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Challenges of diagnosis in fetal alcohol syndrome and fetal alcohol spectrum disorder in the adult.

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American Journal of Medical Genetics Part C (Seminars in Medical Genetics) 145C:261 – 272 (2007)
Challenges of Diagnosis in Fetal Alcohol
Syndrome and Fetal Alcohol Spectrum
Disorder in the Adult
Adults with fetal alcohol syndrome (FAS) and the subsets of individuals with attenuated phenotype subsumed
under the umbrella term of fetal alcohol spectrum disorder (FASD) provide clinicians with a challenge.
Compounding this, FASD is different from most genetic syndromes since a specific diagnostic biological test is not
available. The diagnosis first needs to be suspected and confirmation requires a diagnostic assessment that is best
carried out in the context of a multi-disciplinary team approach. There is surprisingly little research published on
the prevalence, natural history, medical, and social complications relevant to adults with FASD. The evidence that
is emerging suggests that this disorder is common, and that services to diagnose and treat these individuals are
limited. Adults with FASD have a higher incidence of impairments in social adaptive and executive function, and a
higher degree of psychopathology when compared to the general population. The impact of FASD has significant
and serious effects on those affected with FASD, their families, and our communities. There is a need for improved
access to diagnosis, and more research and evaluation of interventions currently in use. In this paper, we describe
the current diagnostic criteria, the differential diagnosis, the prevalence, natural history, the behavioral and
mental health consequences, medical and social management issues, and interventions for adults affected with
this disorder. ß 2007 Wiley-Liss, Inc.
KEY WORDS: fetal alcohol syndrome; fetal alcohol spectrum disorder; adult diagnosis; multi-disciplinary team assessments; dysmorphology;
management; intervention
How to cite this article: Chudley AE, Kilgour AR, Cranston M, Edwards M. 2007. Challenges of
diagnosis in fetal alcohol syndrome and fetal alcohol spectrum disorder in the adult.
Am J Med Genet Part C Semin Med Genet 145C:261–272.
‘‘Fetal alcohol syndrome is not
just a childhood disorder; there is a
predictable long-term progression
of the disorder into adulthood,
in which maladaptive behaviors
present the greatest challenge to
Ann Streissguth, JAMA 1991
It was only in the last half century
that the medical community and society
were convinced of the physical and
central nervous system effects of
excessive alcohol use in pregnancy
resulting in fetal alcohol syndrome
(FAS) [Lemoine et al., 1968; Jones and
Smith, 1973; Jones et al., 1973]. The
diagnosis of FAS and its spectrum is a
medical diagnosis, but its effects on
society are far reaching [Streissguth,
1997]. At one end is the subset of
individuals with FAS, and at the
other end are those individuals with
behavioral and cognitive deficits
who exhibit minimal or no physical
stigmata as a consequence of ethanolinduced prenatal brain injury including those conditions using the
terms described by the Institute of
Medicine (IOM) review of FAS
[Stratton et al., 1996]. Within a decade
of the original description of FAS
[Jones and Smith, 1973; Jones
et al., 1973], substantial behavioral and
cognitive effects of prenatal alcohol
exposure were seen in individuals
who exhibited few sentinel features
and or growth impairment. The
Dr. Chudley is a Professor of Pediatrics and Biochemistry and Medical Genetics at the University of Manitoba. He is the Medical Director of the
Genetics Program in Winnipeg. He has certifications in pediatrics, clinical genetics, and medical genetics. His clinical and research interests are in
the areas of dysmorphology; the recognition, delineation and prevention of birth defects, including fetal alcohol syndrome, and fetal solvent exposure;
the causes of mental retardation, developmental disabilities, and autism spectrum disorders; prenatal diagnosis; gene mapping; and gene
discovery.He has been a consultant to the Manitoba and Alberta governments in issues related to Fetal Alcohol Syndrome Disorder (FASD) and he is a
former member of Health Canada’s Public Health Agency National Advisory Committee on FASD. He is currently President of the Canadian College of
Medical Geneticists.
Dr. Kilgour is an Assistant Professor in Clinical Health Psychology at the University of Manitoba. She is a neuropsychologist with expertise in drug
addiction, brain injury and the diagnosis of FAS in adults.
Megan Cranston is a third year medical student at the University of Manitoba. She has research and clinical interests in FAS.
Michelle Edwards is a fourth year medical student at the University of Manitoba. She has interests in community supports related to FAS in
adolescents and adults.
*Correspondence to: Albert E. Chudley, M.D., F.R.C.P.C., F.C.C.M.G., WRHA Program in Genetics & Metabolism, Departments of Pediatrics and
Child Health, Biochemistry and Medical Genetics, University of Manitoba, Health Sciences Centre, FE 229 820 Sherbrook Street, Winnipeg, Manitoba
R3A 1R9. E-mail:
DOI 10.1002/ajmg.c.30140
ß 2007 Wiley-Liss, Inc.
Within a decade of the original
description of FAS, substantial
behavioral and cognitive effects
of prenatal alcohol exposure
were seen in individuals who
exhibited few sentinel features
and or growth impairment
term fetal alcohol effects (FAE) [Rosett
and Weiner, 1982; Sokol and Clarren,
1989] described this subset. This term is
no longer in vogue [Aase et al., 1995],
and has been replaced by other terms in
the five diagnostic categories recommended by the IOM, an expert panel of
FAS researchers and clinicians in the
United States [Stratton et al., 1996].
These include FAS with prenatal alcohol
exposure confirmed; FAS without prenatal alcohol exposure confirmed; partial FAS [pFAS]; alcohol-related birth
defects [ARBD]; and alcohol related
neurodevelopmental disorder [ARND].
