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8
The Affected Individual:
Clinical Presentation, Intervention,
and Treatment

Despite the apparently large number of affected individuals who are born each year (see Chapter 5), fetal alcohol syndrome (FAS), alcohol-related birth defects (ARBD), and alcohol-related neurodevelopmental disorder (ARND) are rarely diagnosed. Similarly, although developmental problems in children have been demonstrated through prospective studies to be associated with maternal substance use (Streissguth et al., 1993), these problems are often not acknowledged except in the most extreme cases. Because of the difficulty in identification, as well as environmental factors, learning problems and aberrant behaviors can be attributed to other causes. As a result, many affected individuals do not receive correct diagnosis or treatment for their alcohol-related disabilities.

For obvious reasons, the focus of prevention efforts has been on the prevention of maternal alcohol use in pregnancy or on the prevention of pregnancy itself. The logic has been that such activities will be most cost-effective and, ultimately, have the greatest benefit for both mother and offspring. However, despite our best efforts (see Chapter 7), neither universal prevention nor more targeted activities have had a very strong impact on those persons most at risk (Smith and Coles, 1991), and many children are born affected by their teratogenic exposure. For these children, there has been a curious lack of enthusiasm for targeted efforts directed at the prevention of secondary disabilities. Such efforts might prevent some of the more negative outcomes reported to be associated with FAS (Dorris, 1989; Lemoine and Lemoine, 1992; Spohr et al., 1993).

Originally, it was not clear which factors produced these poor developmental outcomes—whether, that is, the observed problems resulted from damage to the nervous system or from poor caregiving. However, there are now convergent



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Page 154 8 The Affected Individual: Clinical Presentation, Intervention, and Treatment Despite the apparently large number of affected individuals who are born each year (see Chapter 5), fetal alcohol syndrome (FAS), alcohol-related birth defects (ARBD), and alcohol-related neurodevelopmental disorder (ARND) are rarely diagnosed. Similarly, although developmental problems in children have been demonstrated through prospective studies to be associated with maternal substance use (Streissguth et al., 1993), these problems are often not acknowledged except in the most extreme cases. Because of the difficulty in identification, as well as environmental factors, learning problems and aberrant behaviors can be attributed to other causes. As a result, many affected individuals do not receive correct diagnosis or treatment for their alcohol-related disabilities. For obvious reasons, the focus of prevention efforts has been on the prevention of maternal alcohol use in pregnancy or on the prevention of pregnancy itself. The logic has been that such activities will be most cost-effective and, ultimately, have the greatest benefit for both mother and offspring. However, despite our best efforts (see Chapter 7), neither universal prevention nor more targeted activities have had a very strong impact on those persons most at risk (Smith and Coles, 1991), and many children are born affected by their teratogenic exposure. For these children, there has been a curious lack of enthusiasm for targeted efforts directed at the prevention of secondary disabilities. Such efforts might prevent some of the more negative outcomes reported to be associated with FAS (Dorris, 1989; Lemoine and Lemoine, 1992; Spohr et al., 1993). Originally, it was not clear which factors produced these poor developmental outcomes—whether, that is, the observed problems resulted from damage to the nervous system or from poor caregiving. However, there are now convergent

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Page 155 data from long-term clinical studies of individuals with FAS gathered from a number of different populations (Lemoine and Lemoine, 1992 [France]; Steinhausen et al., 1993 [Germany]; Streissguth et al., 1991 [Native American]) arguing that outcome can be predicted most effectively by examining the interaction between severity of biological insult (operationally defined as dysmorphia) and environmental risk (operationally defined as caregiving instability and abuse or neglect). This relationship comes as no surprise, because it is well known that in other studies of high-risk children, poor social and caregiving environments exacerbate negative outcomes, whereas middle-class social status (Aylward, 1992) and well-designed early intervention (Bryant and Ramey, 1987) ameliorate these negative effects. However, few systematic attempts have been made to intervene with alcohol-affected children to test the possibility that such strategies would be effective in producing more positive outcomes. It is possible to speculate on reasons for the lack of interest in intervention with this group of children (see Coles and Platzman, 1992). Many of those identified as alcohol-affected are of minority or low socioeconomic status (SES) (Abel, 1995). For these reasons, families often lack the resources that are required to access appropriate services (Anderson and Novick, 1992). It is also well known that most medical and other professionals are not comfortable dealing with substance abuse or with addicts (Chappel, 1973; Robinson and Podnos, 1966). In addition, however, there has been an attitude that ''the damage is done" and that, given the biological nature of the insult to the nervous system, there is little to be done to help affected children. Some clinical studies have appeared to suggest that an optimal rearing environment may not significantly alter the deficits observed in children with FAS (Streissguth et al., 1985). However, others have argued that postnatal environment and experience do, indeed, significantly influence outcome in terms of both behavioral and cognitive development (Brown et al., 1991; Smith and Coles, 1991). Although there are few clinical studies in affected children, animal research suggests that the postnatal rearing environment may have positive outcomes even in alcoholized animals (Hannigan et al., 1993; Weinberg et al., in press). Although one cannot extrapolate directly from findings in animals to the clinical setting, the present data certainly indicate one possible direction for future research on treatment of children exposed to alcohol prenatally. When considered, the view that intervention may not be useful in children affected by alcohol seems odd, because it is inconsistent with the attitude taken toward other groups of high-risk and disabled children, who are the focus of many early intervention and special education efforts (Meisels and Shonkoff, 1990). Children with Down syndrome, for instance, usually are more seriously affected than those with FAS. Nevertheless, such children are regularly identified early and placed in intervention (Farran, 1990), although their developmental scores during the first year often do not qualify them for services. There appear to be several kinds of barriers that have prevented alcohol-affected

