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Diagnosis by DSM-III-R versus ICD-10 criteria

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Journal of Autism and Developmental Disorders, VoL 22, No. 4, 1992

Pervasive Developmental Disorders:

From DSM-III to DSM-III-R 1
Lynn Waterhouse 2
Trenton State College

Lorna Wing
Medical Research Council, London

Robert Spitzer
New York State Psychiatric hTstitute

Bryna Siegel
University of California, San Francisco

The present paper provides a brief histoly of the development of the DSM-III-R
(American Psychiatric Association [APA], 1987) section on Pervasive Devel-
opmental Disorders. It describes the process by which the contents of the text
and criteria for Autistic Disorder and Pervasive Developmental Disorder Not
Otherwise Specified were decided and gives the reasons for the changes from
DSM-III (APA, 1980) categories and criteria. The paper concludes with a short
discussion of critical diagnostic issues.

1We gratefully acknowledge the valuable critical commentary on drafts of this paper provided
by Donald Cohen, Howard Demb, Deborah Fein, Michael Rutter, David Shaffer, Theodore
Shapiro, Peter Szatmari, and Fred Volkmar. Waterhouse's work on this paper was supported
by research grant MH26805 from the National Institutes of Mental Health and by research
grant NS20489 from the National Institute of NeuroLogical Disorder and Stroke. Siegel's
work on this paper was supported by NIMH MH39437 and by the John Merck Fund.
2Address all correspondence to Lynn Waterhouse, Child Behavior Study, 341 Holman Hall,
Trenton State College, Trenton, New Jersey 08650-4700.

525
0162-3257/92/1200-0525506.50 9 1992Plenum l'ublishingCorporation
526 Waterhouse el aL

Table I. DSM-III and DSM-III-R Pervasive Developmental Disorders

Diagnosis Onset Diagnostic criteria

DSM-III

Infantile autism Before 30 months Serious lack of social response

Full syndrome Gross language deficit
Residual state Bizarre features of speech
Absence of thought disorder

Childhood onset 30 months to Severely disturbed emotional

pervasive 12 years relationships
developmental 3 or more of the following:
disorder excessive anxiety;
Full syndrome inappropriate affect;
Residual state resistance to change;
oddities of motor movement;
prosodic abnormalities;
abnormal sensitivity to
sensory stimuli; self-
mutilation
Absence of thought disorder

Atypical Not specified Distortions in the development

pervasive of multiple basic psychological
developmental functions
disorder Does not meet the diagnostic
criteria for infantile autism
or childhood onset pervasive
developmental disorder
DSM-III-R

Autistic Onset during At least 8 of the following 16

disorder infancy or childhood. items are present, these to
Specify if include at least 2 items from
childhood onset A, 1 from B, and 1 from C
(after 36 months
of age). Note: Consider a criterion to
be met only if the behavior
is abnormal for the person's
developmental level.
A. Qualitative impairment in
reciprocal social interaction
as manifested by the
following: marked lack of
awareness of the existence
or feelings of others; no or
abnormal seeking of comfort
at times of distress; no or
impaired imitation; no or
abnormal social play; gross
impairment in ability to make
peer friendships
Pervasive Developmental Disorders 527

Table I. Continued
Diagnosis Onset Diagnostic criteria

B. Qualitative impairment in
verbal and nonverbal communication,
and in imaginative activity, as
manifested by the following: no
mode of communication;
markedly abnormal nonverbal
communication; absence of
imaginative activity; marked
abnormalities in the production
of speech; marked abnormalities
in the form or content of speech;
marked impairment in the ability
to initiate or sustain a conversation

C, Markedly restricted
repertoire of activities and
interests, as manifested by the
following: (a) stereotyped body
movements; persistent preoccupa-
tion with parts of objects;
marked distress over changes
in trivial aspects of environment;
unreasonable insistence on
following routines in precise
detail; markedly restricted range
of interests

Pervasive Onset not This category should be used

developmental specified when there is a qualitative
disorder not impairment in the development
otherw~.se of reciprocal social interaction
specified and of verbal and nonverbal
communication skills, but the
criteria are not met for
autistic disorder, schizophrenia
or schizotypal or schizoid
personality disorder. Some people
with this diagnosis will exhibit
a markedly restricted repertoire
of activities and interests, but
others will not.

INTRODUCTION

I n D S M - I I I - R t h e r e a r e t w o d i a g n o s e s f o r s e v e r e d e v e l o p m e n t a l dis-
o r d e r s i n v o l v i n g i m p a i r m e n t in t h e d e v e l o p m e n t o f r e c i p r o c a l social i n t e r -
528 Waterhouse et al.

