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During pregnancy, ingestion of alcohol, a known teratogen, can cause harm to the fetus. Prenatal alcohol exposure is one of the leading causes of birth defects, developmental disorders, and mental retardation in children. The fetal central nervous system is particularly vulnerable to alcohol; this vulnerability contributes to many of the long-term disabilities and disorders seen in individuals with prenatal alcohol exposure. Diagnoses associated with prenatal alcohol exposure include fetal alcohol syndrome (FAS), partial fetal alcohol syndrome, fetal alcohol effects, alcohol-related neurodevelopmental disorder, and alcohol-related birth defects. Once diagnosed, early intervention improves the long-term outcome of affected children. Without documentation of maternal alcohol use, a diagnosis, and consequently treatment, is often difficult to attain. It is imperative that nurses, physicians, and other healthcare providers become comfortable with obtaining a history of, and providing anticipatory guidance and counseling about, alcohol use.

To complement the 2005 Annual Clinical Focus on medical genomics, AFP will be publishing a series of short reviews on genetic syndromes. This series was designed to increase awareness of these diseases so that family physicians can recognize and diagnose children with these disorders and understand the kind of care they might require in the future. The second review in this series discusses fetal alcohol syndrome and fetal alcohol spectrum disorders.

Neuroanatomical and behavioral evidence indicate that the cerebellum is particularly vulnerable to the toxic effects of prenatal alcohol exposure. Recent research has shown impairments in eyeblink conditioning in rats following binge-like neonatal ethanol exposure. The neural substrates of eyeblink conditioning have been localized to the cerebellum and related brainstem mechanisms. The present study considered whether heavy prenatal alcohol exposure would result in similar impairments in eyeblink conditioning in children. A related purpose was to determine if eyeblink conditioning could discriminate between children with prenatal alcohol exposure and children diagnosed with attention deficit hyperactive disorder or developmental dyslexia. Fifty-three age-matched children [10 prenatal alcohol exposure (FAE), 16 attention deficit hyperactive disordered (ADHD), 14 children with dyslexia (DYS), 13 normal controls] were assessed on eyeblink conditioning in the delay paradigm. Children in the FAE and DYS groups failed to learn the conditioned response, producing longer latencies and poorly timed responses to the conditioning stimulus. Children with ADHD were impaired on measures of adaptively timed responses, although conditioned responses matched normal controls. The results suggest that children prenatally exposed to alcohol have deficits in cerebellar processing similar to those with dyslexia, and that these functional deficits are related to disabilities in learning.

We report a newborn with fetal alcohol syndrome with severe feeding intolerance and failure to thrive due to pyloric stenosis. This illustrates the importance of early recognition of pyloric stenosis in fetal alcohol syndrome to improve nutrition and growth. We speculate that pyloric stenosis in neonates results from the absence or immaturity of intrinsic nitric oxide synthase-containing neurons in the pyloric muscle in children of alcohol-addicted mothers.

Purpose: Speech-language pathologists frequently address social communication difficulties in children with diverse clinical profiles. The purpose of this study was to investigate the feasibility of a social communication intervention for a school-age child with a complex cognitive and behavioral profile secondary to diagnosis of a fetal alcohol spectrum disorder., Method: A case study is presented to describe the implementation of the intervention targeting mental state verb production and social cognitive skills. The intervention included group role play of social scripts and a checklist to elicit the participant's statements about others' perspectives and strategies for completing the social script. Treatment data monitored the participant's responses to the checklist questions. Probe sessions, consisting of theory of mind false belief tasks, were used to examine mental state verb use., Results: Treatment data demonstrated that the participant stated more strategies in response to checklist questions. The participant did not produce any mental state verbs during baseline probes, but did produce mental state verbs during the treatment phase., Clinical Implications: The results support use of this intervention to change children's linguistic and social cognitive skills. Suggestions for extending this intervention to include a generalization plan targeting classroom social communication interactions are provided.

I discuss a newborn whose mother is addicted to alcohol. On the third day of life, the newborn was found to have ventricular tachycardia. After spontaneous termination of the abnormal rhythm, the duration of the corrected QT interval was 0.48 s. During the next days, the duration of the interval normalized, and has now remained stable for 5 years. I conclude that the so-called "alcohol withdrawal syndrome of the newborn" might cause postnatal prolongation of the QT interval.