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Page 156 children from receiving appropriate intervention and treatment services. These problems may include the following: (1) The characteristics of the children themselves have not been well understood, so it has been difficult to understand how to intervene. (2) The nature of the insult to the developing child is such that, often, these children do not qualify for existing services. (3) Some services that might benefit mothers and children do not exist or are not widely available. (4) It is difficult for most professionals to deal with substance abuse due to lack of training, denial, and other social or emotional reactions. (5) There are many barriers to the interaction of the systems that serve children and those that serve recovering mothers so that the needs of the family often are overlooked (Coles and Platzman, 1992). These issues are explored in this chapter. The chapter begins with a description of clinical issues, including a description of what is currently know about the medical, behavioral, and social problems documented in people with FAS. These are discussed in a chronologic manner, beginning with infancy, in which most information has been gathered, and ending in adulthood, a period for which little information is available. Key questions about these issues that are relevant for planning interventions are described. The chapter then goes on to discuss what is known about interventions (medical, educational, and family-oriented initiatives) and the possibilities for decreasing secondary disabilities. The chapter concludes with a discussion on the limitations and barriers to the provision of services to people with FAS. CLINICAL ISSUES IN INDIVIDUALS WITH FAS, ARBD, OR ARND Medical Overview: FAS Health Issues In general, children with fetal alcohol syndrome require little more than routine medical care. However, a number of physical problems have been reported to be related to alcohol exposure and should be considered specifically. These include cardiac defects, urogenital problems, skeletal abnormalities (Streissguth et al., 1985), visual problems (Stromland, 1981), hearing deficiencies (Church and Gerkin, 1988), and dental abnormalities (Barnett and Schusterman, 1985). Necessary attention to these problems varies with the age of the child. In infancy, children with fetal alcohol syndrome should be carefully examined for associated major malformations. Associated defects of the heart and skeletal system can be excluded through a careful physical exam. Problems of the urogenital system, including hydronephrosis and kidney anomalies, cannot be excluded without imaging studies. Because no accurate frequencies for renal anomalies in FAS are established, it is not clear if routine ultrasound evaluations of the renal system are cost-effective in asymptomatic patients. Certainly, renal evaluations are warranted after any urinary tract infection or when other major malformations are found.