action and communication skills and a markedly restricted repertoire of ac-

tivities: (a) autistic disorder (AD); and (b) pervasive developmental disor-
ders not otherwise specified (PDDNOS). In DSM-III the same range of
psychopathology was subclassified as infantile autism (IA), IA residual state,
childhood onset pervasive developmental disorder (COPDD), COPDD re-
sidual state, and atypical pervasive developmental disorder (APDD).
Table I outlines features of PDD in DSM-III and DSM-III-R. In sum-
mary there are five key changes. First, COPDD has been eliminated. Sec-
ond, the absolute criterion for AD of onset before 30 months has been
eliminated. Third, a more comprehensive developmentally organized set of
revised criteria for IA, now called Autistic Disorder, has been specified.
Fourth, APDD has been replaced with PDDNOS. Fifth, the conditions un-
der which a joint diagnosis of schizophrenia and autism can be made have
been specified, and the diagnostic boundaries of AD/PDD with other dis-
orders (mental retardation, severe language development disorder, schizo-
typal disorder) have been considered.
Waterhouse and Wing provided the initial draft of the diagnostic
criteria and text. Spitzer chaired the Advisory Committee meeting, and
coordinated the field trial of the diagnostic criteria, which has been re-
ported elsewhere (Spitzer & Siegel, 1990). Siegel provided a historical per-
spective of the committee process by reviewing the theoretical papers that
were read by the committee, letters between members, and a transcript
of the committee meeting. Although this paper attempts to portray in an
unbiased manner the thinking that guided the Advisory Committee in
making its proposals for the classification of these disorders, it should be
understood that it is not an official report of that committee. The members
of the committee were Dennis Cantwell, Donald Cohen, Howard Demb,
Martha Denckla, Deborah Fein, Rachet Gittleman-Klein, Jack Levine,
Robert Nover, Judith Rapoport, Judith Rumsey, Michael Rutter, Eric
Schopler, Robert Spitzer, A. Hussain Tuma, Fred Volkmar, Lynn Water-
house, Janet Williams, and Lorna Wing. (Also present were Robert Emde,
Stanley Greenspan, Klaus Minde, and Sally Provence, who were working
on the reformulation of Reactive Attachment Disorder of Infancy.)
A draft of this paper has been circulated to all committee members and
we have worked to incorporate their commentary and perspectives on the proc-
ess. However, this paper represents our views and is not committee consensus.

WORK OF THE ADVISORY COMMITTEE

The first effort at reformulating the DSM-III criteria for the PDD
section was made on September 11, 1984, at an ad hoc meeting sponsored
Pervasive Developmental Disorders 529

by the Work Group to Revise DSM-III and the Clinical Research Branch
of the National Institute of Mental Health. The meeting was organized by
Spitzer with the help of Cantwell, Denckla, and Rapoport.
Prior to this meeting, papers on classification, published and unpub-
lished, were circulated within the group. During the discussion at this meet-
ing nine areas were seen as presenting important problems: (a) clinical
features of AD; (b) effects of development on AD symptom presentation;
(c) age at onset of AD; (d) validity of COPDD; (e) meaning of APDD;
(f) subgroups within PDD; (g) differential diagnosis; (h) IQ and adaptive
functioning; and, (i) organic etiology. The group's consideration of each of
these nine issues and the reasons for the decisions that were made are
presented below.
The structure of the discussion of these issues here is tripartite: first
Advisory Committee concerns are outlined, then reasons for decisions are
delineated, and finally, the implementation of decisions is explicated. It is
important to note that while the Advisory Committee concerns presented
here represent the full range of the issues addressed by that group, the
reasons for decisions considered herein represent our own selection of ra-
tionales. These were selected from positions introduced at the meeting and
from those outlined in letters written to Spitzer. It is also important to
note that the implementation of decisions described here was an incre-
mental process which began with the Advisory Committee and ended with
the work of a subgroup: Cohen, Spitzer, Waterhouse, and Wing.

Clinical Features of AD

Advisory Committee Concerns

Prior to the Advisory Committee meeting, criticism of the DSM-III

IA criteria and PDD subgroups had been expressed by 20 clinicians en-
gaged in research in child psychiatry who were surveyed for a formal evalu-
ation of the DSM-III PDD section (Waterhouse, Fein, Nath, & Snyder,
1987). A meeting of PDD researchers organized by Denckla in the Spring
of 1984 at NINCDS generated concerns regarding the DSM-III PDD sec-
tion and in particular, the IA criteria (Denckla, 1986). At the Advisory
Committee meeting, many group members expressed the belief that greater
detail in description in the specific diagnostic criteria for IA (now AD)
would aid in clinical evaluation, and increase sampling replicability in re-
search.
530 Waterhouse~aL

Reasons for Decisions

Wing and Gould (1979) had formulated a triad of impairments--in

social relatedness, in all modes of communication, and in imagination--
necessary for a diagnosis of autism. In their model, repetitive and stereo-
typic behaviors occur in the absence of, and represent the obverse of, the
normal development of imaginative abilities. Data from Wing & Gould's
(1979) epidemiological study had suggested that impaired social relatedness
and social communication were key features for classification because they
marked a group of individuals distinct from those who were mentally re-
tarded but sociable.
As these findings were in line with results from other research and
clinical work, the Advisory Committee decided that classification should
be based on three core symptom areas: (a) qualitative impairment in re-
ciprocal social interaction; (b) qualitative impairment in verbal and non-
verbal communication and imaginative activity; and, (c) the presence of a
restricted repertoire of activities.

Implementation of Decisions

Criteria for each of the three symptom areas were sketched by the
Advisory Committee at the meeting, but the detailed working out was done
by Wing and Spitzer. The first draft included 21 specific c r i t e r i a - - 7 in
each area. In later drafts, the number of symptoms was reduced to 16, with
some items aggregated with other closely related ones. For example, pro-
nomial reversal, idiosyncratic word use, and repetitive language were in-
itially separated but were later merged into a single criterion. The decision
to merge symptoms was based on clinical judgment of functional similarity
of symptoms. An empirical study of symptom distribution comparing the
original draft symptom set with the final merged symptom set in a sample
of 240 PDD children has been conducted (Morris, 1988) with a detailed
analysis to be reported (L. Waterhouse et al., in preparation).
A cross-national multisite field trial was carried out (Spitzer & Siegel,
1990). Spitzer, Cohen, and Waterhouse analyzed the results and found high
specificity and sensitivity if a minimum of 8 of the 16 criteria were rated
as present, including at least 2 items concerning impaired social relatedness,
at least 1 concerning impaired social communication and imagination, and
1 concerning repetitive and stereotyped behaviors. Requiring 8 out of 16
symptoms with a base of four criteria spread across three symptom domains
gave a high level of agreement with clinicians' diagnoses of Autistic Dis-
order.
Pervasive Developmental Disorders 531

By June 1985, the draft of the DSM-III-R criteria for AD had been
successively revised, behavioral examples suggested and added, and was es-
sentially complete. An initial draft of the text for the PDD section which
was revised and published in the DSM-III-R manual was prepared by Wa-
terhouse. The DSM-III-R criteria for AD represent a reorganization and
elaboration of DSM-III criteria that reflect a return to the criteria of Kan-
ner's (1943) original case study descriptive accounts of impaired sociability,
impaired social communication, and the presence of stereotypies or repeti-
tive behaviors.

