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Stephen V Faraone - One of the best experts on this subject based on the ideXlab platform.
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deficient emotional self regulation and pediatric attention deficit hyperactivity disorder a Family risk analysis
Psychological Medicine, 2012Co-Authors: Joseph Biederman, Thomas J Spencer, Alexandra Lomedico, Helen Day, Carter R Petty, Stephen V FaraoneAbstract:BACKGROUND: Although deficient emotional self-regulation (DESR) is associated with attention deficit hyperactivity disorder (ADHD), little research investigates this association and little is known about its etiology. Family Studies provide a method of clarifying the co-occurrence of clinical features, but no Family Studies have yet addressed ADHD and DESR in children.MethodSubjects were 242 children with ADHD and 224 children without ADHD. DESR was operationalized using an aggregate score ⩾180 and Language: en
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deficient emotional self regulation and adult attention deficit hyperactivity disorder a Family risk analysis
American Journal of Psychiatry, 2011Co-Authors: Craig B H Surman, Joseph Biederman, Thomas J Spencer, Carter R Petty, Dayna Yorks, Carolyn A Miller, Stephen V FaraoneAbstract:Objective:A growing body of research suggests that deficient emotional self-regulation (DESR) is prevalent and morbid among patients with attention deficit hyperactivity disorder (ADHD). Family Studies provide a method of clarifying the co-occurrence of clinical features, but no Family Studies have yet addressed ADHD and DESR. Method:Participants were 83 probands with and without ADHD and 128 siblings. All were assessed for axis I DSM-IV conditions with structured diagnostic interviews. The authors defined DESR in adult probands and siblings using items from the Barkley Current Behavior Scale. Analyses tested hypotheses about the familial relationship between ADHD and DESR. Results:Siblings of ADHD probands were at elevated risk of having ADHD, irrespective of the presence or absence of DESR in the proband. The risk for DESR was elevated in siblings of ADHD plus DESR probands but not in siblings of ADHD probands. ADHD and DESR cosegregated in siblings. The risk for other psychiatric disorders was similar ...
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is attention deficit hyperactivity disorder a valid diagnosis in the presence of high iq results from the mgh longitudinal Family Studies of adhd
Journal of Child Psychology and Psychiatry, 2007Co-Authors: Kevin M Antshel, Stephen V Faraone, Kimberly Stallone, Andrea Nave, Felice A Kaufmann, Alysa E Doyle, Ronna Fried, Larry J Seidman, Joseph BiedermanAbstract:Background: The aim of this study was to assess the validity of diagnosing attention deficit/hyperactivity disorder (ADHD) in high IQ children and to further characterize the clinical features associated with their ADHD. Methods: We operationalized giftedness/high IQ as having a full scale IQ ≥120. We identified 92 children with a high IQ who did not have ADHD and 49 children with a high IQ that met diagnostic criteria for ADHD who had participated in the Massachusetts General Hospital Longitudinal Family Studies of ADHD. Results: Of our participants with ADHD and a high IQ, the majority (n = 35) met criteria for the Combined subtype. Relative to control participants, children with ADHD and high IQ had a higher prevalence rate of familial ADHD in first-degree relatives, repeated grades more often, had a poorer performance on the WISC-III Block Design, had more comorbid psychopathology, and had more functional impairments across a number of domains. Conclusions: Children with a high IQ and ADHD showed a pattern of familiality as well as cognitive, psychiatric and behavioral features consistent with the diagnosis of ADHD in children with average IQ. These data suggest that the diagnosis of ADHD is valid among high IQ children.
Joseph Biederman - One of the best experts on this subject based on the ideXlab platform.
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deficient emotional self regulation and pediatric attention deficit hyperactivity disorder a Family risk analysis
Psychological Medicine, 2012Co-Authors: Joseph Biederman, Thomas J Spencer, Alexandra Lomedico, Helen Day, Carter R Petty, Stephen V FaraoneAbstract:BACKGROUND: Although deficient emotional self-regulation (DESR) is associated with attention deficit hyperactivity disorder (ADHD), little research investigates this association and little is known about its etiology. Family Studies provide a method of clarifying the co-occurrence of clinical features, but no Family Studies have yet addressed ADHD and DESR in children.MethodSubjects were 242 children with ADHD and 224 children without ADHD. DESR was operationalized using an aggregate score ⩾180 and Language: en
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deficient emotional self regulation and adult attention deficit hyperactivity disorder a Family risk analysis
American Journal of Psychiatry, 2011Co-Authors: Craig B H Surman, Joseph Biederman, Thomas J Spencer, Carter R Petty, Dayna Yorks, Carolyn A Miller, Stephen V FaraoneAbstract:Objective:A growing body of research suggests that deficient emotional self-regulation (DESR) is prevalent and morbid among patients with attention deficit hyperactivity disorder (ADHD). Family Studies provide a method of clarifying the co-occurrence of clinical features, but no Family Studies have yet addressed ADHD and DESR. Method:Participants were 83 probands with and without ADHD and 128 siblings. All were assessed for axis I DSM-IV conditions with structured diagnostic interviews. The authors defined DESR in adult probands and siblings using items from the Barkley Current Behavior Scale. Analyses tested hypotheses about the familial relationship between ADHD and DESR. Results:Siblings of ADHD probands were at elevated risk of having ADHD, irrespective of the presence or absence of DESR in the proband. The risk for DESR was elevated in siblings of ADHD plus DESR probands but not in siblings of ADHD probands. ADHD and DESR cosegregated in siblings. The risk for other psychiatric disorders was similar ...