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Page 157 Because growth deficiency is part of FAS, a common medical dilemma remains excluding treatable causes for failure to thrive. There is no standard approach to this problem available in the literature. Children with FAS who are raised in nonabusive and nonneglectful settings and are given appropriate nutrition tend to grow parallel to normal growth curves for length, weight, and head circumference. Therefore, postnatal growth decelerations away from the normal growth curves should not be discounted as simply part of the syndrome. Most frequently, growth deceleration will be due to nutritional insufficiency from poor suck, a lack of interest in feeding, or caregiver neglect. When these problems are excluded and the physical examination does not suggest a specific focus for evaluation, consideration of all the usual reasons for failure to thrive, including problems of infections, absorption, metabolism, tumor, and structure, should be undertaken. Deceleration in the rate of head growth, with or without deceleration in other growth parameters, is very unusual in fetal alcohol syndrome and warrants consideration of brain imaging studies. Finally, it is important to mention that alcohol exposure can occur in gestations already complicated by chromosomal anomalies or other birth defect syndromes. General syndrome assessment and testing should always be considered in dysmorphic infants who were exposed to alcohol with an "atypical" fetal alcohol syndrome presentation. Children with fetal alcohol syndrome are reported to have high rates of visual and hearing problems. Visual acuity may be compromised by the short distance from the lens to the retina (small optic globes) or the shape of the lens. Although retinal anomalies may be found, progressive retinal dysfunction has not been reported. Increased frequencies of both conductive and neurosensory hearing problems are found in children with FAS. The frequency of these difficulties and the ages at which they are most likely to become a problem are not fully established. Routine visual screening prior to school and every two years thereafter would appear to be adequate. Similarly, brain stem auditory evoked response (BAER) testing between 6 and 12 months may be of some use in early identification of hearing loss. However, a history of recurrent otitis media or delays in speech should also alert the clinician to the possibility of hearing loss. The efficiency of hearing screening beyond that routinely offered in schools in asymptomatic patients with FAS has not yet established. Children with FAS frequently have narrow maxillary dental arches and often have Class III occlusion with final mandibular growth. Orthodontic follow-up through middle childhood and transitional dentition may lead to selected dental extractions or other techniques that could prevent more extensive orthodontia or oral surgery. Severe neurologic problems in FAS are relatively rare. Occasionally, late gestational exposure to alcohol is thought to be a cause of spasticity. Abnormalities in EEGs (electroencephalograms) have been reported in infancy; the rate of seizures is not known, but the possibility of seizures needs to be considered and

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Page 158 excluded in patients with histories suggestive of petit mal, absence, or psychomotor seizure forms. Children with FAS appear to go through puberty normally and at the normal age. While there do not appear to be medical problems associated with puberty resulting from prenatal exposure, those young people who are cognitively impaired are at higher risk at this time due to intellectual limitations and impaired judgment. They may also be living in high risk environments. Finally, it is possible that children with FAS may carry a genetic predilection for alcoholism that can become manifest in adolescence with drug and alcohol experimentation. Early warning and modeling of alcohol avoidance may be helpful, and careful observation of behavior in adolescents is strongly advised. Behavioral and Social Issues Research Methodology In understanding how to meet the needs of individuals with FAS, it is first necessary to describe the behavioral characteristics of affected children as well as the social environment in which many affected children live. Information about affected children is derived mainly from two sources: (1) retrospective and clinical studies of clinically referred children with FAS and fetal alcohol effects, and (2) prospective research studies of children exposed to alcohol in utero due to maternal drinking. In most such prospective research studies, maternal drinking is in the light to moderate range, with only a few women drinking in the heavy range. As a result, most of the children in these prospective studies are not dysmorphic and would not, therefore, qualify for a diagnosis of FAS, although in some cases they may have milder effects that are observable through focused testing or the statistical analysis of group data. It is well known that these different methodologies often produce different kinds of data and may, if a reader is incautious, suggest different conclusions. (These studies and their outcomes have been reviewed extensively elsewhere and the interested reader is directed to Coles, 1992; Coles and Platzman, 1993; Russell, 1991; and Streissguth, 1986.) In retrospective studies, there is usually much stronger evidence for the effect of a teratogen than in prospective studies, due to the systematic selection biases that occur when children are referred for special education or medical treatment. However, without statistical and experimental controls, it is difficult to discriminate the effects of the teratogen from that of other, associated factors. Despite these limitations, retrospective clinical studies are of great value because the characteristics of the affected individual can be observed much more clearly than among more moderately exposed children. In addition, the characteristics of clinically affected children include those problems that will require intervention and treatment. In contrast, prospective studies allow some statistical control of confounding variables, as well as the use of contrast groups to control for factors such as social

