Vol. 20, No. 2, pp. 172–189 2007 Wolters Kluwer Health

Infants & Young ChildrenVol. 20, No. 2, pp. 172–189Copyright c© 2007 Wolters Kluwer Health | Lippincott Williams & Wilkins

Responding to the Challengeof Early Intervention for FetalAlcohol Spectrum Disorders

Heather Carmichael Olson, PhD; Tracy Jirikowic, PhD;Deborah Kartin, PhD; Susan Astley, PhD

Prenatal alcohol exposure can lead to significant neurodevelopmental disabilities, now recognizedas fetal alcohol spectrum disorders (FASD). This includes both fetal alcohol syndrome, a lifelongbirth defect, and a wider range of enduring learning and behavior deficits often called alcohol-related neurodevelopmental disorder (ARND). Diagnostic classification systems have been devel-oped to identify children with FASD, and early interventionists from multiple disciplines can becentral in identification and referral for diagnosis, and in providing the known protective influ-ence of intervention early in life. With the recent federal mandates to better address needs ofchildren born prenatally affected by substances, or those impacted by abuse and/or neglect, byreferring them for screening and possible early intervention services, there is heightened need forproviders to understand FASD. There is a growing body of research data describing the teratogeniceffects of alcohol on central nervous system function and physical development, the diversity ofchildren with prenatal alcohol exposure and their families, and the developmental and behavioralcharacteristics of this clinical population. This article reviews the latest research evidence, bearingin mind what is important to early intervention. This article also gives practical guidance on FASDprevention, methods for early screening, and referral of young children for diagnosis of FASD (andreferral for needed services once diagnosed), and how to provide education, support, advocacyassistance, and anticipatory guidance for families raising children with FASD. Key words: early di-agnosis and intervention, fetal alcohol syndrome, alcohol-induced disorders (nervous systems),maternal exposure, teratogen

From the Department of Psychiatry and BehavioralSciences, School of Medicine (Dr Carmichael Olson),the Department of Psychosocial and CommunityHealth, School of Nursing (Dr Jirikowic), theDepartment of Epidemiology, School of Public Healthand Community Medicine (Drs Jirikowic andAstley), and Department of Rehabilitation Medicine,School of Medicine (Dr Kartin), University ofWashington, Seattle.

This work was also facilitated by grant P30 HD02274from the National Institute of Child Health and HumanDevelopment.

The authors gratefully acknowledge the Center on Hu-man Development and Disability, Washington State Di-vision of Alcohol and Substance Abuse, and the Centersfor Disease Control and Prevention for support duringthe preparation of this manuscript.

Corresponding author: Heather Carmichael Olson,PhD, Child Psychiatry Research, 1100 Olive Way, Suite800, Met Park West Bldg, Children’s Hospital Child Psy-chiatry Research, Seattle, WA 98101 (e-mail: [email protected]).

PRENATAL ALCOHOL EXPOSURE can leadto significant developmental disabilities,

now recognized under the umbrella termof “fetal alcohol spectrum disorders” (FASD)(National Organization on Fetal AlcoholSyndrome, 2004). The number of childrenwith the full “fetal alcohol syndrome” (FAS)has been estimated to be 0.5 to 3 per 1000live births, with higher rates in some commu-nities (Stratton, Howe, & Battaglia, 1996). ButFAS is found in only a fairly small proportionof children affected by prenatal alcoholexposure. Many children have alcohol-induced impairments that can be just asserious, or more so, than those seen in FAS(Mattson, Riley, Gramling, Delis, & Jones,1998). The term “alcohol-related neurode-velopmental disorder” (ARND) has beenapplied to this condition (National Instituteon Alcohol Abuse and Alcoholism [NIAAA],

172

Responding to the Challenge of Fetal Alcohol Spectrum Disorder 173

2000). Prevalence rates of the full range ofFASD beyond FAS, including ARND and otheralcohol-related birth defects, are believedto occur about 3 times as often as FAS. Arate of 2 to 6 per 1000 (Centers for DiseaseControl and Prevention [CDC], 2007), andapproach the latest estimated prevalenceof autism spectrum disorders. New regu-lations at the federal level, under both theKeeping Children and Families Safe Act of2003, which amended and reauthorized theChild Abuse Prevention and Treatment Act(CAPTA), and the Individuals with DisabilitiesEducation Improvement Act of 2004, requirethat children involved in substantiated casesof child abuse and neglect be referred toearly intervention systems. IDEA further re-quires early intervention referral for childrenwhose development is impacted by prenatalsubstance exposure. These regulations arecertain to result in increased numbers ofchildren in early intervention systems whoneed referral for FASD diagnosis followed bytailored early intervention.

Clearly, FASD is an important problem thatevery early interventionist will encounter—now more than ever—and potentially playa key therapeutic role. To help guide prac-tice in early intervention, this article summa-rizes current research on FASD and providespractical ideas about prevention, qualifyingchildren for services, supporting families,anticipatory guidance, and a developmentalsystems model useful in thinking about as-sessment and intervention for young childrenwith FASD.

ALCOHOL AS A TERATOGEN AND

FASD PREVENTION

As a neurobehavioral teratogen, alcohol in-terferes with normal fetal growth and devel-opment through multiple actions at differentsites. Researchers are now studying the bio-chemical mechanisms underlying alcohol’s ef-fects, in hopes that pharmacologic treatmentsmight eventually be used to intervene with(or prevent) alcohol-related fetal injury. Re-searchers are also looking at neuroimaging

and physical measures (such as EEGs) to un-derstand more precisely how alcohol dam-ages the brain (NIAAA, 2000). Most impor-tant to early interventionists is the fact thatprenatal alcohol exposure can significantlycompromise central nervous system (CNS)function, leading to a wide range of devel-opmental, learning, and behavior problems.These problems can affect later life success.Indeed, natural history data so far show thatindividuals with FASD have a very high like-lihood of suffering secondary disabilities oflifestyle and daily function in adolescence andadulthood (Streissguth et al., 2004).

