Fetal alcohol syndrome: neuropsychiatric phenomics

Burd, Larry; Klug, Marilyn G.; Martsolf, John T.; Kerbeshian, Jacob

doi:10.1016/j.ntt.2003.07.014

Cited by 159 publications

(129 citation statements)

References 16 publications

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“…Children with FASDs show deficits in language comprehension, reading, spelling, and math [Mattson et al, 1998;Duquette and Stodel, 2005] and are at increased risk for learning disabilities [Burd et al, 2003] as well as problematic classroom behaviors [Carmichael Olson et al, 1992].…”

Section: Educational and Cognitive Interventionsmentioning

confidence: 99%

“…Numerous studies have found individuals with FASDs to be at elevated risk for disruptive behavior problems, mood disorders, substance use or abuse problems, and psychiatric confinement [Famy et al, 1998;O'Connor et al, 2002;Burd et al, 2003;Streissguth et al, 2004;Bhatara et al, 2006;Burd et al, 2007;Walthall et al, 2008]. Given such findings, it is not surprising that children with FASDs often receive pharmacological intervention.…”

Section: Pharmacological Interventionsmentioning

confidence: 99%

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Intervention for individuals with fetal alcohol spectrum disorders: Treatment approaches and case management

Paley¹,

O’Connor²

2009

Dev Disabil Res Revs

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Exposure to alcohol in utero is considered to be the leading cause of developmental disabilities of known etiology. The most severe consequence of such exposure, fetal alcohol syndrome (FAS), is characterized by a distinct constellation of characteristic facial anomalies, growth retardation, and central nervous system (CNS) dysfunction. Some individuals with prenatal alcohol exposure (PAE) do not meet the full criteria for FAS, but instead are diagnosed with partial FAS, alcohol related neurodevelopmental disorder (ARND), or alcohol related birth defects (ARBD). The entire continuum of effects from PAE is increasingly being referred to under the umbrella term of fetal alcohol spectrum disorders (FASDs). An extensive body of research has documented major cognitive, behavioral, adaptive, social, and emotional impairments among individuals with FASDs. Although FAS was identified in the U.S. over 35 years ago, the development, evaluation, and dissemination of evidencebased interventions for individuals with FASDs have lagged behind significantly. Encouragingly, however, in recent years there has been a marked increase in efforts to design and test interventions to remediate the impairments associated with prenatal alcohol exposure. This article will review treatment needs and considerations for individuals with FASDs and their families, current empirically tested treatment approaches, case management issues, and suggestions for future directions in research on the treatment of FASDs. ' 2009 Wiley-Liss, Inc. Dev Disabil Res Rev 200915:258-267.

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Section: Educational and Cognitive Interventionsmentioning

confidence: 99%

Section: Pharmacological Interventionsmentioning

confidence: 99%

Intervention for individuals with fetal alcohol spectrum disorders: Treatment approaches and case management

Paley¹,

O’Connor²

2009

Dev Disabil Res Revs

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“…Researchers have proposed a link between prenatal alcohol exposure and infant irritability (Burd, Klug, Martsolf, & Kerbeshian 2003;Clifford, Campbell, Speechley, & Gorodzinsky, 2002;Coles & Platzman, 1993;Scher, Richardson, Coble, Day, & Stoffer, 1988) mediated by subtle neuronal dysfunctions (Kelly, Day, & Streissguth, 2000). In the most severe cases, maternal drinking leads to fetal alcohol syndrome, which is diagnosed when three criteria are met: (a) growth deficiency in both the prenatal and postnatal periods, (b) structural anomalities and/or functional deficits in the central nervous system associated with mental retardation and behavioral problems, and (c) a distinctive pattern of abnormal facial features (Sokol & Clarren, 1989).…”

Section: Prenatal Alcohol Exposurementioning

confidence: 99%

Infant irritability: The impact of fetal alcohol exposure, maternal depressive symptoms, and low emotional support from the husband