Fetal alcohol spectrum disorder (FASD)
is an ‘‘umbrella’’ term that includes all
these diagnostic categories and describes
the spectrum of ethanol teratogenesis in
man [Koren et al., 2003; Sokol et al.,
2003; CDC, 2005; Chudley et al., 2005].
FASD is not a diagnostic category and
should be used only when referring to
the whole collection of diagnostic terms.
FASD is distinct from many genetic
syndromes in that the disorder is potentially preventable. In affected adults, the
implications and impact of the disease
may involve employers, the criminal
justice system, their partners, and their
The term secondary disabilities, was
introduced by Streissguth et al. [1996,
1997] in a longitudinal study of children
and adults with FAS and FAE. Secondary disabilities are disabilities the client
was not born with and that could be
ameliorated through better understanding and appropriate interventions.
Secondary disabilities were hypothesized to be the result of an interaction
of behavioral and mental health pro-
blems with an adverse environment.
Streissguth et al. [1996, 1997] defined
six secondary disabilities for all ages
(mental health problems, disrupted
school experience, trouble with the
law, confinement, inappropriate sexual
behavior, alcohol and drug problems)
and three additional secondary disabilities that were exclusive to adults
(dependent living, problems with
employment, problems with parenting).
Other studies have verified a common
finding of these secondary disabilities in
their study populations [Famy et al.,
1998; Lemoine, 2003; Clark et al.,
2004]. Common manifestations in
adults may include depression, anxiety,
or psychosis, sexual promiscuity, poor
judgment, poor impulse control, restlessness, poor problem solving skills,
resistance to change, difficulty forming
lasting and meaningful relationships,
gullibility and victimization, inability
to understand or conform to social
norms, and unemployment.
There are several challenges for
clinicians when considering an FASD
related diagnosis in an adult. One
challenge is educating primary care
physicians about the recognition and
possibility of FASD in an adult so that
they may be referred for a diagnostic
evaluation. Another challenge is the
There are several challenges
for clinicians when
considering an FASD
related diagnosis in an adult.
One challenge is
educating primary care
physicians about the
recognition and possibility of
FASD in an adult so that
they may be referred for a
diagnostic evaluation.
awareness of the secondary disabilities
related to individuals who have been
previously diagnosed as children, so that
they can receive the help and intervention needed. The cognitively-impaired
individual who has FAS likely has been
diagnosed as a child and may have many
social security services and supports
in place, including residential care
and vocational training. However, most
FASD individuals have an invisible
disease, since there may be no growth
impairment and few, if any, dysmorphic
features, and these individuals may not
receive a diagnosis until adulthood.
Although FAS is proclaimed to be one
of the leading causes of mental retardation in North America, it is estimated
that less than 50% meet the current
definition of mental retardation [Streissguth et al., 1996, 1997]. There are a
limited number of professionals who
have the training and experience in a
multi-disciplinary approach to making a
FASD related diagnosis.
Yet another challenge to the
process of diagnosing FAS in adults is
that reliable prenatal alcohol exposure
history and informative birth records
may be unavailable or non-existent.
The IOM describes significant alcohol
exposure as ‘‘a pattern of excessive
intake characterized by substantial, regular intake or heavy episodic drinking’’
(the National Institute on Alcohol
Abuse and Alcoholism defines heavy
alcohol use as drinking five or more
drinks per occasion on five or more days
in the past 30 days) [NIAAA, 2000]. As
further research is completed and as, or
if, lower quantities or variable patterns of
alcohol use are associated with ARBD or
ARND, these patterns of alcohol use
should be incorporated into the diagnostic criteria [Stratton et al., 1996].
However, if there is no documentation
of alcohol intake in birth records, and/or
the birth mother is not available for
interview, the amount of alcohol intake
remains unknown.
We have advocated for a multidisciplinary approach to diagnosis, since
these patients have a complex pattern of
disabilities, and the assessments need to
be comprehensive and involve the
collaboration of a number of health
professionals [Chudley et al., 2005].
Thus, a team is necessary in order to
make an accurate diagnosis and
provide multi-dimensional recommendations for management. The assessment process begins with the
recognition of need for diagnosis and
ends with implementation of appropriate recommendations. The multidisciplinary diagnostic team can be
geographical/regional, virtual, or can
accept referrals from distant communities and be evaluated using telemedicine. The members of the team may vary
according to the context of the diagnosis. The team could include knowledgeable physicians, psychologists,
speech and language pathologists, social
workers, and a coordinator. Clinical
geneticists are key members of multidisciplinary diagnostic teams, who have
unique training and skills in syndrome
recognition. Multi-disciplinary teams
work with community partners and
resources to develop and implement
management plans to maximize intervention for the affected individual. Our
experience reveals that in many adults an
important source of information may
be from welfare agents, employers,
vocational teachers, appointed guardians, parole officers, advocacy workers,
and the like. Following the assessment, a
report containing the recommendations
should be generated that would be
available to the affected individual, and
those employers, advocates, and justice
workers who may be involved in
case management, guardianship, or
There is limited information on the
epidemiology and prevalence of FASD
in adults. The full spectrum of prenatal
alcohol effects is difficult to estimate
since there are no reliable biological
markers that readily define those
affected, and therefore, estimates likely
under-represent actual incidence and
prevalence [Sokol et al., 2003]. The
prevalence is related to the frequency of
excessive alcohol use in pregnancy and
thus will vary from population to
population. For the subset of individuals
affected with FAS, the prevalence in
the United States is 0.2–2.0 cases per
1,000 births across various populations
and using various methodologies
[CDC, 2005]. The prevalence of FASD
for children and adults in Seattle
Washington, for the period 1975–1981
is estimated to be 9.1/1,000 [Sampson
et al., 1997]. This is higher than the
combined prevalence of common
genetic disorders and birth defects such
as Down syndrome and spina bifida.
