Evaluation of the Revised Ontario Child Health Study Scales

Boyle, Michael H.; Offord, David R.; Racine, Yvonne; Fleming, Jan E.; Szatmári, Péter; Sanford, Mark

doi:10.1111/j.1469-7610.1993.tb00979.x

Cited by 258 publications

(200 citation statements)

References 15 publications

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“…At 6 y of age, mothers completed the MacArthur Health and Behavior Questionnaire (HBQ-P), which yielded measures of internalizing, externalizing, over anxious, and inattention behaviors. The HBQ was derived from the Ontario Child Health Study Measure designed to map on DSM-II_R symptom criteria consistent with the dimensions of internalizing and externalizing behaviors (38). The HBQ-P has strong psychometric properties and has been used to assess child mental health across multiple ages from 4.5 into adolescence (39).…”

Section: Child Behavioral Outcomesmentioning

confidence: 99%

Prenatal exposure to serotonin reuptake inhibitor antidepressants and childhood behavior

2015

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Background: Animal research has suggested that prenatal serotonin reuptake inhibitor (SRI) antidepressant exposure causes increased anxiety-like behaviors in adulthood. We examined whether in utero SRI exposure influenced externalizing and internalizing behaviors in children at 3 y and again at 6 y of age. Methods: We recruited women in their second trimester of pregnancy from primary maternity care providers in Vancouver British Columbia, Canada. We compared the internalizing, externalizing, and the anxious and attention subscales of the internalizing behaviors scores of children exposed to SRIs and children not exposed to SRIs at age 3 and age 6. results: We included 110 mother-child pairs (44 exposed to SRI and 66 not exposed). Higher levels of internalizing and anxious behaviors were reported in SRI exposed children at both 3 and 6 y of age compared with children who were not exposed (F = 7.52, P = 0.0072 and F = 7.91, P = 0.0058, respectively). The fully adjusted hierarchical regression models indicated a positive and significant relationship between SRI exposure and increased internalizing and anxious behaviors even when controlling for maternal mood during pregnancy, postpartum and childhood. conclusion: SRI exposure was associated with sustained higher levels of internalizing behaviors in early childhood even when controlling for maternal depression.

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Section: Child Behavioral Outcomesmentioning

confidence: 99%

Prenatal exposure to serotonin reuptake inhibitor antidepressants and childhood behavior

2015

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“…Exclusion criteria were subjects with scores below 80 on both the Performance and Verbal Scales of the WISC-III, 15 had evidence of neurological or chronic medical illness, bipolar affective disorder, psychotic symptoms, Tourette syndrome, or chronic multiple tics. Information for the diagnosis of ADHD and co-morbid conditions was based on a semistructured interview for parents (Parent Interview for Child Symptoms, PICS-IV; Schachar & Ickowicz, unpublished) and teachers (Teacher Telephone Interview-IV, TTI; Tannock & Schachar, unpublished), supplemented with the following questionnaires and child assessments: Conners Parent and Teacher Rating Scales-Revised, 16 the Ontario Child Health Survey Scales-Revised, 17 Wide Range Achievement Test-III, 18 Clinical Evaluation of Language Fundamentals, 3rd Edition, 19 Children's Depression Inventory, 20 and Children's Manifest Anxiety Scale. 21 Children were free of medication for a minimum of 24 h before their assessment.…”

Section: Diagnostic Criteriamentioning

confidence: 99%

Identification of DNA variants in the SNAP-25 gene and linkage study of these polymorphisms and attention-deficit hyperactivity disorder

et al. 2000

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The gene for the synaptic vesicle docking fusion protein, synaptosomal-associated protein of 25 kDa (SNAP-25), has been implicated in the etiology of attention-deficit hyperactivity disorder (ADHD) based on the mouse mutant strain coloboma. This neutron-irradiation induced mouse strain is hemizygous for the deletion of the SNAP-25 gene and displays spontaneous hyperactivity that is responsive to dextroamphetamine. Because of these characteristics, this strain has been suggested to be a mouse model for ADHD. We identified using single stranded conformational polymorphism analysis (SSCP) four DNA sequence variants in the 3Ј untranslated region of the human SNAP-25 gene. We searched for polymorphisms in the 3Ј untranslated region because the intron/exon structure of this gene has not yet been determined. We tested for linkage of this gene and ADHD using two of the identified polymorphisms that change a restriction enzyme recognition site. We examined the transmission of the alleles of each of these polymorphisms and the haplotypes of both polymorphisms using the transmission disequilibrium test in a sample of 97 small nuclear families consisting of a proband with ADHD, their parents, and affected siblings. We observed biased transmission of the haplotypes of the alleles of these two polymorphisms. Our findings are suggestive of a role of this gene in ADHD. Molecular Psychiatry (2000) 5, 405-409.

