INT J LANG COMMUN DISORD, MARCI-APREL 2011,
VoL. 46, NO. 2, 127-137
Discussion
Co-morbidity of autism and SLI: kinds, kin and complexity
Bruce Tomblin
(Communication Sciences and Dison
15, University of Towa, Iowa Cig, 1A, USA
(Recived 3 October 2010; asepted 15 December 2010)
Abstract
‘There has been a long-standing interest in the relationship between specific language impairment (SLI) and autism
spectrum disorder (ASD). In the last decade Tager-Flusberg and colleagues have proposed that this relationship
consists ofa partial overlap between the two. Therefore, among children with ASD there exists a subgroup who have
SLIand ASD which has heen called ‘ALI’. Tager-Flusherg’s laboratory has presented several papers showing similar
language profile: and brain structure abnormalities in both SLI and ALI. Others (Bishop, Whitehouse, Botting,
Williams) have been less convinced that these ALI children have both ASD and SLI. Although they generally agree
that the two groups are grossly similar, careful inspection of the data shows that there are differences. I will argue
that many of the problems in this debate stem from a view of SLI that represents a particular kind of language
learner and therefore a particular and unique profile can be assumed. I argue for recognizing that SLI is not likely
to be a unique kind of language learner. Many of the features reported to he characteristic of SL are also found
in other forms of neurodevelopmental disorders. Other features are the outgrowth of studying clinically identified
children with SLI and thus the profile appears to reflect biases and practices in the clinical service system. Ava result
it may he more reasonable to conclude that there is a large group of children with ASD who have poor language
skills. The question then remains why are there so many children with ASD who also have poor language? There
are several factors that collectively are strong candidates for answers to this question.
Keywords. autism specteum disorders (ASD), specific language impairment (SLI), co-morbidity.
Introduction
Recently, there have been several papers. published
regarding the relationship of the language and
communication problems of children with autism and
autism spectrum disorder (ASD) and children wich
specific language impairment (SLI). The basic question
that has been raised concerns whether there is an excess
of SLI within children with ASD? For the practis-
ing clinician this question may appear to be a bit
esoteric. Within the day-to-day practice of a speech—
language clinician, cach client is largely viewed as a
unique entity. As such, clinical work is much more
about the particular and the individual than it is about
generalities and groups. The clinician is concerned
most about the welfare of each person served and as
such promoting effective communication in each client.
Research is often quite the opposite. In this enterprise
generalities concerning patterns and principles are the
focus. Individuals are important insofar as they provide
information about these patterns: however, the general-
ities are the most important. This results in what could
be viewed as a disparity of purpose between the clinic
and research, even clinical research.
‘One of these debates in clinical research concerns
how we group or organize the types of clinical conditions
that we treat and the relationships among these. The
issue concerning the relationship of SLI and ASD is one
of these kinds of questions and will be the subject of
this paper. Therefore, we need to ask why these issues
may be important for clinical practice, My best answer
to this is that within the clinic and in research laborato-
ries we must assume that the individual differences in
the language and communication of our clients are
largely systematic. Thus, it is not simply by chance
that some children differ from others with respect to
language and communication nor is it by chance that
some children will be more similar to others in particular
ways. This systematic quality of individual differences
is fundamental to our hope that we can learn what
the processes and mechanisms are that give rise 0
these differences, As we learn what these processes and
‘Address correspondence to: Bruce Tom
‘email: -omblin@ iowa edu
- Communication Seienees and Disoidets, Univesity of lowa, 3 WISTIC, lowa Cigy TA, USA:
| aoa fol of Langue Comat Dedemechanisms are, we should be able to develop better
methods of intervention. This basic premise underlies
nearly all fields of clinical endeavour and provides the
basic scientific underpinnings of our discipline. In many
respects, those of us who are engaged in applied or
clinical research must admit that we are a long way
from being able to deliver on his promise, but the fact
that this model has been successful in other disciplines
such as medicine and enginecring suggests that the basic
approach will yield benefits to our field and ultimately
to each of our clients.
