Psychiatric concerns about the consequences of prenatal alcohol exposure

Psychiatric concerns about the consequences of prenatal
alcohol exposure
References omitted: available online.
The Case of Child Mental Health Problems and FASD..."
Canadian Journal of Psychiatry
Tuesday, December 1, 2015 - 00:01 UTC -0500
Misattributions and Potential Consequences: The Case of Child Mental
Health
Problems and Fetal Alcohol Spectrum Disorders [Canadian Journal of
Psychiatry]
McLennan, John D
Received January 2015, revised, and accepted June 2015.
Numerous Canadian agencies have prioritized services for people
diagnosed with FAS and its broader construct FASD. This prioritization
extends to prevention interventions aimed at reducing or eliminating
PAE.
The many difficulties identified as associated with FAS, FASD, and
PAE is one of the justifications for this prioritization.
Mental health symptoms and disorders are among the most commonly
highlighted challenges
experienced by people labelled with FAS or FASD or exposed to alcohol
in utero.
However, the extent of the relation between the FAS, FASD, and PAE
cluster and
mental health symptom and disorder clusters may be inflated secondary
to at least 3
factors: diagnostic criteria overlap and etiologic assumptions, referral
bias, and failure to

control for confounding variables when assessing associations. Lack of
awareness of
these factors may lead to dissemination of misinformation, which could
adversely distort
the development and provision of mental health services.
Diagnostic criteria for conditions falling under the FASD umbrella have
been
operationalized in several different guidelines. The 2005 Canadian
guideline1 aimed, in
part, to harmonize aspects of the 2 leading approaches at the time, that
is, those of the
Institute of Medicine2 and the Washington 4-digit diagnostic code.3
Guidelines typically
include the complete syndrome, FAS, and require positive findings in 4
domains:
problematic patterns of alcohol exposure in utero (for example, from
maternal binge
drinking), growth abnormalities (for example, low birth weight for
gestational age), facial
dysmorphology (for example, short palpebral fissures), and CNS
neurodevelopment
abnormalities (for example, microcephaly at birth).2
Guidelines then typically go on to describe various partial syndromes.
In the case of the Canadian guideline, the following partial syndromes
are included: FAS (without confirmed alcohol exposure), partial FAS,
and ARND.1 Difficulties identified within children with high PAE, but
who do not have classical dysmorphic manifestations, is used to support
the inclusion of partial syndromes.4
However, this broadening likely contributes to problematic overlap with
those children with mental health difficulties for whom PAE may be
present but for whom it is not etiologic. This is particularly problematic
as there is no consensus on a pathognomonic behavioural manifestation
of PAE or FASD.

Although some propose a unique mental health profile linked to FASD,5
such profiles are based on small clinical samples and do not appear to
have been independently replicated using a nonreferred
population. Nevertheless, a resulting 10-item screening tool appears to
be receiving
national promotion in Canada.6
Concerns that weaknesses in the operationalization of partial FASD
syndromes may
lead to misattribution of PAE as causal for various difficulties (for
example, behavioural
problems) has been raised in critiques of the 2 dominant diagnostic
approaches used in
the field,2,3 that is, the US sources for the Canadian guidelines.7 The
ARND diagnosis,
within the Canadian guidelines, requires "evidence of impairment in
three or more of the
following CNS domains: hard and soft neurologic signs; brain structure;
cognition;
communication; academic achievement; memory; executive functioning
and abstract
reasoning; attention deficit/hyperactivity; adaptive behavior, social
skills, and social
communication."1, p S12
However, abnormalities in 3 of the listed domains would also be
commonly found in many children with various mental health disorders.
PAE may not be uncommon in children with such problem clusters.
However, the fraction for whom PAE is primarily etiologic is unknown,
and to assume it is typically the leading etiology is highly problematic.8
Complicating the picture is the inclusion of an etiologic variable, in this
case PAE, in the

diagnostic criteria for FASD. This is at odds with a key direction taken
in psychiatry as
reflected in contemporary versions of the DSM, that is, to avoid
etiologic assumptions
within diagnostic criteria.9
That the DSM-5 has included neurobehavioural disorders associated
with prenatal alcohol exposure under the section "Conditions for Further
Study"10 is perhaps a new exception. Unfortunately, as currently
written, this DSM-5 provisional criteria may contribute to further
diagnostic overlap with mental disorders not
caused by PAE.
This is in part due to the low threshold set for diagnostic criteria for this
provisional disorder. A leading epidemiologist has noted that the
inclusion of proposed
etiological variables in diagnostic criteria may undermine the validity of
epidemiologic
evaluations of such defined disorders.11
Further complicating considerations of diagnostic overlap and (or)
potential comorbidity
is a direction taken by some in the FASD community to label mental
disorder
manifestations in children with PAE or FASD as being secondary
disabilities.12
Although this may be valid in some situations, it is concerning if there is
a general
assumption that manifestations of mental disorders in the context of
PAE or FASD are
typically secondary phenomena.
Relying primarily on the temporal relation is inadequate to make this
linkage. Various mental disorders have different times of manifestation,
regardless of PAE, and always manifest postpartum. It is not clear how a

clinician could determine that the emergence of a mental disorder is
secondary to PAE or FASD and
not a function of genetic or other environmental factors that may
underlie timing of mental disorder emergence.
Leaving the problem of diagnostic criteria overlap and etiologic
assumptions aside,
referral bias (also known as Berksonian or selection bias) may also lead
to
misattribution.
Referral bias may occur when a factor of interest in the clinic population
(for example, psychiatric symptoms) also influences whether a patient is
seen in the clinic.13 This may lead to spurious correlations and
generalizations.
Apparent associations identified from studies using clinic samples that
have not been verified in nonreferred samples warrant considerable
skepticism. Although it is possible that a child may be sent to an FASD
clinic based solely on unique aspects of facial dysmorphology, factors
such as disruptive behaviours are much more likely to drive referrals.
Consequently, specialized FASD assessment clinics are likely receiving
referrals of children and youth with a disproportionally high occurrence
of disruptive behaviours.
Clinicians then experience high rates of co-occurrence, and the
researchers who rely on studies of clinically referred samples may report
strong but potentially spurious associations. Unfortunately, most FAS or
FASD studies appear to rely on clinic samples.
Fortunately, there are a few population-based samples that include an
examination of psychiatric morbidity among children assessed for PAE
and (or) FAS or FASD and that may help identify whether referral bias
underlies some of the high comorbidity noted in clinical populations.
ADHD may be the most studied psychiatric comorbidity in FASD.