Fetal effects of alcohol exposure differ de-pending on the amount, timing, and patternof maternal drinking, so deficits are highlyvariable from one child to another. In gen-eral, the more a pregnant woman drinks, thegreater the severity of persistent neurobehav-ioral deficits. Episodic (or binge) drinking thatcreates higher maternal peak blood alcoholconcentrations is associated with greater fe-tal damage. On an individual basis, however,any amount of drinking during pregnancy cancause harm, and alcohol use at any time dur-ing gestation is associated with a higher riskof CNS dysfunction. Figure 1 provides high-lights from the 2005 U.S. Surgeon General’sAdvisory on Drinking and Pregnancy (2005).Early interventionists can advance the impor-tant goal of FASD prevention by providing thisinformation to the many women with whomthey work who are thinking about pregnancyor are already pregnant, and to women’spartners.

IDENTIFYING THE PROBLEM AND

QUALIFYING CHILDREN FOR SERVICES

Table 1 defines diagnoses on the fetal al-cohol spectrum, and Figure 2 shows the“face” of FAS. These diagnoses are medicalconditions. Current practice guidelines sug-gest that diagnosing physicians work witha multidisciplinary team and follow well-defined FASD diagnostic guidelines. Nationaldiagnostic guidelines have been published inthe United States for FAS (National Center

174 INFANTS & YOUNG CHILDREN/APRIL–JUNE 2007

Figure 1. Highlights of the 2005 surgeon general’s advisory on drinking and pregnancy. From http://

www.surgeongeneral.gov/pressreleases/sg02222005.html.

on Birth Defects and Developmental Disabil-ities [NCBDD], 2004) and in Canada for thebroader spectrum (Chudley et al., 2005).More specific FASD diagnostic systems havebeen developed for clinical and research usewhich provide a method for diagnosing thefull range of conditions that make up the fe-tal alcohol spectrum.

FASD diagnoses commonly co-occur withdevelopmental delays or deficits arising fromother genetic or medical causes, psychiatricdisorders (such as ADHD), and/or academicproblems. A full understanding of an indi-vidual child’s problems requires taking allco-occurring conditions into consideration.Diagnoses on the fetal alcohol spectrum typ-ically add an important dimension to the de-scription of a child’s problems as classifiedby other medical and psychiatric diagnosesgenerated through the use of diagnostic sys-tems such as ICD-10 (World Health Organiza-tion, 2005), DC:0-3-R (Zero to Three, 2005),or DSM-IV (American Psychiatric Association,1994). Knowing that a child has ADHD inthe presence of FASD, for example, can meanthat commonly used interventions for ADHDwill not have expected effects, and that a dif-

ferent combination of treatment techniquesmay be required. Indeed, an understandingthat a child has neurological unpairment aris-ing from alcohol exposure can fundamentallychange a parent’s or provider’s perception ofthe child’s behavior.

Current FASD diagnostic guidelines usuallyrequire evidence of structural, neurologic,and/or functional damage of the CNS. Evi-dence of structural/neurologic damage mayinclude such findings as microcephaly (smallhead size), abnormal neuroimaging, or seizuredisorders. These can sometimes be identi-fied early in life. Evidence of CNS dysfunc-tion includes standardized test scores thatdocument significant global delays or, morecommonly, variability revealed in significantgaps in skills, atypical patterns of develop-ment, or uneven profiles of learning strengthsand weaknesses. Unfortunately, it is often dif-ficult to gather clear evidence of CNS dys-function at a young age. Early developmentaldeficits of alcohol-exposed children may besubtle and yet important precursors of laterproblems. Tests used with young children of-ten cannot detect variability in learning pro-files or subtle problems, so young children


Table 1. Criteria for diagnosing fetal alcohol spectrum disorders∗,†

Diagnosis Diagnostic features

Fetal alcohol syndrome (FAS) Growth deficiency: Height or weight less than 10thpercentile

Cluster of characteristic minor facial anomalies: Smallpalpebral fissures (eyeslits), thin upper lip, smoothphiltrum (groove above the upper lip)

Central nervous system damage (evidence of structural

and/or functional brain impairment)

Reliable evidence of confirmed prenatal alcohol exposure:

Not necessary if the cluster of characteristic facial

features is fully present

Partial FAS (PFAS) Some of the characteristic minor facial anomalies

Growth deficiency: Height or weight less than 10thpercentile



Reliable evidence of confirmed prenatal alcohol exposure

Alcohol-related neurodevelopmental

disorder (ARND)



Reliable evidence of confirmed prenatal alcohol exposure

∗Adapted from the Astley (2004).†The 4-Digit Diagnostic Code (Astley, 2004) is a system used by clinicians and researchers to evaluate the effects of

prenatal alcohol exposure. While the 4-Digit Code maps onto these widely known diagnoses, the system actually uses

different descriptive terms to more precisely describe how children manifest PFAS and ARND. There are other diagnostic

guidelines that also include a category called “Alcohol-Related Birth Defects” (ARBD). ARBD exist in the presence of

confirmed prenatal alcohol exposure, but children who have ARBD do not necessarily show the characteristic facial

features. ARBD are defined as follows: “Any of a number of anomalies (such as heart or kidney defects) present at birth

that are associated with maternal alcohol consumption during pregnancy” (NIAAA, 2000, p. 286).

will less often meet FASD diagnostic criteria.In addition, because alcohol effects may of-ten emerge most clearly as deficits in higherlevel cognitive functions, children’s problemsmay not even become evident until well pastthe window for early intervention, aroundsecond to fourth grades (Olson, Morse, &Huffine, 1998b). Yet there is growing knowl-edge about the plasticity of the CNS, andintriguing findings on the positive develop-mental effects of enriching the motor andlearning environment with alcohol-exposedanimals (eg, Klintsova, Goodlet, & Gree-nough, 1999; Miura, Whinery, Dominguez,Riley, & Thomas, 2005). These strongly im-ply that early identification and interventionfor children who are alcohol-exposed may beespecially important, because CNS functionmight potentially be improved.