There are certain regions and ethnic
groups in which the incidence for
FAS is much higher. The reasons for
these variable rates and the failure to
have accurate prevalence determination
are related to several factors including:
Variable poverty rates between states
or provinces and between countries
(poverty is strongly associated with
alcohol use before and during pregnancy and a high risk for FASD).
Genetic and ethnic differences
(three different alleles of the alcohol
dehydrogenase [ADH2] gene:
ADH2-1, ADH2-2, and ADH2-3
with differing levels of enzymatic
activity which can alter the risk of
prenatal alcohol effects).
Lack of uniformly accepted diagnostic criteria for FAS in the past,
and the need for diagnostic criteria
for those who lack dysmorphic
features in a high proportion
of affected children and adults
Lack of knowledge, skill, training,
and misconceptions among primary
care providers [CDC, 2005].
There are no national statistics on
mortality in adults affected by FASD. In
children the mortality rate has been
suggested to be 6%, and the all-cause
mortality in siblings of children diagnosed
with FAS is increased 530% compared to
controls [Habbick et al., 1997; Burd and
Wilson, 2004; Burd et al., 2004]. It is
assumed that the mortality rate is high in
FASD adults in light of the social chaos,
drug dependency, and high incidence of
mental health problems these individuals
There are several genetic disorders that
could present with features mimicking
FAS or pFAS in children and adults
[Chudley et al., 2005; Hoyme et al.,
2005]. Most of these disorders can be
differentiated from FAS by a detailed
family and pregnancy history, alcohol
exposure history, physical examination
and chromosome analysis, and/or specific molecular testing. For those adults
with FASD and particularly ARND,
many other conditions can lead to
impairments in cognitive function,
memory, executive function, etc., and a
thorough neuropsychological evaluation and a history of prenatal alcohol
exposure is essential in arriving at an
accurate diagnosis.
Some FASD individuals may also
have other genetic or mental health
disorders that coexist independent from
effects of prenatal alcohol exposure. For
instance, an individual with Down
syndrome may also exhibit some dysmorphic features, brain dysfunction, or
brain injury from prenatal maternal
alcohol exposure. It would be a difficult
clinical task to attribute which proportion of physical findings and cognitive
impairment results from the genetic
syndrome, and which component is the
result of the prenatal alcohol exposure.
Nevertheless, clinicians need to be
cognizant of the potential role of
prenatal alcohol effects on the phenotype in adults with genetic syndromes.
The diagnosis of FAS depends on the
presence of the cardinal findings of
dysmorphic facial features, evidence of
brain dysfunction, and prenatal and
postnatal growth deficiency in the presence of prenatal alcohol exposure
[Clarren and Smith, 1978]. The diagnosis is best done by a multi-disciplinary
team as there are several areas of evaluation required that no one discipline
alone can provide [Chudley et al.,
2005]. In the absence of characteristic
growth impairment and facial dysmorphology, the diagnosis of pFAS or
ARND might be considered assuming
cognitive impairments. However, only
FAS can be diagnosed without information on prenatal alcohol exposure.
In individuals with cognitive and
behavioral difficulties without facial
dysmorphology and the absence of
maternal history of prenatal alcohol
exposure, an FASD related diagnosis
cannot be made with our current understanding and assessments.
Evaluating the Face and
Other Physical Findings
Astley and Clarren [1996, 1997, 2000],
using data from the Washington State
Fetal Alcohol Syndrome (FAS) Diagnostic and Prevention Network (DPN)
of clinics, developed the 4-Digit Diagnostic Code. The four digits in the code
reflect the magnitude of expression of
the four key diagnostic features of
fetal alcohol syndrome in the following
order: (1) growth deficiency; (2) the fetal
alcohol syndrome facial phenotype,
using the palpebral fissure length percentiles (Fig. 1), and the shape of
the philtrum and upper lip (Fig. 2); (3)
central nervous system damage/dysfunction; and (4) gestational alcohol
exposure. The 3rd edition of the DPN
4-Digit Diagnostic Code Manual [Astley, 2004a] is available and is being used
for diagnosis, screening, and surveillance
efforts in all Washington State FAS DPN
clinics. Modifications of the 4-Digit
Code are being used in many clinics
throughout North America for use in
the diagnosis of children and adults.
Table I illustrates how the 4-Digit
Code can be integrated with the IOM
Diagnostic categories.
The sentinel facial features consist
of short palpebral fissure lengths (pfl), a
poorly formed philtrum and a thin
vermilion border of the upper lip. Ideally
and traditionally, a short pfl is considered
to be less than 1.5–2 standard deviations
(or approximately 10th centile and 2nd
centile); for an adult this is typically pfl of
less than 27 mm. We based this measurement on extensive experience with
adults, as well as a study using three
methods to evaluate the pfl; a clear
plastic ruler, a slide precision caliper, and
the photographic analysis using the
software program available through
the University of Washington DPN
[Astley and Clarren, 1996]. The landmarks for pfl measurements are key
in the evaluation (Fig. 1), and require
training and practice. In our study of 50
adults (Canadian medical students) of
mixed ethnic background, the mean
and standard deviation of the pfl
was 29.3 1.37 mm with the ruler
and an almost identical finding with
the computer photographic method
[Cranston, 2006]. The pfl using the
caliper measurements were consistently
0.5 mm longer when compared to the
Figure 1. Landmarks used to measure the palpebral fissure lengths of both eyes.
