Subtypes of Language Disorders in School-Age Children With Autism (Developmental Neuropsychology (34, 1, (66-84) )

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Subtypes of language disorders in school-age children with autism

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Developmental Neuropsychology
ISSN: 8756-5641 (Print) 1532-6942 (Online) Journal homepage: http://www.tandfonline.com/loi/hdvn20
Subtypes of Language Disorders in School-Age

Children With Autism
Isabelle Rapin MD , Michelle A. Dunn , Doris A. Allen , Michael C. Stevens &

Deborah Fein
To cite this article: Isabelle Rapin MD , Michelle A. Dunn , Doris A. Allen , Michael C. Stevens
& Deborah Fein (2009) Subtypes of Language Disorders in School-Age Children With Autism,
Developmental Neuropsychology, 34:1, 66-84, DOI: 10.1080/87565640802564648
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DEVELOPMENTAL NEUROPSYCHOLOGY, 34(1), 66–84
Copyright © 2009 Taylor & Francis Group, LLC
ISSN: 8756-5641 print / 1532-6942 online
DOI: 10.1080/87565640802564648
Subtypes of Language Disorders in School-Age

Children With Autism
Downloaded by [Yeshiva University Libraries - Cardozo - Einstein - YU] at 10:00 18 October 2015
Isabelle Rapin
Saul R. Korey Department of Neurology, Department of Pediatrics, and Rose F. Kennedy
Center for Research in Mental Retardation and Human Development
Albert Einstein College of Medicine, Bronx, New York
Michelle A. Dunn
Saul R. Korey Department of Neurology and Rose F. Kennedy Center for Research in
Mental Retardation and Human Development
Doris A. Allen†
formerly Division of Child Psychiatry, Department of Psychiatry,
Michael C. Stevens
Institute of Living, Hartford, Connecticut
Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut
Deborah Fein
Department of Psychology
University of Connecticut at Storrs, Storrs, Connecticut
Cluster analysis of test scores on expressive phonology and comprehension of words and sentences in
7–9-year-old children with preschool diagnosis of Autistic Disorder yielded 4 clusters. Cluster 1 (N = 11):
phonology and comprehension both low; Cluster 2 (N = 4): phonology low, near average comprehension;
Cluster 3 (N = 40): average phonology, comprehension low to low average; Cluster 4 (N = 7): average or
better phonology and comprehension. The clusters support two major types of language disorders in au-
tism driven by impaired expressive phonology, each divisible by comprehension ability. The clusters refute
a single language disorder in autism and are consonant with earlier-defined clinical subtypes.
Communication impairment is the second of three deficient behavioral domains defining the
Autism Spectrum Disorders (ASDs)—Pervasive Developmental Disorders (PDDs) in the current
Correspondence should be addressed to Isabelle Rapin, MD, K 807 Albert Einstein College of Medicine, 1300 Morris
Park Avenue, Bronx, NY, 10461. E-mail: rapin@aecom.yu.edu
This article was supported in part by NINDS grant # 20489.
A list of abbreviations is presented at the end of the article.
†Deceased
LANGUAGE SUBTYPES IN CHILDREN WITH AUTISM 67
Diagnostic and Statistical Manual of Mental Disorders (4th ed. [DSM-IV-TR]; American Psychi-
atric Association, 2000) and International Classification of Diseases (ICD 10) (World Health Or-
ganization, 1992)—referred to as ASDs or autism in this article. The three descriptors of language
inadequacy in the DSM focus on conversational use of language (verbal and nonverbal prag-
matics), verbal perseveration and idiosyncratic word choices, and delayed or absent expressive
language/speech. Besides pragmatics, language entails three other encoded components: phonol-
ogy (phonemes—the smallest acoustically distinct units of speech, and prosody or intonation),
grammar (morphology—grammatical word markers and function words, and syntax—word or-
der), and semantics (vocabulary assembled into well formed meaningful utterances) (Bates, Thal,
Finlay, & Clancy, 2003).
Interaction of these components for proper language development and use calls for complex,
hierarchically structured, rule-governed brain operations, including interacting bi-hemispheric
circuitry operating in conjunction with other distributed networks subserving attention, memory,
cognitive, executive, affective, and motor operations (Caramazza, 2004). At its most schematic,
language can be considered a one-way dedicated input-processing-output system, with phono-
logic decoding and encoding its initial and final operations. The reality is far more complex of
course, with feed-forward and feedback loops at every node of language circuitry. These loops
support the concurrent bottom-up and top-down operations that make possible the speed, auto-
maticity, and overlap in time of the decoding, comprehension and evaluation, decision-making,
programming, and execution of language in the context of on-going, potentially competing, neu-
ral activities (McClelland, Mirman, & Holt, 2006). However, from a conceptual as well as a mea-
surement standpoint it is helpful to consider these components as separate hierarchical levels of
language, including of language in autism.
Language deficits that do not involve the so-called structural or lower order language abili-
ties—phonology and grammar—are widely referred to as higher order language processing disor-
ders. These higher deficits impact comprehension, processing, and programming of semantics,
that is, the meaning of words and connected speech (discourse), and pragmatics or conversational
use of language. Pragmatic impairment of variable severity is a universal—thus defining—and
life-long feature of language in autism, regardless of phonologic and grammatical abilities
(Baltaxe, 1977; Tager-Flusberg, 1981). It is the key feature that distinguishes communication im-
pairment in autism from that of the great majority of children with developmental language disor-
ders (DLDs). Pragmatic deficits involve the comprehension and production of verbal and nonver-
bal indicators of communicative intent and comprehension such as deviant eye-gaze, lack of
response to being addressed or called by name, deficient interpretation and production of facial
expression, tone of voice, and communicative gestures, and grossly inadequate conversational
skills. These higher order semantic and, especially, pragmatic language deficits are those included
in the DSM/ICD systems. They intersect with the impaired social and cognitive skills of autism
and have been extensively described as the language characteristics of verbal children with ASDs
(Tager-Flusberg & Caronna, 2007).
Some early investigators compared the language of verbal children with ASDs and DLDs (e.g.,
Bartak, Rutter, & Cox, 1975, 1977; Bartolucci, Pierce, Streiner, & Eppel, 1976; Beisler, Tsai, &
Vonk, 1987) and theorized that language impairments in ASD might constitute actual language
disorders, including some involving deficient phonology and grammar. Tager-Flusberg (1981) re-
viewed studies of the four components of language in at least somewhat verbal children with au-
tism and concluded that, albeit often delayed, phonologic and syntactic development followed ex-
68 RAPIN ET AL.
pectations, whereas semantics and pragmatics were affected selectively. Wide acceptance of this
view induced most investigators to focus on the peculiarities of expressive language of verbal chil-
dren, notably echolalia, pronominal reversal, use of scripts, and aberrant prosody, relating them to
cognitive level, inadequate social skills, and theory of mind (e.g., Barrett, Prior, & Manjiviona,
2004; Bishop, 1989). Standardized language tests in 89 children with autism who had at least 2
word utterances reopened the question of lower language deficits in autism (Kjelgaard &
Tager-Flusberg, 2001; Tager-Flusberg & Joseph, 2003). Among the 44 children with high func-
tioning autism (HFA) testable with the Clinical Evaluation of Language Fundamentals (CELF),
mean expressive phonology for words was average but mean Repetition of Non-Words (Korkman,
Kirk, & Kemp, 1997), a sensitive marker for residual deficit in phonologic processing in DLD,
was marginal in the 34 (77%) with low or borderline mean CELF scores. Although there was no
difference at the word level, comprehension of higher order language was more severely impaired
than expression in children with deficient language scores. This more recent work suggests that
there are definable language subgroups in autism, although others (e.g., Whitehouse, Barry, &
Bishop, 2008) question the specificity of language deficits resembling those of DLD in children
with HFA because their language scores correlated with the pervasiveness of their autism and their
errors differed.
Based on the input-processing-out model of language processing and four components of lan-
guage (phonology, grammar, semantics, and pragmatics) applied to unselected verbal or nonver-
bal preschool children with DLD and ASD, Allen, a developmental psycholinguist, and Rapin, a
child neurologist, developed a classification of language disorders in young children suitable for
clinicians in their offices (Allen, 1988; Rapin, 1996a; Allen, Rapin, & Wiznitzer, 1988). They
classified language disorders into three types, each with two subtypes. They used clinical judg-
ment to decide whether children’s language comprehension and production deviated from ex-
pected language development in typical children (Brown, 1973; Fenson et al., 1993). They at-
tended to speech intelligibility, to the grammar, length, and complexity of spontaneous utterances
and richness of the vocabulary, to whether the child used language conversationally and whether it
contained the notoriously aberrant features of autistic communication. They noted whether verbal
and nonverbal children answered simple requests, concrete or more abstract questions verbally or
with gestures like pointing, nodding, or carrying out commands.
Allen and Rapin then compared receptive and expressive communication skills in 229 unse-
lected consecutive mostly preschool children with DLD and 262 with ASD, including some non-
verbal or minimally verbal children in both groups (Allen and Rapin, 1992). A major difference
was that comprehension was deemed deficient in all ASD children, whereas 35% of those with
DLDs fit subtypes with adequate comprehension but impaired expression. They assigned 37% of
children with ASDs (vs. 15% of those with DLDs) to higher order language processing subtypes
with adequate expressive phonology and syntax, and 63% (vs. 50% of those with DLDs) to mixed
receptive/expressive (phonologic-syntactic) subtypes in which impaired phonologic decoding
jeopardizes all downstream processing, thus resulting in more or less severe global language im-
pairment. Another study closely replicated these assignments in 197 young children with ASDs
without severe or profound mental retardation (Tuchman, Rapin, & Shinnar, 1991).
The multidisciplinary study (Rapin, 1996b) of a large sample of uniformly selected and studied
preschoolers recruited between 1985 and 1989 and followed at ages 7 or 9 years provided the op-
portunity to test the validity of the clinically defined types and subtypes of language disorders in
ASDs by using standardized language and neuropsychologic measures. The importance of identi-
TABLE 1
Allen-Rapin Clinically Defined Types and Subtypes of Language Disorders in Young
Children with Inadequate Language Developmenta
Type A: Mixed Receptive/Expressive or Global Disorders (DLD and ASD Children)
– Deficient phonology, grammar, & semantics, ± pragmatics.