Some states recognize the full FAS as a di-agnosed condition with a high probabilityof developmental delay, thus deserving earlyintervention. But there are many additionalchildren impacted by prenatal alcohol expo-sure, and new diagnostic guidelines recog-nize conditions across the full fetal alcoholspectrum. Literature review later in this ar-ticle strongly indicates that children affectedby prenatal alcohol, but without the full syn-drome, have diagnosable conditions that alsocarry a high likelihood of developmental de-lay and later significant problems in adaptivefunction. Because of this, providing early in-tervention services for all children diagnosedwith FASD should be strongly encouraged.An even broader approach to qualifying de-velopmentally vulnerable young children forearly intervention is to classify them “at-risk”


Figure 2. The 3 diagnostic facial features of fetal alcohol syndrome are as follows: (1) palpebral fissure

length (eyeslit length) of 2 or more SD below the mean; (2) smooth philtrum (the vertical groove be-

tween the nose and the upper lip) (rank 4 or 5 on Lip-Philtrum Guide); (3) thin upper lip (rank 4 or 5 on

Lip-Philtrum Guide). Used with permission from Susan Astley.

because of prenatal alcohol exposure coupledwith evidence of emerging learning problemsand/or environmental risk if this approachfits into IDEA implementation in the statewhere the child resides. One strategy thatdoes not fit with current evidence is assum-ing that an alcohol-exposed child will “growout of”apparently mild early delays, and there-fore not providing services or developmentalmonitoring. Instead, if an exposed child doesnot qualify for early intervention, or improvesafter intervention and then no longer quali-fies, a better approach lies in careful moni-toring and reevaluation at key developmen-tal transitions. This will address the possibleemergence of later cognitive, language, andsocial difficulties.

YOUNG CHILDREN WITH PRENATAL

ALCOHOL EXPOSURE AND THEIR

FAMILIES

What does current scientific evidence sayabout young children with prenatal alcoholexposure, and what are the implications forearly intervention? At present, data for youngchildren born prenatally exposed to alcoholcome from several well-designed prospectivelongitudinal studies of the impact of moderateor higher levels of prenatal alcohol exposureconducted in various locations in the UnitedStates, Canada, and selected other countries(with varying ethnic compositions and lev-els of environmental risk). There are also afew small but carefully investigated clinical


samples of young children with FASD. Justnow emerging are data from larger clinicalsamples composed of patients seen in FASDdiagnostic clinics. All these studies are thesource of research findings reviewed here,given the focus of this article on the di-rect impact of prenatal alcohol exposure, aproven neurobehavioral teratogen, on childand family outcome. Also available in the lit-erature are longitudinal studies of young chil-dren born polydrug-exposed, including alco-hol, who typically have lives characterized byhigh levels of postnatal environmental risk.Findings from these latter studies are referredto briefly but not reviewed here, becausethese studies primarily provide insight intothe impact of illicit drug exposure coupledwith the larger issues of very high risk fami-lies and the impact of chemical dependency,rather than the impact of alcohol exposure be-fore birth.

To begin, we briefly summarize new dataon a large number of young children, agedbirth to 8, and their families (N = 781), fromthe Washington State FAS Diagnostic and Pre-vention Network (FAS DPN). The FAS DPN is astatewide clinic network operating since 1993that uses an interdisciplinary team diagnosticprocess and a carefully developed diagnosticsystem called the “4-Digit Diagnostic Code”(Astley, 2004; Astley & Clarren, 2000). TheFAS DPN data discussed here come from thelargest clinical database of children born pre-natally alcohol-exposed believed to be in exis-tence at this time, and includes a large numberof young children. There are no national dataon this set of neurodevelopmental disabili-ties, so the FAS DPN database is an excellentsource of information useful to early interven-tionists even though conclusions are some-what limited by geographical context. Com-pared to the population of Washington State,the overall FAS DPN database includes some-what fewer females and, in terms of ethnic-ity, slightly underrepresents Caucasians (in-cluding those of Hispanic origin) and slightlyoverrepresents African Americans. Largely be-cause of referral patterns (perhaps because ofcultural differences in recognition of the prob-

lem and willingness to refer), the FAS DPNdatabase includes somewhat more NativeAmericans and fewer Asians than in the largerpopulation of Washington State. It shouldbe noted that the FAS DPN database likelyunderrepresents the subset of children withFASD still living with parents grappling withchemical dependency. Research is needed onthe prevalence of FASD in this high-needgroup.

Age of identification and important

demographic characteristics

FAS DPN data show that the average age ofreferral for FASD diagnosis overall is 91/2 years.This means that identification of problems re-lated to alcohol exposure often occurs ratherlate in children’s lives. Younger children, agedbirth to 8, comprise only half of those re-ferred. Of these, the average age of identifi-cation is just more than 5, with only about athird brought in before age 4. This indicatesthat two thirds of younger children missed thechance for true early intervention. Improvedrecognition of FASD by early interventionistscould bring more young children in for earlydiagnosis. Early diagnosis has been identifiedas a crucial protective factor in this popula-tion, because it is associated with more posi-tive outcomes in adolescence and adulthood(Streissguth et al., 2004).

Many children referred for FASD diagno-sis are not in the care of their birth parents.In the FAS DPN database, more than 70%of those referred for FASD diagnosis are infoster/adoptive homes. Interestingly, almosthalf of young children referred (and thosediagnosed with FAS or Partial FAS [PFAS])are at least third born (or later), which fitswith observations that the impact of prena-tal alcohol exposure may be greater for laterborns. Children referred for FASD diagnosishave various racial and ethnic backgrounds.Half of those referred (and those diagnosedwith FAS/PFAS) are considered Caucasian,fewer than expected given Washington Statedemographics, while the others come from avariety of ethnic backgrounds.