‘Those children who present with developmental
language disorders come with 2 variety of language
abilities and limitations. As noted above, we can assume
that these variations are not just there by chance, but
reflect systematic processes that shape the development
oflanguage and communication in these children. Thus,
we can ask, how many different ways ate there for
children to have poor development of language and
communication? In recent years a debate has surfaced
around this question with respect to children with
SLI and ASD. Children with SLI and ASD share the
common feature of poor spoken communication skills
"Thhus, che question arises as to whether SLI and ASD are
related in some fashion. At the extremes we could say
that these are distinctly different forms of developmen-
tal communication disorder or we could say that these
ate closely related if not the same. As we will see, each
of these positions has been posed as well as variations in
between,
Defining and characterizing SLI and autism
SLI
Currently, most clinicians and researchers distinguish
between SLI and ASD. SLI is a common neurodevel-
opmental disorder that involves persistent limitations
in the acquisition and use of spoken language. The
actiology of SLI is unknown; however, in the past
several years there has been a growing body of evidence
supporting a genetic contribution (Tomblin 1996). The
diagnostic standards for SLI involve language achieve
ment levels below cut-off values of-1.0 to-1.5 standard
deviations of age expectations. Additionally, minimum
non-verbal IQ levels as high as 85 have often been
employed, although this standard has been questioned
by several researchers (Tager-Flusberg and Cooper 1999,
Plante 1998). These criteria may be viewed as inclusion.
ary criteria in that a child must meet these conditions
for a diagnosis of SLI. Additionally, children with SLI
are requited to be free from developmental or sensory
impairments. This last criterion has been referred to as
an exclusionary criterion and ordinarily, ASD is viewed
as an exclusionary condition for SLI. In this regard,
Bruce Tomblin
SLI and ASD cannot overlap. But this exclusionary
condition may be forcing SLI to be different from other
communication disorders on arbitrary grounds.
‘The standard diagnostic conceptualization of
language with the diagnosis of SLI has not distinguished
between particular aspects of language: however, as
research has been conducted with these children, a
common profile has emerged. A large number of
studies have shown that these children are_particu-
larly weak with respect to grammatical development,
Tt has been within grammar that one finds particularly
strong debate as to whether SLI represents a distinctly
different type of learner or just a less adept learner.
Several researchers who have examined the grammat-
ical problems of children with SLI have concluded
that these children have distinctive deficits with regard
to grammar (Clahsen 1999, Gopnik 1990, Rice and
Wexler 1996, van der Lely and Battell 2003). One
grammatical feature involving the failure to mark tense
and aspect in obligatory contexts has been proposed as
a matker for SLI (Rice and Wexler 1996). Additional
markers for SLI have also been proposed with respect
‘to poor sentence repetition and repetition of non-words
(Botting and Conti-Ramsden 2003).
‘The notion that there is a marker for SLI suggests
that there are features of SLI that are distinctive and
largely unique to SLI. This raises a question as to how
wwe conceive of SLI. The idea that there is a marker for
SLI connotes the notion that SLI represents a distinet
category of language learners that are different from
‘other types of learners. Such a view therefore proposes
that SLI is a natural kind, Quine (1969) defined a
natural kind as a class or group that is bound together
by natural law and thus has a common causal system.
“There is some reason to question whether these markers
are unique to SLI. The grammatical problems associated
with SLI are also found in other populations of children
with developmental disorders such as Down syndrome
and even Williams syndrome (for instance, Eadie er al,
2002, Grant et al. 1997). Furthermore, there is lice
evidence that the language skills of children with SLI
are qualitatively distinct from children who are typically
developing other than being simply less well developed
(Dollaghan 2004, Leonard 1987, 1998, Tomblin and
‘Zhang 1999). Findings such as these support the notion
that children with SLI represent a region of poor
grammatical skills that are at one end of a continuum
of ability with children who are very good grammar
learners are at the other end of the spectrum. Underly
ing chis continuum, we might assume, are the same
developmental processes that operate in a graded fashion
‘over the whole continuum and thus generating faster or
slower learning rates.
‘As we consider this notion of a continuum, we need
to consider that the skills that go into communicationCo-morbidity of autism and SLI: kinds, kin and complexity
Figure L.A conceptual model of a chrce-dimensional. space
that contains individual diferences in communication formed by
satlation in language structure, speech-sound production sills and
pragmatice. Those children wich SLI are represented within chit
pace by the checked dis hat reflects limited variation in structural
language, but much greater variation i speech sotind snd pragmatic
abil
may be comprised of multiple continua as shown in
figure 1. This concept is certainly not an original idea.
