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Transcript
EDITORIAL
Reactive Attachment Disorder: An Evolving Entity
Anne L. Glowinski,
T
o put into deserved perspective the contribution
that Gleason and colleagues1 make in this issue
of the Journal, theirs is one of the most extensive
validation studies to date of reactive attachment disorder (RAD). The investigators sought to validate
RAD with approaches derived from the classic 1970
article by Robins and Guze.2 The study focused
primarily on four complementary aspects of validity:
construct validity (i.e., is the current description of
RAD valid?), discriminant validity (i.e., is RAD different from other disorders?), longitudinal stability (i.e.,
is RAD stable across time?), and functional impairment (i.e., does RAD impair function as other serious
psychiatric disorders do?).
This multifaceted validation attempt is a major
step forward. A synthesis of phenomenologic and
theoretical perspectives led to the 1980 introduction of
RAD in the DSM-III.3 Clinical descriptions of infants
and toddlers exposed to severely deviant rearing
environments had long converged to recognize their
high risk for certain patterns of emotional-behavioral
outcomes, specifically a socially disinhibited/indiscriminate pattern, an inhibited/emotionally withdrawn pattern, and a pattern combining features of
social disinhibition and inhibition. RAD subtypes
were first described in the DSM-III-R in 1987.4 By
examining the validity of RAD, the study by Gleason
and colleagues1 tackles several enduring controversies: the postulation that a failure and/or absence of a normative attachment process is the
core etiologic agent for RAD; that its core
dysfunction centers around attachment, which
is more theoretical than empirical at this time
and thus controversial; the conjectural status of
RAD as a bona fide psychiatric disorder; and
whether RAD should be separated into two distinct
subtypes, which has remained preliminary.
The study uses data from the groundbreaking
Bucharest Early Intervention Project (BEIP).5 Together
with other famous studies such as the St. Petersburg
Orphanage Study,6 the BEIP has ushered in an era of
serious research on the sequelae of severe deprivation
and its mediators and moderators. Orphanages are
generally characterized by adverse physical and emotional conditions, where care by too few adults and
limited or terse emotional attention or stimulation are
normative.6 The BEIP was launched to investigate the
social-emotional-behavioral developmental trajectories and sequelae associated with early institutionalization and to examine whether foster
care could remediate or moderate the effects of
institutionalization.5
For this purpose, 187 Romanian children with a
history of institutionalization were screened for participation in a randomized study of institutional versus foster care. Extensive background health and
family-of-origin records were often unavailable; thus,
the main screening procedure consisted of a pediatric
examination to exclude children with obvious syndromes (e.g., fetal alcohol syndrome), neurologic disorders, and/or chromosomal disorders. Such exclusion has allowed a focus on children with a history of
pathogenic care but without obviously confounding
risk factors. Of the remaining 136 children, half were
randomized to continued institutionalization and the
other half to foster care. A control group of neverinstitutionalized children was also enrolled in the
BEIP. All children were assessed at baseline, when
they were 6 to 30 months of age, at 20 months on
average; children were reassessed at subsequent
follow-up waves at 30, 42, and 54 months. The assessment battery was state of the art for evaluating
toddlers and preschool-age children and included
multiple instruments to assess RAD symptoms, attachment security and/or organization, child psychiatric disorders, IQ, caretaker and care environment
quality, impulsivity, and child functional impairment.
The study used baseline and follow-up BEIP data
collected from those children initially randomized to
institutional versus foster care, but not from control
children. Journal readers might observe that the ethics
of randomizing Romanian children to continued
pathogenic care versus a hypothetical improved-care
condition are complex and, if so, may consider perusing a 2006 commentary on the topic.7
JOURNAL
210
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M.D., M.P.E.
OF THE
AMERICAN ACADEMY OF CHILD & ADOLESCENT PSYCHIATRY
VOLUME 50 NUMBER 3 MARCH 2011
EDITORIAL
The study’s most unique and important contributions to the literature are considered. First, based
on these data, the differentiation of two distinct
RAD subtypes, characterized by social inhibition
and by disinhibition, appears warranted. Second,
RAD is distinct from other better-established early
childhood disorders, with a particularly clear separation of the RAD-disinhibited subtype from
attention-deficit/hyperactivity disorder. A fascinating related subfinding is that the social impulsivity seen in the RAD-disinhibited subtype is a
phenomenon quite distinct from the pervasively
poor impulse control seen in attention-deficit/hyperactivity disorder. The RAD-inhibited subtype in
turn separates from major depressive disorder.
However, its symptoms substantially overlap with
depressive symptoms in general, and this degree of
comorbidity calls for continued prospective study
to confirm that this RAD-inhibited subtype is not a
depressive disorder. Third, RAD correlates with
child functional impairment, even after controlling
for key factors such as low IQ. As the authors note,
this rebukes the idea that an indiscriminate socialization pattern represents an adaptive set of coping
skills in children exposed to institutionalization.