Need for referral for FASD diagnosis and

advocacy by early interventionists

Surprisingly, in the FAS DPN database, veryfew families (4.7%) of young children arereferred for FASD diagnosis from school orearly intervention settings, but instead comefrom other referral sources such as medi-cal, psychological, or social service providers.This low referral rate could be raised byincreased awareness among early interven-tion providers of referral signs and the haz-ards of alcohol exposure, and by recognizingthe importance of subtle early deficits whenprenatal alcohol exposure is present (whicheven the children’s parents may not fullyappreciate).

Young children in this database receiveFASD diagnoses across the whole spectrum, atrates consistent with population-based stud-ies. This fits with wide variation in prenatal al-cohol exposure seen in this population, rang-ing from maternal consumption of a singleglass of wine once in pregnancy to daily in-toxication throughout pregnancy. Of childrenaged birth to 8, only 7.4% receive an FAS ora PFAS diagnosis. It is this surprisingly smallgroup who has the “face” of FAS and who ismost likely to be recognized and qualify forearly intervention. This is true even thoughtheir CNS dysfunction is often no more severethan that of children with ARND. A larger per-centage (25.0%) of young children are diag-nosed with the equivalent of “severe” ARND.While these young children are clearly in needof intervention, their families may not be ableto access help without strong advocacy fromearly interventionists. An even larger percent-age (43.4%) are diagnosed with the equivalentof “mild” ARND. These youngsters may verywell show significant problems later on. Yetthey are far less likely to receive any early in-tervention unless providers are very well in-formed, and have the chance to serve thesechildren within an “at-risk”category.

Early indicators suggesting referral for

an FASD diagnosis

FAS DPN data suggest that the simple pres-ence of prenatal alcohol exposure may be

the most important reason to refer for diag-nosis, with higher levels of exposure espe-cially worrisome. Behavior problems in thepresence of prenatal alcohol exposure arealso an important referral sign. FAS DPN dataalso reveal that some indicators commonlyused by providers to prompt early identifica-tion of problems may not be as useful in sig-naling the need to refer for FASD diagnosis.For example, the average gestational age forchildren referred to FAS DPN clinics is veryclose to full term at 37.3 weeks. As another,very striking example, only just over half ofthe children show marked developmental de-lay in the first 3 years of life—even amongthose who receive an FAS/PFAS diagnosis. In-deed, more than one fourth of referred chil-dren have developmental profiles well withinnormal limits, with an additional third whoshow only mildly abnormal developmentalscores. Some familiar indicators of early riskdo characterize this group. Data from the FASDPN show that most of these young children(84.5%) are also exposed to cigarettes or illicitdrugs, and most (82.6%) have experiencedsome degree of postnatal environmentalrisk.

FAS DPN data reveal that some importantearly signs for referral for FASD diagnosis thatproviders could use, with training, are oftenbeing missed. It was surprisingly rare foryoung children to be referred for concernsabout facial anomalies or growth. Indeed, di-agnostic referral because of FAS-like facial fea-tures occurred for only about a tenth of theseyoung children. Yet with careful diagnosticmeasurement about three quarters of youngchildren referred showed at least 1 or more ofthe “sentinel” physical features. If early inter-ventionists were more aware of these charac-teristic features, and/or if facial features wereregularly screened as part of an early interven-tion intake process, diagnostic referral mightoccur more often. FAS DPN data do suggestthat it remains important to pay close atten-tion to even mild impairments of body growthand, especially, to small head size (≥2 SD be-low the mean). Children with microcephalyshow more developmental problems than thegeneral population (Dolk, 1991), and over


two thirds of young children diagnosed withFAS/PFAS had microcephaly.

THE EFFECTS OF PRENATAL ALCOHOL

EXPOSURE ON DEVELOPMENT IN

YOUNG CHILDREN

An overview, including problems in

sensory processing

What is known about the effects of pre-natal alcohol exposure on development inyoung children? It is well established thatheavy levels of prenatal alcohol exposure leadto neurobehavioral deficits, but the effects oflower levels of alcohol exposure are less clear(NIAAA, 2000). Neurobehavioral deficits aris-ing from alcohol exposure are lifelong, buttheir impact on adaptive function emergesmore clearly over time—and can likelybe improved or made worse by postnatalexperiences.

A good overview of clinically relevant find-ings is provided by a recent, careful studyusing FAS DPN data that compare a clinicalsample of twenty-five 5- to 8-year-olds to anage-, gender-, and ethnicity-comparable groupof 26 typically developing peers (Jirikowic,2003). Children with FASD performed signif-icantly more poorly than comparison peersacross measures of IQ, adaptive behavior, aca-demic performance, and sensory-motor devel-opment. A main contribution of this studywas findings of sensory processing problemsin the children with FASD, which validatedand extended findings of an older nonstan-dardized questionnaire study (Morse, Miller,& Cermak, 1995). Using a standardized par-ent questionnaire coupled with direct test-ing, Jirikowic (2003) found clinically signif-icant difficulties among children with FASDin tactile, auditory, and visual sensitivity, un-derresponsiveness to sensory information andsensation-seeking behaviors, and auditory fil-tering. Although as a group overall motor per-formance was in the low average range, spe-cific difficulties were seen in sensory-motortasks involving eye-hand coordination andtimed responses, and on tests revealing per-sistent minor neurologic soft signs. Children

with FASD showed generally lowered earlyacademic performance (though still in the av-erage range), with significantly low mathe-matics skills and early spelling skills. Overalladaptive level was lower than among childrenwith typical development, but quite variableacross alcohol-exposed individuals. For chil-dren with FASD, relative strengths in adaptivebehavior were seen in ratings of motor func-tion, and poorer performance in socializationand ability to follow the rules of daily living.Both teachers and caregivers also endorsedsignificantly more behavior problems amongchildren with FASD than among typically de-veloping peers. Interestingly, analysis of thiscarefully constructed and diagnosed samplerevealed no differences in performance be-tween girls and boys in the group with FASD.Gender differences have almost never been as-sessed in other studies.