One review found an overall ADHD prevalence of 48% in children with
FASD14; however, most source studies in that review used clinic-
referred samples. In contrast, a nonreferred, school-sampled study found
a combined-type ADHD prevalence of 8.7% among children with FASD
based on teacher ratings, compared with 5.3% among children without
FASD, a nonsignificant difference.15
The marked differences in ADHD prevalence found in children with
FASD in this population-based study, compared with the review of
clinic-based studies, may lead to the hypothesis that a substantial portion
of ADHD found in children with FASD in referred clinic samples have
ADHD as a function of a wider range of possible etiologies.16
Unfortunately, prevalence of other psychiatric disorders have not been
reported from population-based studies of FASD; however, referral bias
is also likely for other conditions that are apt to precipitate referrals (for
example, aggression, conduct disorder, and developmental delays).
Whether such distortions extend to internalizing problems and disorders
is unknown.
Confounding variables may also contribute to an overestimation of the
strength of relations between the FAS, FASD, and PAE cluster and
mental health problems.
Children referred to FASD clinics are often found to have had many risk
exposures in addition to PAE, such as being victims of physical or
sexual abuse and exposure to parental substance use after birth.17 It is
unclear how clinicians can attribute mental health presentations to the
PAE, compared with one or more of the other risk
exposures.
In some assessment and advocacy contexts, mental health symptoms and
disorders may be framed as primarily or entirely explained by PAE.
Such assumptions do not seem to hold up as suggested by findings from
numerous studies aimed at examining the extent to which PAE
independently explains adverse child outcomes
relative to other known risk factors for child mental health problems.

For example, in a FASD study within a school-based sample, measures
of PAE explained only a modest
portion of cognitive and behavioural outcomes and these association
were no longer significant once other risk factors (for example, lower
maternal education) were included in the multivariate model.18
Another study, based on a sample derived from a maternity clinic, found
PAE was related to child behavioural problems at follow-up but
explained only 0.6% to 1.7% of outcome variance; in contrast, a
measure of maternal
psychopathology explained 13.0% to 29.1% of the variance.19
In a population-based study examining the impact of low-to-moderate
PAE, the association with ADHD symptoms became statistically
insignificant once the multivariate model factored in measures of social
adversity.20
Finally, another large populationbased study attempted to consider
genetic and other environmental contributions beyond PAE by including
siblings and cousins with variable PAE.21 They found that the
significant differences in attentional and impulsivity problems between
children with and without PAE for unrelated families was not found
within related family.21 However, this study did find some evidence for
a significant relation between PAE and conduct problems after
controlling for family membership.21 Although measurement issues and
epidemiologic-based findings may, at times, seem disconnected from
clinical practice, in this case, failure to appreciate these underlying
patterns may have distorting effects on services and policies.
For example, at a service level, if a comorbid psychiatric disorder is
inaccurately attributed to FASD, this may lead to an inappropriate
diversion to a newly designed FASD specialty intervention that lacks
evidence of effectiveness for the comorbid psychiatric problem rather
than being directed to an evidence-based
intervention specific to the identified psychiatric comorbidity.
For example, use of evidence-based behavioural interventions or
medications for ADHD may be discouraged if the presenting attentional
problem is attributed to FASD.

A second example may include the setting of eligibility for certain
services and supports based on the presence of an FASD diagnosis rather
than a given identified need that may not be specific to FASD (for
example, a social skills deficit). This may reinforce unsubstantiated
assumptions made about children with FASD (for example, they all have
social skill deficits) and compromise access to a service for a child who
may have a need for additional services (for example, social skills
training) but who had, say, prenatal polysubstance exposure rather than
PAE.
A further concern is a potential for harm. It has been proposed that
flawed causal models that may be employed within some FASD-focused
clinics may violate the ethical principle of nonmaleficence.8 More
specifically, assumptions made about causes may inadvertently revive
past psychiatric frameworks that emphasized maternal behaviour as
etiologic in child psychiatric
disorders.8
Finally, the failure to consider an epidemiologic perspective may also
distort prevention efforts which may, for example, overemphasize a
single risk exposure (for example, elimination of drinking during
pregnancy) in efforts to improve child mental health in the population.
This may result in relative neglect of other important risk factors
contributing to child mental health problems, such as poverty.22
None of the preceding argument proposes that PAE is not an important
risk exposure that can adversely impact child development or that FAS
is not an important medical disorder.
However, as legitimately concerned as advocates, clinicians, and
researchers may be about PAE, learnings from epidemiology have the
potential to improve the evidence base of our understanding of child
mental health and, by extension, improving intervention services and
health policies.

To ignore such evidence raises the risk for misattribution, lost
opportunities, and potential harm. It is also critical to retain attention on
the relative impacts of multiple etiological factors contributing to mental
health and to be wary of approaches emphasizing single risk factor
models.
Acknowledgements
Thanks to Dr Peter Braunberger, Dr Kathy Georgiades, and Dr Michael
Boyle for critical feedback on earlier drafts of this paper, as well as
recommendations by the anonymous reviewers that helped improve the
final paper. In addition, thanks to several people who have previously
raised the issue of potential misattribution in the field of FASD, such as
Dr Elizabeth M Armstrong, Dr Ben Gibbard, and Dr Barry Zuckerman.
No funding was provided for this research and the author has no
conflicts of interest to declare.
Clinical Implications
* Clinicians and researchers should attend to diagnostic criteria overlap
and etiologic assumptions, referral bias, and potential influence of
confounders when considering associations between different disorders,
symptom clusters, and purported risk factors.
* Some mental health problems in children diagnosed with FASD may
be inaccurately attributed to in utero alcohol exposure and (or) FASD. *
In some cases, children with mental health disorders may be
mismanaged secondary to misattributing most or all
their difficulties to FASD.
Limitations
* This paper is not based on a systematic literature review.
* The number of high-quality source documents to evaluate the relation
between FASD and child mental health disorders is sparse.
References
John D McLennan, MD, MPH, PhD, FRCPC1 1 Associate Professor,
Departments of
Pediatrics, Psychiatry, and Community Health Sciences, Cumming
School of Medicine,
University of Calgary, Calgary, Alberta

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Re. Misattributions and Potential Consequences: The Case of Child
Mental Health
Problems and Fetal Alcohol Spectrum Disorders. John D. McLennon.
Canadian Journal of Psychiatry. Vol 60, No 12, December 2015
Dear Sir/Ms
Dr McLennon’s perspective requires comment and clarification: point
by point.
Keywords
PAE- Prenatal Alcohol Exposure
FAS- Fetal Alcohol Syndrome
FASD- Fetal Alcohol Spectrum Disorder
DSM- Diagnostic and Statistical Manual
Phenotype
Mental Health
Epidemiology
Epigenetic
I know of no Canadian agency that has “prioritized” services for people
diagnosed with FAS….”
- Prioritize: to organize things so that the most important thing is done or
dealt with first.[1]
In Canada there are some programs relating to FASD, none of which
have priority over programs relating to other health conditions: The
Province of Ontario has no programs for FASD at all, at this time.