Lemola

Stadlmayr

Grob

2009

Infant Mental Health Journal

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Objectives: The aim of this study was to investigate the impact of fetal alcohol exposure, maternal depressive symptoms, and low emotional support from the husband on infant irritability in the first one and a half years of life. Four models describing the interplay of these factors were assessed: A direct effect model, an interaction or threshold model, a mediational model and a transactional model. Method: A sample of initially 458 women was assessed in a prospective 3-wave study across the first 17 months after childbirth. Fetal alcohol exposure was questioned retrospectively six weeks after birth. Infant irritability was reported by the mothers and fathers. Results: Support for the direct effect model and the interaction model could be found: Fetal alcohol exposure and low emotional support from the husband were associated with increased infant irritability at 5 months. The impact of fetal alcohol exposure was moderated by postnatal depressive symptoms. More irritability was reported if both risk factors, prenatal alcohol exposure and maternal depressive symptoms, were present. Infant irritability and maternal depressive symptoms were associated cross-sectionally. At the age of 17 months only a main effect of prenatal alcohol exposure on irritability could be found. Conclusion: Direct effects of fetal alcohol exposure, maternal depressive symptoms, and low emotional support from the husband on infant irritability as well as an interaction between fetal alcohol exposure and maternal depressive symptoms were revealed. The interaction can be understood in terms of a diathesisstress model. However, no longitudinal associations between maternal depressive symptoms and infant irritability could be found. Objetivos: La meta de este estudio fue investigar el impacto que el haber estado el feto expuesto al alcohol, los síntomas de la depresión maternal, y el bajo apoyo emocional de parte del esposo tienen sobre la irritabilidad del infante en el primer año y medio de vida. Se evaluaron cuatro modelos que describen el interjuego de estos factores: un modelo de efecto directo, un modelo de interacción o de entrada, un modelo de meditación y un modelo transaccional. Método: Un grupo muestra de 458 mujeres fue evaluado en un estudio de tres etapas futuras a través de los 17 meses después del nacimiento del niño. El haber estado el feto expuesto al alcohol fue investigado retrospectivamente seis semanas después del nacimiento. Las madres y los padres reportaron la irritabilidad del infante. Resultados: Se puede encontrar apoyo para el modelo directo y el modelo de interacción: se asociaron la exposición al alcohol del feto y el bajo apoyo emocional del esposo con el incremento de la irritabilidad del infante a los 5 meses. El impacto de la exposición del feto al alcohol fue moderada por los síntomas depresivos postnatales. Se reportó más irritabilidad si ambos factores de riesgo, la exposición del feto al alcohol y los síntomas de depresión maternal, se encontraban presentes. La irritabilidad del infante y los s...

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“…The Detroit study indicates effects on aggressive behavior in 7-year-olds down to levels of approximately 1 drink/ week (or 0.3 AA/day) when using average ounces of absolute alcohol per day (AA/day) as the dose metric (Sood et al, 2001). Other studies have shown a significant relationship between alcohol exposure in utero and neuropsychiatric disorders or aberrant social behavior later in life (Burd et al, 2003;Kelly et al, 2000). However, it should be noted that although this population had relatively low average levels of drinking, they tended to consume alcohol on average 2 days per week.…”

Section: Rat Humanmentioning

confidence: 99%

Computational models of ethanol‐induced neurodevelopmental toxicity across species: Implications for risk assessment

Gohlke

Griffith

Faustman

2007

Birth Defects Research Pt B

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Computational, systems-based approaches can provide a quantitative construct for evaluating risk in the context of mechanistic data. Previously, we developed computational models for the rat, mouse, rhesus monkey, and human, describing the acquisition of adult neuron number in the neocortex during the key neurodevelopmental processes of neurogenesis and synaptogenesis. Here we apply mechanistic data from the rat describing ethanol-induced toxicity in the developing neocortex to evaluate the utility of these models for analyzing neurodevelopmental toxicity across species. Our model can explain long-term neocortical neuronal loss in the rodent model after in utero exposure to ethanol based on inhibition of proliferation during neurogenesis. Our human model predicts a significant neuronal deficit after daily peak BECs reaching 10-20 mg/dl, which is the approximate BEC reached after drinking one standard drink within one hour. In contrast, peak daily BECs of 100 mg/dl are necessary to predict similar deficits in the rat. Our model prediction of increased sensitivity of primate species to ethanol-induced inhibition of proliferation is based on application of in vivo experimental data from primates showing a prolonged rapid growth period in the primate versus rodent neuronal progenitor population. To place our predictions into a broader context, we evaluate the evidence for functional low-dose effects across rats, monkeys, and humans. Results from this critical evaluation suggest subtle effects are evident at doses causing peak BECs of approximately 20 mg/dl daily, corroborating our model predictions. Our example highlights the utility of a systems-based modeling approach in risk assessment. Birth Defects Res (Part B) 83: 1-11, 2008.

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Fetal alcohol syndrome: neuropsychiatric phenomics

Cited by 159 publications

References 16 publications

Intervention for individuals with fetal alcohol spectrum disorders: Treatment approaches and case management

Intervention for individuals with fetal alcohol spectrum disorders: Treatment approaches and case management

Infant irritability: The impact of fetal alcohol exposure, maternal depressive symptoms, and low emotional support from the husband

Computational models of ethanol‐induced neurodevelopmental toxicity across species: Implications for risk assessment

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