Bishop (2000) has put forth very similar multidimen-
sional accounts for communication disorder. As noted
above, children with SLI are very likely to have poor
grammatical skills and this is usually accompanied by
poor vocabulary. Thus, these two aspects of language
may arguably be a single dimension around which
children can vary. In the literature on ASD and SLI this
dimension has been called structural language. Bates
and Goodman (2001) have clearly argued that these
ise from a single system and thus represent a single
dimension, As noted eatlie, Pinker (1997) as well as van
der Lely and Stollwerck (1997) have argued that these are
istinctsystems. Tomblin and Zhang (2006) have shown
that these systems appear to be highly related, although
inolder children vocabulary becomes less associated with
grammar, no doubt because grammatical development
becomes limited whereas vocabulary does not.
“There has been less certainty about whether speech,
sound disorder or expressive phonology is also a
part of the language profile of SLI and thus as
well perhaps a component of the same dimension as
grammar and vocabulary. In an early study, Bishop
and Edmundson (1987) proposed that speech-sound
production (phonology) occupied the same dimension
as grammar and semantics. In their model, these
systems were differentially vulnerable and therefore one
would find children with speech sound problems but
spared grammar and semantics, but not the other way
around. Therefore, all these aspects of language were
related to each other and the strength or weakness
of children’s skills could be placed along a single
129
dimension, In recent years it has become more likely
that the expressive phonological skills (speech-sound
production) of children seem to be fiee to vary somewhat
independently of vocabulary and grammar (Pennington
and Bishop 2009, Shriberg er al. 1999, Tomblin et a
2004). Thus, we may provisionally consider speech
sound production abilities co be a separate dimension
that can vary among children largely independently
from their grammatical and vocabulary abilities.
‘A third dimension of communication is concerned
with the social use of language subsumed within the
notion of pragmatics. Pragmatic development and skills
are difficult to quantify and to portray in developmental
terms in conteast with phonological, lexical or grammat-
ical abilities. In concrast with their grammatical skills,
the pragmatic skills of children with SLI have often been
reported to be a relative strength (Craig and Evans 1993,
Leonard et al, 1982, Schaeffer 2003), although this
does not mean that social communication is unscathed
in these children. Studies do show that they are less
skilled in conversations and in their ability to adapt
information content to the listener (Farrant e¢ al 2006,
‘Adams and Bishop 1989, Marcon et al, 2005). Some of
these differences may be the outgrowth of theit limited
lexical and grammatical skills, but some social difficul-
ties remain even when language skills are accounted for
(Botting and Conti-Ramsden 2008).
Within the perspective just outlined, we have
evidence that individual differences in spoken
communication development seem to occur within a
thrce-dimensional space. One dimension is defined by
‘grammar and vocabulary and we can call this structural
Tanguage. The next is speech-sound production; and
the third is social communication or pragmatics. These
dimensions are not completely independent of each
other, but children are moderately free to vary in their
accomplishment on each. Within this model SLI then
occupies a region of individual differences primarily on
the language dimension. In this regard, I am saying
that SLI does not represent a natural kind of language
learner. In fact, I would say that SLI only represents
a convenient, arbitrarily constructed group of language
learners who by this grouping are more similar to each
other than learners who fall in some other region of the
three-dimensional space just described.
I have just proposed that there appear to be
three dimensions that contain individual differences in
communication development. Each of these dimensions
seems to be somewhat independent of the other
and if this is correct then we might conclude that
cach dimension has its own set of developmental
mechanisms. This perspective has to be incorrect on
wo grounds. First, thete is no reason that some
mechanisms can be shared across dimensions; but
even more importantly, it is hard co believe that the130
developmental status of one system such as speech-
sound production does not influence another such as
structural language. It is quite reasonable in my mind
to believe that poor intelligibility will have an effect on
scructural language development. Thus, although these
dimensions have the potential to be independent across
a wide range of ability, there may be local effects in
this relationship where poor ability in one domain has a
direct effect on another domain. This interactive effect
is likely non-linear and could therefore warp the local
individual differences space much the way a gravita-
tional field can warp the linear trajectory of light. This
warping effect will have the effect of creating elevated
rates of co-morbidity within what otherwise might be a
set of relatively independent dimensions of communi-
cation development. This same notion of possible local
interactions that could generate elevated co-morbidity
will come up again when we begin co consider the
relationship of SLI and ASD.