Problems in early cognitive skills and

learning, and sleep

Although there is a wide variety in thetype and extent of deficits, problems in cogni-tion, learning and memory, attention, and aca-demic achievement have consistently beenfound among preschool (eg, Janzen, Nanson,& Block, 1995; Jirikowic, 2003) and olderchildren with FASD (eg, Coles et al., 1997;Howell, Lynch, Platzman, Smith, & Coles,2006; Mattson & Riley, 1998). In clinical sam-ples with FASD, there are consistent findingsof deficits in attention, wide-ranging difficul-ties in higher order cognitive processes called“executive functions,” visual-spatial process-ing deficits and other problems in informa-tion processing speed and efficiency, and dif-ficulties with mathematical problem-solvingand achievement (NIAAA, 2000). Also of spe-cial interest are newer findings of alcohol ef-fects on basic conditioned learning and othercognitive functions that reveal an impact onspecific brain regions (such as the cerebel-lum) (eg, Jacobson et al., 2005). An interestingemerging area is potential alcohol effects onsleep, with likely sleep difficulties in respira-tory control and/or circadian rhythms relatedto problems in brain development, and alsoto physical problems in midface development


leading to possible breathing obstruction (M.Chen, personal communication, January 3,2006).

Prenatal alcohol exposure has been asso-ciated with cognitive and learning difficul-ties into adolescence (eg, Goldschmidt,Richardson, Cornelius, & Day, 2004;Streissguth, Barr, Sampson, & Bookstein,1994) and beyond, though not all longitudi-nal studies find effects (Greene et al., 1991).Prenatal alcohol has been associated withmildly decreased performance on the BayleyMental Scale in infancy (eg, Jacobson et al.,1993) and with mildly lowered IQ scores inpreschoolers (eg, Streissguth, Barr, Sampson,Darby, & Martin, 1989). Newer longitudinalresearch with wider ethnic diversity andsomewhat more highly exposed samples(using more sensitive measures) has foundan association between alcohol exposureand early, specific cognitive and achievementdifficulties. For example, infants prenatallyexposed to alcohol have shown deficitsin information processing and efficiency(Jacobson, Jacobson, & Sokol, 1994). Thesepersist into the early elementary years, withadditional findings of a distinctive prenatal al-cohol effect on number processing (Burden,Jacobson, & Jacobson, 2005).

Deficits in speech, language, and

communication

A variety of speech, language, and commu-nication problems have been described forclinical samples of school-aged children withheavy prenatal alcohol exposure, includingdelays in speech acquisition, impaired recep-tive and expressive language, and problemsin speech production (Church & Kaltenbach,1997). Some school-aged children with FASDshow discrepancies between relatively betterverbal abilities (eg, vocabulary, basic syntax),and diminished capacity to use these skillseffectively in social communication (whichis an important foundation for developingsocial relationships and exchanging informa-tion) (Coggins, Friet, & Morgan, 1998). Therehas so far been limited clinical or longitu-dinal study of language and communication

in infants and young children with prenatalalcohol exposure, although this is an areaof intense research interest. Current clinicalthinking is that young children with FASD canoften acquire basic linguistic skills in a typi-cal manner, but have difficulty becoming so-cially competent communicators later on and,as they grow older, show deficits in higherorder language skills. These include difficul-ties in the more complex syntax, metacog-nitive abilities, and narrative skills that aretied to their cognitive difficulties in executivefunctions (eg, Coggins, Olswang, CarmichaelOlson, & Timler, 2003).

Problems in motor development and

neurologic soft signs

Alcohol-exposed individuals consistentlyshow impairments in the development of mo-tor control (NIAAA, 2000). In infancy, clin-ical studies reveal motor delays occurringmore often and/or with increased severityin the presence of heavy alcohol exposure(eg, Autti-Ramo & Granstrom, 1991). Amongyounger children with FASD, delays in motorskills are generally mild to moderate in ex-tent, and poor movement quality (decreasedspeed, efficiency, and control; abnormal bal-ance) is often seen (eg, Osborn, Harris, &Weinberg, 1993). Significant deficits in visual-motor development (but not in motor-freevisual perception), and in fine motor coor-dination, have been described in samples ofyounger children with FAS in comparison tothat of typically developing peers (Adnams etal., 2001; Janzen et al., 1995).

Some longitudinal researchers have foundno discernable impact of more moderate lev-els of social drinking on motor developmentin infancy (eg, Richardson, Day, & Gold-schmidt, 1995) or early childhood (eg, Chan-dler, Richardson, Gallagher, & Day, 1996; Fried& Watkinson, 1990; Larrouque & Kaminski,1998). Other long-term studies have foundclinically significant effects, but only amonginfants at high exposure levels—withqualitative differences in motor behav-iors (eg, deficits in imitating movements,standing, and walking) noted in infants


with lower exposure levels whencompared to those with no exposure(Jacobson et al., 1993). In early childhood,longitudinal research has identified increasedlevels of minor neurologic soft signs amongalcohol-exposed preschoolers (Larrouqueet al., 1995), and a positive associationbetween greater alcohol exposure and in-creased deficits in fine motor steadiness andbalance (Barr, Streissguth, Darby, & Sampson,1990).