FASD is not a “construct”, i.e. an idea or theory not formed from
empirical evidence.
There is overwhelming empirical evidence for the existence of FASD.
[2,3,4]
For those who think a priori: most if not all the research that has been
done on the effects of alcohol on the developed brain surely applies to
the developing brain.
FASD is not “broader” anything of FAS; rather, FAS is one of the many
phenotypes of FASD. [5]
FAS is not a label: it is a phenotype of FASD, as such the term FAS has
been replaced by “FASD with Sentinel Facial Features”. [5] This change
reflects the increasing clarification and understanding of the effects of
alcohol on the developing brain.
The association of DSM diagnoses to FASD was established 20 years
ago [6,7,8]. Confirmation of this association has continued clinically,[9]
neurologically [10] and epigenetically.[11] However, these associations
have not been acknowledged by Psychiatry, nor researched to establish
further the nature of these associations.
“Problematic overlap” will always be the case until PAE is excluded or
included as an etiological factor in DSM diagnoses.
I know of no evidence that the diagnosis of FASD negatively impacts
mental health services: the reverse is not the case however. For those
with FASD DSM diagnoses are often multiple: I have seen as many as
six. [12]
When the diagnosis of FASD is finally made the common reaction is
one of relief: relief, because it offers an explanation for a chaotic life
that multiple symptomatic DSM diagnoses have failed to provide.

These DSM diagnoses are made in good faith by psychiatrists. The
question needs to be asked: how could one individual fulfill the
requirements for so many DSM diagnoses?
There has to be a common factor. [13]
It is likely that there will never be a pathognemonic behavior for FASD,
which is a spectrum of phenotypes.
The diagnoses in the DSM 5 are defined by behavior alone. Increasingly
however, individuals are being identified as having more than one type
of DSM diagnostic behavior. [14] What is the cause of these DSM
overlaps?
Reference 5, “Identifying the behavioural phenotype in fetal alcohol
spectrum disorder: sensitivity, specificity and screening potential”,
relates only to ADHD. I am not aware of any publications that links only
one DSM diagnosis specifically to FASD. On the contrary, a number of
DSM diagnoses have been linked to FASD. [7,15]
There are many non-referred population studies of FASD and PAE,
some of which are of large populations. [12,16,17]
Screening tools have been developed with great diligence. None of them
include DSM
diagnoses as a criteria.
I agree, … “abnormalities in 3 of the listed domains would also be
commonly found in many children with various mental health
disorders”: if they are looked for.
In my experience neuropsychological assessments are rarely done in the
context of Psychiatry, or not considered if available: in keeping with the
lack of publications on the subject.
Surely assessment of information processing, memory etc. should be
routine for those
with DSM diagnoses.

I agree, …. “the fraction for whom PAE is primarily etiologic is
unknown”: therefore it
needs to be explored.
Is it not problematic to ignore the overwhelming associations between
PAE and mental illness? [15]
“Complicating the picture is the inclusion of an etiologic variable, in this
case PAE, in the diagnostic criteria for FASD.”
Without PAE there is no FASD. This fundamental diagnostic principle is
applied in Psychiatry e.g. grouping under the common etiological factor
of stress.[18,19,]
The threshold referred to is actually high in that many of the effects of
PAE are not captured. There is no threshold at which PAE will have no
deleterious effect on the developing fetus.[21]
Etiological variables are a fact of life: Epidemiology has to deal with it.
[22]
“Secondary”, coming after, is a reasonable word to describe the mental
disorders that affect 98% of individuals diagnosed with FASD.
With or without PAE as an etiological factor one would expect that
various mental illnesses would always manifest postpartum, and not
prepartum!
It has always been acknowledged that other environmental factors
contribute to the secondary disabilities of PAE. [7,23]
We now understand that the process of disruption of brain development
by PAE is largely through epigenetic changes of gene expression
[24,25,26,27], and that manifestation of those disruptions may occur at
different times and be influenced by other environmental factors.

So far as clinic bias is concerned: the various DSM diagnoses are not
made in the few available FASD diagnostic clinics. The DSM diagnoses
are made separately by psychiatrists and other practitioners throughout
Canada, both before and after the diagnosis of FASD is made: they make
no reference to FASD. It follows that Berksonian bias does not apply.
[28]
Up to now the attribution of DSM diagnoses has not been part of the
screening or diagnostic process for FASD. However, the overwhelming
associations make it reasonable that it should be the case. [29,30,31,32]
The recent updating of the Canadian Guidelines does now include
previous DSM diagnoses.[5]
The associations between FASD and DSM diagnoses satisfy the
requirements of Bradford Hill’s causal inference in epidemiologic
studies, especially in the light of recent neurological and epigenetic
research. [7,29]
It should be noted that many children who are exposed to prenatal
alcohol, fulfill the requirements for the diagnosis of FASD, have been
adopted at birth and have not experienced abuse or neglect, yet still
receive diagnoses from the DSM.[30]
We know that an early diagnosis and a positive environment mitigates
the secondary disabilities of FASD:[7] mitigate is the correct word, since
in spite of positive adoptive parental efforts significant negative
outcomes may still occur, including multiple DSM diagnoses.
Research into the effectiveness of FASD interventions for DSM
comorbid symptoms is required. I find it difficult to see how such
interventions might be counterproductive for those with DSM diagnoses.
However, the reverse is not the case, especially in relation to
psychotropic medications. Cardiac birth defects are associated with
PAE/FASD. Also, there is an increased risk of suicide. Yet ADHD is the

most common other diagnosis for children with FASD, many of whom
are prescribed psychostimulants such as Ritalin.
All those diagnosed with FASD have social skills deficits. The
neuropsychocgical deficiencies required for the diagnosis are such that
social skills deficits are inevitable, but their impact can be improved.
[33,34,35]
Lack of social skills may not be due to such permanent
neurodevelopmental disabilities. In such cases training and management
may be different; this is all the more reason why PAE and FASD should
be excluded.
FASD Awareness and Prevention programs always emphasize the
significance of risk factors such as poverty. [36]
Pursuing the diagnosis and understanding PAE/FASD is not
synonymous with ignoring research into mental illness. On the contrary,
the more research into the neurological origins of mental illness the
more associations with PAE are found.
No one is emphasizing a single risk factor model for mental illness.
However any risk model should include PAE as a risk factor: but this is
not happening as is demonstrated by the absence of references to
PAS/FASD in most Psychiatric publications.
The criteria for the diagnosis of mental illness needs to be extended into
the 21st
century.
It is time to move on. [37]
The day will come when the genes that control individual aspects of
brain function will be identified. Changes in gene expression will be
related to clinical presentations, such as those in the DSM5: the
generation at which those changes occurred will be determined.