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is attention deficit hyperactivity disorder a valid diagnosis in the presence of high iq results from the mgh longitudinal Family Studies of adhd
Journal of Child Psychology and Psychiatry, 2007Co-Authors: Kevin M Antshel, Stephen V Faraone, Kimberly Stallone, Andrea Nave, Felice A Kaufmann, Alysa E Doyle, Ronna Fried, Larry J Seidman, Joseph BiedermanAbstract:Background: The aim of this study was to assess the validity of diagnosing attention deficit/hyperactivity disorder (ADHD) in high IQ children and to further characterize the clinical features associated with their ADHD. Methods: We operationalized giftedness/high IQ as having a full scale IQ ≥120. We identified 92 children with a high IQ who did not have ADHD and 49 children with a high IQ that met diagnostic criteria for ADHD who had participated in the Massachusetts General Hospital Longitudinal Family Studies of ADHD. Results: Of our participants with ADHD and a high IQ, the majority (n = 35) met criteria for the Combined subtype. Relative to control participants, children with ADHD and high IQ had a higher prevalence rate of familial ADHD in first-degree relatives, repeated grades more often, had a poorer performance on the WISC-III Block Design, had more comorbid psychopathology, and had more functional impairments across a number of domains. Conclusions: Children with a high IQ and ADHD showed a pattern of familiality as well as cognitive, psychiatric and behavioral features consistent with the diagnosis of ADHD in children with average IQ. These data suggest that the diagnosis of ADHD is valid among high IQ children.
Sylvia Stockleripsiroglu - One of the best experts on this subject based on the ideXlab platform.
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molecular characterisation and neuropsychological outcome of 21 patients with profound biotinidase deficiency detected by newborn screening and Family Studies
European Journal of Pediatrics, 2003Co-Authors: Dorothea Moslinger, R Baumgartner, Terttu Suormala, Adolf Muhl, Sylvia StockleripsirogluAbstract:Early recognition by newborn screening and oral biotin supplementation may prevent clinical and neurological deficits in profound biotinidase deficiency (residual plasma biotinidase activity <10%). In order to evaluate possible correlations of molecular characteristics, onset and continuation of treatment and clinical outcome, we investigated 21 patients detected by newborn screening and consecutive Family investigations. In 18 patients found by newborn screening, the range of biotinidase activities was 0%–9% residual activity. Application of a sensitive HPLC assay enabled us to discriminate five patients with residual biotinidase activities <1%. Two patients with zero activities were homozygous for the G98:d7i3 mutation and three patients with activities <1% carried mutations G98:d7i3, R157H, and Q456H. The mutation spectrum of the remaining patients included T532M, A171T+D444H, V62M,C432W, and D444H. Evaluation of clinical and neuropsychological outcome showed that only patients with biotinidase activities <1% exhibited characteristic clinical symptoms within the first weeks of life whereas five patients with residual activities of 1.2%–4.6% did not develop clinical symptoms even when not treated until 3.5–21 years. In all patients treated with biotin within the first weeks of life, neuropsychological outcome was normal whereas abnormal in three out of five patients tested for IQ and treated after the age of 3.5 years. Conclusion:the clinical and molecular spectrum of profound biotinidase deficiency is heterogeneous. Early onset of symptoms is predicted by the presence of zero residual activity as measured by sensitive assays and by homozygosity for the G98:d7i3 mutation. In patients with higher residual activities and variable mutational spectrum, correlation with the onset and severity of symptoms cannot be made.