– Associated oromotor deficits frequent.b

1. Verbal auditory agnosia (VAA): most severe disorder; little or no comprehension of speech (language by ear); little
or no speech; distorted phonology, very impoverished grammar and vocabulary.
2. Phonologic-syntactic disorder: speech sparse, poorly articulated; short agrammatical sentences; impoverished
vocabulary. Comprehension impaired but equal to or better than expression. Severity ranges from mild to very severe.
Type B: Higher Order Processing Language Disorders (DLD and ASD Children)
– Comprehension and expression affected.

– Deficient semantics ± pragmatics, phonology, and grammar adequate.
1. Lexical-syntactic disorder (language programming disorder): delayed expression (± simplified grammar, word
finding problems, dysfluency, and jargon early on). Elicited language worse than spontaneous utterances.
Comprehension of connected speech (discourse) impaired.
2. Semantic-pragmatic disorder: speech not delayed, fluent, large atypical vocabulary, expressive phonology, and
grammar unimpaired. Comprehension of discourse worse than spontaneous expression. Pragmatic deficits mild in
DLD, universal and often blatant in ASD.
Type C: Expressive Phonology ± Grammar Disorders (DLD Children Only?)
– Deficient phonologic expression, ± impoverished vocabulary, ± word finding problem.

– Comprehension and pragmatics unaffected, clear drive to communicate verbally or by gesture.
1. Phonologic programming deficit disorder: speech poorly articulated, in some cases to the point of an unintelligible
jargon. Speech fluent or dysfluent.
2. Verbal dyspraxia: Children mute or speech very dysfluent, effortful; grossly distorted production of single words in
which most consonant sounds may be missing. Associated oromotor deficits frequent.
aInadequate verbal and nonverbal pragmatics (conversational use), lack of compensatory gestures, and aberrant pros-
ody distinguish children on the autism spectrum (ASD) from children with developmental language disorders (DLDs/spe-
cific language impairments—SLIs). ASD children likely to have atypical features (e.g., echolalia, pronominal reversal,
perseveration, repeated questioning, idiosyncratic word choices).
bOromomor deficits (oromotor dyspraxia), that is, impaired voluntary control of the oromotor musculature for nonver-
bal tasks like swallowing, chewing, moving the tongue to command, and so on. Frequent in dysfluent children with global
language disorders or verbal dyspraxia. Not causative but likely to contribute to poor speech (e.g., slurred, dysrhythmic,
unintelligible, or even absent). Due to neurologic disorders that do/do not affect language circuitry.
fying valid homogeneous phenotypic subtypes (endophenotypes) has become pressing with the
current emphasis on their genetic and neurobiological substrates (e.g., Belmonte et al., 2004)
METHOD
Participants
The current study draws on 118 children with autism available for testing at school age. They be-
longed to an original cohort of 176 preschool children with DSM III-R Autistic Disorder (AD)
who participated in a multi-site NINDS-supported study of autism compared to non-autistic de-
70 RAPIN ET AL.
velopmental disorders. The original sample was enrolled at four sites charged to recruit children in
different diagnostic groups: Boston MA: AD, the Bronx NY: AD and DLD, Cleveland OH: DLD,
and Trenton NJ: AD, with all sites recruiting some nonautistic children with low IQs (see Rapin,
1996b, p. 37). A small minority of the children from the Bronx were included in the Allen and
Rapin (1992) and Tuchman et al. (1991) studies.
To be selected for the autism sample, preschool children had to fulfill criteria for DSM III-R
AD. Diagnosis was based on an interview of the child and parent by experienced psychiatrists,
trained together to ensure uniformity of diagnostic criteria. Details of all original selection and
data collection procedures at preschool are published (Rapin, 1996b, pp. 31–57). Briefly, we dis-
qualified children with hearing losses, diagnosable neurological conditions associated with their
autism, overt sensorimotor deficits such as cerebral palsy, uncontrolled epilepsy, large doses of
anticonvulsant or psychotropic medication, and non-English speaking families. The Institutional
Review Board at each site granted permission for the study, the parents signed informed consents,
and children who were able to do so assented to the study.
Of 176 children with AD recruited at preschool, only 118 were available for school-age testing
between 1988 and 1992, either because parents could not be contacted or refused further partici-
pation. Attrition among the sites ranged from 14.3% to 36.1% but did not differ significantly by
site (Pearson χ2 = 1.57, ns). The reasons for attrition (58 of 176, or 33.0%) over a several year pe-
riod in partially deprived urban areas with high mobility are unknown. A comparison of the
symptomatology of children who did and did not return at school age revealed no differences in ei-
ther preschool intellectual ability (returning children’s average (SD) nonverbal IQ ratio = 63.9
(33.7) versus attrition = 58.9 (32.2), t = –.927, ns) or preschool autistic severity—average symp-
tom count on the Wing Autistic Disorder Interview Checklist (WADIC) (Wing, 1996) (returning =
13.8 (4.0) versus attrition = 14.0 SD (3.4), t = -0.328, ns), suggesting broad comparability. Thirty
six of the 118 children (30.5%) had incomplete test scores on the two clustering measures (see be-
low) and were therefore ineligible for clustering, leaving 82 children for study.
We did not include in the clustering 20 of the 82 children who obtained floor scores on both cluster-
ing measures because we could not determine whether their lack of performance was due to inability,
lack of compliance, or some other reason. These 20 participants, whom we retained for comparison,
did not differ from the final sample of 62 by age (t = 1.68, ns) or gender (Pearson χ2 = 0.32, ns).
The parent project called for children to be reassessed twice at school age—once at 7 and again
at 9, but not all participants returned for both assessments. So as not to weight more heavily 14
children with complete data on both clustering variables at both ages and to increase age homoge-
neity, we used only the 9-year data unless a child’s 7-year data for the other variables needed for
the study were significantly more complete. Of the 62, 19 were assessed within a few months of
age 7 and 43 of age 9. Mean age at testing was 8.6 years. There were 46 boys (85.7%) and 16 girls
(14.3%).
Measures
We used videotapes to ensure methodologic uniformity between sites and examiners. Investiga-
tors and research assistants met quarterly to review procedures and data and met yearly with an