The agent that caused those changes, with other environmental factors,
will be identified.
Then we will understand to what degree alcohol has determined the
nature of mental illness.
Barry Stanley MB ChB. F.R.C.S. [C]
Feb. 2016
Submitted to the CJP: not published
A Critique of the New Canadian Fetal Alcohol Spectrum Disorder
Guideline
John D. McLennan, MD, PhD and Peter Braunberger, MD, PhD
Scientist, Children’s Hospital of Eastern Ontario – Research Institute;
Research Chair in Child and Adolescent
Psychiatry, Department of Psychiatry, University of Ottawa; Adjunct
Associate Professor, Department of Pediatrics,
University of Calgary
Assistant Professor, Northern Ontario School of Medicine, Thunder Bay,
Ontario
Corresponding E-Mail: jmclennan@cheo.on.ca
Received 2016 Dec 7; Accepted 2017 May 24.
Copyright © 2017 Canadian Academy of Child and Adolescent
Psychiatry
Abstract
A new Fetal Alcohol Spectrum Disorder (FASD) guideline was
published in the Canadian Medical
Association Journal in 2016. This is relevant to the mental health field as
mental health symptoms and
psychiatric disorders are often identified as associated with and/or part
of FASD presentations.

Unfortunately, the new guideline has not advanced understanding of the
interface between FASD and
mental health problems; rather it may contribute to additional confusion.
For example, a new
recommendation to include additional mental health symptoms, such as
anxiety and affect
dysregulation, as manifestations contributing to a diagnosis of FASD is
particularly concerning given
the paucity of evidence supporting this assertion and the potential to
distort delivery of mental health
interventions for mental health problems. In addition, the guideline
recommendation for introducing an
“at risk for FASD” designation is not without risk. An appeal is made
for greater scrutiny in the
construction of diagnostic criteria and guidelines and for a more careful
delineation of causal
relationships and comorbidities to better inform the delivery of
evidence-based mental health care.
Keywords: fetal alcohol syndrome, practice guidelines, comorbidity,
diagnosis, mental disorders
Introduction
A new Canadian diagnostic guideline for Fetal Alcohol Spectrum
Disorder (FASD) was published in
the Canadian Medical Association Journal in 2016 (Cook et al., 2016a).
Whereas there is little
disagreement regarding the potential teratogenicity of prenatal alcohol
exposure (PAE), there are many
unanswered questions about the construct of FASD and how human
service sectors should best
respond. Unfortunately, aspects of the new Canadian guideline appear to
further compromise clarity
rather than advance an evidence-based approach.

Overview of the new Canadian guideline
This new guideline replaces the 2005 Canadian version (Chudley et al.,
2005) and joins five other
published efforts identified as FASD guidelines [a German, (Landgraf,
Nothacker, & Heinen, 2013) an
Australian, (Watkins et al, 2013) and three US versions (Stratton, Howe
& Battaglia, 1996), (Hoyme et
al., 2005), (Hoyme et al., 2016)]. All guidelines to date are largely
focused on assessment and
diagnosis, although some include points on management and follow-up.
A particular challenge
confronting those developing FASD guidelines is the variable
manifestation, in persons with PAE, of
the physical features described in the classical fetal alcohol syndrome
(FAS). This includes variability
in the manifestation of the sentinel facial dysmorphic features of short
palpebral fissures, smooth
philtrum and thin upper lip (del Campo & Jones, 2016). Furthermore,
growth impairment (e.g.,
intrauterine growth restriction), another of the core dimensions of the
original syndrome (Jones &
Smith, 1973), has been dropped in the new guideline (Cook et al.,
2016b) because of inconsistent
associations with PAE (O’Leary, Nassar, Kurinczuk, & Bower, 2009).
Given inconsistent
manifestations of these physical features, an accurate operationalization
of neurodevelopmental criteria
is then particularly critical for FASD guidelines.
Within the Canadian guidelines, achievement of the neurodevelopmental
criteria for FASD requires
severe impairment in three or more of ten neurodevelopmental domains
(e.g., academic achievement,
attention, affect regulation) (Cook et al., 2016a). Impaired affect
regulation, a newly added domain, can

be achieved by meeting criteria for one of several DSM-5 disorders
(e.g., Disruptive Mood
Dysregulation Disorder, Generalized Anxiety Disorder) (Cook et al.,
2016a). Also new is that attention
is separated from hyperactivity/impulsivity (the latter now being housed
under the executive function
domain) (Cook et al., 2016a). Presumably this could lead to a scenario in
which a child with a
combined presentation of ADHD could, through this one diagnosis
alone, achieve two of the three
required neurodevelopmental criteria.
The 18 guideline recommendations are housed within domains that
range from “screening” to
“management and follow-up.” “Strength of the recommendation” and
“quality of the level of evidence”
ratings are given for 17 of the 18 recommendations (Cook et al., 2016a).
The “strength of the
recommendation” is rated as “strong” for all 17 (Cook et al., 2016a). Ten
recommendations receive a
“high” rating for quality of evidence (Cook et al., 2016a). Within the
recommendations, a three
category classification system is proposed: (i) FASD with sentinel facial
features; (ii) FASD without
sentinel facial features; and, (iii) a new proposed “designation” of “At
risk for Neurodevelopmental
Disorder and FASD, associated with PAE”(Cook et al., 2016a).
Critique 1: Questionable aspects of the neurodevelopmental criteria for
an FASD diagnosis
Perhaps the most concerning aspect of the new guideline is the inclusion
of an expanded array of
mental health symptoms within the neurodevelopmental criteria, in
particular, incorporation of
difficulties with affect regulation and specific DSM diagnoses. While a
linkage between PAE and affect