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clinical and neuropsychological outcome in 33 patients with biotinidase deficiency ascertained by nationwide newborn screening and Family Studies in austria
European Journal of Pediatrics, 2001Co-Authors: Dorothea Moslinger, Terttu Suormala, Adolf Muhl, Sylvia Stockleripsiroglu, S Scheibenreiter, Monika Tiefenthaler, Rainer Seidl, W Strobl, Barbara Plecko, Regula E BaumgartnerAbstract:Newborn screening for biotinidase deficiency (BD) provides prevention of neurological sequelae in patients with low residual enzyme activity by early treatment with oral biotin substitution. Screening 1.1 million newborns in Austria and consecutive Family Studies led to the identifcation of 21 patients with profound BD (residual activity 1%–<10% (n=16) respectively. Evaluation of clinical and neuropsychological outcome showed that only patients with a biotinidase activity <1% (n=3/5) exhibited characteristic clinical symptoms within the first weeks of life, while five patients with a residual activity of 1.2%–4.6% did not develop clinical symptoms even when not treated until 3.5–21 years. In all patients with residual activity <10% and biotin substitution within the first weeks of life, neuropsychological outcome was normal, while abnormal in three out of five patients tested for IQ and treated after the age of 3.5 years. In five out of nine patients with poor compliance or delayed or no treatment, visual and brainstem auditory evoked potentials were measured and were within age-related normal values. All patients with partial BD available for follow-up remained clinically and neuropsychologically asymptomatic without treatment at ages 2.5–10 years.
Dorothea Moslinger - One of the best experts on this subject based on the ideXlab platform.
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molecular characterisation and neuropsychological outcome of 21 patients with profound biotinidase deficiency detected by newborn screening and Family Studies
European Journal of Pediatrics, 2003Co-Authors: Dorothea Moslinger, R Baumgartner, Terttu Suormala, Adolf Muhl, Sylvia StockleripsirogluAbstract:Early recognition by newborn screening and oral biotin supplementation may prevent clinical and neurological deficits in profound biotinidase deficiency (residual plasma biotinidase activity <10%). In order to evaluate possible correlations of molecular characteristics, onset and continuation of treatment and clinical outcome, we investigated 21 patients detected by newborn screening and consecutive Family investigations. In 18 patients found by newborn screening, the range of biotinidase activities was 0%–9% residual activity. Application of a sensitive HPLC assay enabled us to discriminate five patients with residual biotinidase activities <1%. Two patients with zero activities were homozygous for the G98:d7i3 mutation and three patients with activities <1% carried mutations G98:d7i3, R157H, and Q456H. The mutation spectrum of the remaining patients included T532M, A171T+D444H, V62M,C432W, and D444H. Evaluation of clinical and neuropsychological outcome showed that only patients with biotinidase activities <1% exhibited characteristic clinical symptoms within the first weeks of life whereas five patients with residual activities of 1.2%–4.6% did not develop clinical symptoms even when not treated until 3.5–21 years. In all patients treated with biotin within the first weeks of life, neuropsychological outcome was normal whereas abnormal in three out of five patients tested for IQ and treated after the age of 3.5 years. Conclusion:the clinical and molecular spectrum of profound biotinidase deficiency is heterogeneous. Early onset of symptoms is predicted by the presence of zero residual activity as measured by sensitive assays and by homozygosity for the G98:d7i3 mutation. In patients with higher residual activities and variable mutational spectrum, correlation with the onset and severity of symptoms cannot be made.
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clinical and neuropsychological outcome in 33 patients with biotinidase deficiency ascertained by nationwide newborn screening and Family Studies in austria
European Journal of Pediatrics, 2001Co-Authors: Dorothea Moslinger, Terttu Suormala, Adolf Muhl, Sylvia Stockleripsiroglu, S Scheibenreiter, Monika Tiefenthaler, Rainer Seidl, W Strobl, Barbara Plecko, Regula E BaumgartnerAbstract:Newborn screening for biotinidase deficiency (BD) provides prevention of neurological sequelae in patients with low residual enzyme activity by early treatment with oral biotin substitution. Screening 1.1 million newborns in Austria and consecutive Family Studies led to the identifcation of 21 patients with profound BD (residual activity 1%–<10% (n=16) respectively. Evaluation of clinical and neuropsychological outcome showed that only patients with a biotinidase activity <1% (n=3/5) exhibited characteristic clinical symptoms within the first weeks of life, while five patients with a residual activity of 1.2%–4.6% did not develop clinical symptoms even when not treated until 3.5–21 years. In all patients with residual activity <10% and biotin substitution within the first weeks of life, neuropsychological outcome was normal, while abnormal in three out of five patients tested for IQ and treated after the age of 3.5 years. In five out of nine patients with poor compliance or delayed or no treatment, visual and brainstem auditory evoked potentials were measured and were within age-related normal values. All patients with partial BD available for follow-up remained clinically and neuropsychologically asymptomatic without treatment at ages 2.5–10 years.
Larry J Seidman - One of the best experts on this subject based on the ideXlab platform.