Identify the inner corner or endocanthion (en) and outer corner or exocanthion (ex) for
each eye. The ex can be clearly seen if the patient is asked to gaze upward. Measure with a
clear flexible ruler in the horizontal plane the length of each ex–en interval immediately
below the eye, being careful not to touch the eye or eyelashes. Look at the eyes
perpendicular to the pupil; looking at the side will give a false reading. Plot the result
using an appropriate nomogram chart to identify the centile or standard deviation for
each eye. (From Chudley et al., CMAJ, 2005 with permission.)
two other tools. The normative data on
adults published in Hall et al. [1989],
and used in the computer software
package calculation for the standard
deviation ranking from photographic
measurements, are based on data
from Farkas [1994] who used calipers
for the pfl measurements and were
derived from Caucasian adolescents
and adults from southern Ontario,
Canada. Therefore, using the published
graph standards when measurements
involve the use of the ruler or the
calculation from photographic computer
program analysis gives a result that
is about 1 standard deviation more
than from our study and our clinical
experience. To correct for this, one needs
to add 1 standard deviation to the standard
deviation calculated on the photographic
computer program analysis or plotted
on Hall et al. published graph.
Using the published graph
standards when measurements
involve the use of the ruler or the
calculation from photographic
computer program analysis
gives a result that is about
1 standard deviation more
than from our study and
our clinical experience. To
correct for this, one needs to
add 1 standard deviation
to the standard deviation
calculated on the photographic
computer program analysis
or plotted on Hall et al.
published graph.
The lesson here is that if one uses the
published norms, the method or tool
used to acquire the measurement needs
to be the same as the method that
generated the normative data! Clinically,
we recommend either the use of the
plastic clear ruler or the photographic
tool, and correct for the 1 standard
deviation difference in the published
norms. Pfl do not change after
16 years of age. Data for pfl in adults from
Clinically, we recommend
either the use of the plastic clear
ruler or the photographic tool,
and correct for the 1 standard
deviation difference in the
published norms.
other ethnic backgrounds have not been
A poorly formed philtrum is
defined as a 4 or 5 score on the lipphiltrum pictorial guide (Fig. 2), and a
thin vermilion border of the upper
lip is defined as a 4 or 5 score on
the lip-philtrum pictorial guide, or a
circularity score that is only used in
conjunction with the photographic software program The evaluation of the
philtrum and the vermilion of the
upper lip in adults can be a challenge
if the patients sport a moustache.
The final rank score is derived
from a ABC score obtained using the
three sentinel facial features (Fig. 3).
The growth ABC score and other tables
are available from the 4-Digit Code
manual [Astley, 2004a] and are also on
the back of the lip-philtrum pictorial
There is some controversy concerning whether the dysmorphic
features in FAS children persist into
adulthood. Some are of the opinion that
the sentinel features in classical FAS do
Figure 2. Lip-philtrum pictorial guides; left, Caucasians, right, Black Americans.
(Courtesy Dr. Susan Astley, University of Washington, Seattle, WA.)
persist [Streissguth et al., 1991; Streissguth, 1994]. Others believe that the
diagnosis of FAS and the expanded
phenotype is most accurately done
between the ages of 2 and 11 years
[Stratton et al., 1996], due to changes
with maturation. There are few published reports on dysmorphology in FAS
adults. Streissguth et al. [1991] assessed
61 adolescents and adults with FAS.
They stated that ‘‘The characteristic
facies of children became less distinctive
TABLE I. The IOM Diagnostic Categories and the Corresponding DPN 4-Digit Code Rankings
IOM nomenclature
FAS (with confirmed exposure)
Partial FASa (with confirmed exposure)
FAS (without confirmed exposure)
ARND (with confirmed exposure)
2, 3, or 4
1, 2, 3, or 4
2, 3, or 4
1, 2, 3, or 4
Alcohol history
3 or 4
2, 3 or 4
3 or 4
3 or 4
3 or 4
3 or 4
3 or 4
Occasionally rank score of 2 for the brain for those less than age 6 years can be used in difficult cases or in whom no standardized scores are
readily available, using clinical judgment) Modified from Chudley et al. [2005].
hood, and should be considered reliable
markers for possible prenatal alcohol
Evaluating the Brain
Figure 3. Chart located on back of the lip-philtrum guide to determine the ABC
score for the three sentinel facial features to establish the rank score for the face. (Courtesy
Dr. Susan Astley, University of Washington, Seattle, WA.)
with increasing age, but that in many
cases the eye anomalies, short palpebral
fissures and abnormalities of the philtrum and lips remain useful diagnostic
features in adolescents and adults.’’ The
facial pattern of changes are what is
expected during and after normal puberty as the face elongates, the mid-face
and chin lengthen and grow outward
(Fig. 4). Lemoine [2003] re-contacted
and re-examined 105 now-adult cases
from his original report on 125 alcohol
affected children [Lemoine et al., 1968]
and noted that the facial anomalies had
changed, ‘‘often with a large nose and
large chin (contrary to the newborn);
the statural and ponderal hypotrophy
were attenuated; the microcephaly
persisted significantly; the intellectual
deficits persisted, as did the maladaptive
behavior’’. Lemoine [2003] did not
report on the pfl on objective measurement nor on the philtrum or upper
lip appearances. Our own experience
suggests that the physical features in
children with FAS persist into adult-
There are several ways in which the brain
in FASD needs a detailed evaluation,
which is as critical as a proper evaluation
searching for evidence of dysmorphic
features. The Canadian and American
guidelines for FASD assessment have
recommended the evaluation of several
brain domains [CDC, 2005; Chudley
et al., 2005]. These domains include
the documentation of structural,
neurologic, and functional abnormalities.