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“…Interviews were supplemented with information about behavior, development, and medical history derived from standardized parent and teacher questionnaires including the Conners Parent and Teacher Rating Scales-Revised 36 and the Ontario Child Health Survey Scales-Revised. 37 Children were assessed for anxiety (Children's Manifest Anxiety Scale 38 42 ). Children were included if they met DSM-IV criteria for one of the three ADHD subtypes (inattentive, hyperactive/impulsive, combined) and were excluded if they scored below 80 on both the Performance and Verbal Scales of the WISC-III, had evidence of neurological or complex medical illness, Tourette syndrome, chronic multiple tics, bipolar affective disorder, psychotic symptoms, or had comorbid anxiety, depressive or developmental disorder that could better account for the behaviors (as specified by DSM-IV).…”

Section: Diagnostic Instrumentsmentioning

confidence: 99%

Evidence for the serotonin HTR2A receptor gene as a susceptibility factor in attention deficit hyperactivity disorder (ADHD)

et al. 2000

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A recent study demonstrated that treatment of hyperactive mice with psychostimulants and serotonergic agents produced a calming effect that was dependent on serotonergic neurotransmission and was not associated with any changes in extracellular dopamine levels. 1 The complex interaction between the serotonergic and dopaminergic neurotransmitter systems suggests that a balance between the two systems may be necessary for mediating hyperactive behaviour. Defects in serotonin system genes, therefore, may disrupt normal brain serotonin function causing an imbalance between these neurotransmitter systems leading to the development of attention deficit hyperactivity disorder (ADHD). Attention deficit hyperactivity disorder (ADHD) is a common childhood disruptive behavioral disorder affecting between 3-5% of school age children who display persistent patterns of inattention and hyperactivity/impulsivity causing impairment in academic, social, and emotional development. 2 ADHD children frequently exhibit a variety of other comorbid conditions such as learning disorder, mood disorder, and other disruptive behavior disorders including oppositional defiant disorder (ODD) and conduct disorder (CD).While the exact mechanisms for the disorder are unknown, research has suggested abnormalities in the catecholaminergic and serotonergic systems. Support for a catecholaminergic hypothesis has been based on evidence from neuroimaging studies which have suggested reduced functioning in frontal-striatal regions, whose pathways are rich in catecholamines, notably dopamine. 3 Furthermore, stimulant medications, such as methylphenidate (Ritalin™), whose primary site of action is the dopamine transporter, have shown widespread clinical success in the treatment of ADHD. The significant interaction between the dopaminergic and serotonergic systems, 4 however, suggests that dopamine dysfunction may not be the sole basis for the development of ADHD.Evidence for the serotonergic hypothesis began two decades ago when it was found that whole blood and serum serotonin (5-HT) concentrations were decreased in children with ADHD. 5,6 These results have been further supported by a recent study that also found a tendency towards low platelet serotonin in a sample of children with severe ADHD. 7 Additional support for a serotonin hypothesis is demonstrated by the moderate efficacy of several serotonin enhancing agents in the treatment of ADHD including selective serotonin reuptake inhibitors (SSRIs) 8 and certain selective monoamine oxidase inhibitors. 9 Several lines of evidence have indicated abnormal serotonergic function in children with disruptive behaviour disorders (ADHD, ODD, CD) who display marked problems with hyperactivity, impulsivity, and aggression. [10][11][12][13][14] Animal models of ADHD have also been useful in implicating a role for serotonin in the control of attention, impulsivity, and hyperactivity. Rodents that had poorer performance on a task measuring attention and impulsivity had a greater index of serotonin utilization in t...

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Evaluation of the Revised Ontario Child Health Study Scales

Cited by 258 publications

References 15 publications

Prenatal exposure to serotonin reuptake inhibitor antidepressants and childhood behavior

Prenatal exposure to serotonin reuptake inhibitor antidepressants and childhood behavior

Identification of DNA variants in the SNAP-25 gene and linkage study of these polymorphisms and attention-deficit hyperactivity disorder

Evidence for the serotonin HTR2A receptor gene as a susceptibility factor in attention deficit hyperactivity disorder (ADHD)

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