Clinical descriptions of patients with Fetal Alcohol Syndrome (FAS) and Fetal Alcohol Effects (FAE) suggest major problems with adaptive behavior. Five operationally defined adverse outcomes and 18 associated risk/protective factors were examined using a Life History Interview with knowledgeable informants of 415 patients with FAS or FAE (median age 14 years, range 6-51; median IQ 86, range 29-126). Eighty percent of these patients were not raised by their biological mothers. For adolescents and adults, the life span prevalence was 61% for Disrupted School Experiences, 60% for Trouble with the Law, 50% for Confinement (in detention, jail, prison, or a psychiatric or alcohol/drug inpatient setting), 49% for Inappropriate Sexual Behaviors on repeated occasions, and 35% for Alcohol/Drug Problems. The odds of escaping these adverse life outcomes are increased 2- to 4-fold by receiving the diagnosis of FAS or FAE at an earlier age and by being reared in good stable environments., (Copyright 2004 Lippincott Williams and Wilkins, Inc.)

People with fetal alcohol spectrum disorder (FASD) present challenges to those who work in the criminal legal system. Prenatal exposure to alcohol can cause physical, neurological, and psychological impairments. It is vital to understand the individual offender in order to address the underlying reasons for criminal behavior. Individuals with FASD often come from dysfunctional backgrounds, and may have mental illnesses and substance use disorders. A comprehensive medical-legal report, prepared by a professional experienced with FASD, can help judges and lawyers understand how complex the interactions are among brain damage, genetics, and the environment. The person with FASD can be misunderstood in court, victimized in jails, and mismanaged in the transition back to the community, unless those working with the individual are aware of FASD and its implications.

Fetal alcohol syndrome in association with RETT syndrome: We report on a girl with neonatal dystrophy, microcephaly, heart defect, and the characteristic features of alcohol embryopathy. Later, she developed distinctive features of RETT syndrome including loss of early acquired developmental skills and presented typical symptoms of RETT syndrome as reduction of communication skills, reduction of hand function, hyperventilation, and grinding of teeth. Molecular analysis of the MECP2 gene revealed the c.808T>C (R270X) mutation located in the nuclear localisation signal sequence of the gene. Our report highlights the importance of considering the diagnosis of RETT syndrome even in patients who are already suffering from a defined disease.

Fetal alcohol syndrome (FAS) is a common developmental disorder with impairments in multiple neuropsychiatric spheres of varying severity. Few population-derived studies of the behavioral phenotype are available. The purpose of this study was to estimate the prevalence of neuropsychiatric disorders in three groups: subjects who met criteria for FAS (n=152); subjects who met criteria for partial FAS/ARND (n=150); and referred subjects who did not meet criteria for either FAS or partial FAS/ARND (n=86). Each subject had a standardized evaluation by a medical geneticist. All subjects were from North Dakota. We found increases in the prevalence rates of neuropsychiatric disorders in subjects with FAS compared to subjects with partial FAS/ARND and the lowest rates in the group that did not meet criteria for either FAS or partial FAS/ARND. Comorbid attention deficit hyperactivity disorder occurred in 73% of cases with FAS, in 72% cases with partial FAS/ARND, and in 36% subjects who did not meet criteria for either. For other neuropsychiatric disorders, a similar distribution of comorbidity was found. This study supports the concept of a continuum of impairment resulting from prenatal alcohol exposure. The presence of complex cognitive, behavioral, and physical symptomatology in the affected subjects with prenatal alcohol exposure would seem to fit well under the diagnostic rubric of fetal alcohol spectrum disorder (FASD). Diagnosis and long-term management will require increasing access to multidisciplinary child development teams including mental health professionals who treat children and adolescents. Adults will require care primarily from teams with expertise in mental health and developmental disabilities.

The prevalence and magnitude of effect of individual risk markers for specific developmental disorders vary widely across diagnostic category. The four study cohorts for this project were patients from four diagnostic registries in North Dakota for fetal alcohol syndrome (FAS), autism, sudden infant death syndrome (SIDS), and Tourette syndrome. These four cohorts were used to estimate prevalence and magnitude of effect of parental risk markers in patients with developmental disabilities. Cases with North Dakota birth certificates were matched with controls. Using birth certificate data, we then examined five parental risk markers for each cohort and estimated direct and indirect effects for each risk marker by cohort. The authors found two significant paternal risk markers (age in SIDS and education in FAS). Significant maternal markers were age in SIDS, education in FAS, autism, and SIDS. Marital status was a significant risk marker in FAS. Effect sizes were estimated using paired t tests, odds ratios, and population attributable risk (PAR) for both direct and indirect effects for each marker. We estimated both direct and indirect effects to allow for direct comparisons of the differential effect estimates of each of these markers. The direct effect of parental markers differs across diagnostic cohorts of patients. Use of cohorts from similar denominator populations obtained from prevalence studies is a useful methodological tool for estimating the prevalence and magnitude of effect of risk markers.