Difficulties in adaptive behavior and

social-emotional development

Difficult behaviors and social skill deficitsthat persist across time are an overarchingconcern among individuals of all ages withprenatal alcohol exposure in both clinicaland longitudinal samples (eg, Olson et al.,1997; Olson, Feldman, Streissguth, Sampson,& Bookstein, 1998a; Spohr & Steinhausen,1996). Mental health problems have beenreported for a very large majority of individ-uals with FASD in natural history research(Streissguth, Barr, Kogan, & Bookstein, 1996),and elevated rates of psychiatric disorders area concern (eg, Fryer, McGee, Matt, Riley, &Mattson, 2005; Murray, Olson, & Montague,2005; O’Connor, Kogan, & Findlay, 2002a).For school-aged children with FASD, studiesusing questionnaires and child behaviorchecklists often show clinically elevatedattention, social, and sometimes internalizingproblems (eg, Mattson & Riley, 2000; Roebuck& Riley, 1999), and sometimes also problemswith externalizing behavior and aggression(eg, Olson, Brooks, Davis, & Astley, 2004).Adaptive behavior and social skills amongpre–school-aged and young school-agedchildren with FASD are reported as lowerthan expected for age and intellectual level(Mattson, Lee, Hayden, & Riley, 2005;Thomas, Kelly, Mattson, & Riley, 1998). Itappears that children exposed to alcoholshow relatively greater deficits in adaptivefunction than do clinic-referred peers afterthe age of 8 (Whaley et al., 2001). Clinicalstudies of children with FASD use terms suchas impulsive, distractible, and “always on the

go” to describe behavior in the preschooland elementary years (Janzen et al., 1995). Inaddition, while younger children with FASDhave been described as engaging, verbal, ap-parently alert, and “bright-eyed” (Streissguth,1997), and appear more functional than theyactually are, they seem to lack social bound-aries (Olson, 1994). There is wide variabilityin the level of these deficits, ranging fromsubtle to severe.

Longitudinal studies focused on infancy re-port early problems in behavioral regulationassociated with prenatal alcohol exposure, in-cluding mild to moderate irritability, poor ha-bituation, sleep problems, and feeding diffi-culties (Eyler & Behnke, 1999; Streissguth,Barr, Martin, & Herman, 1980). Amongpreschoolers, limited longitudinal data sug-gest that prenatal alcohol exposure has beenassociated with functional compromise thatincludes mild to moderate inattention and hy-peractivity, and subtle to moderate impulsiv-ity, and behavior problems (eg, Streissguth,Bookstein, Sampson, & Barr, 1993, 1995).

Developmental systems thinking adds toour understanding of the direct “main”effectsof alcohol on child outcome, to better explainthe reverberating impact of prenatal alcoholexposure and maternal drinking on social-emotional development across infancy andearly childhood. O’Connor and her colleagues(eg, O’Connor et al., 2002b) described a trans-actional process in which alcohol-exposed in-fants show increased negative affect, theirmothers have difficulty responding to thesebabies (perhaps because of their own de-pression that may be associated with a ten-dency to drink, and/or because of difficultiespresented by the child), attachment securityis compromised, and these alcohol-exposedchildren grow into preschoolers who show in-creased levels of depression at around 4 to 5years of age. This has been shown in middle-income families, and even more clearly inlow-income families who have additional riskfactors that increase severity of this negativecycle. Additional analyses of middle-incomefamilies through age 6 revealed this processas most important for girls, but also found


separate trends or significant direct effectsof prenatal alcohol exposure on outcome inboth boys and girls (O’Connor, 2001). Fur-ther research taking a developmental systemsapproach, and examining issues such as gen-der and socioeconomic differences, is crucialto creating targeted, empirically based earlyintervention for children who are alcohol-exposed or have FASD diagnoses.

Cumulative risk and FASD

The impact of prenatal alcohol exposureis often coupled with that of other prenataldrug exposures, poor prenatal care, and lifewith parents who struggle with chemical de-pendency. Children may live in environmentswith health and safety concerns, relationshipproblems, and chaotic lifestyles. Longitudinalstudies (eg, Arendt et al., 2004; Butz, Pulsifer,Leppert, Rimrodt, & Belcher, 2003; Singeret al., 2004) have tracked the often nega-tive developmental outcomes of children withprenatal substance exposures in these high-risk situations. Clinical studies have examinedthe difficult lives of children and the poten-tial impact of intensive interventions throughcomprehensive chemical dependency treat-ment programs serving women with children(eg, Division of Alcohol & Substance Abuse,1999), long-term and very intensive familysupport programs for the highest risk mothers(eg, Grant, Ernst, Streissguth, & Stark, 2005),and intensive early intervention with familysupport (eg, Butz et al., 2001; Nair, Schuler,Black, Kettinger, & Harrington, 2003; Schuler,Nair, & Kettinger, 2003). These studies aresharp reminders that children with FASD mayoften spend at least some of their early years inan environment of cumulative risk. A develop-mental systems approach emphasizes that cu-mulative risk could be especially harmful fora child made biologically vulnerable by pre-natal alcohol exposure. With the implemen-tation of CAPTA amendments and the IDEAImprovement Act of 2004, early interventionproviders will more often be linked with thechild welfare system and see children who notonly experience cumulative risk but also haveprenatal exposures. As a result, the need to

refer children for FASD diagnosis or to referthose children who are diagnosed for appro-priate supplementary services will increase—and specialized training and systematic link-ages with service systems that work specifi-cally with these families will be needed.

TAKING ON THE CHALLENGE OF FASD

IN EARLY INTERVENTION

A developmental systems model

and its usefulness in guiding practice

and research

Developmental systems thinking can guidepractice for young children with FASD or withprenatal alcohol exposure, and makes clearwhy early intervention for this population isespecially important. A useful developmen-tal systems model was created for early in-tervention with children who have specialneeds (Guralnick, 2001). Applying this modelto FASD, prenatal alcohol exposure can beseen as placing a child at risk for (or cre-ating) biological vulnerability and “disablingchild characteristics,”such as sensory sensitiv-ities or unusual learning deficits. Such deficitsare individually variable and arise in multipledomains of development (perhaps in subtleways), and may emerge more clearly or be-come more debilitating over time, and thesechild deficits (and compensatory strengths)must be comprehensively assessed.