regulation could constitute a reasonable hypothesis to be studied, it is
premature for a practice
guideline to advocate this as a domain with sufficient evidence of
causality to include it as a symptom
pattern contributing to achievement of FASD diagnostic criteria.
Unfortunately, many studies
identifying associations between mental health symptoms and FASD or
PAE are fraught with
methodological limitations, including referral bias and uncontrolled
confounders (McLennan, 2015).
These limitations may contribute to an overestimate of the strength of
relationships between mental
health symptoms and PAE or FASD (McLennan, 2015).
Also questionable are proposed cut-points for criteria attainment in
various domains. This includes the
repeated recommendation to rely on two standard deviations (SD) from
the mean on various normed
behavioural and developmental scales as the threshold for
neurodevelopmental criteria (Cook et al.,
2016b). While this is more conservative than the new US guideline
which proposes a cut-point of 1.5
SD (Hoyme et al., 2016), both are arbitrary. Similarly, the proposal to
use DSM-5 criteria to establish
thresholds for some neurodevelopmental domains (e.g., meeting criteria
for Separation Anxiety
Disorder for the affect regulation domain) (Cook et al., 2016b) is also
without empirical evidence.
Again, these could be hypotheses to be investigated, i.e., whether such
thresholds result in greater
diagnostic accuracy and, more importantly, whether such thresholds lead
to effective service matching.
However, it seems unwarranted at this point to advocate their use as
evidence-based criteria.
The guideline algorithm proposes that neurodevelopmental compromise
(at the proposed thresholds) in

the absence of physical criteria, but occurring in the context of
significant PAE, is adequate for an
FASD diagnosis. Unfortunately, it is not clear how a person whose
neurodevelopmental symptoms
secondary to other causal factors, but who also has PAE, might avoid
being categorized as FASD; in
other words, the risk for false positive FASD diagnoses is not addressed.
Of note, the guideline itself acknowledges that “no neurodevelopmental
deficits are considered
pathognomonic for, or specific to, FASD” (p. 195) (Cook et al., 2016a).
How clinicians might
determine whether a given neurodevelopmental problem is attributable
to PAE, and, more importantly,
how such a distinction benefits the recipient of an FASD diagnosis are
important and unfortunately
unaddressed questions.
Although Hoyme, et al. (2016) expresses concern that FASD might be
misdiagnosed as another
disorder, the possibility that another mental health or medical diagnosis
is misdiagnosed as FASD or
missed because of an FASD diagnosis is similarly concerning. Now that
mood and anxiety diagnoses
are added to the list of neurodevelopmental criteria, and physical
abnormalities are not required, the
risks of misdiagnosis and missed diagnoses are potentially amplified and
as such warrant further
scrutiny.
Additional complexities of psychiatric diagnoses were also not
addressed. For example, it is not clear
how changes in psychiatric presentations over time might be managed
(e.g., Should a past history of
major depressive disorder, now in remission, be counted towards the
affect regulation domain?). Nor is
it clear how associated or correlated symptoms should be addressed
(e.g., cognitive deficits have been

identified in those who have or have had depression [Rock, Roiser,
Riedel, & Blackwell, 2014];
learning disabilities and academic underachievement are commonly
comorbid with ADHD [DuPaul,
Gormley, & Laracy, 2013]). It is a concern that common associated
features or comorbidities may be
attributed or misattributed twice towards FASD.
Critique 2: Risks from the newly proposed “at risk for
neurodevelopmental disorder”
designation
A second concern is the new category of “at risk for neurodevelopmental
disorder and FASD,
associated with PAE” proposed by the Canadian guideline. This
classification can be achieved in two
ways: (i) children with concerning PAE, but who do not meet criteria for
sentinel facial features, nor
for CNS impairment, and for whom the assessment is deemed
“inconclusive,”; and, (ii) children < six
years old with known or unknown PAE with sentinel facial features, but
without apparent or
measurable CNS impairment (Cook et al., 2016a). This approach may
facilitate increased surveillance
of persons who may be at higher risk for subsequent difficulties.
However, whatever advantage this
affords needs to be balanced against potential adverse consequences of
labelling a number of persons
“at risk.” Some of these “at risk” persons will not subsequently develop
any concerns, while others
may develop problems that may not be a function of PAE. In the latter
case, the “at risk” status may
prime an approach that encourages attributing emerging concerns as
likely to be a function of PAE, and
potentially downplaying the contribution of other causal factors. A bias
against the role of other

contributing factors may increase the risk of missing potentially
modifiable variables influencing child
development. Of interest, this is the one of the 18 recommendations
which did not include strength of
recommendation or quality of evidence ratings.
Critique 3: Unsupported ratings of “strong” recommendation and “high”
quality evidence
Although the Appraisal of Guidelines, Research, and Evaluation
(AGREE) framework was referenced
in the new Canadian guideline, it is important to note that AGREE itself
“do[es] not evaluate the
clinical appropriateness or validity of the recommendations” (p. 840)
(Brouwers, et al., 2010). Rating
tools from the Grading of Recommendations, Assessment, Development
and Evaluation (GRADE)
were also cited (Guyatt, et al., 2011). However, it was often not clear
how the resulting
recommendations attained “strong” and “high” ratings despite reviewing
the additional materials
available in the guideline supplement (Cook et al. 2016b).
For example, the first recommendation calls for universal screening of
all pregnant and postpartum
women for alcohol consumption (Cook et al., 2016a). Proposals for
universal screenings require
assessment of multiple factors including cost, implication of false
positives and false negatives, and the
imperative to demonstrate improved outcomes as a function of the
proposed screening. The guideline
and its supplement contained no critical discussion of the risks and costs
of screening all pregnant and
postpartum women for alcohol consumption, nor empirical evidence that
such an initiative would result
in substantial health benefits. It is surprising then that this
recommendation was rated as “strong” and

the quality of evidence “high” (Cook et al., 2016a). (Note, the issue
questioned here is the impact of
screening, not the impact of reducing alcohol consumption in
pregnancy). This is unfortunately similar
to other well-intentioned promotions of large-scale psychosocial risk
screening which lack critical
scrutiny (McLennan & MacMillan, 2016). An informative exception is
the thorough deliberations by
the Canadian Task Force on Preventive Health Care regarding
systematic depression screening in
primary care (Thombs, et al., 2012).
In contrast to the number of strong/high ratings in the Canadian
guideline, similar recommendations in
the Australian (Watkins et al., 2013) and German (Landgraf et al. 2013)
guidelines received
consistently lower ratings. For example, the Australian guideline rated
the recommendation of
requiring a “comprehensive interdisciplinary team” for diagnostic
assessment as conditional and of low
quality evidence (Watkins et al., 2013) while, without further
explanation or citation of empirical
evidence, the Canadian guideline rated this recommendation as strong
and of high quality (Cook et al.,
2016a).
There are additional concerns related to the application of AGREE to
this particular guideline. The
guideline authors indicate that the criteria for all 23 AGREE items were
met by listing “yes” (Cook et
al., 2016b). However, the AGREE manual stipulates that criteria should
be rated on a 7-point Likert
scale, from “strongly disagree” to “strongly agree” (Brouwers et al.,
2013). The authors’ decision to
reduce this to a dichotomous “yes/no” classification may have obscured
the extent of supporting
evidence, or lack thereof.