Effects of Development on Autistic Disorder Symptom Presentation

Advisory Committee Concerns

A central issue of the discussion at the meeting, introduced by Wing,

was the differential expression of symptoms over the course of develop-
ment. She proposed rating symptoms only if they were abnormal for de-
velopmental level. The group accepted Wing's proposal, and it was
therefore decided that each diagnostic criterion would be judged taking
into account the patient's mental age, although the method for ascertaining
mental age was not circumscribed. The desirability of rating adaptive func-
tioning was considered and was judged to be of potential value as an ad-
junct to diagnosis but not necessary for establishing a diagnosis.

Reasons for Decisions

There are two issues involved in consideration of the influence of

developmental changes on symptomatology. First, many autistic-like behav-
iors are exhibited by very young normal children in the course of develop-
ment. A normal 2-year-old might be echolalic. Imaginative play does not
normally emerge until around 18 months. Therefore as diagnostic criteria
for AD are meant to index impairment or abnormality, they should be
coded as such only when inappropriate for mental age. Second, as the ex-
pression of impairment or abnormality in AD often changes across devel-
opment (DeMyer, Hingtgen, & Jackson, 1981; Kanner, 1949; Morris, 1988),
it is important to specify diagnostic criteria that span the range of devel-
opment and capture key aspects of symptom variation.
532 Waterhouse et al.

Implementation of Decisions

Within each of the three symptom areas, the items are arranged in
order of probable developmental sequence (Wing, 1985, 1987). This occurs
in two ways nested within the criteria. First, for each specific item, the
examples are arranged in developmental sequence. For example, the third
item of the first symptom category is "no or impaired imitation." This item
is illustrated by the following: "does not wave bye-bye; does not copy
mother's domestic activities; mechanical imitation of others' actions out of
context." A younger or more developmentally impaired child may fail to
wave goodbye, a teenager or adult may express impaired imitation by the
mechanical copying of another's behavior in an inappropriate context.
Second, across the list of items for each of the three symptom areas
there is a developmental sequence implied. Within the first symptom area
for example, Item 1, "marked lack of the awareness of feelings in others"
may be developmentally earlier than Item 5, "gross impairment in the abil-
ity to make peer friendships." These sequences are not intended, however,
to suggest that there is an implicit uniform developmental sequence within
AD or PDD, nor are these orderings intended to index a Guttman scaling
(cumulative and subsumptive progression) of the severity or absolute num-
ber of symptoms. The developmental framework of the AD criteria is in-
tended to aid clinical description and diagnosis.

Age at Onset of Autistic Disorder

Advisoly Committee Concerns

In DSM-III, age of onset had been a major part of the differential

diagnosis of IA and COPDD as the diagnosis of IA could not be made if
the age of onset was determined to be after 30 months.
Rutter pointed out that the issue is not the age of onset of autistic
symptoms as such, but whether there has been a period of unambiguously
normal development that extends up to age 3 years. If the age differentia-
tion is excluded from the diagnostic criteria, Rutter had noted that re-
searchers lose the opportunity of studying different groups which may have
different etiologies. Emphasizing the importance of age of onset may have
the advantage of encouraging clinicians to give special attention to obtain
a careful developmental history. Furthermore, excluding age of onset as a
diagnostic criterion leads to overlooking the disintegrative disorders.
Wing disagreed that eliminating age at onset would discourage re-
search into etiology. She argued that acknowledging the similarity of the
Pervasive Developmental Disorders 533

basic autistic syndrome regardless of age of onset should encourage re-

searchers to study questions of etiology, as has been the case with the con-
cept of mental retardation, which is defined descriptively, regardless of
whether it has its onset at birth or at some later stage prior to full devel-
opment.
After much discussion, two proposals were considered. The first
proposal was that AD would require onset prior to 3 years of age. Even
if an identical clinical picture developed after 3 years, a different diag-
nosis would have to be given. The majority of the group supported this
proposal. A second proposal was that the same diagnosis could be given
regardless of the age of onset, but that the diagnosis would be further
qualified as either infantile onset or childhood onset (after 3 years) or
not known. This latter proposal, since it did allow for distinguishing age
at onset, was supported unanimously. (In the final DSM-III-R, the clas-
sification notes that when onset is after 3 years, it should be further
qualified as "childhood onset.")

Reasons for Decision

Research findings suggest three arguments for preserving the require-

ment of onset of symptoms before 30 or 36 months of age.
The first argument posits that as most children with AD symptoma-
tology have shown aberrant behaviors before 30 or 36 months (Volkmar,
Stier, & Cohen, 1985; Waterhouse, Fein, et al., 1987; Wing, 1988), there-
fore, the criterion should be established as a fixed syndrome boundary. But,
as Widiger, Hurt, Frances, Clarkin, and Gilmore (1984) and others (Meehl,
1986) have argued, fixed boundaries introduce the possibility of excluding
positive cases from diagnosis. Past clinical practice, in fact, has been marked
by underdiagnosis of AD and PDD, rather than the too liberal application
of these categories (Wing, Yeates, Briefly, & Gould, 1976). Many parents
have difficulty in recalling and describing the details of their child's early
development. When cases present for the first time in adult life there may
be no one available to give information concerning the individual's infancy
and childhood.
The second argument claims that, as later onset may be associated
with milder symptomatology (Rutter & Schopler, 1988; Wing, 1988),
later onset cases should not be diagnosed as having AD. Milder symp-
tomatology - - of the same symptom s e t - - h o w e v e r , does not argue for
a fixed onset boundary unless it is clearly associated with a differentiable
set of risk factors. This has not yet been determined for the Ad/PDD
diagnoses. In the absence of a clear bimodal assorting of risk factors
534 Waterhouse~aL

