Recognition of the Fetal Alcohol Syndrome in Early Infancy

Jones, KennethL.; Smith, Dale E.

doi:10.1016/s0140-6736(73)91092-1

Cited by 2,411 publications

(1,163 citation statements)

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“…Although FAS was identified in the U.S. over 35 years ago [Jones and Smith, 1973], the development, evaluation, and dissemination of evidencebased interventions for alcohol-exposed individuals have lagged behind significantly. A review by Premji et al [2006] highlighted the paucity of researchbased interventions for this population, and further noted that the few extant studies were characterized by small sample sizes and methodological limitations.…”

Section: Interventions For Fasdsmentioning

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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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: Interventions For Fasdsmentioning

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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“…In mice, exposure to ethanol on gestational day (G) 7 or G8 increases the expression of markers for cell death (Dunty et al, 2002;Kilburn et al, 2006). More impressive is that mice exposed to ethanol during gastrulation (Sulik et al, 1981;Dunty et al, 2002;Da Lee et al, 2004) exhibit craniofacial malformations like those that characterize human children with fetal alcohol syndrome (FAS) (Lemoine et al, 1968;Jones and Smith, 1973). Similar time-dependent vulnerability is evident in the monkey (Astley et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Time-specific effects of ethanol exposure on cranial nerve nuclei: Gastrulation and neuronogenesis

Mooney

Miller

2007

Experimental Neurology

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During the development of the central nervous system, neurons pass through critical periods or periods of vulnerability. We explored periods of vulnerability for cranial nerve nuclei by determining the effects of acute exposure to ethanol during development on the number of neurons in mature brainstem. Long-Evans rats were injected with 2.9 g ethanol/kg body weight on one day between gestational day (G) 7 and G13, inclusive. Two hours later, animals received a second injection of 1.45 g/kg. Controls were injected with equivalent volumes of saline. Brainstems of 31-day-old offspring were cryosectioned and stained with cresyl violet. Stereological methods were used to determine the volume and numerical density of neurons in three trigeminal sensory nuclei (the principal sensory nucleus of the trigeminal nerve, and the oral and interpolar subnuclei of the spinal trigeminal nuclear complex) and three motor nuclei (the trigeminal, facial, and hypoglossal nuclei). The numbers of neurons in most nuclei were lower following early (on G7 and/or G8) or later (on G12 and/or G13) exposure. Only the trigeminal interpolar nucleus was affected by neither early nor late ethanol exposure. Thus, prenatal exposure to ethanol affects the number of neurons in brainstem nuclei in a time-dependent manner. Windows of vulnerability coincide with gastrulation (G7/G8) and the period of neuronal generation (G12/G13).

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“…31 Phenotypic abnormalities of FASD include neurological, craniofacial, cardiac, and limb malformations, as well as generalized growth deficits and mental retardation. 32 The mechanisms proposed to underlie the spectrum of birth defects caused by fetal alcohol exposure include: apoptosis, 33 cell adhesion defects, 34 accumulation of free radicals, 35 dysregulation of growth factors, 36 and altered retinoic acid biosynthesis. 37 Some simple and essential questions have not been well explained by these hypotheses, for instance, how one or, at most, a few social drinks, cause fetal defects, why alcohol preferentially induces defects targeting some organs and tissues and not others, or why the pattern of defects seen in FASD is predictable and reproducible.…”

mentioning

confidence: 99%