Critique 4: Utility of FASD specific recommendations for management
and follow-up
A fourth concern relates to management and follow-up
recommendations. Consistent with a very thin
evidence base for FASD specific interventions, the authors fittingly
rated the evidence for these
recommendations as low. But one might then understandably ask the
question “should there be stronger
evidence for the benefits of receipt of an FASD diagnosis and/or benefits
of specific FASD
interventions before disseminating a diagnostic guideline in the first
place?”
Presumably the purpose of a specific diagnosis in a clinical setting is to
inform the selection of
evidence-based interventions that would not otherwise be received if it
were not for the receipt of this
specific diagnosis. A similar challenge was raised in a paper entitled
“Why ask why? Logical fallacies
in the diagnosis of Fetal Alcohol Spectrum Disorder” (Price & Miskelly,
2015). This disconnect might
be captured by the guideline authors’ own algorithm which proposes
“developmental care as needed”
for the patient that does not meet criteria for FASD (Cook et al., 2016a),
a recommendation that
presumably could be made for all patients whether or not they have PAE
or have met the proposed
FASD diagnostic criteria.
Although the evidence-base is thin for FASD specific interventions, this
need not lead to therapeutic
nihilism. Mental health symptoms and disorders in those receiving an
FASD diagnosis might still be
addressed with established evidence-based interventions for given
mental health problems. For

example, a study of standard medication treatment of ADHD symptoms
in a cohort of children
diagnosed with FASD demonstrated substantial symptom improvement
(Doig, McLennan, Gibbard,
2008). Similarly, a social skills intervention which had already
demonstrated a positive impact in a
non-FASD mental health population (Frankel, et al., 2010) also
demonstrated positive impacts with a
sample of children diagnosed with FASD (Reid, et al., 2015). These
findings may suggest that a mental
health approach focused on symptom clusters to inform treatment
provision may continue to be
reasonable rather than an approach driven by hypothesized etiological
factors.
Conclusions
The new guideline has not provided clarity or compelling new evidence
to reduce the confusion around
the pattern and strength of the relationship between PAE and many of
the neurodevelopmental criteria.
Further, the new guideline does not shed light on the extent to which
mental health disorders seen in
persons diagnosed with FASD ought to be considered part of FASD,
rather than as comorbidities. It is
also not clear how an FASD diagnosis will improve outcomes of persons
with neurodevelopmental
difficulties.
Implementation of guideline recommendations has health care service
planning and delivery
implications. The potential for service and policy distortions in pursuing
carved-out separate service
approaches for persons diagnosed with FASD versus integrated services
based on matching individual
needs to evidence-based interventions has previously been raised
(McLennan, 2010). Such concerns

were not addressed by the new Canadian guideline.
The rigour of practice guidelines needs to be improved. One proposed
approach to improve the quality
of guidelines is to better operationalize a clear analytic framework to
strategically inform the
development of guidelines as described elsewhere (Woolf, Schünemann,
Eccles, Grimshaw, &
Shekelle, 2012). Within such an analytic framework there is a call to be
“as explicit as possible in
defining outcomes of interest…[and determining] … what specific
outcomes need to be affected to
arrive at a recommendation” (p.2) (Woolf et al., 2012). Unless we
increase the level of scrutiny of our
well-intentioned ideas and recommendations, we will fail to move
forward in reducing the confusion in
this and other health fields which may ultimately impede the delivery of
effective care to those in need.
Acknowledgements / Conflicts of Interest
The authors have no conflicts of interest to disclose.
J Can Acad Child Adolesc Psychiatry. 2018 Apr; 27(2): 83–87.
Published online 2018 Apr 1.
PMCID: PMC5896521
PMID: 29662519
Response to “A critique for the new Canadian FASD diagnostic
Guidelines”
Jocelynn L. Cook, PhD, MBA, Courtney R. Green, PhD, Christine
Lilley, PhD, R. Psych, Sally Anderson,
PhD, Mary Ellen Baldwin, Dip CS, R. Psych, Albert E. Chudley, MD,
Julianne Conry, PhD, Nicole LeBlanc,
MD, Christine A. Loock, MD, Bernadene Mallon, MSW, RSW, Audrey
McFarlane, BED (CED), MBA,
Valerie Temple, PhD, and C. Psych

The Society of Obstetricians and Gynaecologists of Canada (SOGC),
University of Ottawa, Ottawa, Ontario
Canada FASD Research Network, Department of Obstetrics and
Gynaecology, University of Ottawa, Ottawa,
Ontario
Compass Clinic, Vancouver, British Columbia
National Institutes of Health, Bethesda, Maryland, USA
Fetal Alcohol Spectrum Disorders Clinic, Child Development Services,
Alberta Children’s Hospital, Calgary,
Alberta
Department of Pediatrics, University of Manitoba, Winnipeg, Manitoba
Emerita University of British Columbia, Vancouver, British Columbia
Dr. Georges-L.-Dumont University Hospital Centre, Moncton, New
Brunswick
FASD Centre of Excellence, Université de Moncton and Université de
Sherbrooke, Moncton, New Brunswick
Department of Pediatrics, University of British Columbia, Vancouver,
British Columbia
Glenrose Rehabilitation Hospital, Alberta Health Services, Edmonton,
Alberta
Lakeland Centre for FASD, Cold Lake, Alberta
Surrey Place Centre, Toronto, Ontario
Corresponding author.
Corresponding E-mail: jcook@sogc.com
Copyright © 2018 Canadian Academy of Child and Adolescent
Psychiatry
Fetal alcohol spectrum disorder (FASD): A guideline for diagnosis
across the lifespan (Cook et al.,
2016b) was published to provide updated recommendations for
diagnoses related to prenatal alcohol
exposure. As part of the AGREE process to update the 2005 guideline,
the authors undertook a
literature review, as well as, a broad consultative process that involved
input from national and

