimate diagnoses were obtained. Results were as follows: First, ADHD combined type (ADHD-C) had an excess of externalizing and internalizing Axis I disorders, suggesting a gradient-of-severity relationship between it and ADHD inattentive type (ADHD--I). Second, ADHD--C and ADHD--I did not differ in frequency of Axis II disorders. Third, however, ADHD overall was associated with increased rates of Axis II disorders, compared with rates in non-ADHD control participants, including both Cluster B (primarily borderline personality disorder) and Cluster C disorders. Fourth, ADHD incrementally accounted for clinician-rated global assessment of functioning scores above and beyond comorbid conditions or symptoms on either Axis I or Axis II. Results further inform nosology of ADHD in adults. Keywords: attention-deficit/hyperactivity disorder (ADHD), comorbidity, DSM-IV subtypes, personality disorders, functional impairment

This study examined neuropsychological deficits among children with bipolar disorder while attending to its comorbidity with attention-deficit/hyperactivity disorder (ADHD). Seventy-three unmedicated children (ages 6-17 years) with Diagnostic and Statistical Manual of Mental Disorders (4th ed.; American Psychiatric Association, 1994) bipolar disorder plus ADHD (BPD + ADHD) were compared with 102 unmedicated children with ADHD without bipolar disorder, and 120 children without bipolar disorder or ADHD. Ninety-four percent of participants were Caucasian, 58% were male, and 42% were female. On average participants were of middle to upper socioeconomic status. Participants were assessed with a comprehensive neuropsychological battery and measures of academic achievement, school failure, and special education placement. Participants with BPD + ADHD and with ADHD were impaired in interference control, verbal learning, and arithmetic achievement and had higher rates of special school services. Across all of the measures of neuropsychological functioning, the only difference observed between youths with BPD + ADHD and youths with ADHD was that youths with BPD + ADHD performed more poorly on one measure of processing speed. Thus, comorbidity with ADHD may account for many of the neuropsychological deficits observed in children with bipolar disorder. Keywords: neuropsychology, bipolar disorder, child, ADHD, processing speed

The association between executive function deficits (EFDs) and functional outcomes were examined among children and adolescents with attention-deficit/hyperactivity disorder (ADHD). Participants were children and adolescents with (n = 259) and without (n = 222) ADHD, as ascertained from pediatric and psychiatric clinics. The authors defined EFD as at least 2 executive function measures impaired. Significantly more children and adolescents with ADHD had EFDs than did control participants. ADHD with EFDs was associated with an increased risk for grade retention and a decrease in academic achievement relative to (a) ADHD alone, (b) controlled socioeconomic status, (c) learning disabilities, and (d) IQ. No differences were noted in social functioning or psychiatric comorbidity. Children and adolescents with ADHD and EFDs were found to be at high risk for significant impairments in academic functioning. These results support screening children with ADHD for EFDs to prevent academic failure.

Within families, co-occurring attention-deficit/hyperactivity disorder (ADHD) in parents and children may be common. The authors evaluated the hypothesis that parental ADHD may lead to a reporting bias of ADHD symptoms in offspring. They combined 2 family case-controlled studies of ADHD using structured interviews. They compared rates of maternal reported ADHD symptoms among 3 groups of ADHD children: no parental ADHD (n = 231), mother with ADHD (n = 63), and father with ADHD (n = 57). With the exception of 1 symptom, the rates of reporting between groups did not differ. There was no evidence that the discrepancy between maternal reports and self-reports of symptoms differed by parental ADHD. Results were similar across child gender or referral status. These results do not support the notion that parental ADHD affects maternal reports of offspring ADHD.

Tobacco use is significantly associated with schizophrenia. However, it is not clear if smoking is associated with the illness itself, treatment, or underlying vulnerability to the disease. Smoking was studied in a sample of schizophrenic probands (n = 24), their unaffected co-twins (n = 24), and controls (n = 3,347). Unaffected co-twins had higher rates of daily smoking than controls. Probands and co-twins were more frequently unsuccessful in attempts to quit than controls. Probands reported shaky hands and depression following smoking cessation more often than controls, whereas unaffected co-twins reported difficulty concentrating, drowsiness, nervousness, and headache following smoking cessation more often than controls. Results are consistent with the hypothesis that nicotine use is influenced by familial vulnerability to schizophrenia, not just clinical schizophrenia per se.

A study was conducted to analyze the overlap between mania and conduct disorder (CD) in consecutively referred youths. The premises that neither CD nor manic symptoms were secondary to the other disorder and that children supporting two disorders have correlates of both were examined. Results indicated that the co-occurrence of mania and CD in children correlates with a correct diagnosis and that CD symptoms should be associated as secondary to mania and manic symptoms.

In a prior study of 54 relatives of patients with schizophrenia and 72 control participants, 3 neuropsychological functions met the criteria for risk indicators of the schizophrenia genotype: executive functioning, memory, and auditory attention. In an assessment of the stability of these findings, the sample was reexamined 4 years after the initial assessment. Three test scores were found to differ between groups (Immediate Verbal Memory, Delayed Verbal Memory, and Dichotic Listening Digits Detected) or to show a significant Group x Gender interaction (immediate and delayed verbal and visual memories). None of the test scores showed Group x Time interactions, suggesting that the discriminating power of the tests was stable over time. Evidence for deficits in working memory and role learning on the object alternation test was also found. These results support the idea that neuropsychological dysfunction among relatives of patients with schizophrenia is a stable trait caused by the familial predisposition to schizophrenia.