Ethnic differences in parental detection of externalizing disorders.

Zwirs BW, Burger H, Buitelaar JK, Schulpen TW.

Dept. of Paediatrics, University Medical Centre, P.O. Box 85090, 3508 AB, Utrecht, The Netherlands, b.zwirs@wkz.azu.nl.

Eur Child Adolesc Psychiatry. 2006 May 9; [Epub ahead of print]

BACKGROUND: Previous research has reported lower treatment rates for externalizing disorders among non-Western children as compared to Western children. Ethnic differences in parental detection may be an explanation for this discrepancy. AIMS: In a cross-sectional study among the four largest ethnic groups in the Netherlands, namely Dutch, Moroccan, Turkish and Surinamese, we examined the influence of ethnicity on parental detection of behavioural disorders.

METHOD: A total of 270 children (aged 6-10 years) and their parents were interviewed regarding psychiatric disorders and socio-demographic data. Sensitivity and specificity were calculated by using standard definitions, with adjustment for parental educational level.

RESULTS: Sensitivity to detect any externalizing disorder and ADHD in particular was significantly lower among Moroccan and Surinamese parents when compared to Dutch parents. Sensitivity to detect ADHD tended to be lower among Turkish parents. Specificity to detect any externalizing disorder was higher among Moroccan and Turkish parents. Specificity to detect ADHD was higher among Moroccan parents and tended to be higher among Turkish parents.

CONCLUSIONS: The detection rate of externalizing disorders is markedly lower among non-Dutch parents than among Dutch parents. This finding emphasizes the importance of taking parents' cultural context into account when appraising their report on possible externalizing disorders in their children.

Autism Spectrum Disorders and Attention-Deficit/Hyperactivity Disorder in Boys with the Fragile X Premutation.

Farzin F, Perry H, Hessl D, Loesch D, Cohen J, Bacalman S, Gane L, Tassone F, Hagerman P, Hagerman R.

1Medical Investigation of Neurodevelopmental Disorders (M.I.N.D.) Institute, University of California, Davis, Medical Center, and Department of Psychology, University of California, Davis, Sacramento 2Medical Investigation of Neurodevelopmental Disorders (M.I.N.D.) Institute, University of California, Davis, Medical Center, Sacramento 3Medical Investigation of Neurodevelopmental Disorders (M.I.N.D.) Institute and Department of Psychiatry and Behavioral Sciences, University of California, Davis, Medical Center, Sacramento 4School of Psychological Science, La Trobe University, Melbourne, Australia 5Fragile X Alliance Clinic, Victoria, Australia 6Medical Investigation of Neurodevelopmental Disorders (M.I.N.D.) Institute, University of California, Davis, Medical Center and Department of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento 7Medical Investigation of Neurodevelopmental Disorders (M.I.N.D.) Institute and Department of Pediatrics, University of California, Davis, Medical Center, Sacramento, California.

J Dev Behav Pediatr. 2006 Apr;27(2 Suppl 2):S137-S144.

ABSTRACT.: Fragile X syndrome (FXS) is caused by a full mutation expansion (>200 CGG repeats) in the FMR1 gene that results in a deficiency of the fragile X mental retardation protein. Although most individuals with the premutation (55-200 CGG repeats) are considered unaffected by FXS, recent case studies have documented children with the premutation who have cognitive deficits, behavioral problems, and/or autism spectrum disorders. The objective of this study was to compare the prevalence of autism spectrum disorders (ASD) and attention-deficit hyperactivity disorder (ADHD) symptoms in boys with the premutation who presented as probands, in brothers with the premutation who did not present as probands, and in normal brothers of premutation and/or full mutation carriers. Participants included 43 male children: 14 probands who presented to clinic, 13 nonprobands who were identified through cascade testing (routine genetic testing of family members after identification of a proband) and confirmed to have the premutation, and a control group of 16 male siblings of individuals with the fragile X premutation or full mutation who were negative for the FMR1 mutation. Participants came from 1 of 2 collaborative sites: University of California, Davis and La Trobe University in Australia. Parents completed the Conners' Global Index-Parent Version for assessing symptoms of ADHD and the Social Communication Questionnaire (SCQ) for identifying symptoms of ASD. Children who were in the ASD range on the SCQ (n = 13) underwent further evaluation with either the Autism Diagnostic Observation Schedule-Generic (n = 10) or the Autism Diagnostic Interview-Revised (n = 3). A final diagnosis of ASD included clinical assessment utilizing DSM-IV-TR criteria in addition to the standardized assessments. There was a higher rate of ASD in boys with the premutation presenting as probands (p < 0.001) or nonprobands (p < .04) compared with sibling controls without the premutation. In addition, probands had a significant increase in ADHD symptoms compared with controls (p < .0001). Of the probands, 93% had symptoms of ADHD and 79% had ASD. In the nonproband premutation group, 38% had symptoms of ADHD and 8% had ASD. Thirteen percent of sibling controls had symptoms of ADHD and none had ASD. IQ scores were similar in all 3 groups (p = .13), but the use of psychotropic medications was significantly higher in probands with the premutation compared with that in controls (p < .0001). Developmental problems have been observed in premutation carriers, particularly those who present clinically with behavioral difficulties. Although this study is based on a small sample size, it suggests that premutation carriers, even those who do not present clinically, may be at increased risk for an ASD and/or symptoms of ADHD. If the premutation is identified through cascade testing, then further assessment should be carried out for symptoms of ADHD, social deficits, or learning disabilities.