for more severe versus more mild cases, the presence of a grading of
behavioral severity of the same symptom set argues for a neurodevelop-
mental spectrum approach to PDD in general (Waterhouse, Wing, &
Fein, 1989; Wing, 1988).
The third argument for preserving age of onset as a fixed boundary
is that late onset AD cases are likely to be the result of organic etiology
(Kolvin, 1971; Rutter, 1988). Rutter and Schopler (1988) stated that
"Occasional cases of autistic-like disorders do occur after the age of
three but they are rare and usually due to acquired brain disease or
genetic disorders of later manifestation such as cerebral lipoidoses. For
the moment it seems useful to separate those late onset conditions from
'classic' "autism" (p. 412). Cohen, Paul, and Volkmar (1987) have sug-
gested a tripartite division of Axis III of the DSM wherein the presence
of symptoms suggestive of CNS disorder be catalogued as either (a) idi-
opathic (no CNS signs or symptoms present), or (b) stigmatic (associated
with significant but nondiagnostic CNS factors), or (c) syndromic (sign
and symptoms are related to a recognized CNS disturbance) (1987, p.
25). If used in research this might lead to a better understanding of the
relationship of onset, symptomatology, and life course found for PDD.
At present, however, there is not enough evidence to argue con-
clusively that later onset disorders are associated with a distinct subset
of etiological agents (Ornitz & Ritvo, 1976; Prior & Werry, 1986). Evi-
dence for "organic" etiology appears at all reported points of onset, and
etiology also appears to be mixed for samples at all reported points of
onset (Coleman & Gillberg, 1985). As it is increasingly clear that all
children diagnosed as having AD or PDDNOS have neurological dys-
function stemming from a wide variety of etiological agents, it seems
that requirement of a fixed onset boundary would not specifically elimi-
nate any of the possible specific organic causes of these disorders. In
fact, many severe organic insults occur prenatally but their effects unfold
developmentally in variations dependent on type, locus, and severity of
the insult as well as on genotypic individual variability in brain structure,
function, and maturation patterns.

Implementation of Dec&ions

In DSM-III-R age at onset is not a criteria for AD as it was in DSM-

III for IA. In DSM-II1-R if onset is determined to be after 36 months, the
AD diagnosis should be specified as "childhood onset."
Pervasive Developmental Disorders 535

Validity of Childhood Onset Pervasive Development Disorders

Advisory Committee Concerns

Although research had not provided definitive evidence that COPDD

was an invalid or null category, it was the consensus of committee members
and P D D researchers surveyed (Waterhouse, Fein, et al., 1987) that
C O P D D was not a clinically useful concept. Therefore, the committee's
decision was to eliminate this category. A portion of the COPDD diagnostic
criteria have been subsumed as criteria for AD: disturbed emotional be-
havior (COPDD, AI); resistance to change (COPDD, B3); stereotypies
(COPDD, B4); prosodic impairment (COPDD, B5). Another portion has
been listed in the text under the discussion of associated features of AD:
excessive anxiety (COPDD, B1); inappropriate affect (COPDD, B2); ab-
normal sensitivity to sensory stimuli (COPDD, B6); self-injurious behavior
(COPDD, B7).

Reasons for Decision

There are two arguments supporting the elimination of COPDD: Few

cases are found and those given this classification cannot be distinguished
from AD, apart from reported age of onset.
Both clinical practice and empirical research (Cohen, Paul, & Volk-
mar, 1986; Morris, 1988; Waterhouse, Fein, et al, 1987; Wing, 1988) have
suggested that children diagnosed as COPDD represent a small fraction
of any PDD population. Green et al. (1984) reported that their clinic had
seen only one child diagnosable as COPDD in 5 years. More recently Mor-
ris (1988) has reported that in a PDD sample of nearly 200 children, fewer
than 3% were diagnosable as COPDD.
In clinical practice and in research studies, those individuals diag-
nosed as having COPDD included (a) children who met criteria for DSM-
III IA except for the criterion of onset to be reported before 30 months,
and (b) children who exhibited a mild expression of IA symptomatology
or a limited set of IA symptomatology (Provence & Dahl, 1987). These
variations do not argue for a separate syndrome definition but are more
appropriately captured either as part of AD itself or as part of a remainder
category (PDDNOS). Dahl, Cohen, & Provence (1986) were unable to dis-
tinguish COPDD from the autistic spectrum using cluster analytic methods.
In a study of 274 preschool children, Rescorta (1986) found that distin-
guishing COPDD from AD was extremely difficult.
536 WaterhouseaaL

A related problem in DSM-III was that the fixed upper boundary of

onset for IA (30 months) was the lower boundary of COPDD. Thus a di-
agnosis based on problematic onset data would lead to false negative cases
of IA and simultaneously to false positive cases of COPDD. Furthermore,
if two children had nearly identical symptomatology, a 1-month difference
in reported onset would mean that one child had IA and the other
COPDD.
More important, the distribution of requisite diagnostic symptomatol-
ogy between IA and COPDD in DSM-III is not consonant with clinical
experience. Wing (1988) has argued that IA and COPDD divide diagnostic
criteria, all of which appropriately belongs to autistic spectrum disorders.
She cites as an example the fact that in DSM-III IA has echolalia as a
criterion, while COPDD has abnormal movements such as tiptoe walking
as a criterion, although both are seen in cases of IA. Rutter (1988) has
also argued that the COPDD criteria are not "satisfactory."
In fact, COPDD appears to be an artifact of a process of creating a
tight system for diagnosis where coverage for post-30 months onset was
needed. COPDD has no history under that name and has been interpreted
in a wide variety of ways by researchers and clinicians to reflect a range
of previously outlined syndromes such as childhood schizophrenia, mild
atypical disorder, high-functioning autism, late onset autism, and early on-
set psychosis (Waterhouse, Fein, et al, 1987).

