Alcohol Syndrome Disorders Research Articles

The Clinical Application of Applied Behavior Analysis in a Child With Partial Fetal Alcohol Syndrome

The current case study describes the longitudinal assessment of a young child diagnosed with Partial Fetal Alcohol Syndrome and pervasive developmental disorder–not otherwise specified. The patient participated in an applied behavior analysis (ABA)–based Verbal Behavior treatment program to target communication impairments and functional skill deficits. Because ABA-based interventions have demonstrated efficacy in improving levels of functioning across various developmental disabilities, it was reasonable to assess the clinical utility of these same strategies when applied to a patient presenting with fetal alcohol spectrum disorder and associated developmental delays. The current study relied on quasi-experimental single-subject design methods to measure treatment outcomes and to inform clinical decision making. Dependent measures in the study included standardized, norm-referenced assessments of cognitive and adaptive functioning, as well as behavioral data collected throughout treatment to measure gains across skill areas. Outcomes included rapid skill acquisition across several areas of functioning (e.g., expressive and receptive language, visual-performance, and adaptive emotional/behavioral functioning). The impact of treatment on global areas of functioning will be reported.

Фетальный алкогольный синдром и краткосрочное психологическое вмешательство как метод его профилактики

This article presents brief intervention method, conducted with childbearing age women, aimed at fetal alcohol syndrome prevention. The article describes a model of intervention, provides the principles and successive steps. This method was developed in the framework of an international research grant project R01AA016234 «Prevention of fetal alcohol syndrome and neurodevelopmental disorders in Russian children».

Cortical Thickness in Fetal Alcohol Syndrome and Attention Deficit Disorder

Cortical Thickness in Fetal Alcohol Syndrome and Attention Deficit Disorder

Congenital malformations in newborns of alcoholic mothers

To identify the presence of fetal alcohol syndrome, other alcohol-related congenital defects, and/or neurodevelopment disorders in newborns of mothers who consumed alcohol during gestation. In a public maternity in the city of São Paulo, 1,964 puerperal women were interviewed and 654 had consumed alcohol at some point during gestation. The newborns were clinically and laboratorially examined in order to identify the occurrence of fetal alcohol syndrome, congenital defects or neurodevelopment disorders related to alcohol. Three children were found with fetal alcohol syndrome (1.5/1,000 live births), 6 with congenital defects related to alcohol (3.0/1,000 live births), and 67 with developmental disorders related to alcohol (34.1/1,000 live births). The congenital malformations found in these children were thin or absent corpus callosum, brain cyst, asymmetry of the cerebral ventricles, meningomyelocele, cleft lip, anteverted nose, low-set ears, megaureter, hydronephrosis, polydactyly, congenital clubfoot, aphalangia of the toes, cryptorchidism, and hypospadia. Newborns of mothers who consumed alcohol may have congenital malformations of various organs and systems, and early diagnosis is fundamental for a probable and occasional more effective resolution and progress.

Fetal Alcohol Syndrome, Tourette Syndrome, and Hyperactivity in Nine Adopted Children

Much attention has been paid in recent years to the role of prenatal exposure to alcohol. Fetal alcohol syndrome is one of the most severe afflictions resulting from such exposure. The present report documents the cases of adopted children diagnosed with fetal alcohol syndrome who developed both Tourette syndrome and attention deficit-hyperactivity disorder. Out of a population of 138 adopted children with behavior issues whose clinical histories were reviewed retrospectively, 9 children (6.5%) presented this constellation. Epidemiologic data, clinical data, neurologic examination findings, complementary testing, and developmental data were recorded. All nine patients studied had initial psychomotor retardation, despite the frequent case of subsequent intelligence quotient normalization. From a behavioral perspective, half of the cases presented obsessive-compulsive disorder and problems with social relations. Aggressive behavior was common. These cases also presented a high degree of severity of both tics and hyperactivity. The most common drug treatment was methylphenidate. This constellation of fetal alcohol syndrome, Tourette syndrome, and attention deficit-hyperactivity disorder is scantly reported in the literature and is likely underdiagnosed. This particular constellation poses its own prognosis and requires its own treatment.

Binge Drinking During Pregnancy: Long-Term Effects on Offspring

The consequences of prenatal exposure to alcohol include a heightened risk for fetal alcohol syndrome and alcohol-related developmental disorders

Alcohol Brain Damage and Neuroinflammation: Is There a Connection?