External Review Board. Because the original design was longitudinal, preschool diagnostic as-
signments, clinical evaluation procedures, and tests had been retained at school age. For this
cross-sectional clustering study, the available measure of expressive phonology was the Photo Ar-
ticulation Test (PAT) (Pendergast, Dickey, Selmar, & Soder, 1984), which yields a score for cor-
rect speech sounds produced in naming photographs of objects. We created a composite score of
language comprehension from two subtests of the Comprehensive Evaluation of Language Fun-
damentals–Revised (CLEF–R) (Semel, Wiig, & Secord, 1987), Word Classes to evaluate compre-
hension and use of vocabulary, and for comprehension at the sentence level either Sentence Struc-
ture (for age 7) or Semantic Relations (for age 9), the corresponding age-appropriate subtests. We
transformed PAT scores into age-normalized scaled scores so they would have the same metric as
the CELF–R scaled scores (both with a mean of 10, standard deviation of 3, and floor score of 3).
We assessed the concurrent validity of the cluster solution with reference to clinical and cogni-
tive schoolage measures not used for the cluster analysis. The Stanford-Binet Intelligence Scale,
Fourth Edition (S-B) (Thorndike, Hagen, & Sattler, 1986) supplied measures of verbal and non-
verbal cognitive ability and the school-age WADIC (Wing, 1996) of the severity of autistic
symptomatology. Details of the methods and subtests used to generate scores of verbal and non-
verbal cognitive skills over a wide range of abilities at preschool are detailed in Rapin (1996b pp.
48–51). The same approach was used at school age. The WADIC is a 21-item parent interview that
overlaps many items of the DSM III-R amd of the Autism Diagnostic Inventory (ADI) (Le
Couteur et al., 1989), neither published at the start of the preschool phase of the study. Each item is
scored on a 3 point scale (0 = normal to 2 = severe). The Vineland Adaptive Behavior Scales
(VABS) Social Domain (Sparrow, Balla, & Cicchetti, 1984) provided a measure of functional so-
cial ability, and the VABS Communication Domain a gauge of functional language. The Peabody
Picture Vocabulary Test–Revised (PPVT) (Dunn & Dunn, 1981) and Expressive One Word Pic-
ture Vocabulary Test (EOWPVT) (Gardner, 1979) indexed receptive and expressive language at
the word level. The neurologists’ mean scores for intelligibility and for oromotor function the as-
sessment of which is detailed in Rapin (1996b, p. 106) (0 = normal to 2 = severe impairment) were
also used. Only a general comparison was possible between language clusters and the Allen and
Rapin clinical language classification (Table 1) because individual study children had not been
classified clinically.
Data Analyses, Clustering
Dr. Robin Morris of Atlanta supervised the cleaning, pooling, and compiling of data from all sites
for original analyses. We performed hierarchical clustering with SPSS version 14 using squared
Euclidean distance measures and between-groups linkages to determine cluster membership. The
hierarchical clustering method produces a dendrogram graphing a series of possible cluster struc-
tures. We determined the best fit for our sample by examining the heights of links among branches
relative to higher levels to detect natural break points among distance measures among groups of
cases. Analysis of variance was used for comparisons between cluster means with significance set
at p < .05.
RESULTS
Visual inspection of the 2, 3, 4, and 5 cluster dendrograms suggested that the 4-cluster solution
provides the best separation among groups. This solution, which we adopted, is shown in Figure 1,
which gives each child’s scores on the measures of expressive phonology (PAT) and comprehen-
72 RAPIN ET AL.
FIGURE 1 Scatter plot of individual school-age children’s scaled scores on the Photo Articulation Test and re-
ceptive composite scores from the Clinical Evaluation of Language Fundamentals–Revised (CELF–R). Thick
lines mark means and thin lines lower limit of average (–1 standard deviation) in the normative populations. Floor
score = 3 on both measures. SS = scaled scores.
sion at the word and sentence levels (CELF–R composite) and Table 2 displays mean PAT and
CELF–R scores in the 4 clusters. The 2, 3, and 5 cluster solutions had specific weaknesses. The
PAT score partitioned the 62 children into 2 clusters, one of 15 children whose expressive phonol-
ogy was impaired (PAT 4.1 ± 1.5) and a cluster of 47 in whom it was not (PAT 10.6 ± 1.2). The 2
cluster solution, based entirely on the PAT, ignored major differences in receptive language ability
TABLE 2
Comparison of Mean ages and Scaled Scores (SD) Among Children with Autism (N = 62)
Clustered by Measures of Phonologic Production (PAT) and Language Comprehension (CELF–R)
Significance of
Cluster 1 Cluster 2 Cluster 3 Cluster 4 F Differences
(N = 11) (N = 4) (N = 40) (N = 7) (p value) Between Clusters
Mean age (years) 8.4 (1.11) 9.0 (0.76) 8.6 (0.90) 9.0 (1.60) 0.58 (ns)
Photoarticulation Test (PAT) 4.6 (1.57) 3.0 (0.0) 10.4 (1.24) 11.9 (0.38) 112.95 (p < .001) 1, 2 < 3 < 4
(SS)
Clinical Evaluation of 3.7 (0.44) 8.0 (1.78) 5.99 (2.22) 11.7 (1.38) 27.02 (p < .001) 1 < 2, 3 < 4
Language Fundamentals–
Revised (CELF–R)
composite (SS)
Analysis of variance with post hoc comparisons using Bonferroni correction for multiple comparisons; significance levels set
at least p < .05 after correction. N: number of children in clusters; SD: standard deviation; SS: scaled score: mean = 10, SD of 3,
floor score 3.
(CELF–R 4.7 ± 2.2, range 3–10 in the first and 6.8 ± 2.9, range 3–13 in the second). The next
partitions were driven by scores on the CELF–R which yielded a 3 cluster solution with the 47
phonologically unimpaired children divided into a group of 7 children (i.e., Cluster 4) with nor-
mal language ability on both measures (PAT 10.40 ± 1.24, CELF–R 11.7 ± 2.22), and a group of
40 children (i.e., Cluster 3) with average phonology and low to borderline CELF–R scores (PAT
10.4 ± 1.24, CELF–R 5.99 ± 2.22, range 3–10). This solution left the phonologically impaired
children in one group, with comprehension scores ranging from severely impaired to average.
The 4 cluster solution divided these 15 children into two groups, a cluster of 11 severely glob-
ally impaired children (i.e., Cluster 1, PAT mean 4.55 ± 1.57, CELF–R 3.59 ± 4.40) and a small
cluster of 4 children (i.e., Cluster 2) with average or close to average comprehension (CELF–R
mean 8.00 ± 1.80) despite profoundly impaired phonology, all with a basal level of 3 on the PAT.
Because of the broad range of comprehension in Cluster 3, we also tried a 5 cluster solution,
which divided it into a group of 20 with clearly impaired comprehension (CELF–R 4.05 ± 0.9)
and a group with low average comprehension (CELF–R 7.93 ± 1.20). Visual inspection of the
