Developmental Language Disability As a Consequence of Prenatal Exposure to Ethanol

PEDIATRICS ◽  
1981 ◽  
Vol 68 (6) ◽  
pp. 850-855 ◽  
Author(s):  
Sally E. Shaywitz ◽  
Barbara K. Caparulo ◽  
Elizabeth Susan Hodgson

Two pre-school-aged patients with a history of prenatal exposure to ethanol had abnormal head size and developmental delay. Both children were strikingly similar in physical appearance, behavior, and cognitive dysfunction. Facial features were typical of fetal alcohol syndrome. Head circumference >97th percentile without hydrocephalus and no evidence of prenatal or postnatal growth failure were unusual for ethanol teratogenicity. Each child had a similar pattern of verbal and behavioral dysfunctions characterized by (1) marked hypervigilence, (2) distractability, and (3) cognitive confusion manifested as anxiety and behavioral disorganization. It is suggested that a history of prenatal exposure to ethanol associated with (1) large head circumference, (2) facial features of fetal alcohol syndrome, and (3) early developmental delay, particularly in language acquisition, and impaired modulation of attention and arousal may represent a possible new effect of alcohol teratogenicity.

2007 ◽  
Vol 31 (10) ◽  
pp. 1707-1713 ◽  
Author(s):  
Elizabeth S. Moore ◽  
Richard E. Ward ◽  
Leah Flury Wetherill ◽  
Jeffrey L. Rogers ◽  
Ilona Autti-Rämö ◽  
...  

Human Nature ◽  
2004 ◽  
Vol 15 (1) ◽  
pp. 101-117 ◽  
Author(s):  
Katherine L. Waller ◽  
Anthony Volk ◽  
Vernon L. Quinsey

Key Points FASD is a continuum of physical, growth, and neurobehavioral abnormalities that occur as a result of prenatal exposure to alcohol and other disorders in FASD include: Partial fetal alcohol syndrome (PFAS)Alcohol-related birth defects (ARBD)Alcohol-related neurodevelopmental disorder (ARND)Diagnosis of FAS and other FASD is established by history and physical examination.Early recognition and treatment is crucial for better outcomes.Multidisciplinary team approach is recommended for management.


The Lancet ◽  
1977 ◽  
Vol 310 (8051) ◽  
pp. 1292-1293 ◽  
Author(s):  
Lusia Hornstein ◽  
Carol Crowe ◽  
Ralph Gruppo

PEDIATRICS ◽  
1994 ◽  
Vol 93 (2) ◽  
pp. 211-215
Author(s):  
Margaret A. Pearson ◽  
Mary E. Rimsza ◽  
H. Eugene Hoyme ◽  
Laurie H. Seaver

Objective. To determine if maternal toluene abuse produces any structural or developmental disabilities in the developing fetus, a cohort of toluene-exposed infants was ascertained and examined. Methodology. Eighteen infants with a history of in utero toluene exposure were examined at birth. Nine of these infants were reexamined 3 to 36 months after their initial evaluations. The clinical findings in these patients were compared with those of similarly exposed children from the literature and with patients who had the fetal alcohol syndrome. Results. Thirty-nine percent of all toluene-exposed infants described in this and other studies were born prematurely, and 9% died during the perinatal period. Fifty-four percent were small for gestational age, and 52% exhibited continued postnatal growth deficiency. A 33% incidence of prenatal microcephaly, a 67% incidence of postnatal microcephaly, and an 80% incidence of developmental delay were observed. Eighty-three percent of the patients had craniofacial features similar to the fetal alcohol syndrome, and 89% of these children had other minor anomalies. Conclusions. Data from the patients herein described and the available scientific literature suggest that the mechanism of alcohol craniofacial teratogenesis may be nonspecific, with a variety of teratogens, including toluene, giving rise to phenotypic facial abnormalities similar to those of the fetal alcohol syndrome. We propose a common mechanism of craniofacial teratogenesis for toluene and alcohol, namely a deficiency of craniofacial neuroepithelium and mesodermal components due to increased embryonic cell death.


PEDIATRICS ◽  
1992 ◽  
Vol 89 (1) ◽  
pp. 67-77
Author(s):  
Susan J. Astley ◽  
Sterling K. Clarren ◽  
Ruth E. Little ◽  
Paul D. Sampson ◽  
Janet R. Daling

The association between fetal marijuana and/or alcohol exposure and facial features resembling fetal alcohol syndrome was investigated in a sample of 80 children. Standardized lateral and frontal facial photographs were taken of 40 children, 5 to 7 years of age, whose mothers reported frequent use of marijuana during the first trimester of pregnancy and 40 children whose mothers reported no use of marijuana during pregnancy. The marijuana-exposed and unexposed children were group-matched on alcohol exposure prior to and during pregnancy, sex, race, and age at the time of assessment. The photographs were assessed clinically by a study staff dysmorphologist and morphometrically by computerized landmark analysis. Fetal alcohol syndrome-like facial features were not associated with prenatal marijuana exposure in this study sample. No consistent patterns of facial features were identified among the marijuana-exposed group. Maternal consumption of two or more ounces of alcohol per day, on average, in early gestation was found to be associated with fetal alcohol syndrome-like facial features identified both clinically and morphometrically. Cocaine use reported by 13 of the 80 women was independently associated with mild facial dysmorphic features of hypertelorism and midfacial flattening. The results demonstrate the usefulness of this diagnostic technique for quantifying anomalies apparently unique to fetal alcohol syndrome and for targeting clusters of anomalies in new conditions for future evaluation.


PEDIATRICS ◽  
1974 ◽  
Vol 53 (4) ◽  
pp. 490-494
Author(s):  
R. Heather Palmer ◽  
Eileen M. Ouellette ◽  
Lyle Warner ◽  
Sandra R. Leichtman

Three cases in one family—a girl and monozygotic girl twins, the offspring of a chronic alcoholic mother —are presented. They show a pattern of prenatal onset of growth deficiency and developmental delay, with microcephaly, small palpebral fissures, and multiple minor anomalies, recently described in a series of 11 unrelated cases by Jones et al. and named by them the "fetal alcohol syndrome." After considering alternative theories, we conclude, with them, that the cases demonstrate an association between the maternal alcohol intake and the abnormalities found in the offspring. We report these three cases in confirmation of their findings.


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