international multidisciplinary experts in the field of FASD. In our
deliberations, we explored the
alternative diagnostic approaches with respect to our Canadian
population, evidence and expertise. The
final document, and its associated recommendations, was the result of
two years of national and
international consultations, reviews of multiple drafts and the available
evidence-base at the time.
This Clinical Commentary is a response to the critique Fetal Alcohol
Spectrum Disorder: Canadian
guidelines for diagnosis, written by McLennan and Braunberger
(McLennan & Braunberger, 2017).
Testing the reliability and validity of guidelines is an essential part of
adapting to new high-quality
evidence and ensuring that recommendations remain strong. The revised
diagnostic guideline authors
have met and appreciate the opportunity to review and reflect on their
methods in response toMcLennan and Braunberger’s paper (McLennan
& Braunberger, 2017).
The Diagnostic and Statistical Manual of Mental Disorders, Fifth
Edition (DSM-5) have proposed
criteria for Neurobehavioral Disorder Associated with PAE (ND-PAE)
as part of its defined
mental/psychiatric diagnoses. It is important to note that the purpose of
the updated Canadian FASD
diagnostic guidelines was not to advance the pathophysiological
relationship of FASD and mental
disorders; diagnosis is merely an identification process and not a
replacement for the scientific process
of understanding pathogenesis of disease.
Critique #1: Questionable aspects of the criteria for an FASD diagnosis
Affect regulation criterion

McLennan and Braunberger begin by stating that the most concerning
aspect of the new diagnostic
guidelines is inclusion of an Affect Regulation (AR) domain in the
neurodevelopmental criteria for
diagnosis. They concede that it is reasonable to hypothesize a link
between AR and FASD, but feel that
the available evidence is fraught with methodological challenges and
should be viewed with caution. A
deficit in AR (as defined by the guidelines) is present when an
individual meets the DSM-5 criteria for
a depression or anxiety disorder.
Response: A large number of studies have found high rates of affective
disorders in individuals with
FASD (Barr et al., 2006; Famy, Streissguth, & Unis, 1998; O’Connor &
Paley, 2009; O’Connor et al.,
2002; Pei, Denys, Hughes, & Rasmussen, 2011). There is also robust
evidence from animal models that
directly links PAE and increased neuroendocrine response to stress
(Hellemans, Verma, Yoon, Yu, &
Weinberg, 2008; Weinberg, Sliwowska, Lan, & Hellemans, 2008), with
PAE permanently affecting
neuro-adaptive mechanisms that mediate the stress response, which can
lead to hyper-reactivity to
stress across the lifespan. Hyper-reactivity to stress, in turn, may
predispose individuals with PAE to
affect dysregulation and disorders such as anxiety or depression. We
note that these studies do face
some methodological challenges and should be viewed with caution and
we do agree with McLennan
and Braunberger that the category of AR requires further discussion,
refinement, and research in the
context of FASD diagnosis.
Neurodevelopmental categorization

The critique suggests that the neurodevelopmental categorization in the
new guidelines was necessary
in view of inconsistent manifestations of facial and growth features.
Response: The decision point was evidence of the domains’
predictability for an FASD diagnosis,
rather than the variability suggested by the authors. The literature was
extensively reviewed for each
brain domain, specifically, with national and international experts
convening to draft the
recommendations and criteria. It is recommended that each domain is
evaluated using a step-wise
process. When results on standardized measures fall at or below minus
two standard deviations, the
domain is considered to be significantly impaired.
In studies at the University of Washington (Astley, 2013), the criteria of
minus two standard deviations
(-2 SD) on at least three domains was associated with brain changes that
could be detected using
imaging techniques. Similarly, -2 SD has been used to identify
intellectual disabilities. As was
described in the 2005 guidelines, we recognize that, in standard
neuropsychological practice, less
stringent levels may indicate subtle brain impairment and these are an
important part of the individual’s
profile. However, for the purposes of an FASD diagnosis, and the
certainty that the scores represent
injury caused by alcohol, the more extreme cut-off is recommended.
Certainly, the interpretation of any score at −2 SD requires clinical
judgment. Clinical consensus, along
with standardized measures, have traditionally been used to develop
criteria for many DSM-5
diagnoses. Consensus diagnoses that offer reliability and consistency
across diagnosticians are
necessary to achieve strong evidence.

PAE as the primary deficit
The algorithm developed for FASD diagnosis focusses on PAE as the
largest contributing factor to the
individual’s issues. Patients/clients with mental health symptoms arising
from other causes will be
misdiagnosed as FASD.
Response: The concerns expressed that comorbidities will lead to a
misdiagnosis of FASD is not
supported by any evidence. This assumes a mechanistic use of the
algorithm and guidelines. The
contrary is more likely, as earlier versions of the DSM did not recognize
the influence of PAE, and
FASD manifestations were diagnosed as other DSM conditions.
Related to this are various studies among those with FASD who were
found to have additional DSM
diagnoses after a thorough semi-structured interview. This contradicts
the authors’ position as it is the
FASD that could be misdiagnosed, or go undiagnosed, if the secondary
mental health diagnosis was
given without consideration of the PAE. Traditional psychiatric
interventions may be ineffective if the
underlying brain dysfunction is not recognized.
Critique #2: Risks from the newly proposed “At-Risk for
neurodevelopmental
disorders” designation
The “At-Risk” category was developed to ensure that individuals with
significant PAE, who do not yet
meet the criteria for an FASD diagnosis, are not lost for follow up, but
are flagged for management and
interventions. A main concern from clinicians in the field was that these
patients became “lost in the
system” and were never fully assessed, precluding them from receiving
the services that would

improve outcomes for them and their families. This can occur when
patients are too young for a
comprehensive assessment or when they have other issues in their lives
that must be prioritized ahead
of a comprehensive assessment (e.g., homelessness; mental health;
addiction).
McLennan and Braunberger argue that potential adverse consequences
of “labelling” may bias against
the role of other contributing factors that potentially are modifiable.
Response: In practice, the designation affords several important benefits.
For infants or preschoolers,
the designation flags them for a comprehensive assessment when they
are at an appropriate age and/or
when the child’s social situation has stabilized. A management plan for
the child would include a
targeted date for the complete neurodevelopmental assessment, as well
as a plan for early interventions
and strategies, as indicated. It is notable that many very young children
with PAE are not living with
their biological parents and may be candidates for adoption, or may be
living in poverty with
inconsistent access to medical care and developmental supports. While it
is true that the “At-Risk”
designation does carry some risk of self-fulfilling prophecy, and we take
that seriously, we feel that the
risk is justified by the importance of emphasizing consistent care and
early intervention services given
the social instability that many such children are facing.
We have never argued that more symptom-specific diagnosis or other
causes of disability are neither
important nor deserving of treatment. We are very concerned about the
potential that an FASD
diagnosis may de-emphasize other possible risk factors, especially
physical and psychological trauma.