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Page 159 class and race, and also allow examination of factors that can be obscured in clinical studies. However, as described above the sample selected for inclusion in prospective studies is often different from that included in retrospective and clinical studies. The level of prenatal alcohol exposure tends to be less than that found in retrospective studies of identified FAS individuals. This can lead to problems in interpretation of the findings. In interpreting the results of such studies, the problems of overgeneralization and interpretation of multiple comparisons should be considered. For these reasons, in the current review, the type of study from which the information is derived is identified. Developmental Differences in Clinical Presentation Children with the full FAS syndrome are distinguished by dysmorphic facial features, growth retardation, and some evidence of damage to the central nervous system (CNS). On average, individuals with the full syndrome are mildly mentally retarded, with IQ scores in the 60s (Streissguth, 1986). However, there is wide variability in presentation, and scores can range from the severely disabled through the average range (85 to 115). Individuals with partial FAS, ARBD, or ARND may have some of the characteristic physical features, while others are absent, or they may have behavioral effects in the absence of physical features. These individuals often have IQs in the "borderline" range (i.e., 70 to 85), and are frequently described in the scientific literature and popular press as having "normal" intelligence. In fact, having intellectual abilities in this range can be very disabling socially and adaptively, particularly if accompanied by the other kinds of problems often found in children growing up in alcoholic families (Brown, 1991; Sher, 1991). Behavioral deficits have been described by many clinicians. A number of problems have been identified, including (1) attentional problems or hyperactivity (Morse, 1991; Nanson and Hiscock, 1990); (2) academic problems, including specific deficits in mathematics and memory skills (Streissguth et al., 1993); (3) very specific language deficits (Abkarian, 1992); and (4) problems with adaptive functioning that grow more significant with age (Lemoine and Lemoine, 1992; Streissguth and Randels, 1989). Although it is possible to have only one or two behavioral difficulties, in most individuals with a diagnosis of FAS, most of these problems co-occur, which makes an appropriate intervention program hard to implement. While such patterns are often reported to be characteristic of affected individuals, they are not always seen. Even some dysmorphic children do not show all of these traits (Coles et al., 1994a,b), and in prospectively followed samples of moderately exposed children, few such problems may be seen (N. Day, personal communication, 1994; Greene et al., 1991; Boyd et al., 1991). Although a teratogenic etiology for these patterns is usually assumed, the relationship between

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Page 160 specific neurological damage and particular behaviors or patterns of behavioral development has not been well established (see below). Finally, because of the nature of the developmental process, the behavioral, as well as the physical, manifestations of the teratogenic effect can change over time. Such apparent inconsistencies make diagnosis and treatment difficult and often lead observers to suggest that effects are unrelated to prenatal exposure. However, a better understanding of the meaning of the presentation of behavioral symptoms may also provide a key to their nature. Newborn and Infancy Although it would be best to identify affected individuals as early as possible, it is frequently difficult in the newborn period because of the lack of development of specific facial features that are often thought to be more recognizable during the preschool period (Clarren et al., 1987; Egeland et al., submitted for publication; Graham et al., 1988). It has been established (Abel et al., 1993; Coles et al., submitted for publication) that trained observers can identify both the facial features and the behavioral signs associated with prenatal alcohol exposure during this period. Behavioral patterns characteristic of alcohol-exposed neonates are often those associated with withdrawal from a CNS depressant (Coles et al., 1984, 1985; Nugent et al., 1990; Robe et al., 1981). During the first week of life, infants exposed to sufficiently high amounts of alcohol throughout pregnancy may show excessive arousal, disturbed sleep patterns (Sher et al., 1988), hyperactive reflexes, gastrointestinal symptoms, and other signs of abstinence syndrome. Children who were exposed only during the first part of pregnancy (Coles et al., 1985) or to lower doses (Richardson et al., 1989) may not demonstrate behavioral changes. Behavioral effects, including overarousal and sleep disturbances, may persist over the first month of life (Coles et al., 1987) or longer (Havlicek et al., 1977; Ioffe and Chernick, 1990). Other studies have identified specific behavioral differences in neonates (e.g., habituation deficits relative to controls [Streissguth et al., 1983]; effects on the cry acoustics [Nugent et al., 1990]). (See Coles and Platzman, 1993, for an exhaustive review of effects in infancy and childhood.) Fewer studies have examined effects in the first two years of life and, often, there have been no effects demonstrated, particularly in samples of children without the full syndrome (e.g., Richardson et al., in press; Streissguth et al., 1980). Growth measures, the metrics of which are more direct and precise than those of behavior, have been found to withstand statistical manipulations sufficiently to allow identification of effects of moderate exposure (Day et al., 1994). Behavior, however, is more slippery to measure and more poorly defined in relation to teratogenic exposure. For that reason, at least, in part only children who are clearly affected (i.e., dysmorphic or growth retarded) or those who are participating in well-controlled prospective studies (Jacobson et al., 1993) have shown effects on global developmental tests during this period.