comprehension scores of these two groups suggested continuity rather than discontinuity (see
Cluster 3 in Figure 1), so we concluded that the 4 cluster solution was the most parsimonious
and clinically interpretable.
Table 3 shows mean scores for the 4 clusters on other cognitive, social, and language tests. The
clusters did not differ by age. Cluster 1 includes children with significant impairments on all func-
tions, including expressive phonology, comprehension, verbal and nonverbal IQ, social and com-
municative adaptive skills, receptive and expressive vocabulary, and a high level of autistic
symptomatology. Cluster 2 comprises the small number of children with profoundly impaired ex-
pressive phonology with, surprisingly, borderline comprehension, average nonverbal IQ, mild im-
pairments of functional communication and receptive vocabulary, and good scores on expressive
vocabulary, with a high number of autism symptoms and impairments in socialization. Cluster 3
children, by far the largest group, had good expressive phonology and normal nonverbal IQ, im-
paired comprehension, verbal IQ, receptive vocabulary, and socialization, and a moderate number
of autism symptoms. Expressive single word vocabulary in Cluster 3 was normal. Cluster 4
groups children who performed at average or above average levels on all cognitive and language
measures. Although all 7 met criteria for AD when they entered the study at preschool, at this
point, age 9, parents reported few autism symptoms and mild socialization impairments.
We considered the possibility that deficient PAT and CELF–R scores might merely be proxies for
the overall severity of the autism, as suggested by Whitehouse et al. (2008), rather than indexing the
specific language deficits we favor. If so scores on both tests should be strongly and similarly related
to measures of autism severity. To clarify this issue, we used stepwise regression to examine the rela-
tionship of PAT and CELF–R scores to ASD symptom domains quantified on the WADIC (Wing,
1996). These models found significant but varying relationships of PAT and CELF–R scores with
Wing A (social), Wing B (language/communication), and Wing C (odd behavior) domains. PAT was
significantly correlated with Wing A (t = –2.336, p = .022), Wing B (t = –2.942, p = .005), but not
Wing C (t = –1.357, p = .180). CELF–R was highly correlated with all three domains (p < .001 for
each). The shared variance between PAT and CELF–R was particularly noticeable in their joint rela-
tionship to Wing A socialization impairment scores, where the inclusion of CELF–R into the step-
wise model rendered PAT non-significant. This shared variance was present to a lesser degree for the
prediction of Wing B, but PAT remained significant at a trend level in this stepwise model. In sum,
these supplementary analyses indicate that despite a degree of shared variance in predicting relation-
74 RAPIN ET AL.
TABLE 3
Comparison of the Mean (SD) Severity of the Autism, Social, and Cognitive, and Language
Deficits Among the 4 Clusters
Significance of
Cluster 1 Cluster 2 Cluster 3 Cluster 4 F Differences in
Measures (N = 11) (N = 4) (N = 40) (N = 7) (p value) Impairment
WADIC (mean number 12.2 (4.58) 10.2 (7.84) 8.0 (5.95) 2.0 (2.16) 5.08 (<.01) 1, 2, 3 > 4
of symptoms out of (N = 11) (N = 4) (N = 35) (N = 7)
a total of 21)
Vineland 67.1 (20.44) 67.5 (5.44) 74.0 (17.58) 85.6 (16.58) 1.53 (ns)
Socialization (N = 9) (N = 4) (N = 35) (N = 6)
Domain (SS)
S-B Nonverbal IQ 76.5 (12.94) 100.0 (5.94) 96.2 (17.67) 119.0 (15.06) 10.03 (<.001) 1 > 3, 4;
(SS) (N = 11) (N = 4) (N = 39) (N = 7) 3>4
S-B Verbal IQ (SS) 66.8 (10.85) 84.2 (12.52) 81.7 (18.92) 109.0 (8.02) 9.30 (<.001) 1, 2, 3 > 4
(N = 11) (N = 4) (N = 39) (N = 7)
Vineland 62.1 (13.42 76.2 (10.71) 79.5 (18.63) 102.1 (17.38) 6.43 (p < .001) 1 > 4; 3 > 4
Communication (N = 9) (N = 4) (N = 35) (N = 6)
Domain (SS)
Peabody Picture 59.0 (14.21) 71.0 (14.16) 75.4 (19.58) 106.2 (11.85) 10.19 (p < .001) 1, 2, 3 > 4
Vocabulary Test (N = 11) (N = 4) (N = 39) (N = 7)
(SS)
Expressive One Word 75.2 (10.45) 104.7 (14.15) 99.3 (22.87) 125.2 (19.72) 8.85 (p < .001) 1 > 3; 1 > 4;
Picture Vocabulary (N = 11) (N = 4) (N = 39) (N = 7) 3>4
Test (SS)
Analysis of variance with post hoc comparisons with Bonferroni correction for multiple comparisons; significance levels set at
least p < .05 after correction. Groups not displayed or separated by “>” are not statistically different. Abbreviations: N: number of
children with data in cell; S-B: Stanford-Binet IV; SD: standard deviation; SS: scaled score; WADIC: Wing Autistic Disorder In-
terview Checklist.
ships to specific autism symptoms, PAT and CELF–R each had a unique relationship to overall au-
tism severity and contributed unique variance to different aspects of language.
Because the PAT drove the clustering, we compared the clusters on correlates of phonologic
impairment. Clusters 1 and 2 children spoke first words later (21 and 23 months) than the phono-
logically unimpaired children in Clusters 3 and 4 (17 months). Neurologists’ scores were conso-
nant with PAT scores: suboptimal intelligibility in 64% and 75% of children in Clusters 1 and 2
compared to 20% and 14% of those in Clusters 3 and 4, and oromotor function inadequate in 27%
and 50% in Clusters 1 and 2 compared to 22% and 14% in Clusters 3 and 4. Although expressive
deficits in children in Cluster 1 might be viewed as a correlate of global impairment, the normal
intelligence of the small Cluster 2 children belies this interpretation and points to a specifically
compromised circuitry.
Finally, we examined scores of the 20 children (mean age 8.19 ± 1.10) we excluded from the
clustering because of their floor scores on both the clustering variables in order to determine how
substantially they differed from the globally impaired children in Cluster 1. In general, their mean
scores indicated greater impairment. Their S-B Nonverbal IQ was much lower than Nonverbal IQ
in Cluster 1 (52.8 compared to 76.5), their mean WADIC score of 15 was approximately equal to
12.2 in Cluster 1, but VABS Socialization of 51.5 was lower than 67.1. Their VABS Communica-
tion was 41.6 compared to 62.1 and PPVT 46.5 compared to 59.0. Thus they were more severely
impaired overall than children in Cluster 1, without being globally untestable.
DISCUSSION
This study supports the existence of two major types of language disorders in school-age children
with autism, based on their scores on the PAT, an index of expressive phonology (correctly articu-
lated single words), which drove the first partitioning of the sample. The first type (Clusters 1 and
2), accounting for 24% of the sample, is characterized by persistently and severely impaired ex-
pressive phonologic skill at age 8½. The 4 children in Cluster 2, only 6% of the sample, differed