Implementation of Decisions

In sum, as both research findings and clinical experience suggest that

the problems in the concept of COPDD far outweigh its possible clinical
or research usefulness, COPDD was eliminated as a diagnostic classifica-
tion.

Meaning of Atypical Pervasive Developmental Disorder

Advisory Committee Concerns

There were three concerns with APDD. First, the label "atypical" was
seen as problematic because it carried associations with Rank's (1949)
"atypical personality development." Second, the APDD diagnostic category
had been intended as a remainder category, but the label "atypical" sug-
gested that the diagnosis would generate a more cohesive phenomenology
than that of a remainder category. Finally, a structural concern was that
Pervasive Developmental Disorders 537

remainder categories across DSM-III-R should carry parallel labels. There-

fore APDD became PDDNOS: PDD not otherwise specified.

Reasons for Decision

Although it is of value to have a diagnostic remainder category clearly

indexed as such, a label does not confer phenomenological clarity, and the
presence of individuals in this remainder category remains a problem for
research. Sparrow et al. (1986) suggested that PDDNOS has many symp-
toms in common with AD. Waterhouse and Fein (1984) also found that
children who would meet criteria for PDDNOS but not AD followed a
developmental course similar to that found in those classified as AD. This
similarity of developmental pattern for AD and PDDNOS cases, and symp-
tom congruity, suggests that the remainder category may be capturing many
individuals whose clinical picture and development are not significantly dis-
tinct from those of individuals diagnosed as having AD.
Another problem is that establishing a central diagnosis (AD) and re-
mainder diagnosis (PDDNOS) tacitly implies that all clinical phenomenology
has been accounted for within this diagnostic framework (D. Shaffer, personal
communication 1989). This is unlikely to be the case. Future research may
reveal other currently unknown aspects of the phenomenology as well as un-
cover biological markers which in turn may suggest new ideas on classification.
Despite these difficulties a majority of the Advisory Committee mem-
bers considered that AD should be defined more narrowly than the full
range of PDD. As it was also d e c i d e d - - f o r reasons discussed in the fol-
lowing s e c t i o n - - n o t to delineate other subgroups of PDD, therefore all
PDD not classified as AD is categorized as PDDNOS.

Implementation of Dec&ions

In DSM-III-R APDD becomes PDDNOS. This change eliminates as-

sociation problems with the "atypical" label, and establishes a remainder cate-
gory label congruent with the other remainder category labels in DSM-III-R.

Subgroups Within Pervasive Development Disorder

Advisory Committee Concerns

There was much discussion about possible subgroups within the autis-
tic spectrum and a great deal of disagreement about nosology. However,
538 Waterhouse~aL

there was consensus that subgroups probably existed. The possible inclusion
of Asperger syndrome (Asperger, 1944) as a milder, high-functioning, later
onset PDD syndrome was considered. The possible inclusion of disintegra-
tive psychosis as a later onset PDD syndrome with associated neural de-
generation over life course was also considered. There was a lack of
consensus about which subgroups could be reliably delineated, and the de-
cision was made to adopt only one diagnostic category: AD.

Reasons for Decision

In establishing only one diagnosis (AD) and a remainder category

(PDDNOS), DSM-III-R is clearly underspecifying possible syndromes.
However research evidence and diagnostic models for proposed subgroups
other than Autistic Disorder were deemed inadequate at present.
In fact, conceptualization and identification of valid subgroups poses
two initial problems: What is the larger "metadiagnostic" domain from
which the subgroups are drawn? And what is the basis (etiology, neuro-
logical deficit, behavioral phenomenology) on which the subgroups are to
be discriminated?
Historically there have been subgrouping debates which conceptual-
ized the metadiagnostic domain quite differently than is now done. In ear-
lier views, the key subgrouping issue was the relationship between autism
and childhood schizophrenia. For example, it has been argued that autism
and childhood schizophrenia are polar variants of a single generalized
sphere of deficit (Ornitz & Ritvo, 1976). The Group for the Advancement
Psychiatry (GAP; 1966) diagnostic system supported a distinction between
autism and childhood schizophrenia (Table II), but DSM-II (APA, 1968)
offered only the diagnosis "childhood schizophrenia" and did not include
the label autism as a separate diagnosis: Thus autism and childhood schizo-
phrenia were not differentiable within the bounds of its classification. Al-
though concern for understanding the nature of childhood schizophrenia
per se has persisted (Cantor, 1988), the metadomain encompassing Autistic
Disorder (i.e., PDD) excludes thought disorder and therefore excludes
childhood schizophrenia.
At present PDD is inadequately described. Though most Advisory
Committee members believed that early developmental emergence of im-
pairment in social functioning and communication (in the absence of iden-
tified thought disorder) characterized the autistic spectrum of disorders
currently captured as PDD, most members were dissatisfied with the fuzzy
boundaries of this spectrum.
Pervasive Developmental Disorders 539

Table II. Diagnostic Classification of Severe Childhood Psychopathology

ICD-9 (1977)

299 Psychoses with origin specific to childhood

299.0 Infantile autism (=childhood autism, infantile psychosis, Kanner's syndrome)
299.1 Disintegrative psychosis (=Heller's syndrome)
299.8 Other (=atypical childhood psychosis)
299.9 Unspecified (=child psychosis NOS, childhood schizophernia NOS) (excludes
schiz, of adult type occurring in childhood)

ICD-10 (1989)