We employed a computerized (virtual) Morris water task (VMWT) to measure place learning and cued-navigation in eight adolescent males (9.5-16.5 years old) diagnosed with Fetal Alcohol Syndrome (FAS). Eight adolescent males matched for age and ethnicity with no history of prenatal alcohol exposure served as controls. Participants were trained to navigate to a hidden platform in a fixed location relative to a set of four conspicuous extramaze cues. After 20 hidden platform trials, a single no-platform probe trial was conducted, followed by 8 trials during which the platform was visible (cued-navigation). The FAS group traveled further than controls to navigate to the hidden platform during training. During the probe trial, controls navigated more directly to the platform region and persisted in searching where the platform had been more than the FAS group. Cued-navigation was comparable in both groups, suggesting that group differences in place learning were not attributable to visual-motor or motivational deficits in the FAS subjects. This pattern of impaired place learning and spared cued-navigation is similar to that reported in rats exposed to ethanol during periods of prenatal or early postnatal brain growth, as well as in animals with hippocampal damage.

A sample of 12 children (seven males, five females; mean age 6 years 7 months, SD 2 years 6 months, range 2 years 4 months to 12 years 1 month) with moderate-to-severe foetal alcohol syndrome (FAS) and another sample of 26 children (12 males, 14 females; mean age of 6 years 2 months SD 2 years 10 months, range 2 years 6 months to 12 years 8 months) with mild FAS or foetal alcohol effects (FAE) as well as a sample of 15 age- and sex-matched control children with unspecific intellectual disability were compared using the Developmental Behaviour Checklist (DBC). There were significant differences (p=0.01) between the groups on five of six subscales of the DBC with controls scoring lower on the disruptive, self-absorbed, anxiety, antisocial behaviour, and communication disturbance scales. The DBC profiles of the two foetal alcohol exposed groups did not differ from each other. It is concluded that quantitative behaviour measurement provides insights into specific behavioural phenotypes of FAS/FAE.

Alcohol constitutes one of the main risk factors for the health of the newborn infant and is also one of the leading causes of cognitive deficit. The distinctive pattern of abnormalities that characterizes fetal alcohol syndrome (FAS) includes: pre- and postnatal growth retardation, cognitive deficit, behavior and language disorders, cerebral malformations (schizencephaly, polymicrogyria, agenesis of the corpus callosum), facial changes (short palpebral fissures, low nasal bridge, anomalies of the auricle, maxillary hypoplasia, cleft lip and palate) and organ anomalies (heart defects, renal and skeletal malformations). As occurs with any teratogenic agent, the variability of phenotypic expression is wide and depends on dose, gestational stage, duration of exposure, maternal and fetal metabolism and other environmental and genetic factors. This study describes 6 subjects with FAS who express various characteristics of the clinical spectrum of the syndrome.

Midaortic syndrome (MAS) is an uncommon condition characterized by progressive narrowing of the abdominal aorta and its branches and impressive formation of collateral circulation. It affects children and young adults and presents predominantly as untreatable hypertension. Fetal alcohol syndrome (FAS) refers to a constellation of physical, behavioral, and cognitive abnormalities secondary to alcohol exposure in utero. The authors present an unusual association between a hypoplastic abdominal aorta and fetal alcohol syndrome. The patient discussed in this article presented with severe hypertension that was successfully treated with renal angioplasty.