drastically from those in Cluster 1 by better or even low average language comprehension and av-
erage nonverbal IQ in the face of profoundly impaired phonologic expression. The severity of
Cluster 2’s expressive phonologic problem despite reasonable comprehension is bolstered by pro-
ject neurologists’ confirmation of impairment and by mothers’ preschool report of an average age
of 23 months at first words, when the MacArthur Inventories (Fenson et al., 1993) indicate that
typically developing 23-month-old boys have a vocabulary of 230 words (range 56–633), girls
350 (38–612).
Note that the 20 children excluded because of floor scores on both clustering measures were
found to be low or lower functioning than the children in Cluster 1. Because there was no way to
distinguish “could not do” from “would not do”— a frequent situation in autism testing (Man-
delbaum et al., 2006)—we did not include them in the cluster analysis, but it is likely that the per-
cent of children assigned to Cluster 1 is an underestimate as some or most of the 20 excluded chil-
dren probably belong to this group.
In contrast, the 76% of children of the second type (Clusters 3 and 4) had borderline/low aver-
age to better than average expressive phonology, confirming that by school age the majority of
children with ASDs do not have conspicuous “structural” language deficits (Tager-Flusberg, Paul,
& Lord, 2005). This does not mean that their language skills are uniformly appropriate because
comprehension at the lexical and sentence level, as indexed by variable CELF–R composite
scores, ranged from severely impaired to above average. The 14.9% of children in Cluster 4 stand
out because their scores for both phonology and comprehension were at least equal to the average
of the standardization samples. Based on these criteria, this small group does not fulfill criteria for
any language disorder, with the caveat that the study provided no data on pragmatics or abnormal-
ities such as echolalia, aberrant word choices, or prosody which, even when subtle, are strongly
suggestive of an ASD (Adams & Bishop, 1989; Lewis, Murdoch, & Woodyatt, 2007). Although
children in Cluster 4 showed the mildest VABS socialization deficits, there was no significant dif-
ference in socialization among the clusters, including Cluster 4. This suggests that parents of most
of the children in Cluster 4 were aware of persistent social difficulties despite their children’s in-
telligence and adequate communication skills and despite the children no longer showing frankly
autistic symptoms (Kelley, Paul, Fein, & Naigles, 2006; Stevens et al., 2000)
The second goal of this study was to determine how well empirically defined language clusters
would map onto Allen and Rapin’s clinically defined types and subtypes of language disorders
(Table 1). Clustering identified two main types of language disorders, one with impaired phonol-
ogy (Clusters 1 and 2) and one without (Clusters 3 and 4). These are congruent with the major clin-
ical types, the global expressive-receptive type and the higher order processing type. Cluster 1
76 RAPIN ET AL.
maps perfectly onto the phonologic/syntactic deficit syndrome, whereas the small Cluster 2, with
floor scores on the PAT and only mildly low to low normal comprehension scores on the CELF–R,
was not detected clinically. The clustering study thus indicates that comprehension may not be as
universally defective in school-age children with autism as Allen and Rapin had suggested clini-
cally at preschool. Reasons for the disagreement may be improvement with maturation, more
challenging comprehension demands in a conversational setting which is likely to call for answers
to “wh-” questions, a wider vocabulary, and more difficult grammar than do the well standardized
CELF–R subtests, although conversation runs the risk of making age-inappropriate demands.
The major difference between Cluster 1 and the clinical phonologic/syntactic deficit subtype is
prevalence, that is, 17.7% in Cluster 1 compared to two thirds to three quarters in the mostly youn-
ger clinically scored children (Allen & Rapin, 1992; Tuchman et al., 1991) This much lower pro-
portion may reflect the expected improved phonologic production with age in both typical pre-
schoolers (Bates et al., 2003) and those with DLD (Conti-Ramsden & Botting, 1999; Stothard,
Snowling, Bishop, Chipchase, & Kaplan, 1998; Whitehurst & Fischel, 1994) or ASD (Paul,
1987). Several minutes of conversation provides more opportunities for mispronounciations than
the single words of the PAT—albeit selected to include most consonant sounds of English. The ex-
clusion of the 20 children with floor scores probably contributed to amplifying prevalence differ-
ences between this study and clinical descriptions.
Cluster 3 is the largest (65%) and most diverse in terms of comprehension, compared to the
37% of Allen and Rapin’s higher order language deficit subtypes (Allen & Rapin, 1992). At pre-
school, comprehension of discourse is typically quite deficient in autism. Variable CELF–R com-
posite scores in Cluster 3 indicate that by school-age comprehension improves substantially in
some—but not all—verbal children on the spectrum. Inclusive longitudinal studies will be re-
quired to elucidate the maturational trajectories of phonology and comprehension in autism.
Cluster 3 corresponds to the clinically defined higher order processing deficit type, which Al-
len and Rapin proposed to divide into the lexical-syntactic and semantic-pragmatic deficit sub-
types (Table 1). We cannot determine how closely Cluster 3 maps onto either of these clinical sub-
types because information on word elicitation, delayed development—especially of grammar, and
production of jargon, often prominent at preschool in the lexical-syntactic subtype, is lacking in
the present study.
As stated earlier, by the criterion of test data, children in Cluster 4 no longer have a language
disorder, but the study provides no information on the classical semantic and pragmatic features of
high functioning, fluent, talkative autism/Asperger syndrome. It is likely that some Cluster 4 and,
probably, higher scoring Cluster 3 children correspond to the clinically defined semantic-prag-
matic deficit subtype (Bishop & Norbury, 2002). Their easily demonstrable preschool compre-
hension deficits by schoolage may be limited to the semantic peculiarities and residual pragmatic
deficits evident in their conversational speech (Adams & Bishop, 1989; Lewis et al., 2007). Some
may paradoxically remain deficient in nonword repetition (Bishop et al., 2004) or reading
(Bishop, 2001). Deficiency in nonword repetition and reading is linked to a locus on 16q (SLI
Consortium, 2004), but does not appear to be genetically inherited in ASD, even in those with im-