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Page 161 In contrast, when FAS is identified as clinically significant in infancy and babies are followed medically, there are a number of characteristic problems associated with fetal alcohol exposure, including failure to thrive (often associated with feeding difficulties), delays in development, motor dysfunction, otitis media, and cardiac problems. Behaviorally, infants are often described as having what Greenspan and Wieder (1993) call "regulatory" problems, as well as delays in acquisition of skills. Unfortunately, clinically referred children are often victims of abuse and neglect as well as prenatal exposure and, for that reason, may also suffer from behavioral problems associated with those conditions (e.g., reactive attachment disorder [American Psychiatric Association, 1994] or the behavioral effects of stress), and it can be difficult to discriminate one behavioral effect from another, particularly among individual children in a clinical setting (Zeanah et al., 1993). Preschool During the preschool period, usually defined as from 2½ to 6 years of age, there are relatively few studies of prospectively followed alcohol-exposed children. Those that have been done are not entirely consistent in their findings across most areas studied, including cognition (Greene et al., 1990; Streissguth et al., 1989), attention (Boyd et al., 1991; Brown et al., 1991; Streissguth et al., 1984), and behavior (Brown et al., 1991; Landesman-Dwyer et al., 1981; Morrow-Tlucak and Ernhart, 1987). In clinically identified groups, presentation varies, depending on the child's caregiving environment, as well as other factors. However, cognitive deficits are observed frequently, and attention-deficit hyperactivity disorder (ADHD) is often identified (Conry, 1990; Nanson and Hiscock, 1990). Children of this age have been described both as lively, friendly, and socially interested (Streissguth and Giunta, 1988) and also as exhibiting hyperactivity, ADHD, language dysfunction, perceptual problems, and behavioral disturbances (Morse, 1991). Morse et al. (1995) also reported on the frequency of sensory integration problems in a study of a 100 children with FAS and an equal number of controls, finding that parents of children with FAS reported more problems than other parents. Language Development. The possibility that there are deficits in language development as a result of prenatal alcohol exposure has been examined, particularly in young children. In children with cognitive deficits, language delays are often noted before other problems and are usually associated with general developmental delay. Of more interest is the possibility that specific language deficits are associated with alcohol exposure. Again, this possibility has been explored both by the examination of children with the diagnosis of FAS and those who clearly have alcohol-related disabilities and by prospective examination of exposed children through identification of maternal drinking prenatally. In a comprehensive statistical analysis of the first seven years of data from the prospectively followed Seattle sample, Streissguth et al. (1993) concluded

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Page 162 that "language disabilities are generally absent from the lists of fetal alcohol effects revealed by these analyses" (p. 198). However, they noted that in clinically referred samples, young children had "good but superficial language skills" that masked the "early neuromotor deficits that foreshadow later school problems" (p. 198). Similarly, a prospective study (Greene et al., 1990) in Cleveland that specifically explored language development in children aged 4 years, 10 months, using both observation and standardized tests, found no evidence of deficits in the exposed groups in comparison with other low-income children. In a cohort of low-income African-American children in Atlanta, Coles and colleagues also found that language skills were preserved relative to visual or spatial skills and memory (Coles et al., 1991a, 1994a,b). In these studies, language was assessed only as part of a cognitive battery and was confined to measures of vocabulary and fluency, so more subtle deficiencies in language skills may not have been detected. In another sample, however, Russell et al. (1991) looked at 6 year olds whose middle-class mothers had been identified during gestation as "heavy" drinkers. Among social and moderate drinkers, no significant effects were found on tests of intelligence or on auditory information processing. However, among children of "problem" drinkers (defined from the results of a screening test called Indications of Problem Drinking), scores on the verbal portion of the Weschler Intelligence Scale for Children-Revised (WISC-R), the Token Test (a receptive language measure), and a dichotic listening task were significantly lower than in other groups. When descriptions of clinical samples of alcohol-affected children's language problems are examined, there is an apparent discrepancy between the child's vocabulary and fluency and the general ability to communicate effectively. Difficulties appear to involve comprehension and social discourse or the pragmatics of speech. These issues were examined by Abkarian (1992), who reviewed the available literature on speech and language disabilities in alcohol-affected children. He concluded that affected children had deficits in the quality of semantics and syntax and in the pragmatic aspects of speech. For instance, although they easily engaged in conversational interactions and understood the need for turn taking, their responses often had little relationship to the initial statements (Hamilton, 1981). In dysmorphic children (Becker et al., 1990), there were indications of articulation deficits associated with structural as well as functional defects. Abkarian (1992) found that in comparing the experimental and the clinical literature on FAS and alcohol effects, a pattern of communication dysfunction could be identified. This is described as "social but dysfunctional communicative interaction" (p. 232), with individuals being fluid, but superficial, in their speech and having an awareness of the necessity for turn taking without the ability to communicate effectively. Because there are a number of potential reasons for such deficits, the author concludes with a plea for treatment research