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early childhood iq trajectories in individuals later developing schizophrenia and affective psychoses in the new england Family Studies
Schizophrenia Bulletin, 2015Co-Authors: Jessica Agnewblais, Stephen L Buka, Garrett M Fitzmaurice, Jordan W Smoller, Jill M Goldstein, Larry J SeidmanAbstract:Individuals who develop schizophrenia in adulthood exhibit, on average, deficits in childhood cognition relative to healthy controls. However, it remains unclear when in childhood such deficits emerge and whether they are stable across childhood or change (increase or decrease) across development. Importantly, whether the trajectory of childhood cognition differs among youth who later develop affective psychoses (AP) vs schizophrenia as adults remains unresolved. Subjects in the Collaborative Perinatal Project were administered the Stanford-Binet IQ test at age 4 and the Wechsler Intelligence Scale for Children at age 7. A total of 9809 (54.7%) participants in the New England Study sites were tested at both ages, including 37 who later developed schizophrenia spectrum psychoses (SSP) and 39 who later developed AP. Logistic regression models examined the association of level of and change in childhood IQ and later SSP or AP. Lower overall childhood IQ was associated with higher risk of SSP. Additionally, there was a small mean increase in IQ in the SSP group relative to a mean decrease in the control group from age 4 to 7 such that positive change in IQ was significantly associated with a higher risk of SSP. Neither overall level nor change in IQ was associated with risk of AP. The results are consistent with neurocognitive impairment throughout early childhood specifically for children who later develop schizophrenia, affirming the theory of atypical neurodevelopment in premorbid schizophrenia.
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neuropsychological performance and Family history in children at age 7 who develop adult schizophrenia or bipolar psychosis in the new england Family Studies
Psychological Medicine, 2013Co-Authors: Larry J Seidman, Jessica Agnewblais, Jill M Goldstein, Sara Cherkerzian, Ming T Tsuang, Stephen L BukaAbstract:BACKGROUND Persons developing schizophrenia (SCZ) manifest various pre-morbid neuropsychological deficits, studied most often by measures of IQ. Far less is known about pre-morbid neuropsychological functioning in individuals who later develop bipolar psychoses (BP). We evaluated the specificity and impact of Family history (FH) of psychosis on pre-morbid neuropsychological functioning. METHOD We conducted a nested case-control study investigating the associations of neuropsychological data collected systematically at age 7 years for 99 adults with psychotic diagnoses (including 45 SCZ and 35 BP) and 101 controls, drawn from the New England cohort of the Collaborative Perinatal Project (CPP). A mixed-model approach evaluated full-scale IQ, four neuropsychological factors derived from principal components analysis (PCA), and the profile of 10 intelligence and achievement tests, controlling for maternal education, race and intra-familial correlation. We used a deviant responder approach (<10th percentile) to calculate rates of impairment. RESULTS There was a significant linear trend, with the SCZ group performing worst. The profile of childhood deficits for persons with SCZ did not differ significantly from BP. Neuropsychological impairment was identified in 42.2% of SCZ, 22.9% of BP and 7% of controls. The presence of psychosis in first-degree relatives (FH+) significantly increased the severity of childhood impairment for SCZ but not for BP. CONCLUSIONS Pre-morbid neuropsychological deficits are found in a substantial proportion of children who later develop SCZ, especially in the SCZ FH+ subgroup, but less so in BP, suggesting especially impaired neurodevelopment underlying cognition in pre-SCZ children. Future work should assess genetic and environmental factors that explain this FH effect.
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is attention deficit hyperactivity disorder a valid diagnosis in the presence of high iq results from the mgh longitudinal Family Studies of adhd
Journal of Child Psychology and Psychiatry, 2007Co-Authors: Kevin M Antshel, Stephen V Faraone, Kimberly Stallone, Andrea Nave, Felice A Kaufmann, Alysa E Doyle, Ronna Fried, Larry J Seidman, Joseph BiedermanAbstract:Background: The aim of this study was to assess the validity of diagnosing attention deficit/hyperactivity disorder (ADHD) in high IQ children and to further characterize the clinical features associated with their ADHD. Methods: We operationalized giftedness/high IQ as having a full scale IQ ≥120. We identified 92 children with a high IQ who did not have ADHD and 49 children with a high IQ that met diagnostic criteria for ADHD who had participated in the Massachusetts General Hospital Longitudinal Family Studies of ADHD. Results: Of our participants with ADHD and a high IQ, the majority (n = 35) met criteria for the Combined subtype. Relative to control participants, children with ADHD and high IQ had a higher prevalence rate of familial ADHD in first-degree relatives, repeated grades more often, had a poorer performance on the WISC-III Block Design, had more comorbid psychopathology, and had more functional impairments across a number of domains. Conclusions: Children with a high IQ and ADHD showed a pattern of familiality as well as cognitive, psychiatric and behavioral features consistent with the diagnosis of ADHD in children with average IQ. These data suggest that the diagnosis of ADHD is valid among high IQ children.