F84 Pervasive developmental disorders

F84.0 Childhood autism
F84.1 Atypical autism
F84.2 Rett syndrome
F84.3 Other childhood disintegrative disorder
F84.4 Overactive disorder associated with mental retardation and stereotyped movements
F84.5 Asperger syndrome

DSM-II (1968)

295.8 Schizophrenia, childhood type

GAP (1970)

Psychotic disorders
a. psychoses of infancy and early childhood
1. early infantile autism
2~ interactional psychotic disorder (symbiotic)
3. other psychosis of infancy and early childhood

b. psychoses of later childhood

1. schizophreniform psychotic disorder
2. other psychosis of later childhood

c. psychoses of adolescence
1. acute confusional state
2. schizophrenic disorder, adult type
3. other psychosis of adolescence

DSM-III (1980)

Pervasive developmental disorders

299.0x Infantile autism (full syndrome or residual)
299.9x Childhood onset pervasive developmental disorder (full syndrome or residual)
299.8x Atypical pervasive developmental disorder
Adult-type schizophrenia with onset in childhood

DSM-III-R (1987)

Pervasive developmental disorders

299.00 Autistic disorder
299.80 Pervasive developmental disorder-not otherwise specified
540 WaterhouseaaL

The second major problem in selecting subgroups of PDD (such as

Asperger, Rett syndrome, or other) for inclusion in a classification system
is that many subgroups that have been proposed have been defined on a
mixed basis (genetic, neurological deficit, behavioral), and the mixtures are
not the same across subgroups proposed.
Fragile X, for example, is a disorder defined by the presence of an
observable fragile site on the X chromosome. A significant subset of indi-
viduals positive for fragile X are diagnosable as having AD; another subset
of fragile X individuals are diagnosable as PDDNOS. Thus a fragile X sub-
group of AD could be defined on the basis of specified observable chro-
mosome damage in conjunction with AD symptomatology. At the same
time, another group of fragile X positive individuals could be defined as
a subgroup of PDDNOS.
As can be seen in Table II, the current ICD-10 draft for PDD iden-
tifies six subgroups. The six subgroups are (a) Rett syndrome; (b) other
childhood disintegrative disorder; (c) childhood autism; (c) Asperger syn-
drome; and two new subgroups, not previously included in any classification
system, (e) atypical autism, and (f) overactive disorder associated with men-
tal retardation and stereotyped movements.
Although all six subgroups are behaviorally defined within ICD-10,
there are implicit differences in the basis for identifying at least two of the
six subgroups proposed. First, Rett syndrome is defined as a genetic dis-
o r d e r - - i n d e p e n d e n t of its definition as a subgroup of PDD in ICD-10.
There are Rett syndrome cases with autistic-like (i.e., PDD) symptomatol-
ogy, and Rett syndrome cases without autistic-like symptomatology. There-
fore, if the intersection of Rett syndrome features with PDD behaviors is
defined as a subgroup of PDD, should not a fragile X subgroup be defined
as well? Of course the presence of those two subgroups within PDD would
suggest an additional internal axis for diagnosis.
The second ICD-10 subgroup that raises problems for comparability
of subgroups is Other Childhood Disintegrative Disorder which carries
course features that imply the presence o f neurological deficit. Albeit a
current working assumption of the field is that all PDD subgroups describe
phenomenology attributable to neurological deficit, nonetheless, the special
implication of disintegrative course marks a separate distinguishable basis
for subgroup formation.
Identifiable subgroups are beginning to emerge at all levels of analy-
sis, but most~ of the range of PDD phenomena cannot yet be reliably and
validly subclassifiedr It can be argued that mixing these different levels in
a classification system t~resents difficulties for both research and clinical
practice because they are~not mutually exclusive. For example, a Rett's case
will follow a disintegrative course, and may express behavior which would
Pervasive Developmental Disorders 541

permit a diagnosis of either childhood autism or atypical autism: As such,

one case could conceivably support four ICD-10 PDD diagnoses. More gen-
erally, another problem arises from the reality that overt behavior patterns
can vary independently of the underlying etiology.
It has been argued that the DSM-III section on PDD created prob-
lems expressly because there were too many ill-validated and unreliable
diagnostic distinctions (Gould, Shaffer, Rutter, & Sturge, 1988; Quay, 1985;
Waterhouse, Fein, et al, 1987; Werry, 1985). ICD-10 has gone in the di-
rection of expanding the list of possible subgroups. DSM-III-R has gone
in the opposite direction of a more unitary conceptualization of one core
behaviorally defined syndrome (AD) within the broad category of PDD
(despite recent advances in the identification of specific etiologies, such as
Rett syndrome and fragile X). In the present state of knowledge, each of
these solutions has advantages and disadvantages.
A way of resolving the problems arising from the mixed basis for sub-
group formation that may become possible with future advances in research
is to specify subsyndromes of AD/PDD on the basis of clinically significant
and empirically determined associations between etiology, neurological
deficits, and behavioral features of subsyndromes (Fein, Pennington, Mark-
owitz, Braverman, & Waterhouse, 1986; Rescorla, 1988; Siegel, Anders,
Ciaranello, Bienenstock, & Kraemer, 1986; Waterhouse et al., 1989).

Implementation of Decisions

DSM-III-R outlines only AD within the PDD spectrum. AD is de-

fined as a behavioral syndrome. It is assumed that AD may be associated
with a wide range of etiologies, as well as a wide range of neurological
deficits, and is therefore not a "disease" entity.