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Page 163 both to describe the nature and extent of any alcohol-related speech and language problems and to identify appropriate methodologies for intervention. Such studies have not yet been done. School Age School age covers that time from the beginning of school (usually 6 years of age) until early adolescence (13 years). At this age, clinically referred, affected children are described as unable to sit still in class and pay attention to school work. They are said to find it difficult to deal with multiple sensory inputs, particularly auditory information, and to show significant difficulties in peer relationships (Morse, 1991; Streissguth et al., 1985). Beginning at school age, children have also been reported to "lack remorse," to fail to learn from mistakes, to lack judgment, to be unusually aggressive, and to be unable to maintain friendships (Streissguth, 1992). Despite the importance of this period of children's academic and intellectual development and socialization, there are few empirical studies of the effects of prenatal alcohol exposure during this time. Those controlled research studies that do exist have focused on cognitive performance, academic achievement, and attention or hyperactivity. There is no research-based information available on social and emotional status or other aspects of development in these children. Cognitive and Academic Performance. In prospective studies it is at school age that deficits in cognitive performance begin to appear reliably (Coles et al., 1991a; Nanson and Hiscock, 1990), and these have been found even in the absence of physical dysmorphia (Day, personal communication, February 1995; Streissguth et al., 1990). Streissguth and her colleagues reported that at age 7, cognitive effects, including lower IQ scores on the WISC-R, were associated with heavier drinking during pregnancy in a sample of middle-class, predominantly Caucasian children (Streissguth et al., 1990). In understanding these data, it is important to note that the vast majority of the exposed children were performing in the average range and would not have been identified as showing clinical symptoms. Areas of relative weakness included memory, problem solving, mental flexibility, visual or motor performance, academic skills (measured with the Wide Range Achievement Test [WRAT]), and particularly math skills. These authors also noted that such deficits were more evident under more stressful environmental conditions (e.g., in single-parent families, in large families, and in lower-SES groups). Due to the large sample size, these investigators were able to control most potentially confounding factors. Similar outcomes were found in a low-SES predominantly African-American sample in Atlanta (Coles et al., 1991a). More impaired performance on the Kaufman-Assessment Battery for Children (K-ABC) was found in children with greater exposure to alcohol. Sequential processing and preacademic skills, particularly

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Page 164 precursors to math, were most affected, with language relatively preserved. Attention. Considerable confusion continues to exist over "attention" as a psychological construct and "attention" as a component of attention-deficit hyperactivity disorder. The latter is defined in the fourth edition of the American Psychiatric Association's Diagnostic and Statistical Manual (DSM-IV) as a constellation of behaviors reported by parents or teachers, and it represents one of the most common problems of childhood. In contrast, attention as the psychological construct is measured by using a variety of tests (e.g., continuous performance [CPT] or vigilance tasks). Children with ADHD do not necessarily exhibit problems in attention, the psychological construct (see Shaywitz et al., 1994, for more extensive discussion of this issue). Although clinicians frequently report disturbances in attention in the offspring of alcoholic women, results from the few systematic studies that address attention in FAS have been difficult to interpret. Thus, Streissguth et al. (1986) found that greater fetal alcohol exposure was associated with poorer test performance on a vigilance task, particularly greater distractibility and more impulsivity. Academic and behavioral deficits consistent with a diagnosis of ADHD were noted in the same children. A sample from the Atlanta cohort was tested at age 5 years, 10 months (Brown et al., 1991), and a second group of children was tested at 7 ½ years (Coles et al., 1994a,b), by using two different vigilance paradigms. At 7 ½ years, a contrast group of children with a confirmed diagnosis of ADHD, who responded therapeutically to stimulant medication, was also tested. At 5 years, 10 months, children whose mothers continued to drink throughout pregnancy showed a relative weakness in sustaining attention across trials but did not demonstrate impulsivity. Hyperactivity and impulsivity were also assessed through standard checklists, videotaped observations, and cognitive measures, and no other ADHD-type effects were noted on any of these measures. At 7 ½ years, when a more comprehensive assessment of vigilance performance was possible, children with FAS showed better performance on these computerized tasks than did non-alcohol-exposed ("normal") children, while the ADHD-diagnosed children were significantly impaired. Based also on standard checklists and observation of behavior, children with an ADHD diagnosis could be discriminated but children with alcohol exposure were no different from controls. Similarly, Fried et al. (1992) reported that alcohol exposure (among middle-class, white, social drinkers in Ottawa) resulted in lower levels of impulsivity on a standard CPT task, a finding that is consistent with those in the Atlanta sample but inconsistent with those of Streissguth et al. (1986) and Nanson and Hiscock (1990), who used a group of clinically referred, Native American children in Canada. With a sample of lower-class white and African-American children in Cleveland, Boyd et al. (1991) found no effects of alcohol exposure on attention at age 4 years, 10 months.