Autism Spectrum Disorder (ASD)
‘The diagnosis of ASD has come to be defined in terms
of a triad of developmental deficits involving qualita
tive impairments of social interaction, communication,
and restricted, repetitive and stereotyped behaviour (for
instance, Happe and Ronald 2008). ‘The language and
communication profiles of children with ASD ate highly
variable across and within aspects of language and
communication. As noted above, considerable research
over the past several decades has taught us that pragmatic
abilities appear to vary at least somewhat indepen-
dently from structural aspects of language (phonology
and grammar). This perspective has been reflected in
Bishop's (2002) distinction between pragmatic disorder
and SLI. Children with ASD are characteristically
challenged with respect to pragmatic ability. In contrast,
wwe find considerable variation among these children
with respect co their structural language abilities where
some children are non-speaking, others present with
poor language while still others have solid skills wich
respect to phonology, grammar and vocabulary. Incerest-
ingly, the aspects of communication chat are character-
istically limited in SLI—scructural aspects—are most
variable in ASD, and vice versa. This kind of profile
contrast has often been used in neuropsychology as a
double dissociation, which is used to argue that the two
disordersare independent and therefore different natural
kinds.
“We can see this view of ASD as a natural kind rather
clearly in the accounts of the actiologies of ASD. It has
been common to view ASD as a distinct form of child
psychopathology that has a single unilying core deficit
such as an impaired Theory of Mind (ToM), Cencral
Coherence (CC) or Executive Function (EF). In this
Bruce Tomblin
way of thinking there is a particular causal account
for why children present with ASD that is different
from one used with children who ate typically develop-
ing, mentally disabled or who are SLI. Such a view of
ASD has been challenged over the years simply by the
recognition of the extent of variability in behaviours of
children. We might ask whether ASD is a composite
of several semi-independent dimensions such as we
observed with speech and language disorders and that
there may a continuum along which people can vary on
these dimensions.
Anearly form of this perspective arose out of research,
‘on the family members of individuals with autism that
resulted in the notion of a Broader Autism Phenotype
(BAP) (Cox etal. 1975, Bolton er al. 1994, Le Couteur
et al. 1996, Landa et al, 1996, Folstein er al 1999,
Fombonne er al. 1997). The BAP has been described by
Bolton et al. (1994) as dysfunction in communication,
social or stercotyped behaviours, and thus represents a
lesser variant of autism that will be expressed in one or
more of these domains. Thus, these researchers hypothe-
sized that the triad of symptoms of autism were both
dimensional in terms of severity and could be disassoci-
ated from one another. Furthermore, it was thought
thac different causal factors could influence each of
these dimensions. More recently, others have presented
a similar view. Studies are now showing that the traits
that comprise ASD can be extended into the normal
population and that there is lite evidence that there is
a discontinuity at some clinical boundary (Constantino
and Todd 2003, Skuse etal. 2005). Furthermore, Ronald
ct al. (2006a, 2006b) have shown that these traits have
considerable freedom to vary independently. This leads
us to question whether ASD is properly viewed as a
natural kind as well
SLI and autism: a long debate over kinship
If SLI and ASD are natural kinds of developmental
disorders, then it makes sense to consider whether they
are in some way related. By definition, children with
SLI cannot present with ASD; however, ASD does not
exclude SLI and therefore this form of overlap has
become a central issue of debate. Diagnostic overlap
is often referred co as co-morbidity. Co-morbidity is the
‘concept that two or more diseases occur together at rates
that exceed chance levels. Classically, co-morbidity has
referred to the co-occurrence of two or more indepen-
dent diseases; however, this term is also used co refer
to diseases that may be partially related (for instance,
Neale and Kendler 1995) and it is in this sense that I
will be using the term. If two clinical conditions with
unknown aetiologies ate co-morbid, we can hypothe-
size that they ate likely to share common risk factors oF
aetiologies. Therefore, the question of co-morbidity ofCo-morbidity of autism and SLI: kinds, kin and complexity
SLI and ASD will ultimately rest on whether there are
shared underlying mechanisms for the language deficits
in these two conditions.