Structural Brain and
Neurological Abnormalities
The brain is vulnerable to the
adverse effects of prenatal alcohol exposure through all three trimesters of the
pregnancy, although different effects
may be observed depending on the
amount of alcohol consumed, the blood
alcohol level achieved, the duration of
exposure, and the stage of gestation
during which alcohol is consumed.
No specific anatomical region of
the brain appears to be targeted,
although malformations seen include
migration abnormalities including
Figure 4. Patient diagnosed with FAS as an adult. A: At age 5 years. B: At age 10 years. C: At age 19 years.
gray matter heterotopias or variable
degrees of lissencephaly, abnormalities
in the size, shape, and position of the
corpus callosum, cerebellar vermis
hypoplasia, hypoplasia of the basal ganglia and hippocampus, and microcephaly
[Streissguth et al., 1991; Mattson et al.,
2001]. Most individuals with FAS show
no gross anatomical abnormalities on
brain imaging. However, many may
have neurologic damage, and exhibit
seizures, soft neurological signs such as
poor coordination and balance, and
visual motor difficulties. Thus a careful
neurological examination is warranted
[CDC, 2005; Chudley et al., 2005].
Neuropsychological Assessments
The Canadian guidelines [Chudley
et al., 2005] recommend assessment of
hard and soft neurological signs (including sensory-motor); brain structure
(OFC, MRI scans, etc.); general intellectual ability (IQ); communication:
receptive and expressive; academic
achievement; memory; executive functioning and abstract reasoning; attention
and adaptive behavior, social skills, and
social communication. The assessment
should include and compare basic and
complex tasks in each domain, as
appropriate. Although the domains are
assessed as though independent entities,
where there is overlap, experienced
clinical judgment is required to decide
how many domains are affected. A
domain is considered ‘‘impaired’’ when
on a standardized measure scores are two
standard deviations or more below the
mean, or there is a discrepancy of at least
1 standard deviation between subdomains. For areas where standardized
measurements are not available, a clinical
judgment of ‘‘severely abnormal’’ is
made, taking into consideration that
important variables, including age, mental health factors, social-economic
factors, and disrupted family/home
environment (e.g., multiple foster placements, history of abuse and neglect) that
may affect development but do not
indicate brain damage [Chudley et al.,
On neuropsychological assessments, exposed individuals show
deficits on tasks related to the function
of the prefrontal cortex and hippocampus, characterized by deficiencies
in executive functions, working memory, information processing, attention,
and place learning [Mattson and Riley,
On neuropsychological
assessments, exposed
individuals show deficits
on tasks related to the
function of the prefrontal
cortex and hippocampus,
characterized by deficiencies
in executive functions,
working memory,
information processing,
attention, and place learning.
1998; Mattson et al., 2001; Hamilton
et al., 2003]. FAS adults, who do not
have mental retardation and have an IQ
in the normal range, exhibit clear deficits
in measures sensitive to complex attention, verbal learning, and executive
function [Kerns et al., 1997].
Recent work assessing functional
memory in both adults and children with
FAS and ARND show impairments in
spatial working memory on functional
MRI analysis compared to controls
[Malisza et al., 2005]. Whether these
findings are specific to FASD individuals
and a potential tool in diagnosis has yet
to be determined. Fagerlund et al.
[2006] studied the brains of adolescents
and adults with FASD using magnetic
resonance spectroscopy (MRS), and suggested that prenatal alcohol exposure
appears to permanently alter brain metabolism in a long-standing or permanent
manner in multiple brain areas. These
findings agreed with previous findings
from structural and functional studies.
Most of the metabolic alterations
involved changes in the glial cell pool
rather than in the neurons.
From the neuropsychological perspective, the most difficult diagnoses are
those in which severe deficits are not
found across all diagnostic criteria. It is
becoming more recognized that fullblown FAS will manifest with significant
impairment across at least three domains
of cognitive functioning [Chudley et al.,
2005], including reduced general IQ, as
well as at least two other areas mentioned
below. Those individuals whose Full
Scale IQ scores are below 70, and show
impaired adaptive functioning may be
diagnosed with mental retardation.
However, many FASD affected individuals do not meet these severe criteria.
The Committee on Substance Abuse
and Committee on Children with
Disabilities [2000] recognized that
cognitive, behavioral, and psychosocial
manifestations of FASD may vary with
age and current life circumstances
and that each individual may display a
somewhat different constellation of
deficits. There is no neurocognitive
profile specific to FASD, although some
research [Greenbaum et al., 2002] is
emerging that shows fairly consistent
patterns. For example, Full Scale IQ may
fall in the low average to average range,
however, it is not uncommon for
Performance IQ to be within normal
limits, but observe significantly lower
Verbal IQ. As well, when assessing
academic achievement, word reading,
and spelling may be within the normal
range, however, mathematical skills tend
to be considerably reduced when compared to age-matched controls.
Evidence of significant impairment
in three domains is necessary for diagnosis and, in terms of diagnostic code
would be equated to a score of 3 or 4 in
the 4-Digit Code depending on the
severity. A score of 2 is reserved for those
individuals with mild impairment that
may or may not reflect brain dysfunction
from prenatal alcohol exposure and
would not normally lead to a diagnosis
in any category of FASD. This is a
conservative approach and the threshold
that has been established may exclude
some individuals that may be mildly
impaired from prenatal alcohol exposure. Until there are tests that can better
differentiate alcohol brain injury from
other etiologies, establishing a cut-off
is justifiable. Furthermore, individuals
who score 3 or 4 on the brain assessment
may have other reasons for their impairment, and these could include genetic
factors, brain injury from other pre- and
post-natal environmental exposures,
head injury, and drug abuse.