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Page 183 of measurement. From infancy through early school age, cognitive deficits are usually "mild" and motor deficits are relatively subtle compared to those usually treated in early intervention programs. Generally, to receive therapeutic services, children must meet state or district criteria, which usually involve standardized testing. Often, to receive services, infants and preschool children must score less than 70 (2 standard deviations [SD] below the mean) on a standardized test in at least one area of functioning (usually cognitive, motor, or language development) or, in some cases 1.5 SD in two areas. Because alcohol-exposed infants may not score in this deficit range during the first year, many do not qualify for services during that time. It might be assumed, given that children do not perform poorly on standardized tests during this time, that they are not really damaged by their prenatal exposure but by other environment factors. However, children with other conditions associated with later deficits (e.g., Down syndrome) may not always score in the deficit range during the first year due to the problem of measurement associated with infant tests. Because the prognosis for children with Down syndrome is well known, however, such children are usually not denied services. Similar problems can occur when the child is older, as well. Many of the indicators of adult cognitive and emotional functioning are, by definition, missing in infants and preschool children (e.g., language, ability to care for one's self). In currently available data from several sources, alcohol-affected children who will later show mild retardation at school age, score in the low-average range at 12 months and in the borderline range at 24 months (Platzman et al., 1986). These patterns do not result solely from deficits in the validity of test instruments or from poor reliability, but from the nature of the developmental process itself and, probably, from the impact of negative social environments and the particular kinds of brain damage caused by fetal alcohol exposure (see above). If further research confirms this pattern of declining scores with age, children who need services might not be identified early enough during development to receive preventive treatment but must wait until more severe deficits become manifest. This raises concern, because it is much more difficult to provide useful treatment (see Campbell and Ramey, 1994). Inconsistency in Follow-Up Inconsistency in follow-up may be due to many factors. To receive high-quality services, parents of developmentally delayed children must be able to act as advocates with educational and social service systems. When children remain with their biological parents or with relatives, they can be influenced by dysfunction within these families. Because of family problems, which may include the impairments associated with substance abuse, these families can be inconsistent in providing well-baby checkups and immunizations and in following up on medical or educational recommendations (Wilson et al., 1984). Unless severe

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Page 184 abuse or neglect brings the child to the attention of authorities, children often will not be noticed until they begin to fail at school or suffer from behavior problems (usually externalizing) that bring them to attention. By this time, usually early school age, it may be difficult to overcome the combined effects of prenatal exposure and lack of educational or medical intervention. When children are in the foster care system, they also may not receive adequate services, for many well-known reasons. Even when developmental delays are noted, health and educational professionals may not be experienced in dealing with alcohol-abusing parents or with the kind of family dysfunction that often accompanies addiction (Beckwith, 1990). As a result of ineffective interactions with the child's caregivers, treatment recommendations may not be followed. Wilson et al. (1984) identified a number of children with FAS who needed medical and social services. Mothers were noted to have poor psychological adjustment, and half of them were still using alcohol. Because of their own difficulties, mothers were found to be ineffective both in parenting and in their ability to make use of medical or other available services that were needed by their affected children. In another study of low-SES school-aged children prenatally exposed to alcohol, Coles and colleagues (unpublished data) found that although there was a high incidence of medical problems noted in children who could be diagnosed with FAS or possible alcohol-related effects, the use of health care, including checkups, acute care visits, and emergency room visits, was lower in this group than in SES controls. SUMMARY: INTERVENTION AND TREATMENT Although the most desirable way of dealing with fetal alcohol syndrome, ARBD, and ARND is through prevention of the birth of an affected child, provisions must be made for affected children when such efforts fail. Efforts to prevent secondary disabilities will involve coordination of several levels of identification, intervention, and treatment in order to maximize the child's postnatal development. Such efforts will also require changes in professional education, application of special educational methods, and changes in some public policy agendas. As such efforts are undertaken, it is important to recognize that although children are affected by prenatal exposure to alcohol, a great deal of neurological development occurs postnatally, and if child care, nutrition, and environment are adequate, it is probable that alcohol-exposed children can make considerable progress. This is particularly true when the insult has not been severe. Among other groups of high-risk children, adequate education and training, together with protection from negative child rearing environments and attention to predictable crises at various developmental stages, can make the difference between achieving a reasonable degree of independence and life satisfaction and more negative outcomes (Campbell and Ramey, 1994). Negative reports of developmental outcomes for children affected by prenatal