Differential Diagnosis

Advisory Committee Concerns

Committee members raised questions about differential diagnosis in

four cases: (a) AD and mental retardation (MR); (b) AD and schizophrenia
that first develops in childhood; (c) AD and reactive attachment disorder
of infancy; and (d) AD and residual states of AD. For the first three cases,
the decision was made to include a discussion of the difficulties inherent
in differential diagnosis in the DSM-III-R PDD text, and to provide for
hierarchical positioning of the diagnosis of AD in relation to those disor-
ders.
542 Waterhouse~aL

The committee members expressed dissatisfaction with the DSM-III

"residual state" category. Rapoport argued that even though an individual
originally diagnosed as having AD might undergo changes in form and de-
gree of social impairment, this did not mean that the individual was really
in a residual state of the disorder, but rather that the symptoms of AD
had evolved into another form. Committee members agreed and it was de-
cided that the category "residual state" would be eliminated in DSM-III-R.

Reasons for Decisions

Standardizing rules concerning the hierarchy of assignment of diag-

noses is necessary for a system of classification such as DSM, but, of course,
does not resolve the empirical questions that remain: Given the presence
of multiply assignable symptomatotogy in individuals with severe develop-
mental disorders, what are the most valid distinct syndromes; and, what is
the biological significance in regard to neural development of the overlap
of symptom sets?
It has been argued that "there is no doubt that autism constitutes a
valid and meaningfully distinct psychiatric syndrome; indeed the evidence
on its validity is stronger than for any other psychiatric condition in child-
hood" (Rutter & Schopler, 1988, p. 411). However, it has also been argued
that (a) autism is a man-made syndrome (Tanguay, 1984); (b) that there
are serious boundary problems for AD versus PDDNOS and versus other
disorders (Waterhouse, Fein, et al, 1987; Waterhouse et al., 1989); and (c)
that the utility, validity, and syndrome distinction (of AD) have yet to be
established (Prior & Werry, 1986). It is clear that the "internal" relationship
of AD to PDDNOS and to other possible subgroups within the PDD spec-
trum (Cohen et al., 1986; Szatmari, Bartolucci, & Bremner, 1989; Wing,
1981), and the "external" relationship of AD to MR (Freeman et al., 1981;
Waterhouse et al., 1989), of AD to severe language disorders (Cohen, Ca-
parullo, & Shaywitz, 1977; Paul & Cohen, 1984; Prizant, 1988; Rapin,
1987), and of AD to schizophrenia with onset in childhood (Creak, 1963;
Creak et al., 1961; Goldfarb, 1964; Petty, Ornitz, Michelman, & Zimmer-
man, 1984; Tanguay & Cantor, 1986) remain important unresolved issues
for future research.
The greatest increase in new data concerning AD and PDD has been
the firmer establishment of these disorders as a behavioral expression of
a neurodevelopmental deficit (Fein, Humes, Kaplan, Lucci, & Waterhouse,
1984; Golden, 1987; Maurer & Damasio, 1982; Rapin, 1987). Unfortunately
the increasing understanding of the range of neurological deficits associated
with AD and PDD has not led to increased diagnostic clarity.
Pervasive Developmental Disorders 543

Implementation of Decisions

In DSM-III-R some of the pragmatic questions of possible concurrent

diagnoses of AD and other disorders are resolved by proscribing preemp-
tive relationships. The diagnoses of Schizoid and Schizotypal personality
disorders (in which there are deficits in interpersonal relatedness) are
preempted by a diagnosis of AD. A diagnosis of Reactive Attachment Dis-
order of Infancy or Early Childhood is preempted by a diagnosis of either
AD or PDDNOS. Diagnosis of either AD or PDDNOS also preempts di-
agnoses of Developmental and Receptive Language Disorders and Atten-
tion Deficit Hyperactivity Disorder.
AD/PDDNOS diagnoses, however, do not preempt diagnosis of Men-
tal R e t a r d a t i o n . Individuals who meet criteria for MR and AD or
PDDNOS are to be given both diagnoses. The diagnosis of Schizophrenia
with onset in childhood preempts a diagnosis of PDDNOS but does not
preempt a diagnosis of AD. Individuals diagnosed as having AD who show
clear evidence of delusions or hallucinations are to be given the additional
diagnosis of Schizophrenia.
Finally, in DSM-III-R, the residual state diagnosis was eliminated.

IQ and Level of Adaptive Functioning

Advisoly Committee Concerns

Spitzer questioned whether some level of intellectual or adaptive

functioning should be included as a diagnostic criterion for the PDD di-
agnoses. The committee agreed that knowledge of the level of the individ-
ual's cognitive functioning was important, but that it was not crucial for
diagnosis. The committee also decided that there should be no minimal
cutoff IQ for diagnosing AD or PDDNOS, but that degree of mental re-
tardation (mild, moderate, severe, profound, or unspecified) should always
be included in the clinical diagnosis of AD and PDDNOS. The committee
further decided that adaptive functioning-- independent of cognitive func-
t i o n i n g - m i g h t be indexed as an adjunct of diagnosis but was not crucial
for diagnosis.
Related to this issue the committee debated whether autism should
be identified as an Axis I or Axis II disorder, and it was agreed that PDD
(AD and PDDNOS) should be an Axis II disorder.
544 WaterhouseaaL

Reasons for Decisions

It has been argued that there may be two subgroups of AD based

on I Q - - b e l o w IQ of 70 and above IQ of 70 (Prior, 1979; Rutter, 1983).
And it has further been argued that those with AD whose IQs are above
70 express the syndrome of autism in "a 'pure' form, not associated with
mental retardation" (Rutter, 1983, p. 521). If a specific IQ cutoff would
form two distinct subgroups of AD, then logically IQ level should not be
coded as part of a separate diagnosis on the same Axis (as in MR) but
should be included in the diagnostic criteria of AD directly, for the for-
mation of two diagnostic subgroups of AD. The former subgroup would
have a double diagnosis: AD and MR; the latter would have the single
diagnosis of AD. If, however, IQ is understood as a continuum of cognitive
functioning expressed against a relatively fixed set of behavioral impair-
ments in PDD then it would be best to have it coded separately (Water-
house, Fein, et al., 1987).
A further problem rests in the use of the diagnostic label Mental Re-
tardation. MR represents two things: a syndrome label for diagnosing in-
dividuals who have a range of developmental delays and impairments
without severe impairment in social relatedness; and a term to index level
of cognitive functioning in individuals who have met criteria for other di-
agnoses. The first is the Axis II syndrome; the second is what the Axis II
MR severity subgroups (mild, moderate, etc.) mean when used in conjunc-
tion with diagnosis of PDD and other disorders.