Streissguth et al. [2004] reported on an
update of the secondary disabilities in
adolescents and adults with FASD from
their ongoing longitudinal study.
The life span prevalence was 61% for
Disrupted School Experiences, 60% for
Trouble with the Law, 50% for Confinement (in detention, jail, prison, or a
psychiatric or alcohol/drug inpatient
setting), 49% for Inappropriate Sexual
Behaviors on repeated occasions, and
35% for Alcohol/Drug Problems. Poor
outcomes are increased two- to fourfold
when diagnosis is after age 12 years and
by unstable, poor home environments.
In a British Columbia study, Clark et al.
[2004], showed a remarkably similar
proportion of secondary disabilities in
adults with FASD.
Adults with FASD are at substantial
risk for mental health illness. One study
assessed 25 adults with FASD who had
Full Scale IQ’s above 70 for psychopathology. These individuals underwent
structured clinical interviews for psychiatric and personality disorders [Famy
et al., 1998]. Drug or alcohol dependence was seen in 15 subjects, depression
in 11 subjects, and psychotic disorders
in10 subjects. The most common personality disorders were Avoidant in six
subjects, Antisocial in four subjects, and
Dependent in three subjects.
Barr et al. [2006] noted that young
adults exposed to one or more binge
alcohol episodes in utero had twice the
odds of having substance dependence or
abuse disorders and passive-aggressive
and antisocial personality disorders compared to non-exposed control adults.
The authors conclude that prenatal
exposure to alcohol may be a risk factor
for specific psychiatric disorders and
traits in early adulthood, even in a nonclinical group, where a diagnosis of
FASD was not present.
There are few published reports on
the risk of suicide in the FASD adult
population [Kelly et al., 2000; Devlin,
2001]. It is unclear whether the risk for
this is based on the postnatal environment or derived from the prenatal
alcohol exposure and resulting brain
damage [Kelly et al., 2000]. However,
in light of the high incidence of mental
illness, the social chaos, physical and
mental abuse, poverty in which many of
these individuals have come from or
remain in, the high unemployment, the
problems with the law with incarceration, and the high substance dependency
and abuse rates, we suspect the risk of
suicide is high.
A recent report on Town Hall Meetings
related to FASD suggests that our
systems of care provide supervised living
arrangements for those who have sustained brain damage in accidents, but
this does not extend to someone who has
sustained brain damage prior to birth
[Ryan et al., 2006]. Some adults who
have a FASD do live independently with
proper assistance, such as appropriate
housing, vocational rehabilitation, and
income support (e.g., Supplemental
Security Income, Social Security
Disability Insurance). Many adults with
FASD are ineligible as their IQs often are
within the normal range, which can
disqualify them from support in
many states and provinces despite their
impairments. There was a recognized
need for increased access to existing
services, such as income support,
housing, vocational rehabilitation, and
developmental disabilities services.
They often are perceived as ‘‘normal,’’
although their neurological problems
result in functioning at levels that are
far below normal [Ryan et al., 2006].
Perhaps the best accounts illustrating the impact on the FASD individuals,
their families and the community are
found in two classical publications on
this subject authored by adoptive parents; Michael Dorris’s book The Broken
Cord [Dorris, 1989] and Bonnie
Buxton’s book Damaged Angels: A mother
discovers the terrible cost of alcohol in
pregnancy [Buxton, 2004]. Healthcare
providers participating in the evaluation
and treatment of FASD individuals and
their families need to read these books.
Both books give a personal account, the
grief and hardship and the joy and
success, of living with an FASD child
and adult.
The question of management issues
for the adult with FASD highlights the
need for the multi-disciplinary approach
that includes a neuropsychological
assessment. Such an approach will
outline both the individuals’ deficiencies, as well as relative strengths. Therefore, individual programs can be tailored
to meet the specific needs of each
The diagnosis of a FASD related disorder
is predictive of a high risk for trouble
with the law and confinement [Boland
et al., 2003]. The crimes vary from theft
to murder. The typical pattern is nonviolent crime with repeated offences of
failed compliance to parole conditions
resulting in recidivism. It is unclear to
what extent state, provincial and federal
prisons house FASD individuals. Streissguth et al. [2004] report that 60% of
adolescents and adults in a sample of 253
FASD affected individuals, had some
contact with the law and 35% had been
incarcerated. The onset of trouble with
the law started at a mean age of 12.8
years. Fast et al. [1999] estimated that
within a sample of young offenders
remanded to a forensic psychiatric
inpatient assessment unit, 23% were
diagnosed as FASD. This study involved
a highly select group who were
remanded for further assessment, and
does not represent the rate within the
young offender population. Burd et al.
[2004], in a US study of 43 state or major
cities’ corrections systems, distributed a
questionnaire to determine the prevalence of FAS and ARND in the offender
population, the availability of screening
and diagnostic services to identify offen-
ders with FAS, and staff training needs
related to FAS. Only four programs
(7.4%) reported having access to diagnostic services for FAS in the corrections
facilities. Of the 3,080,904 offenders,
only one offender was reported to have a
diagnosis of FAS. The authors concluded that correctional facilities have
high, unmet needs to screen, identify,
and treat offenders with FAS and
ARND. In a similar study that surveyed
Canadian corrections facilities, 13 of
148,797 offenders were reported to have
a diagnosis of FAS [Burd et al., 2003].