The notion that ASD was related to SLI extends
back to at least 1967 when Rutter (1967) hypothe-
sized that language impairment served as the primary
abnormality in autism and that this abnormality might
be similar to that of a severe receptive aphasia. In
this respect ASD was a severe variant of receptive
language impairment and thus the two were one and
the same. In fact, Rutter considered the social difficul-
ties in ASD to arise from the very poor language
skills and therefore were secondary to language deficits
Rutter and colleagues tested this idea by contrasting
the language and cognitive characteristics of children
with receptive aphasia and children with autism (Bartak
eral. 1975, 197). ‘They found that these two clinical
groups were similar wich regard to deficits in vocabulary
and syntax; however, differences in the communica-
tion profiles of these children were found with respect
to the use of gestures and spoken language for social
communication purposes. That is, they identified the
profile features described earlier wherein children with
ASD were most prominently impaired in pragmatics
and less affected in the structural aspects of language.
Numerous other studies have demonstrated the marked
impairment of social aspects of language in children with
autism (Baltaxe 1977, Tager-Flusberg 1994). Because
the profiles of ASD and receptive aphasia (SLI) were
not the same particularly with respect to pragmatic
skills, most researchers and clinicians recognized them
as representing different developmental disorders.
SLI and ASD as co-morbid
Recognizing that two disorders are different; however,
this does not necessarily mean they cannot be comorbid,
As noted above, it remains possible for children with
ASD to also present with SLI and this viewpoint
was put forth about a decade ago by Tager-Flusberg
and colleagues. In so doing, Tager-Flusberg’s claim has
stimulated considerable debate over the last decade. This
view was frst expressed by Kjelgsard and Tager-Flasberg
(2001) who emphasized the variability in structural
language skills even among children with ASD who were
verbal. ‘This variabilicy presented itself as a continuum
from normal to very low structural language stills,
‘They further noted that this variability in language
contrasted with generally poor pragmatic skills and
generally preserved speech-sound production abilities.
In this respect children with ASD as a group presented
with a different profile than children with SLI; however,
a subgroup of children with ASD shared poor structural
language problems with children with SLI, as depicted
in figure 2
Langeage Structure a
Figure2. A conceptual model ofthe same thice-dimensional space
described in figure I, but now with populations of children with SLI
(checkerboard disk) and ASD (disk with a grid) placed inthis space
‘The intersection of these swo disks reflect the overlap with rexpect
to sructurl impairments
These authors then focused on the dimension
of variability that comprised structural language that
provided this overlap. The continuum of language
ability was therefore cu-up into three groups based on
the Peabody Picture Vocabulary Test with cut-points
placed at —1 and —2 SD, where normal levels were
above —1 SD (ALN) and impaired levels (AL were
below —2 SD, and those between —1 and —2 were
borderline, They reported that 50 of the 82 children
were in the ALI category, whereas only 22 were ALN.
In a sample of 82 children we would expect that less
than 3% of the population would score below —2 SD,
and yet in this sample 61% scored below this threshold.
‘This shows a substantial excess of children with poor
language. Not only was there an excess of poor language
learners, but also the authors presented data that argued
that the language profiles of these children in the
borderline group and impaired group match profiles
reported for children wich SLI. Additionally, they also
noted that both SLI and ASD had been shown to be
heritable and thatthe research on the BAP had suggested
that near relatives of children with autism were prone
co language-learning disorders. So they hypothesized
that a subgroup of children with ASD presented with
comorbid SLL. As such, SLI and ASD were therefore
likely co have related if not shared aetiologies at least
within this subgroup. Subsequent to this paper, Tager-
Flusberg and Roberts (2003) expanded on this idea by
bringing together literature on cognition neuroimaging
and genetics in ASD to show greater evidence that a
subgroup of children with autism may also have SLI
“Two pieces of evidence in that paper focused on studies
that examined for the presence of two markers of SLI
poor tense use and poor non-word repetition, In these
studies they compared children with ASD and normal132
language (ALN), children with ASD and apparent SLI
(ALD, and a group of children with SLI. Tager-Flusberg
(2006) as well as ‘Tager-Flusberg and Roberts (2003)
described the non-word repetition skills of children
with ALI and ALN. Although both groups showed very
good speech-sound production abilities on the Goldman
Fristoe ‘Test of Articulation, the ALI children were
less capable of repeating syllable strings in non-words.