Disabling child characteristics can disruptexisting family interaction patterns, creatinginformation and resource needs for parents,threats to parenting confidence, and bothcaregiver and family stress. Comprehensiveassessment of these “environmental risk fac-tors,” and risks uniquely important in thispopulation, are also essential. One unique riskfactor identified through clinical experiencecenters around inappropriate caregiver reac-tions to deficits of the child with FASD—deficits caregivers may not easily recognize asa result of alcohol-induced CNS dysfunction,but see as willful disobedience. Other pivotalfamily risk factors have been documented innatural history research. For this population,


past or current parental substance use, andpoor quality of attachment security or poorquality of the childhood caregiving environ-ment, is significantly associated with poor lifeoutcomes (Streissguth et al., 2004). Protectivefactors hypothesized as important to this tar-get population, such as the parent’s level ofoptimism and parenting efficacy, use of spe-cialized parenting practices, advocacy skill,and knowledge of FASD, or appropriate link-age to community resources (Olson et al.,2005), must also be assessed.

Early intervention should then aim to con-currently reduce the impact of disabling childcharacteristics and cumulative environmen-tal risk, while at the same time enhancingprotective factors. For the diagnosed child,a comprehensive intervention program canbe developed and implemented, providingresource, social, and information supports,and direct intervention to enhance family in-teraction patterns, adjusted to the family’sunique needs and targeted to the disability.For example, if a child with FASD has sensorysensitivities and processing speed deficits aris-ing from prenatal alcohol exposure, then en-vironmental modification and supportive OTservices, caregiver education, and advocacyfor later special education, might be neces-sary. Home visiting or clinical services to helpcaregivers understand alcohol-related braindamage, modify attitudes, learn specializedparenting skills, and learn effective advocacyto access existing community supports maybe required when children with FASD haveespecially difficult behavior problems. Inter-vention models for such services have beendeveloped and show promising findings insystematic research with somewhat older chil-dren with FASD (eg, Olson et al., 2005). For“at-risk”young children with prenatal alcoholexposure who may or may not yet show clin-ically concerning behaviors, preventative in-terventions are needed. For example, if attach-ment security is compromised in a very youngchild, intervention focused on enhancing se-cure attachment may be helpful—but mayhave to be adjusted for a biologically vulner-able child and the family structure (eg, foster,

birth) in which the child is being raised. Earlyintervention models are being developed thatincorporate a variety of child- and family-focused intervention strategies as needed (eg,Coles, Kable, Dent, & Lee, 2003; Gurwitch,Mulvihill, & Chaffin, 2003).

Of course, research on FASD preventionand on biological methods to amelioratethe impact of prenatal alcohol exposure onchild development (such as nutritional sup-plements) is important. But many childrenare born exposed to, and affected by, pre-natal alcohol, so intervention research is es-sential. Developmental systems thinking canalso guide intervention research. Specific “dis-abling child characteristics” of children withFASD (or prenatal alcohol exposure) must beidentified. For deficits amenable to change,targeted intervention strategies must be stud-ied. For example, young children with FASDor prenatal exposure likely have behavior reg-ulation problems, and targeted interventionsmight involve teaching caregivers special-ized techniques to calm their alcohol-exposedchild or help the child self-sooth. It is also im-perative to conduct research on the effective-ness of more comprehensive early interven-tion services. These reduce “environmentalrisk factors” that have already been identifiedand increase hypothesized protective parent-ing and family factors. Such research is al-ready under way through, for example, col-laborative research by several research groupsfunded by the Centers for Disease Controland Prevention (eg, Bertrand, Sidhu, & Floyd,2003).

Educating early intervention

professionals about FASD and

improving service delivery

To best serve children with FASD or pre-natal substance exposure, what training isrecommended for all early intervention pro-fessionals? As a start, this article presentsimportant information about the disability.But there are additional needs for special-ized preservice education and continuing ed-ucation in the field, with training recom-mendations presented in Table 2. Training


Table 2. Suggested training topics for early intervention providers working with childrenaffected by parental substance abuse, including alcohol∗,†

How to ask questions about prenatal exposure

The process of addiction and recovery; harm reduction and relapse prevention

How to provide FASD prevention information

How to recognize and screen for the characteristic facial features of FAS, small head size, and mild

or greater growth impairment

Key behavioral symptoms signaling need for diagnostic referral when in the presence of alcohol

exposure

Advocacy skills to help children at risk continue to be monitored or qualify for services even with

subtle deficits, and to promote services in the next intervention setting

Neurodevelopmental disabilities, and specifics about FASD; how brain development and function

are affected by prenatal alcohol exposure

How to provide appropriate early intervention given current data on FASD, with a focus on

environmental modification and antecedent-based positive behavior support planning

The family experience of raising children with FASD, and differences between different family

structures

How parental substance abuse affects children’s lives

CAPTA and IDEA regulations, and interagency efforts to improve services for children affected by

parental substance abuse

Systems of care for chemical dependency treatment, FASD diagnosis, child welfare, crisis

placement, foster care, adoption, adult corrections, and adult developmental disabilities service.

∗Contact Drs Carmichael Olson and Jirikowic for more information on training program.†FASD indicates fetal alcohol spectrum disorders; FAS, fetal alcohol syndrome; CAPTA, Child Abuse Prevention and

Treatment Act; and IDEA, Individuals with Disabilities Education Act.

is an essential foundation to help providersdevelop skills to screen for FASD, guidefamilies in obtaining a diagnosis, and effec-tively support the children with a diagnosisand their caregivers. Such training programsare under development and continuing ed-ucation about some of these topics alreadyexists. Beyond training, early interventionproviders can build working relationships andformal connections with service provider sys-tems that specialize in this area, such aswoman-oriented chemical dependency treat-ment centers, FASD diagnostic clinics, FASDintervention programs, FASD parent sup-port/advocacy organizations, and the childwelfare system. At the state and local lev-els, interagency efforts can set up methodsto raise awareness and train providers, fa-cilitate smooth diagnostic and service refer-rals, modify categorical service requirementsas needed, enhance collaborative care, and

strengthen supports for these children andfamilies.