Previous work conducted in vitro suggests that nitric oxide (NO) protects developing neurons against the toxic effects of alcohol. We tested the hypothesis that neonatal mice carrying a null mutation for neuronal nitric oxide synthase (nNOS), the enzyme which synthesizes NO in neurons, have increased vulnerability to alcohol-induced microencephaly and neuronal loss. Wild-type mice and mutant (nNOS(-/-)) mice received a single intraperitoneal injection of ethanol (0.0, 2.2, 3.3, or 4.4 g/kg) daily over postnatal days (PD) 4-9 and were sacrificed on PD 10. Peak blood alcohol concentrations were approximately 170, 280, and 385 mg/dl for the 2.2, 3.3 and 4.4 g/kg/day treatment groups, respectively, and did not differ significantly between wild-type and nNOS(-/-) strains. Exposure to alcohol induced dose-dependent reductions in total brain weight, forebrain weight and cerebellum weight in both strains of mice. However, the reductions in brain weight were significantly more severe in the nNOS(-/-) mice than in wild type. Quantification of cerebellar neurons revealed that alcohol-induced losses of Purkinje cells and granule cells were both significantly greater in the nNOS(-/-) mice than in wild type. The increased vulnerability of nNOS-deficient neurons to alcohol-induced cell death was confirmed in vitro. Cerebellar granule cell cultures derived from nNOS(-/-) and wild-type mice were exposed for 24 h to 0, 100, 200 or 400 mg/dl ethanol. At each alcohol concentration, the nNOS(-/-) neurons had a significantly greater cell loss than did the wild-type neurons. The results demonstrate that deficiency of nNOS decreases the ability of developing neurons to survive the toxic effects of alcohol. Because NO upregulates intracellular cGMP, which can activate cGMP-dependent protein kinase (PKG), we hypothesize that the NO-cGMP-PKG pathway has a neuroprotective role against alcohol toxicity within the developing brain.

Physical and behavioral difficulties can beset the child exposed to alcohol in utero. Timely intervention can lessen their severity.

Foetal alcohol syndrome (FAS) is a collection of signs and symptoms seen in children of women who consume alcohol during pregnancy. With the increasing incidence of FAS, there is a great variation of its clinical features different from that described in the standard textbooks. This article aims to report on the unusual clinical features of FAS. It also aims to explain the mechanism of action of alcohol as a teratogenic agent.

The fetal alcohol syndrome (FAS) is caused by maternal alcohol misuse during pregnancy and is characterized by pre- and postnatal growth retardation, central nervous system anomalies and a wide spectrum of malformations, the most typical being the craniofacial features. The eye is a sensitive indicator of the adverse effects of environmental agents, and the ocular abnormalities observed in children with FAS indicate that the developing eye is particularly affected by alcohol. The external signs include short palpebral fissures, telecanthus, epicanthus, blepharoptosis, microphthalmos and strabismus. Within the eyes, the signs and symptoms most commonly detected are optic nerve hypoplasia, increased tortuosity of the retinal vessels and impaired vision. Experimental models of FAS, closely reproducing characteristics of human FAS, have contributed to our understanding of the cellular and molecular basis of the action of alcohol in the developing visual system. As there is such a high frequency of eye signs and symptoms in FAS, an ophthalmological examination is important when making the diagnosis, as well as in the management of the disorder. Current knowledge of ophthalmological involvement in FAS in humans is presented, as well as a review of findings using animal models specially designed for studying ocular developmental changes induced by alcohol.

Alcohol is much more slowly eliminated in the fetus than in the mother (< 50%). The ethanol and its derivative the acetaldehyde have a constant dose-effect on the development of the nervous system central. The individual susceptibility to alchol teratogenic effect in utero is responsible of variable clinical phenotype. This teratogenicity is constant during all the development of the central nervous system. The diagnosis of fetal alcohol syndrome (FAS) associates three criteria: delay of pre- and postnatal growth, abnormal development of the central nervous system, craniofacial abnormalities. Cerebral malformations are extremely variable, being to relate to the various stages of development of the nervous system central. Neurochimic abnormalities interest mainly the mono-aminergic system. The backwardness is the best known consequence of SAF (34 to 851%). It is not constant. Facial dysmorphic results of joint abnormalities whose none is pathognomonic but whose grouping is evocative. Psychomotor instability is the most frequent expression on the behavioral phenotype.

Two brothers with severe mental retardation of unknown origin were found to share several physical anomalies, including large round head, small concave nose, downslanted palpebral fissures, and gingival hyperplasia. In addition to relative macrocephaly, magnetic resonance imaging (MRI) showed severe cerebral atrophy, especially fronto-temporally. The brothers also had a thin corpus callosum and atrophic caudate nuclei. The reduced white matter showed patchy periventricular signal intensity changes. The lateral and third ventricles were large, but the fourth ventricle was of normal size. The boys had large cisterna magna, communicating widely with the fourth ventricle, but no vermian hypoplasia. Both boys had Lennox-Gastaut spectrum type epilepsy. No chromosomal anomalies were found, despite the suggestive clinical picture. Some of the clinical findings resembled fetal alcohol effects/fetal alcohol syndrome (FAE/FAS), which was also suggested by history. Current diagnostic criteria for FAE/FAS, however, excluded full-blown FAS in these cases and failed to explain the entire clinical picture in the boys. We argue that these boys had an unidentified inherited syndrome, possibly modified by fetal alcohol exposure., (Copyright 2001 Wiley-Liss, Inc.)