Fourth, RAD is at least moderately stable over time
(e.g., there is a peak correlation of 0.49 in disinhibited RAD at from 42 to 54 months of age). Importantly, prevalence rates of the disinhibited subtype
remain very stable after 30 months, with a prevalence of 18% through 54 months, after a high of 32%
at baseline. The inhibited subtype is far less common, with a prevalence ranging from a trough of
1.6% at 42 months of age to highs of 4.6% at
baseline and 4.1% at 54 months. Because longitudinal stability was examined only in children randomized to institutional care (to minimize confounds related to changes in caretaking conditions),
this validates the enduring pathogenic nature of
orphanages but highlights a continued risk of de
novo RAD emergence through 54 months of age.
Taken together, these longitudinal results should,
ideally, have major international policy implications
because a staggering 1 million children currently live
in orphanages worldwide. Last but not least, there are
critical findings regarding the core conceptualization
of RAD. As noted previously, an RAD diagnosis has
implied disordered attachment as an etiology and as
an outcome. However, the finding that many children with disinhibited RAD show organized attachment patterns at 54 months of age further supports
the idea that placing attachment insecurity and/or
disorganization at the core of RAD is misguided. This
extends previously published BEIP results8 already
challenging attachment as a core substrate for RAD
(see Rutter et al.9 for an extensive commentary). The
study also questions another current RAD construct,
by showing that concurrent caretaking quality is
inversely associated to inhibited RAD but has a minimal relation to disinhibited RAD.
These findings should shape a research agenda to
identify novel and/or better predictors of new
and/or continued RAD. Related to improved prediction, familial aggregation, a usual hallmark of psychiatric disorders,2 was shown in 2007, when a large UK
twin study reported substantial genetic factors underlying RAD and its two presumptive subtypes.10 This
finding does not invalidate that RAD is a disorder
related to environmental deprivation, but rather that
such a concept is overly reductionistic. The idea that
genetic variations and other currently understudied
factors play a role in determining vulnerability to
RAD needs to be disseminated and investigated
further.
The related clinical take-home message is that we
should be weary of over-focusing disinhibited RAD
evaluations on attachment patterns and treatment on
current caretaking quality. Also, we must remember
the variety of risks associated with a wide range of
common child behavioral syndromes. RAD diagnoses must be made with parsimony, never reflexively,
in adopted and/or fostered patients exposed to deprivation, because these results should be measured
against the extraordinary conditions endured by orphanage children.
Regarding the DSM-V, empirical findings support
the inclusion of two distinct subtypes of socialemotional-behavioral disorders related to early
pathogenic care. Although the inhibited subtype is
possibly related to attachment, the disinhibited subtype appears to be a disorder of abnormal social
interaction in need of further research and may perhaps benefit from a name change. &
JOURNAL OF THE AMERICAN ACADEMY OF CHILD & ADOLESCENT PSYCHIATRY
VOLUME 50 NUMBER 3 MARCH 2011
Accepted December 20, 2010.
Dr. Glowinski is with the Washington University School of Medicine,
St. Louis, MO.
Disclosure: Dr. Glowinski reports no biomedical financial interests or
potential conflicts of interest.
Correspondence to: Anne L. Glowinski, M.D., M.P.E., Washington
University School of Medicine, CID Building, 4560 Clayton
Avenue, Suite 1000, Office 1125, St. Louis, MO 63110; e-mail:
[email protected]
0890-8567/$36.00/©2011 American Academy of Child and
Adolescent Psychiatry
DOI: 10.1016/j.jaac.2010.12.013
www.jaacap.org
211
GLOWINSKI
REFERENCES
1. Gleason MM, Fox NA, Drury S, et al. The validity of evidence—
derived criteria for reactive attachment disorder: indiscriminately
social/disinhibited and emotionally withdrawn/inhibited types.
J Am Acad Child Adolesc Psychiatry. 2011;50:216-231.
2. Robins E, Guze SB. Establishment of diagnostic validity in psychiatric illness: Its application to schizophrenia. Am J Psychiatry.
1970;126:983-987.
3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 3rd ed. Washington, DC: American
Psychiatric Association; 1980.
4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 3rd rev ed. Washington, DC: American
Psychiatric Association; 1987.
5. Smyke AT, Zeanah CH Jr, Fox NA, Nelson CA. A new model of
foster care for young children: the Bucharest Early Intervention
Project. Child Adolesc Psychiatr Clin North Am. 2009;18:721734.
6. The St. Petersburg–USA Orphanage Research Team. The effects
of early social-emotional and relationship experience on the
development of young orphanage children. Monogr Soc Res
Child Dev. 2008;73(3):vii-295.
7. Wassenaar DR. Commentary: ethical considerations in international research collaboration: the Bucharest Early Intervention
Project. Infant Mental Health J. 2006;27:577-580.
8. Smyke AT, Zeanah CH, Fox NA, Nelson CA, Guthrie D. Placement in foster care enhances quality of attachment among young
institutionalized children. Child Dev. 2010;81:212-223.
9. Rutter M, Kreppner J, Sonuga-Barke E. Emanuel Miller Lecture:
attachment insecurity, disinhibited attachment, and attachment
disorders: where do research findings leave the concepts? J Child
Psychol Psychiatry. 2009;50(5):529-543.
10. Minnis H, Reekie J, Young D, et al. Genetic, environmental and
gender influences on attachment disorder behaviours. Br J Psychiatry. 2007;190:490-495.
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AMERICAN ACADEMY OF CHILD & ADOLESCENT PSYCHIATRY
VOLUME 50 NUMBER 3 MARCH 2011