P300 differences exist between Tourette's syndrome with and without attention deficiency and hyperactivity disorder in children.

Yan Z, Po-Zi L, Kai-Man L, Lin-Yan S, Da-Xing W, Ming Z.

Mental Health Department, The Second Affiliated Hospital (Yu Quan Hospital) of Medical School, Tsinghua University, Beijing, China.

World J Biol Psychiatry. 2006 Jun;7(2):91-98.

Objective: To study the characteristics of P300 in Tourette's syndrome (TS) with and without attention deficiency and hyperactivity disorder (ADHD).
Method: Auditory evoked P300 were recorded in 19 TS only (TS-ADHD) children, 15 TS with ADHD (TS + ADHD) children and 20 unaffected control subjects, and their waveforms, amplitudes, latencies and topographies were compared at Fz, Cz, C3, C4 and Pz.

Results: The TS + ADHD group showed shorter latencies than control subjects at all electrode sites (P&lt;0.05 or 0.01), and the TS-ADHD group at CZ and PZ (P&lt;0.05); however, there was no significant difference between control subjects and the TS-ADHD group. The TS-ADHD group showed smaller amplitudes than the control group at all electrode sites (P&lt;0.05), and the TS + ADHD group at Cz (P&lt;0.05); however, there were no significant differences between control subjects and the TS + ADHD group. There was no significant difference in the prevalence of abnormal waveforms between the control, TS, TS-ADHD and TS + ADHD groups, but there were significant differences in the variability of localization of P300 between the control and the TS group (P=0.003), control and TS + ADHD groups (P=0.000), and the TS-ADHD and TS + ADHD groups (P=0.039). P300 in the TS + ADHD group tended to spread out to the left and that of the TS-ADHD group tended to spread out to the right.

Conclusions: P300 differences exist between TS-ADHD and TS + ADHD in children. These suggested that establishment different development defects or delay of communications between different structures rather than a delay in maturation of the structures themselves may be involved in TS + ADHD and TS-ADHD children and ADHD symptoms in TS patients are likely a trait rather than adventitious or acquired within the TS syndrome.

Behavior and orofacial characteristics of children with attention-deficit hyperactivity disorder during a dental visit.

Atmetlla G, Burgos V, Carrillo A, Chaskel R.

Universidad Latina de Costa Rica. gatmetlla@yahoo.com

J Clin Pediatr Dent. 2006 Spring;30(3):183-90.

ADHD is a neuropsychological disorder, affecting attention, impulsiveness and activeness. The study included 36 children with ADHD, 47 without, and two silent observers. A dental form, SNAP-IV and ADHDT symptom checklists were used. Statistically significant differences were observed in hospitalization histories, oral habits, tongue characteristics, and facial biotype. Differences in orofacial characteristics and behavior between the groups were confirmed.

Sleep-disordered breathing, behavior, and cognition in children before and after adenotonsillectomy.

Chervin RD, Ruzicka DL, Giordani BJ, Weatherly RA, Dillon JE, Hodges EK, Marcus CL, Guire KE.

Sleep Disorders Center, Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA. chervin@umich.edu

Pediatrics. 2006 Apr;117(4):e769-78.
http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=16585288

OBJECTIVES: Most children with sleep-disordered breathing (SDB) have mild-to-moderate forms, for which neurobehavioral complications are believed to be the most important adverse outcomes. To improve understanding of this morbidity, its long-term response to adenotonsillectomy, and its relationship to polysomnographic measures, we studied a series of children before and after clinically indicated adenotonsillectomy or unrelated surgical care.

METHODS: We recorded sleep and assessed behavioral, cognitive, and psychiatric morbidity in 105 children 5.0 to 12.9 years old: 78 were scheduled for clinically indicated adenotonsillectomy, usually for suspected SDB, and 27 for unrelated surgical care. One year later, we repeated all assessments in 100 of these children.

RESULTS: Subjects who had an adenotonsillectomy, in comparison to controls, were more hyperactive on well-validated parent rating scales, inattentive on cognitive testing, sleepy on the Multiple Sleep Latency Test, and likely to have attention-deficit/hyperactivity disorder (as defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition) as judged by a child psychiatrist. In contrast, 1 year later, the 2 groups showed no significant differences in the same measures. Subjects who had an adenotonsillectomy had improved substantially in all measures, and control subjects improved in none. However, polysomnographic assessment of baseline SDB and its subsequent amelioration did not clearly predict either baseline neurobehavioral morbidity or improvement in any area other than sleepiness.

CONCLUSIONS: Children scheduled for adenotonsillectomy often have mild-to-moderate SDB and significant neurobehavioral morbidity, including hyperactivity, inattention, attention-deficit/hyperactivity disorder, and excessive daytime sleepiness, all of which tend to improve by 1 year after surgery. However, the lack of better correspondence between SDB measures and neurobehavioral outcomes suggests the need for better measures or improved understanding of underlying causal mechanisms.