We do not downplay these important factors and, in fact, the guidelines
instruct the diagnostic teams to
consider the effects of PAE in the context of multiple factors affecting
the development of the
individual.
On the contrary, the effects of PAE are well-established and cannot be
ignored. We do not argue that
FASD is the complete story for any patient, but as with other risk factors
that cause broad
neurodevelopmental differences such as a genetic syndrome or acquired
brain injury, FASD must be
included in diagnostic formulations. We also hope that future empirical
research will proceed as these
critics urge, so that the next guidelines can be informed by even more
high quality evidence. One need
only look back at the historical descriptions of Fetal Alcohol Syndrome
(Jones & Smith, 1973) to
appreciate the sophistication of diagnosis that has evolved.
In Summary, this new designation was in direct response to the feedback
received from the
comprehensive survey of all Canadian FASD diagnostic clinics, who
indicated a need for a
classification that addresses current and emerging needs for patients,
who did not meet the criteria for
FASD, but who had confirmed PAE. This would enable them to begin
providing strategies and
supports.
Critique #3: Unsupported ratings of “strong” recommendation and
“high” quality of
evidence
McLennan and Braunberger question how the AGREE II process was
applied to the recommendations.
Response: The CMAJ provided strict instructions for how the AGREE II
process was reported and the

GRADE categorization of the strength of evidence. As part of the
submission process, we detailed how
our process for guideline development met each step of the AGREE II
criteria and how we applied the
GRADE methodology to evaluate the evidence. All steps were followed
and justified. The guidelines
were informed by a comprehensive analytic framework for development,
as described in the Woolf et
al. (2012) publication (Woolf, Schunemann, Eccles, Grimshaw, &
Shekelle, 2012); however, due to
strict page limitations, it was not possible to expand or to provide more
detail on the process and
procedures. Below, we will provide additional information.
A table of the evidence and GRADE evaluation was produced and has
been shared around the world
with interested parties. Of note, because there is little Canadian data,
evidence was often used from
other countries with large cohort studies. We went beyond the AGREE
II process by having three
national/international consultative workshops focused on specific
aspects of the diagnosis. Two
iterations of the draft guidelines were also extensively reviewed by
national and international experts in
the field, who were acknowledged in the manuscript itself. A companion
review paper was also drafted
that provided more detail about the specific evidence, but because of
strict publishing limitations, it
was not included in the guideline document itself. It is available on the
CanFASD’s website:
www.canfasd.ca.
Finally, the exhaustive consultation process cannot be overestimated, as
the CMAJ had significant
trouble identifying reviewers for the guideline, who had not contributed
to the final recommendations

through the variety of opportunities afforded to them by the authorship
group.
Critique #4: Utility of FASD specific recommendations for management
and followup
The fourth critique questioned the utility of disseminating new
guidelines when the evidence is weak
and that there was little value in providing a diagnosis without evidence-
based interventions. They also
question whether there should be stronger evidence for the benefits of an
FASD diagnosis and
interventions before guidelines for diagnosis are disseminated. They
suggest that treatment could focus
on symptom clusters without relying on an etiology.
Response: As with others in the field who are grappling with the same
published evidence, we strongly
believe that although evidence continues to evolve, a fair and objective
assessment still provides
guidance for those seeking best practice. We support that diagnosis can
improve outcomes, which has
been well-described in the literature (and earlier diagnosis is associated
with significantly improved
outcomes for affected individuals (Streissguth, 1997; Streissguth et al.,
2004). We know that early
interventions significantly improve outcomes (Loock, Conry, Cook,
Chudley, & Rosales, 2005), and
this has also been described not only in the FASD field, but also in the
early child development
literature (Einfeld, Tonge, & Clarke, 2013; Petrenko, 2013; Position
Statement: Early Intervention for
Children with Developmental Disabilities, 2013; Vitrikas, Savard, &
Bucaj, 2017).
There is emerging evidence on successful interventions for individuals
with neurocognitive deficits and

for individuals specifically with FASD. These include a broad range of
approaches such as
occupational therapy (Paley & O’Connor, 2011), social skills training
(O’Connor et al., 2006) and math
interventions (Kable, Coles, & Taddeo, 2007). These were addressed in
the guidelines and the science
in the field continues to evolve. Without an initial diagnosis, further
evidence cannot be collected on
the efficacy of FASD interventions.
Conclusion
This critique has helped to draw attention to the need to maintain
scientific rigor in guideline
development, which will benefit not only the FASD field, but also
medical practice, in general. The
relationship between mental disorders, PAE and FASD remains one that
only interdisciplinary and
constructive collaborative research will bring the clarity required to help
many caught in the interface.
We agree that strategies to manage false positive FASD diagnoses
should be in place and that scientific
investigation, for the criteria for the AR domain in clinical samples, is
needed. We note that without
standardized diagnostic criteria, investigation will not be possible at all.
The critique tends to downplay the role of ten years’ experience with the
existing 2005 guidelines and
the knowledge we gained from studying the pros and cons of other
diagnostic systems and their
applicability to diagnosis in the Canadian context [e.g. the University of
Washington 4 Digit Diagnostic
Code (Astley, 2013; Astley & Clarren, 2000). Considerable clinical data
was reviewed to evaluate
divergence and implications of applying different diagnostic schemata
and the subjective experience of

many clinicians in the field was sought in the process of writing these
guidelines.
It is now widely accepted that the complexity of an FASD diagnosis
requires a multidisciplinary team.
As in the original 2005 guidelines, the updated guidelines (Cook et al.,
2016b) are meant to be used by
members of multidisciplinary diagnostic teams in Canada, who have
acquired the necessary expertise
and experience, to conduct a thorough medical and neurodevelopmental
FASD assessment. The
updated 2016 diagnostic guidelines for FASD will hopefully contribute
to advancing the field with the
rigor and specificity described in the full text version (Cook et al.,
2016a)
http://www.cmaj.ca/content/cmaj/suppl/2015/12/14/cmaj.141593.DC1/a
pp1.pdf (e.g., PAE; age ranges;
thresholds; direct and indirect assessment guidelines).
The authors recognize the critical importance of service provision and
support following an FASD
diagnosis, but it is important to point out that these are not part of the
diagnostic criteria – nor are they
predictive of FASD – and are addressed in other programs, including the
Canada FASD Research
Network’s online training curriculum related to diagnosis
(https://estore.canfasd.ca/).

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