This correlates to a prevalence rate of
0.087 per 1,000, below the estimated
incidence rate of the American and
Canadian population of FAS or FASD
of 1–3 per 1,000 and 9.1 per 1,000,
respectively. Clearly there are many that
are undiagnosed FASD individuals.
There is a need to efficiently and
reliably identify at risk individuals and
bring them into a diagnostic process.
Some have advocated screening tools in
prisons for this purpose [Burd et al.,
Because of their disabilities, individuals with FASD do not typically
respond to the standard cognitive therapy that is currently in place in the
prisons and in the community [Boland
et al., 1998]. Thus, standard programs
do not work for these individuals. This
mismatch between therapeutic modality
and the abilities of the individual
to respond to such treatment adds
to the frustration experienced by both
the affected individual and those
attempting to assist him or her. In a
correctional setting, for example, the
affected individual may find their parole
revoked or experience some other
negative consequence for non-compliance, when, in fact, their cognitive
limitations disallow what is considered
‘‘appropriate response’’ to treatment.
Non-compliance may not be the issue.
Unless there are better means to identify
the FASD individual, and determine the
true extent of the prevalence of FASD in
our prisons, there will be no incentive
to develop and adapt more effective
intervention and substance abuse programs to address the needs of individuals
with brain injury.
The manifestation of suboptimal parenting skills reflects the particular constellation of cognitive challenges the affected
individual faces. The most cognitivelyintact parent has difficulties at times
parenting their child(ren). Ideally, a
parent displays consistency, patience,
affection, but firm consequences for
misbehavior. These characteristics can
be a challenge for all. However, imagine
a parent who experiences attention and
memory deficits. How can they apply
consistent responses to their child(ren)?
If life-long deficits include reduced
judgment and insight, the individual
may not have the cognitive capacity to
recognize poor judgment applied to
FASD individuals frequently have
children and the results show that to be
successful as parents they require additional supports and resources. Streissguth et al. [1996] has demonstrated that
in her cohort of 253 FASD individuals,
17% were parents, at an average age of 18
years. Those who became parents had a
higher rate of living in unstable homes,
were more likely to have been homeless,
and were more likely to have experienced domestic violence. A high proportion of these parents gave up
parenting, or the children were apprehended by child protection services. An
alarming 40% of the affected mothers
had a history of drinking in the their
pregnancy and 17% of their children had
a FASD related diagnosis, suggesting that
this group is at very high risk for having
FASD affected children themselves.
Recognizing these women as a high risk
group should trigger an offer to refer the
patient for counseling and support, and
this may lead to an overall reduction in
the chance of them having an alcohol
affected child. There have been few
studies that have demonstrated the
effectiveness of treatment and prevention strategies in FASD. However, there
are valid strategies for recognizing the atrisk mother in clinical practice [Loock
et al., 2005], and, successful programs
such as the network of clinics and
prevention mentorship programs that
have been developed in the State of
Washington; Astley, 2004b].
The FASD adult needs to be looked
upon as a neurologically impaired individual with a brain injury. They are
vulnerable to physical violence and
sexual abuse. They frequently get ‘‘lost’’
in the system, and have few family or
friends who could advocate for their
needs. They often have limited insights
into of their lack of abilities and limitations, and frequently over-represent
their capabilities to others and themselves. The ideal situation for an
FASD individual is to have a mentor or
proctor who offers structure and order,
and functions as an ‘‘external brain’’,
since most FASD individuals have
poor judgment and adaptive skills.
The ideal situation for an
FASD individual is to have a
mentor or proctor who offers
structure and order, and
functions as an ‘‘external
brain’’, since most FASD
individuals have poor judgment
and adaptive skills.
They would act as advocates and oversee
their client’s daily living activities, assist
in acquiring living accommodations,
money management, offer advice and
encouragement, remind them of their
appointments or vocational duties, and
assure their client’s safety and protection.
With an appropriate multi-disciplinary
assessment, the intensity of intervention
required could match the actual need
of the individual. The more severely
affected individual may require 24-hr
supervision, whereas less severe ARND
manifestations may only require a
situation with daily check-in and/or
telephone contact with a mentor.
Unfortunately, many FASD adults
encounter difficulties with the law
and experience a prison environment.
Although it is temporally structured, it is
noisy, over stimulating, and requires that
new coping skills be learned quickly.
There are many opportunities to be
misled by other offenders looking for
people to participate in illegal activities.
Alternative sentencing, having parole
conditions that take into account
their disability, and having mentors or
proctors, will likely lower recidivism.
More resources will have to be introduced to, or reallocated within, the
social services systems to improve the
outcome and quality of life for these
Jennifer was born in a rural community.
At 1 year of age she and two of her older
siblings were apprehended by the Child
Protection Agency in their community.
She had experienced several placements
in foster homes before being adopted at
3 years of age. She attended school
regularly but struggled with academics
and problems with behavior. She was
held back in grade two, and had major
difficulties with mathematics and language arts. She failed to complete most
assignments, and often interrupted the
teacher and was generally disruptive in
the classroom. She was referred to a
school psychologist at age 9 years and
was diagnosed with attention deficit
disorder and was placed in a modified
school program. A stimulant medication
was prescribed and she took this medication for 5 years with some benefit.
During high school, she was placed in a
vocational stream classroom, but
dropped out of school in grade 11. She
had few friends in school, and was
considered to be violent and a troublemaker. Her adoptive parents noted that
she often would not come home on
weekends. She broke curfews, and
would run away frequently for several
days in a row. She struggled with alcohol
and drug addiction. At 20 years of age
she was hospitalized for a short period
after being assaulted by her boy friend.