paired reading of nonwords (Bishop et al., 2004). A number of individuals with ASD use a
non-phonologic strategy for reading, which may contribute to the frequent association of hyper-
lexia with autism (Grigorenko, Klin, & Volkmar, 2003).
This discrepancy between repetition and reading in autism, together with results of direct tests
of verbal and nonverbal memory, is consonant with the hypothesis that inadequate short-term au-
ditory memory is a major contributor to impaired acquisition of the phonologic code (Adams &
Gathercole, 2000; Whitehouse, Barry, & Bishop, 2007). Electrophysiology points to other poten-
tial contributors to phonologic decoding, such as preattentive influences on detection of auditory
signals, auditory discrimination, allocation of attention, speed of processing, short-term auditory
working memory, procedural memory, and atypical lateralization of temporal auditory association
cortices (Bishop, 2007; Ceponiene et al., 2003; Dunn, Gomes, & Gravel, 2008; Lepisto et al.,
2005; Oram Cardy, Flagg, Roberts, & Roberts, 2005; Ullman & Pierpont, 2005). Electro-
physiology and advanced morphometric and functional imaging applied to individuals with rigor-
ously defined subtypes of language deficits with and without autism (endophenotypes) are re-
quired for identifying the genetic and neural circuitry contributing to language decoding.
The chief finding of this study—persistence of expressive phonologic deficits at schoolage in a
substantial minority of children with autism—had been documented in some early reports (e.g.,
Bartolucci et al., 1976), then largely ignored until recently (Kjelgaard et al., 2001; Tager-Flusberg
et al., 2003), in part because, typically, only verbal children without overt articulation deficits
were studied, which biased findings. Children in Cluster 2 with severe expressive phonologic defi-
cits yet reasonable comprehension perhaps deserve the label of verbal dyspraxia (Table 1). The
neurologists detected oromotor deficits (oromotor dyspraxia/dysarthria, a motor—not linguis-
tic—deficit) (Hayden, 1994) in Clusters 1 and 2. Oromotor deficits are often associated with, and
may contribute to, dysfluent speech in verbal dyspraxia—an expressive language deficit, and in
the global receptive/expressive DLDs.
In contrast to expressive language subtypes in which earlier language operations are pre-
served, the simplified input-processing-output clinical view of language processing implies
that, by jeopardizing all subsequent language processing, severely impaired auditory phono-
logic decoding at the language learning age impairs not only comprehension and higher order
processing, but also results in impoverished, phonologically and grammatically defective ex-
pression, that is, a global receptive-expressive disorder. Faulty grammar was documented in two
studies of children with HFA and “structural” language disorders (Tager-Flusberg et al., 2003,
Eigsti, Benetto, & Dadlani, 2007) but was not assessed in this study. Impaired grammar and
phonology are regularly associated in the clinical phonologic-syntactic syndrome (Table 1).
This may reflect the hierarchical nature of language processing and not a common genetic basis
despite their joint occurrence in some families with DLD (Bishop, Adams, & Norbury, 2006,
Falcaro et al., 2007). Severely impaired receptive phonology is the unquestioned cause for lack
of speech in non- or minimally verbal children with either developmental (Echenne et al., 1992;
Klein, Tuchman, & Rapin, 2000; Worster-Drought & Allen, 1930), or acquired (Kaga, 1999;
Korkman, Granstrom, Appelqvist, & Liukkonen, 1998; Landau & Kleffner, 1957; Mantovani &
Landau, 1980; Rapin, Mattis, Rowan, & Golden, 1977) verbal auditory agnosia (VAA). In VAA
the deficit is specific to the auditory channel and involves primary and secondary auditory corti-
ces uni- or bilaterally, often—but not necessarily—in the context of epilepsy. VAA, even when
improved, is associated with atypical and delayed auditory event-related potentials (ERPs) in
autistic and non-autistic individuals (Klein et al., 1995). The primacy of impaired phonologic
decoding as a (the?) major cause of inadequate comprehension and defective expression in chil-
dren with mixed receptive/expressive DLDs is their persistent deficits in reading nonwords in
the face of now fully adequate speech articulation mentioned earlier (e.g., Barry, Yasin, &
Bishop, 2007) and the few nonverbal children with autism or DLD in Allen’s nursery who
learned to speak words after they had learned to read them.
78 RAPIN ET AL.
Very severe comprehension deficits (notably VAA) resulting in global failure to acquire lan-
guage are as likely to be causes, as well as consequences, of cognitive incompetence, especially if
associated with the social deficits of autism. Indeed, based on parents’ responses to questionnaires
describing their children’s functional skills, 155 mute Swedish children and adults were judged to
be more severely socially and intellectually impaired than 335 verbal individuals with ASDs
(Miranda-Linne & Melin, 1997). Perhaps some of the 20 cognitively impaired children who were
not included in the clustering, as well as some of those with the lowest comprehension scores in
Cluster 1, would have been classified clinically as having VAA. Although a rare subtype of DLD
(Klein et al., 2000; Worster-Drought et al., 1930), its prevalence needs to be determined in pro-
foundly impaired nonverbal individuals with autism.
Clinical evaluation shows that children with higher order processing disorders often speak
better than they comprehend (Rapin, 1996a; Tager-Flusberg et al., 2007). Kjelgaard and Tager-
Flusberg (2001) found that comprehension was more severely impaired on receptive than expres-
sive subtests of the CELF, although not at the single word level. In the present study, single word
receptive scores (PPVT) were lower than expressive vocabulary (EOWPVT) in all the clusters, in-
cluding Cluster 4. These two tests make differing demands. The EOWPVT (“what is this?”) has a
simple stimulus–response format, whereas the PPVT (“show me X”) requires the child to hold the
word in working memory, scan each of four pictures and compare it to the word, compare the
goodness of fit of each picture to the word, inhibit impulsive or location-driven responses, and
make a pointing response.
Success on tests of receptive skills, like receptive skills in everyday life, requires motivation
and attention, as well as the ability to process connected language in real time, which may be defi-
cient in autism. Newbury, Bishop, and Monaco (2005) argue that deficient nonword repetition is
due not to inadequate auditory discrimination but to impaired short-term auditory working mem-