Objective: Moderate to heavy levels of prenatal alcohol exposure have been associated with alterations in child behavior, but limited data are available on adverse effects after low levels of exposure. The objective of this study was to evaluate the dose-response effect of prenatal alcohol exposure for adverse child behavior outcomes at 6 to 7 years of age., Methods: Beginning in 1986, women attending the urban university-based maternity clinic were routinely screened at their first prenatal visit for alcohol and drug use by trained research assistants from the Fetal Alcohol Research Center. All women reporting alcohol consumption at conception of at least 0.5 oz absolute alcohol/day and a 5% random sample of lower level drinkers and abstainers were invited to participate to be able to identify the associations between alcohol intake and child development. Maternal alcohol, cigarette, and illicit drug use were prospectively assessed during pregnancy and postnatally. The independent variable in this study, prenatal alcohol exposure, was computed as the average absolute alcohol intake (oz) per day across pregnancy. At each prenatal visit, mothers were interviewed about alcohol use during the previous 2 weeks. Quantities and types of alcohol consumed were converted to fluid ounces of absolute alcohol and averaged across visits to generate a summary measure of alcohol exposure throughout pregnancy. Alcohol was initially used as a dichotomous variable comparing children with no prenatal alcohol exposure to children with any exposure. To evaluate the effects of different levels of exposure, the average absolute alcohol intake was relatively arbitrarily categorized into no, low (>0 but <0.3 fl oz of absolute alcohol/day), and moderate/heavy (>/=0.3 fl oz of absolute alcohol/day) for the purpose of this study. Six years later, 665 families were contacted. Ninety-four percent agreed to testing. Exclusions included children who missed multiple test appointments, had major congenital malformations (other than fetal alcohol syndrome), possessed an IQ >2 standard deviations from the sample mean, or had incomplete data. The Achenbach Child Behavior Checklist (CBCL) was used to assess child behavior. The CBCL is a parent questionnaire applicable to children ages 4 to 16 years. It is widely used in the clinical assessment of children's behavior problems and has been extensively used in research. Eight syndrome scales are further grouped into Externalizing or undercontrolled (Aggressive and Delinquent) behavior and Internalizing or overcontrolled (Anxious/Depressed, Somatic Complaints, and Withdrawn) behaviors. Three syndromes (Social, Thought, and Attention Problems) fit neither group. Higher scores are associated with more problem behaviors. Research assistants who were trained and blinded to exposure status independently interviewed the child and caretaker. Data were collected on a broad range of control variables known to influence childhood behavior and/or to be associated with prenatal alcohol exposure. These included perinatal factors of maternal age, education, cigarette, cocaine, and other substances of abuse and the gestational age of the baby. Postnatal factors studied included maternal psychopathology, continuing alcohol and drug use, family structure, socioeconomic status, children's whole blood lead level, and exposure to violence. Data were collected only from black women as there was inadequate representation of other racial groups., Statistical Analyses: Statistical analyses were performed using the SPSS statistical package. Frequency distribution, cross-tabulation, odds ratio, and chi(2) tests were used for analyzing categorical data. Continuous data were analyzed using t tests, analyses of variance (ANOVAs) with posthoc tests, and regression analysis., Results: Testing was available for 501 parent-children dyads. Almost one fourth of the women denied alcohol use during pregnancy. Low levels of alcohol use were reported in 63.8% and moderate/heavy use in 13% of pregnancies. Increasing prenatal alcohol exposure was associated with lower birth weight and gestational age, higher lead levels, higher maternal age, and lower education level, prenatal exposure to cocaine and smoking, custody changes, lower socioeconomic status, and paternal drinking and drug use at the time of pregnancy. Children with any prenatal alcohol exposure were more likely to have higher CBCL scores on Externalizing (Aggressive and Delinquent) and Internalizing (Anxious/Depressed and Withdrawn) syndrome scales and the Total Problem Score. The odds ratio of scoring in the clinical range for Delinquent behavior was 3.2 (1.3-7.6) in children with any prenatal exposure to alcohol compared with nonexposed controls. The threshold dose was evaluated with the 3 prenatal alcohol exposure groups. One-way ANOVA revealed a significant between group difference for Externalizing (Aggressive and Delinquent) and the Total Problem Score. (ABSTRACT TRUNCATED)

Objective: Epidemiologic evidence for the associations of alcohol consumption with eye diseases was gathered., Method: A literature review was conducted., Results: In addition to alcohol-induced ocular anomalies among children with fetal alcohol syndrome, epidemiologic studies in the past two decades have demonstrated that chronic alcoholism is associated with a significantly increased risk of cataract, keratitis, color vision deficiencies and corneal arcus. Moderate alcohol use, however, has been reported to be possibly protective against age-related macular degeneration, cataract and diabetic retinopathy., Conclusions: It is evident that through its biologic effects and effects on nutrient deficits alcohol plays a role in a variety of eye diseases. Information on the patient's drinking history can be clinically valuable and should be collected on a routine basis.