At the age of 21 years she delivered a
baby boy, who was placed for adoption.
She could not hold a job for more than a
few weeks, often being fired because
of frequent absences and difficulties
with co-workers. She depended on her
parents for financial support.
Her parents recognized that her life
was chaotic and she was immature and
was not able to cope with the challenges
in her life. Contact with social services
was made and a social worker suggested
that she might be affected by FASD. A
referral was made for Jennifer to be
evaluated with the FASD Diagnostic
team in their region. Detailed background information was obtained, and
her parents were found to both have
been alcoholics. Heavy prenatal use of
alcohol by the birth mother was confirmed during all three trimesters of the
pregnancy. Her birth parameters were
normal, and apart from the neglect and
suspected abuse she was otherwise
healthy for most of her life. Physical
and dysmorphology assessment confirmed normal height and weight, a
head circumference at the 10th–25th
centile, a normal neurological examination with mild fine motor deficits, short
palpebral fissures (2.6 cm; <3rd centile),
a smooth philtrum, and a thin upper lip
(a score of 4 for both on the lip-philtrum
pictorial guide). A comprehensive neuropsychological evaluation revealed an
overall low average score on cognitive
testing with a significant difference
between verbal and non-verbal performance. Functional memory and attention was severely impaired, and she
had impaired executive function and
social adaptive abilities. A diagnosis of
partial FAS was made and the diagnostic
team referred her to the community
FASD adult program for supportive
She received counseling for her
addiction, taking into consideration that
she had cognitive impairments. She was
connected with a mentor in the program
who helped her understand the nature
of her disability and assisted her with
application for social assistance, budgeting, food allowance and enrollment in
school upgrading and job training. Two
years after the diagnosis and interventions, she was able to live on her own
with ongoing assistance, she was drug
free and she was working as a hair stylist
in her community.
Ultimately, we believe a reliable, multidisciplinary team diagnosis is the first
step in effectively understanding the
issues and identifying the needs of
the affected adult. The diagnosis can
lead to a paradigm shift in attitude
and perception towards the affected
individual from one of a lazy, lying,
obstinate and difficult individual or
sociopath, to that of an individual
who is neurologically impaired and
who needs appropriate assistance, with
specific management and treatment.
Ultimately, we believe a
reliable, multi-disciplinary
team diagnosis is the first step in
effectively understanding the
issues and identifying the needs
of the affected adult. The
diagnosis can lead to a
paradigm shift in attitude and
perception towards the affected
individual from one of a lazy,
lying, obstinate and difficult
individual or sociopath, to that
of an individual who is
neurologically impaired and
who needs appropriate
assistance, with specific
management and treatment.
Although a diagnosis made in an adult
may not offer the same advantage of
preventing the occurrence of secondary
disabilities that is evident when a
diagnosis is made in a young child, a
diagnosis can offer hope and change
lives. A diagnosis may mitigate progression or reduce secondary disabilities,
provide an answer to the individual for
his or her disabilities and failures, and
improve their likelihood of being connected to interventions and services for
FASD adults.
Steven Neafcy writes:
‘‘I was not diagnosed with FASD
until I was 43 yrs old and not
knowing the reasons for my actions
was very frustrating. I was really a
person who wanted to do good!!
I could not understand what drove
me to disappoint those I wanted to
be proud of me. I was so lost! It was
only after I was diagnosed with
FASD that I realized my brain was
like a fuse box on overload without
the current flow that healthy brains
have, to give me the chance to
think before I acted and make a
choice. This was taken away from
me by the alcohol before I was
born. Now where do I go from
here? First it was important for me
to realize the reason I had a short
circuit. With this information I
could pick up from that point and
not keep bashing my head against
the wall trying to be normal and
function like those who don’t have
brain damage. This is impossible!
Now knowing this would I take
advantage of this Knowledge? At
first maybe so, but with a chance to
begin where I am capable and
achieve from that point can only
better my life. Now I might have a
damaged brain and be unable to
make decisions, but by turning to
my higher power, that being (God)
would and could take over for me.’’
[Retrieved from: http://www.acbr.
Having advocates or mentors for
FASD individuals can effectively fill the
gap in services and supports. FASD
adults who have had advocates have
experienced increase in personal
income, received direct services by
being found eligible for existing programs in the system that they did not
know how to access prior to the help,
and they have become empowered to
make changes in their lives [La Berge,
There are many excellent web sites on
FASD that also link to other resources in
print, in video format or on the worldwide web. These are just a few of the sites
that we recommend for clinicians and
FASD websites:
Canadian Centre for Substance
Abuse. Excellent site with FAS Tool kit
and a section on adults affected by FASD.
Adolescents and Adults with FASD.
Contains many links to useful sites.
Teresa Kellerman’s of the FAS
Family resource center of Tucson
FAS Community Resource Center
Information about FAS and FASD.
Fetal Alcohol Drug Unit (Dr. Ann
Streissguth’s research site on FAS at the
University of Washington, Seattle).
FAS Diagnostic and Prevention
Network (Dr. Susan Astley’s site at
the University of Washington, Seattle).
The 4-Digit Code manual is available
from this site.
Department of Health and Human
CDC. Guidelines from CDC here.
FASLink Fetal Alcohol Disorders
Society, an excellent section on Aduts
with FASD.
National Institute on Alcohol
Abuse and Alcoholism. The web page
includes a link to the Interagency
Coordinating Committee on Fetal
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