ory, vulnerable to inattention. Comprehension of connected speech (sentences) too is vulnerable
to short term working memory deficits but depends on many other cognitive and affective vari-
ables, and therefore may be deficient when phonology and grammar are not. In addition, as men-
tioned earlier, children with ASD may have a specific difficulty with wh- questions and other
grammatical forms that they may be able to avoid when programming their own speech, which
tends to be better than the more constrained elicited speech.
Some investigators attribute higher order language processing disorders like semantic and
pragmatic deficits to the social and cognitive impairments of autism (e.g., Dalton et al., 2005;
Charman, 2003; Fisher, Happé, & Dunn, 2005), yet their comprehension deficits share features
with posterior aphasias, for example the production of over-learned phrases, echolalia, and chain-
ing to preceding words. These aberrant productions may help compensate for difficulty self-gen-
erating language and responding to inadequately comprehended discourse.
Morphometric imaging in a small subsample of non-retarded boys from the present study pro-
vides evidence for involvement of language circuitry in at least some individuals with HFA. In-
deed, it revealed rightward brain asymmetry of language- related cortices in both the DLD and AD
boys, as opposed to typically developing controls (Herbert & Ziegler, 2005). Inferior lateral fron-
tal (Broca’s area) and superior temporal cortices were larger on the right than the left in 16 of 17
boys with autism drawn from our school-age sample (Herbert et al., 2002). The brains of the boys
with AD and DLD had more in common than they did with the brains of controls. In another
morphometric study (De Fossé et al., 2004), only the brains of boys with DLD or ASD with low
CELF and nonword repetition scores had reversed asymmetry of Broca’s area, not those of ASD
boys who did well on these two tests or those of typically developing controls. Paradoxically, the
planum temporale of both language impaired groups was larger on the left, but in that study, ex-
pressive phonology was largely unaffected, unlike that of at least some of the boys in the current
study.
These small preliminary imaging studies support parallel involvement of “classic” language
circuitry in some children with ASD and DLD. It is currently unresolved what proportion of au-
tism and DLD, each of which is a behaviorally defined environmentally influenced phenotype and
not a specific “disease,” is or is not on a genetic continuum (“broader autism phenotype”)
(Dawson et al., 2002; Whitehouse et al., 2008). A contemporary view is that there are some “gen-
eralist” genes with common effects on a broad range of developmental disabilities, and others re-
sponsible for discrete deficits, including RNA editing genes responsive to environmental influ-
ences (Mattick & Mehler, 2008). “Generalist” genes might influence early synaptic structure and
function in a range of developmental disorders without disturbing programs for major brain struc-
ture (Crawley, 2007; Zoghbi, 2003). Synaptic dysfunction may contribute to dyssynchrony be-
tween co-activated interconnected circuitry (Welsh, Ahn, & Placantonakis, 2005) and provide a
basis for the currently favored view that impaired connectivity is critical to the pathophysiology of
autism (Geschwind & Levitt, 2007; Minshew & Williams, 2007).
One limitation of the current study is that there was no typically developing control group;
therefore the extent to which similar clusters might be found in unaffected toddlers is un-
known. Although there are very limited data on this question, Bates et al. (1994) reported sa-
liently different styles of early language acquisition among typical young children who might
well cluster with standardized measures. This question is also related to whether the specific
language deficits found in this study represent delay or deviance. Although there are studies
that suggest that phonology and grammar are simply delayed in autism (Tager-Flusberg,
1981), more recent studies suggest deviance in some children (Eigsti et al., 2007; Tager-
Flusberg et al., 2003). The issue is primary dysfunction in dedicated language circuitry in
these children, in addition to the well-documented consequences of the social and cognitive
deficits characteristic of autism.
Other limitations include the restricted sample size and resultant smallness of some of the clus-
ters, although their relative sizes are consistent with clinical experience that by school age, the ma-
jority of verbal children with ASDs do not have overt “structural” language deficits. (Tager-
Flusberg et al., 2005). The rarity of children with much better comprehension than expression
(Cluster 2) may account for why they were not detected clinically at preschool (Allen et al., 1992).
Admittedly, the clinical language subtypes and the clusters do not correspond exactly to those that
emerged from other classification efforts recently reviewed by van Weerdenburg, Verhoeven, and
van Balkom (2006), but no current classification can be considered definitive. Although hierarchi-
cal cluster analysis is widely considered exploratory, clinical congruence with the clusters and the
significance of cluster differences on measures of IQ and socialization not used to determine clus-
ter membership mitigate against this criticism.
A clear strength of this study is that by not excluding children with very compromised expres-
sive phonology it gives a realistic view of the language deficits of autism. Future research will
need to replicate the study’s findings in larger samples to confirm and refine the subtypes
(endophenotypes) of language disorders in children with ASDs. In seeking their biologic corre-
lates with electrophysiologic, neuroimaging, or genetic tools, and to answer questions about the
relationship of language disorders to autism, investigators will need to take into account not only
80 RAPIN ET AL.
the cognitive level and severity of the autistic symptomatology, but also the subtypes of language
disorders identified in children at any given time with their developmental trajectories.
ACKNOWLEDGMENT
This article is dedicated to the memory of the authors’ late colleague and friend Doris A. Allen
who championed the detailed study and subtyping of language disorders in developmentally dis-
ordered children, including those with autism.
The authors thank the children and their parents for their participation in the study. The authors
acknowledge the contributions of Robin Morris, Ph.D. and Lynn Waterhouse Ph.D. and of the
many research assistants who participated in the study.
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ABBREVIATIONS
AD = DSM III-R Autistic Disorder; ANOVA = Analysis of variance; AS = Asperger syndrome;