Implementation of Decisions

In DSM-III-R, individuals can be diagnosed as AD or AD and MR.

Within the MR (Axis II) diagnosis, an individual's level of functioning can
be coded for degree of severity.

Organic Etiology

Advisory Committee Concerns

Spitzer questioned whether it might not be of value to include some

information concerning etiology of AD and PDDNOS cases. As with the
issue of level of IQ and adaptive functioning, the committee felt such in-
formation was important but not crucial for diagnosis, as diagnosis depends
on behavioral manifestations of symptoms regardless of etiology. Therefore
it was decided that while knowledge of putative or possible etiology of AD
Pervasive Developmental Disorders 545

or PDDNOS was important for chart information, it was not a key element
in the diagnosis.

Reasons for Decisions

More information concerning the links between specific etiologies and

the associated behavioral manifestations is being uncovered. Studies of the
fragile X syndrome, studies of multiplex families, and studies of infectious
etiologies associated with the AD or PDDNOS behavioral diagnostic pat-
tern suggest that there will be bases on which to differentiate to some de-
gree those behaviors which tend to aggregate with one syndrome versus
another. This may lead, however, not to a new set of clearly distinct be-
havioral syndromes but to a new method of diagnosis--PDD/Rett form,
PDD/Fra(X) form, and so o n - - i n which the general notion of social im-
pairment, impaired communication, and presence of stereotypies and re-
petitive behaviors is seen as varying in small but specific ways in association
with the differing etiologies.
In such a future diagnostic system, the phenomenology of PDD might
have general boundaries and a general core dysfunction (as social impair-
ment), but etiological or neural system dysfunction variants of the general
PDD pattern could be marked as distinct. Nevertheless, it is necessary to
note that the specific etiologies identified to date as significantly often oc-
curring with autistic-type conditions can all be associated with different de-
grees of severity and different patterns of symptoms within the range of
PDD and, in most eases, with non-autistic-type disorders or even with nor-
mal intelligence and behavior. Much work is still needed to identify for
certain the phenomena that are specific to particular causes.

Implementation of Decisions Concerning Organic Etiology

In the DSM-.III-R PDD diagnoses there is no formal mechanism for

coding type of organic etiology, or for specifying the presence of evidence
for organic etiology.

CONCLUSIONS

Effectively, taken together, three of the five changes in DSM-III-R

--eliminating COPDD, eliminating age at onset for AD, and revision of
the AD criteria--will increase the number of children receiving the diag-
nosis of AD as compared with the number of children who received a di-
546 Waterhouse~aL

agnosis of IA in DSM-III. This has already been shown to be the case

(Hertzig, Snow, New, & Shapiro, 1990; Spitzer & Siegel, 1990; Szatmari,
1989; Volkmar, Bregman, Cohen, & Cicchetti, 1988).
However, as already noted, findings from the national field trial for
PDD (Spitzer & Siegel, 1990) and from a study of 500 children with severe
developmental disorders (220 of whom received diagnoses of AD or
PDDNOS) (Morris, 1988; Waterhouse, Wing, Allen, Fein, & Rapin, 1987)
indicate that clinicians' direct interview judgment of the presence of autism
is consonant with the DSM-III-R AD criteria. This suggests that clinicians
would diagnose a child as having autism whose specific behaviors might
have supported a diagnosis of COPDD or APDD in DSM-III.
Still another issue is the character and structure of the set of 16 cri-
teria for AD. First, clinical interpretation of symptoms across development
remains open to variation (Hertzig et al., 1990). Second, there is formal
diagnostic redundancy in criterial symptoms which nonetheless provide dis-
tinctly different pictures of behaviors for clinicians (Siegel, Vukicevic, EI-
liott, & Kraemer, 1989). These two problems, of course, were also inherent
in the DSM-III criteria.
For clinicians who believe that the DSM-III criteria for IA are a valid
index of a real underlying disorder (Rutter & Shaffer, 1980; Rutter &
Schopler, 1988), the DSM-III-R changes may appear problematic in that
the risk of false positive diagnoses for AD may be increased. However, it
is unlikely from present evidence that the DSM-III criteria have captured
the phenomenology with the greatest accuracy (Cohen et al., 1986; Prior
& Werry, 1986; Waterhouse, Fein, et al, 1987). Furthermore, it is as yet
unclear that there is a single valid underlying core disorder within the PDD
spectrum.
In fact, the DSM-III-R PDD section, in eliminating the diagnosis of
COPDD and the 30-month onset boundary for AD, has moved closer to
the findings of empirical studies (Dahl et al., 1986; Morris, 1988; Provence
& Dahl, 1987; Rescorla, 1986; Siegel et al., 1989; Waterhouse, Wing, et
al., 1987; Wing, 1988). Therefore, making the assumption that the diagnos-
tic criteria (whether IA or AD) are necessarily bound to be fallible, having
fewer categories with a freedom from arbitrary boundaries (e.g., age at on-
set), and having greater descriptive coverage (the revision of the AD cri-
teria) should allow both clinicians and researchers to use the PDD section
to move toward greater clarity in descriptive diagnosis, greater under-
standing of possible etiology, and more effective determination of subsyn-
dromes. The criteria for autistic disorder are by no means a closed book:
Change will come through future research that addresses the range of com-
plexities inherent in the phenomenology.
Pervasive Developmental Disorders 547

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