Screening for FASD

Using a developmental systems approach,screening is an essential first step to iden-tify children who should be referred forFASD diagnosis as young as possible. Screen-ing should take place in all early interven-tion settings. The most efficient and effectivescreening method for FAS is to look for thecharacteristic facial features. Inexpensive anduser-friendly tools are available (Lip-PhiltrumGuides and FAS Facial Photographic Analy-sis Software) and have been used to effec-tively screen high-risk populations for FASsuch as children in foster care (Astley, Sta-chowiak, Clarren, & Clausen, 2002). Screen-ing for ARND requires effective and appropri-ate inquiry about prenatal alcohol exposurebecause, unlike the FAS facial features, there


is no pattern or type of CNS dysfunction thatis specific to prenatal alcohol exposure andcan clearly identify ARND. Providers shouldobtain training on how to ask about women’sdrinking and drug use, know their ownagency guidelines before talking with care-givers about prenatal exposures, and remem-ber that alcohol use at times other than preg-nancy can suggest only the possibility of gesta-tional alcohol exposure. Providers should alsoscreen for behavior problems and growth im-pairment that occur in the presence of alcoholexposure.

Helping families obtain an FASD

diagnostic workup

Early interventionists are well-placed tohelp families find a diagnostic center and ob-tain a workup for an identified child. Diag-nostic services are most likely to be availablein child guidance or child development cen-ters, hospitals specializing in children’s ser-vices, or the growing number of specializedFASD diagnostic clinics. The Substance Abuseand Mental Health Services Administration, agovernmental agency, through its FASD Cen-ter for Excellence, has sponsored a Web sitethat as of 2007 collates all available infor-mation on diagnostic services, intervention,prevention efforts, screening programs, andresearch literature: http://fascenter.samhsa.gov/about/index.cfm.

Understanding and supporting families

through FASD diagnosis

Early interventionists can play a key rolein helping families adjust to the possibilitythat a child may have (or does have) FASD.Caregivers raising a child with FASD and be-havior problems almost all experience highlevels of child-related parenting stress (Olsonet al., 2004). Perhaps more than with otherneurodevelopmental disabilities, FASD carrieswith it an emotional overlay, because it is abirth defect that could have been prevented—and the disruptive influence of addiction will,in some way, be part of the family history.Parents’ emotional reactions to the diagnosis

can range from anger, to refusal to believe orlisten, to acceptance—but almost always in-clude grief, and often a firm (but likely mis-taken) conviction that all problems can bedealt with by nurturing parenting or extraor-dinary efforts at early intervention.

Reactions of birth parents are also influ-enced by whether parent(s) are currentlydrinking or involved in the recovery pro-cess. The emotions of guilt and shame, orthe psychological defense of denial, can cre-ate barriers to problem recognition or offersof intervention. Continued drinking and/oraccompanying illicit drug use can mean in-effective communication and unpredictablelives, and even raise ethical and legal dilem-mas for providers. Working with birth parentsrequires interpersonal sensitivity, and at leastsome specialized training (or access to con-sultation with providers who understand theissues of addiction and recovery). But a basicprecept is that meeting families where theyare, with a respectful, open, nonjudgmental,and supportive stance, is the best responseby providers to the feelings of families. Tomaintain such a stance, however, requires thatan early intervention provider think throughtheir emotional reactions to their own andothers’ substance use, and to the stark realitythat parental alcohol use can compromise anaffected child’s lifelong development.

Foster families in many states often receivetraining on issues related to children’s spe-cial needs, and even specifically about FASD.But a child’s foster placement may be tem-porary, so early intervention providers oftenmust support both foster parents and care-givers who may then receive the child, includ-ing birth parents in recovery. Adoption agen-cies now typically openly disclose to adop-tive families what is known about a child’sprenatal and postnatal risks and any specialneeds, and families may have specifically cho-sen to adopt a child with FASD. But becausealcohol effects may reveal themselves overtime, adoptive families often find themselvesstruggling as they realize what is really meantby a lifelong birth defect. Therefore, they


may need intensive support from early in-terventionists. Furthermore, kinship adoptiveplacements may differ quite dramatically fromnonrelative adoptive placements. Childrenin kinship placements are living in familiestouched directly by addiction. A maternalgrandmother raising her grandson, for in-stance, might also be contending with herdaughter’s ongoing addiction, and the griefand shame (or anger) that arises from boththe ongoing addictive behavior and its conse-quences that impact the child.

Providing anticipatory guidance and a

model for future intervention

Early interventionists individualize and setup appropriate, clear structure and rou-tines, promoting strengths and accommodat-ing each child’s particular deficits. Early inter-vention settings ideally aim to provide family-centered, integrated services that are basedon a developmental framework and attemptto achieve inclusion (Guralnick, 2001). Such

settings are, perhaps, a model for how chil-dren with FASD would best be served evenafter the early intervention period. It is a ma-jor challenge when a child with FASD transi-tions out of the early intervention system tothe schools, and the child and family mustthen deal with the expectations of more inde-pendent function and reduced access to indi-vidualized programming that come with age.Early interventionists can smooth this transi-tion. They can be the first to grasp the realhazards of prenatal alcohol exposure, refer-ring children for diagnosis with FASD as earlyas possible, alerting caregivers to the grow-ing child’s likely emerging neurobehavioraldeficits and increasing struggles with relation-ships, connecting families with needed ad-ditional services (such as alcohol treatmentfor parents)—and showing the family and thechild’s set of care providers what interventionstrategies can really work. Early interventionproviders can be proactive and essential gate-keepers and guides to the future.

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