Background: Even though fetal alcohol syndrome (FAS) has been reported in nonwestern nations, there is a paucity of information on neurodevelopment in the affected children from those nations. This article reports on a study of cognitive-motor development in a group of children with FAS from a community in the Western Cape Province in South Africa., Methods: Thirty-four children with FAS and 34 controls from grade 1 (school entry level) classes participated. The two groups comprised Afrikaans-speaking children of mixed ancestry (South African Colored) and were matched for age, sex, and family income. The Griffiths Mental Development Scales were used to assess cognitive motor development of the participants., Results: A multivariate analysis of covariance was performed to test the group effect on the combined Griffiths subscales adjusting for maternal education. The results showed a significant group effect. Follow-up analyses revealed that a combination of four subscales (Speech and Hearing, Performance, Practical Reasoning, and Eye and Hand Coordination) primarily contributed to the overall effect. Although there was a marginal effect on the Personal-Social subscale, no significant effect on the Locomotor (gross motor) subscale was found., Conclusions: The results showed that the FAS group was markedly deficient only in higher-order cognitive-motor competencies.

Objective: Executive function deficits, including verbal fluency, have been documented in children with histories of prenatal alcohol exposure. Whereas nonverbal fluency impairments have been reported in adults with such exposure, these abilities have not been tested in children. Deficits in both verbal and nonverbal fluency were predicted and assessed in children and adolescents with histories of heavy prenatal alcohol exposure., Method: There was a total of 28 (54% female) subjects; children with heavy prenatal alcohol exposure with (n = 10) and without (n = 8) fetal alcohol syndrome (FAS) were compared to nonexposed controls (n = 10) on the design and verbal fluency measures from the Delis-Kaplan Executive Function System. Both fluency measures consist of three conditions, including a new set-shifting task. All tests require the generation of multiple responses within both rule and time constraints., Results: Data were analyzed using repeated measures analyses of variance and hierarchical regression analyses. Compared to controls, children with heavy prenatal alcohol exposure with and without FAS displayed deficits in both fluency domains, but did not differ from each other. In addition, prenatal alcohol exposure was a significant predictor of performance on the set-shifting design fluency task above and beyond performance on more traditional fluency tasks. IQ was not a significant predictor for the traditional or set-shifting fluency measures, whereas diagnostic group remained a significant predictor when IQ was included in the model., Conclusions: This study adds to the literature on the integrity of executive functions in children with heavy prenatal alcohol exposure, documenting fluency impairment in both verbal and nonverbal domains. It is important to note that these impairments were demonstrated in higher functioning alcohol-exposed children, both with and without FAS, and that diagnostic group explained such deficiencies above and beyond general intellectual ability.

Fetal alcohol syndrome, FAS, is characterized by pre- and/or postnatal growth deficiency, CNS dysfunction, typical facial features and evidence of prenatal alcohol exposure. FAS is often an unrecognized diagnosis and is based on clinical symptoms alone. The cognitive and behavioral disturbances have a great influence on the children's ability to learn and on their adult life. FAS is to a great extent found in areas with less than satisfactory socio-economic conditions. Since ophthalmologic involvement is frequent, an eye examination may be helpful in making a diagnosis. Prevention is essential since the brain damage prevails, despite comprehensive medical and social supportive efforts being made during childhood and in education.

Fetal alcohol syndrome, FAS, is characterized by pre- and/or postnatal growth deficiency, CNS dysfunction, typical facial features and evidence of prenatal alcohol exposure. FAS is often an unrecognized diagnosis and is based on clinical symptoms alone. The cognitive and behavoral disturbances have a great influence on the children's ability to learn and on their adult life. FAS is to a great extent found in areas with less than satisfactory socio-economic conditions. Since ophthalmologic involvement is frequent, an eye examination may be helpful in making a diagnosis. Prevention is essential since the brain damage prevails, despite comprehensive medical and social supportive efforts being made during childhood and in education.