Many neurological disorders include a neuroinflammatory response in the central nervous system (CNS) that contributes to the pathogenesis and progression of the condition. However, the question of whether neuroinflammation plays a role in alcohol-induced brain damage has received little attention. This symposium at the 2004 World Congress on Biomedical Alcohol Research held in Mannheim, Germany considered for the first time the relationship between alcohol neuropathology and neuroinflammation. The organizers and co-chairs were Peter J. Syapin and Cynthia J. M. Kane. Neuroinflammatory responses including glial activation, demyelination, neuronal damage and neurodegeneration may contribute to the neurological deficits associated with alcoholism, alcohol abuse, fetal alcohol syndrome or alcohol-related neurodevelopmental disorder. A substantial body of literature indicates that alcohol directly affects astroglial cell function, including inflammation-related activity. In addition, emerging data indicate that alcohol affects microglial cell development and function in specific ways that interfere with microglial interactions with the immune system and with neurons. This symposium provided alcohol researchers with background information on CNS immunity and inflammatory processes and examined emerging experimental evidence that neuroinflammatory processes might be involved in alcohol-induced brain damage. A brief introduction was followed by four presentations, the first two describing the nature of immune reactions in the CNS and the role of astrocytes and microglia in neuroinflammatory processes. The presentations included: (1) Initiation of inflammation in the nervous system, by William Hickey; (2) Microglia – Interface between immune system and brain, by Helmut Kettenmann; (3) Ethanol and neuroinflammatory response in brain astroglial, by Peter Syapin; and (4) Microglia are targets of alcohol pathogenesis in the developing CNS, by Cynthia Kane.

PAEDIATRICS SELECTIONPediatrics (2000) American Academy of Pediatrics. Foetal alcohol syndrome and alcohol-related neuro-developmental disorders. Vol. 106, No. 2, pp. 358–361.

<b>PAEDIATRICS SELECTION</b><b><i>Pediatrics (2000)</i></b> American Academy of Pediatrics. <i>Foetal alcohol syndrome and alcohol-related neuro-developmental disorders</i>. Vol. 106, No. 2, pp. 358–361.

The role of retinoid metabolism by alcohol and aldehyde dehydrogenases in differentiation of cultured neuronal cells.

Retinoic acid is a morphogen that plays important roles during fetal growth in specification of head and limb bud development (Hofman and Eichele, 1994), and probably also in regulation of neuronal development (Holder and Maden, 1992). Exposure of the developing fetus to ethanol can cause a range of deformities and neurological abnormalities, leading to conditions known in humans as fetal alcohol syndrome (FAS) and alcohol related neurodevelopmental disorder (ARND) (Sampson et al., 1997). Retinoic acid is formed from retinol (vitamin A) via oxidation first to retinal, catalysed by isozymes of alcohol dehydrogenase (ADH) or the short chain dehydrogenase/reductase family. Retinal is then oxidised to retinoic acid by aldehyde dehydrogenase (A1DH), retinal dehydrogenase or microsomal cytochrome P450 1A1 or 1A2 (Duester, 1996). Retinoic acid has its effect on fetal development through binding to nuclear receptors and forming transcription factors which n regulate gene expression (De Luca, 1991; Chambon, 1996). It has been postulated that one of the mechanisms leading to the development of FAS or ARND may be inhibition of retinoic acid production caused by competitive inhibition of alcohol and/or aldehyde dehydrogenases during ethanol metabolism (Duester, 1991, Deltour et al., 1996). e present study was initiated to see whether cultured neuronal cells could be used a model system in which to study the effects of ethanol and acetaldehyde on retinoid- regulated neuronal cell differentiation. A human neuroblastoma cell line, SH-SY5Y, was chosen because it had previously been shown to be responsive to retinoic acid (Pahlman et al., 1984).

Disabled American Indians: A Special Population Requiring Special Considerations

It is well known that the health status of American Indians is below national averages and has been for many years. Identified health difficulties include a pattern of social problems, poverty, and disease that is unparalleled among other ethnic and racial minorities in the United States. The disabled American Indian, however, faces additional disadvantages in the form of major barriers to care and rehabilitation services. Further, the incidence of several serious disabling conditions among some tribes is thought to be well above that reported for the United States population as a whole. Fetal alcohol syndrome (FAS), bacterial meningitis, otitis media, diabetes, accidentsltrauma, alcoholldrug abuse, and mental and emotional disorders cause disabilities among Indians at significantly higher rates than among non-Indians. Major disabilities include seizure disorder, developmental delay, language and speech delay, mental retardation, pulmonary disorders, vision problems, hearing loss, trauma from accidents, diabetesrelated disabilities, and alcoholism. The severity of each problem, however, varies from one Indian group to another. Fetal alcohol syndrome (FAS) and fetal alcohol effect (FAE), disabling conditions which have been identified and categorized only since 1973, consist of a group of physical and developmental abnormalities present in infants, which are caused by maternal