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Page 185 alcohol exposure are distressing, particularly when there have been attempts at intervention and prevention over the child's life span. These outcomes have led to the suggestion (LaDue et al., 1989; Spohr et al., 1993) that interventions, including placement in foster care or adoption, do not change the prognosis for children affected by prenatal alcohol exposure. Such negative ideas have affected the way in which children with FAS, ARBD, or ARND are treated by caregivers, health care providers, educators, and social service agencies (Conn-Blowers, 1991; Streissguth, 1992). Clearly, there is a need for better understanding of these issues. However, this understanding will require a number of changes in the approach to this disorder. First, we must provide for a well-organized strategy directed toward investigation of the clinical needs of affected individuals. RECOMMENDATIONS The committee concludes that there are no specific programs to treat children with FAS, ARBD, or ARND, and other efforts to prevent secondary disability in these children are insufficient and inadequate. Given the known value of early intervention, however, it is important to identify children with FAS, ARBD, or ARND as early as possible. Thus, in the committee's view, action to bring needed programs and efforts to an acceptable level must proceed on a number of fronts. For example, as pointed out in other chapters, there is a critical need for more consistent diagnostic criteria and better surveillance. Application of these criteria requires the availability of well-trained professionals in social services, education, and health care, as well as those charged with developing policies that impact services for special children. The committee, therefore, recommends the following actions to address these needs: • Clusters of high-quality diagnostic and treatment services should be available locally and regionally. • Programs that offer training of professionals and that serve as resource centers for schools and medical clinics should be established. • Programs serving children with FAS, ARND, or ARBD should meet the special, complex needs of such children, including consideration of the families involved and increased availability of parenting training for caretakers (birth parents, foster parents, and adoptive parents). • Community outreach programs should be available to establish appropriate lines of communication with clinicians, judges, police, psychologists, teachers, and both birth and adoptive/foster parents. • Educational materials should be developed for professionals who deal with school-age children to increase their awareness of FAS, ARND, or ARBD as a potential cause of ADHD-like behaviors, including hyperactivity, and to facilitate their referral of such children to other appropriate or needed services.

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Page 186 • Ways should be developed to address the issues of confidentiality that apply to identifying and treating children exposed to alcohol (or other substances) in utero. • Clinical practice guidelines should be developed for follow-up and treatment of children with FAS, ARND, or ARBD. A necessary complement to the above actions is an expanded knowledge base. The committee, thus, views further research as essential to providing adequate treatment of children affected by FAS, ARND, and ARBD. The committee recommends additional research in the following areas: • research to distinguish the role of the postnatal environment in modifying the effects of fetal alcohol exposure, including research on adopted versus nonadopted children with these disorders; • research on the social and emotional status of school age children affected by FAS, ARND, or ARBD and research on the existence of specific impairments associated with these syndromes, particularly impairments in attention, language, sensory integration, and other behavioral problems; • further basic research using animal models to examine the underlying neurobiological mechanisms of behavioral and environmental interventions over the life span; and • evaluation of the effectiveness of educational interventions on children with FAS, ARND, or ARBD, possibly beginning with the examination of educational interventions that look promising in case studies or in studies of children exposed to illicit drugs in utero. REFERENCES Abel EL. Fetal Alcohol Syndrome. Oradell, New Jersey: Medical Economics Co., 1990. Abel EL. An update on incidence in Fetal Alcohol Syndrome: FAS is not an equal opportunity birth defect. Neurotoxicology and Teratology 1995; 17:427-443. Abel EL, Martier S, Kruger M, Ager J, Sokol RJ. Ratings of fetal alcohol syndrome facial features by medical providers and biomedical scientists. Alcoholism: Clinical and Experimental Research 1993; 17:717-721. Abkarian GG. Communication effects of prenatal alcohol exposure. Journal of Communication Disorders 1992; 25:221-240. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: 4th Edition. Washington, DC: APA, 1994. Anderson B., Novick E. Fetal Alcohol Syndrome and Pregnant Women Who Abuse Alcohol: An Overview of the Issue and the Federal Response. Washington, DC: U.S. Department of Health and Human Services, 1992. Aronson M, Kyllerman M, Sabel KG, Sandin B, Olegard R. Children of alcoholic mothers: Developmental, perceptual and behavioural characteristics in children of alcoholic mothers as compared to matched controls. Acta Paediatrica Scandinavica 1985; 74:27-35. Astley S. Diagnostic Criteria for FAS. Paper presented at CDC Data Collaborative Meeting, 1994.

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