Purpose: To describe the experiences of foster parents who are living with a child diagnosed with Fetal Alcohol Syndrome (FAS)., Design and Method: A qualitative approach was selected due to the paucity of knowledge on the topic. Eight foster mothers living with children with FAS were studied. These foster parents had parented a collective total of 17 children with FAS, ranging between the ages of 2 and 16. Each in-depth interview was unstructured and consisted of open-ended questions. Data were analyzed using content analysis., Results: Foster parents described many difficult issues needing attention in children with FAS. Cognitive concerns included diminished memory/comprehension, lack of understanding of consequences, and the absence of fear. Behavioral management was a problem due to the frequent occurrence of hyperactivity, aggressiveness, destructiveness, and high pain tolerance. Parents also described problems in coping with daily realities of life with a child with FAS including the necessity of providing consistency, coping strategies, and fears for the child's future., Clinical Implications: Nurses need to understand the complex problems that face affected children and their families. Understanding the daily realities of living with children with FAS allows nurses to realistically assess childrens' abilities, maximize their development, and provide for their needs more effectively, as well as assisting families to cope with the behavior and cognitive issues so apparent in children with FAS.

We report an 11-year-old boy with fetal alcohol syndrome and immunodeficiency, whose longstanding malnutrition, diarrhoea with steatorrhoea, symptomatic electrolyte loss and eosinophilia were attributed to renal tubular disease and recurrent worm infestation. The symptoms resolved with diagnosis and treatment of infection by the protozoan Isospora belli, although immunodeficiency persisted.

Prenatal alcohol exposure can cause a whole spectrum of central nervous system (CNS) sequelae that persist throughout the life span and manifest in a spectrum of effects from clinically indistinguishable to severely impairing. The greatest impact of alcohol as a teratogen is to the brain-the greatest need is for holistic treatment and management of the associated mental disorders. The interaction of this subtle brain damage with the complex psychosocial circumstances surrounding the birth of a child to a mother with alcohol problems can further compound development and result in costly and devastating social consequences. Research is urgently needed on the chronic neuropsychiatric sequelae of these subtle birth defects of the brain. Identification of these fetal alcohol spectrum disorders (FASD) in the psychiatric nomenclature is a necessary step to focus the attention and resources of the mental health field on this personally and socially significant problem.

Foetal alcohol syndrome is a syndrome with a rather high incidence. It is characterized by mental retardation, growth deficiency, a striking facial appearance (a.o. short palpebral fissures, short, upturned nose, hypoplastic philtrum, hypoplastic maxilla). Malocclusion and a disturbed facial growth may occur. Mental retardation can interfere with dental treatment.

Mental retardation in young children is often missed by clinicians. The condition is present in 2 to 3 percent of the population, either as an isolated finding or as part of a syndrome or broader disorder. Causes of mental retardation are numerous and include genetic and environmental factors. In at least 30 to 50 percent of cases, physicians are unable to determine etiology despite thorough evaluation. Diagnosis is highly dependent on a comprehensive personal and family medical history, a complete physical examination and a careful developmental assessment of the child. These will guide appropriate evaluations and referrals to provide genetic counseling, resources for the family and early intervention programs for the child. The family physician is encouraged to continue regular follow-up visits with the child to facilitate a smooth transition to adolescence and young adulthood.

Although the aetiology of antenatal brain injury is often unclear, procedures can be employed to prevent or reduce the risk of injury. Defective neuropore closure can be prevented by periconceptional administration of folic acid, and the incidence of other severe malformations and genetic disorders can be reduced by early identification and termination of pregnancy. Antenatal identification of IUGR, administration of corticosteroids to cases with pending preterm birth, and treatment of maternal/fetal infections would also reduce the incidence of injury. Mothers can decrease the risk of injury by maintaining a good diet, avoiding smoking, alcohol intake and exposure to TORCH infections during pregnancy., (Copyright 2000 Harcourt Publishers Ltd.)

A disproportionately large number of youth and adults with fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE) seem to be coming into conflict with the legal system. Learning and behavioral difficulties associated with FAS/FAE may make them more susceptible to criminal behavior. This study determined the prevalence of FAS/FAE among youth who were remanded for a forensic psychiatric/psychological assessment. All youth remanded to a forensic psychiatric inpatient assessment unit over a 1-year period were evaluated for FAS/FAE. Of the 287 youth, 67 (23.3%) had an alcohol-related diagnosis: 3 (1.0%) had a diagnosis of FAS and 64 (22.3%) had a diagnosis of FAE. Thus, this group is disproportionately represented in the juvenile justice system, indicating the need for increased education and awareness among those in the criminal justice system involved with these youth.