ASD(s) = autism spectrum disorder(s); CELF–R = Clinical Evaluation of Language Fundamen-
tals–Revised; DLD = developmental language disorder; DSM III–R = Diagnostic and Statistical
Manual of Mental Disorders III–Revised; EOWPVT = Expressive One Word Picture Vocabulary
Test; HFA = high functioning autism, defined as Full Scale or Performance IQ > 70 or 80; IQ = In-
84 RAPIN ET AL.
telligence Quotient; NINDS = National Institute of Neurological Diseases and Stroke; ns = not
significant; PAT = Photo Articulation Test; PDD = Pervasive Developmental Disorder; PIQ =
performance (nonverbal) IQ; PPVT = Peabody Picture Vocabulary Test-Revised; S-B = Stan-
ford-Binet Intelligence Scale, Fourth Edition; SD = standard deviation; VAA = verbal auditory
agnosia; VABS = Vineland Adaptive Behavior Scales; VIQ = verbal IQ; WADIC = Wing Autistic
Disorder Interview Checklist.
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Subtypes of language disorders in school-age children with autism

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Isabelle Rapin Michelle Dunn

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Michael Stevens Deborah Fein

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Subtypes of Language Disorders in School-Age

Isabelle Rapin MD , Michelle A. Dunn , Doris A. Allen , Michael C. Stevens &

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Subtypes of Language Disorders in School-Age

Type A: Mixed Receptive/Expressive or Global Disorders (DLD and ASD Children)

– Deficient phonology, grammar, & semantics, ± pragmatics.

– Associated oromotor deficits frequent.b

– Comprehension and expression affected.

Type C: Expressive Phonology ± Grammar Disorders (DLD Children Only?)

– Deficient phonologic expression, ± impoverished vocabulary, ± word finding problem.

Data Analyses, Clustering

AD = DSM III-R Autistic Disorder; ANOVA = Analysis of variance; AS = Asperger syndrome;

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