Background: Fetal alcohol syndrome (FAS) describes the systemic and ocular anomalies resulting from the teratogenic effect of maternal alcohol abuse during pregnancy. It is a leading cause of preventable birth defects in the U.S., Case Reports: Two case reports illustrate the characteristic findings in FAS. These include growth retardation, cognitive impairment, and facial dysmorphism. Ocular signs are prevalent, including small palpebral fissure, microcornea, strabismus, myopia, astigmatism, and optic nerve hypoplasia., Discussion: Fetal alcohol exposure can lead to a wide spectrum of systemic defects and vision deficits. The increasing frequency of drinking among pregnant women in recent years should call more public attention to this detrimental yet preventable syndrome., Conclusion: The high frequency of ocular manifestations aids in making a diagnosis of FAS, which can be challenging. Eye-care professionals can play an important role in patient management and the educational process.

Alcohol is a teratogen and it can cause lasting birth defects called Fetal Alcohol Syndrome (FAS)/Fetal Alcohol Effects (FAE). FAS is one of the leading causes of mental retardation. FAS/FAE can result in a myriad of behavioral, learning and developmental problems. There are estimates of 12,000 new cases of FAS yearly. The school nurse plays an important advocacy and educational role in helping the child with FAS. Family involvement is important for the child with FAS.

Background: Deficits in attention are commonly identified among patients who have been prenatally exposed to alcohol, and they often affect the ability of the patients to function appropriately in society., Methods: Eleven adult patients with fetal alcohol syndrome (FAS) or fetal alcohol effects (FAE) were compared with nine adult subjects with no history of prenatal alcohol exposure, using four tests of visually and auditorially mediated attention., Results: In relation to the comparison group, patients with FAS/FAE exhibited substantial deficits in both auditory and visual attention; the auditory deficits were greater. We observed two predominant patterns of deficits among patients with FAS/FAE, one involving both auditory and visual attention problems and the other involving less severe auditory problems and even fewer visual problems. Most subjects with FAS or FAE had some manifestations of attention problems in at least one of the tests of attention used in this study. We present a new graphical representation of individual auditory Continuous Performance Test data across a 6-min period, which, compared with conventional scores, more clearly reveals the markedly disrupted and variable attention patterns displayed by some individuals with FAS or FAE., Conclusions: These findings suggest that detailed analysis of the pattern of individual performance for each subject is an important aspect of Continuous Performance Test assessment. Our findings further suggest that intellectual performance (intelligence quotient score) alone is not sufficient to account for the patterns of disrupted attention for individuals with FAS/FAE. Assessment of individuals with FAS or FAE should include measurement of attentional functioning in both the visual and auditory modalities.

Background and Objective: Maternal alcohol addiction in pregnancy causes fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE) in children. At present, little is known about the physical, mental, and social long-term consequences in adulthood., Patients and Methods: Since 1974, 52 children with FAS and FAE, all born to alcohol dependent mothers, were prospectively followed up from birth to adulthood. Height, weight and head circumferences were based on percentile standards; mental and school development were assessed by school reports and by intelligence subtests. By structural interviews, occupational and social follow-up were assessed., Results: Growth retardation continued mainly in severely affected adults with underweight in 26%, underheight in 30%, and microcephaly in 46%. They mostly lived in foster families, only 6/52 were able to live independently. In 56% special schools for handicapped and mentally disabled were attended. In most cases (37/52), simple occupations without vocational training were practised., Conclusions: It is mainly the neurotoxic effects of alcohol in pregnancy that have longlasting developmental significance in adults. Because of the dysmorphic changes over time, it is difficult to diagnose FAS and FAE only in adulthood.

Fetal alcohol syndrome (FAS) refers to a pattern of anomalies that include craniofacial, CNS, growth, and various sensory anomalies. We have observed that FAS is associated with four kinds of hearing disorders: (1) developmentally delayed auditory function, (2) sensorineural hearing loss, (3) intermittent conductive hearing loss owing to recurrent serous otitis media, and (4) central hearing loss. As is the case with other syndromes associated with craniofacial anomalies and hearing impairments, speech and language pathologies also are common in FAS patients. Although auditory and vestibular systems arise from similar embryological tissue, vestibular dysfunction is variable in FAS. Early identification and intervention to treat hearing, language, and speech problems should improve the functional level of FAS in children.