Roberts etal. (2004) used an elicitation task that probed
for tense usage in these children and found the ALI
children and the SLI children were poor on tense usage,
‘These findings that the children with ALI presented
with linguistic characteristics of SLI added additional
support to the view that SLI and ASD were co-morbid,
Twant co remind readers that T previously noted that
grammatical deficits, even those just concerned with
tense marking, are found in poor language users of
other populations, A similar observation can be made
with respect to non-word repetition. Poor non-word
repetition is often observed in children with dyslexia
and, indeed, Catts ral. (2005) have presenced evidence
that poor non-word repetition is more likely a marker
for dyslexia than SLI. Thus, these SLI markers may not
be good markers for identifying a particular nacural kind
of poor language learner but rather are associated with
poor language skills in general. Ifso, then by selecting a
group of children with ASD who have poor language, it
should not be surprising to see that they show the signs
of poor language learners. Having said this, we have not
resolved the question as to why there isan excess of poor
language learners regardless of what we call them.
Brain imaging
Unquestionably, language arises from and through brain
systems. The structural properties of the brains of SLI
and ASD could cherefore reveal underlying biological
markers of SLI in children with ASD. Research into
the brain characteristics of children with ASD has been
extensive; however, far fewer brain studies can be found
for children with SLI, but some general patterns seem
to emerge. Several studies have provided evidence for an
abnormal left-right hemispheric relationship in children
vwith SLI Jernigan etal, 1991, Plante et al. 1989, 1991,
Gauger et. 1997) resulting in smaller than expected left
petisylvian (posterior language areas) volumes relative to
the right hemisphere, However, Preis et al, (1998) did
not find abnormal symmetry in the perisylvian region,
Gauger etal. (1997) also extended the regions of interest
for SLI to the inferior frontal cortex where they also
found the volume of the left hemisphere in this region
to be smaller in children wich SLI than controls.
Tager-Flusberg et al (2004) recently reported a
rightward asymmetry in the inferior frontal cortex of
children with SLI than controls thus replicating the
Bruce Tomblin
Gauger et al study. Also, surprisingly given the prior
results, the planum temporale was found to have more
lefeward asymmetry inthe children with SLI than among
typically developing children in this study. That is,
children with SLI had larger left hemispheric develop-
‘ment than controls. Herbert et al. (2005) performed a
nested hierarchical analysis ranging from whole brain
through major anatomical lobes to smaller regions
defined as parcellation units with images from children
with SLL Similar to De Fosse ef al. (2004), they found
more rightward asymmetry in the frontal language
areas and more leftward asymmetry in the perisylvian
language areas.
"Among the studies of brain structure there isa small
set of studies that have directly contrasted children with
SLI and children with ASD. In addition to reporting
‘on findings concerned with SLI, De Fosse et al. (2004)
‘compared children with SLI with children with ASD
who either presented with poor language (ALD) or had
‘normal language abilities (ALN). Patterns of abnormal
asymmetry in the inferior frontal cortex were found
for the children with SLI and the children with ALI
Likewise both the SLI and children who were ALI
showed the unexpected exaggerated L > R asymmetry
described earlier in the perisylvian area. The children
with normal language and those with ALN did not show
these abnormal asymmetric relationships. Herbert tal
(2005) used children with ASD who were described as
being high functioning and therefore would be likely
to have had normal structural language abilities and
may have been similar to De Fosse et al’s normal
language ASD group. Despite this, they also found
similar patterns of asymmetry to those of De Fosse
eral’ study for both anterior and posterior parcellation
units involved with language. Thus, they also found the
unexpected abnormal exaggerated [> R in both groups
in the perisylvian area, Herbert and Kenet (2007) have
concluded from these findings that autism and SLI share
many, although not all, neurological features and thus
could be viewed as overlapping conditions. I would also
conclude that in studies where children with ALI were
directly compared with children with SLI there is good
evidence of similarity in brain morphology: Ie would
appear that this pattern is more specific to poorlanguage,
possibly SLI, than to autism, It remains unclear as to
why in these studies they found L > R in the perisyl:
vvian region where other studies have usually found the
‘opposite. One likely reason is that both the De Fosse
et al, and Herbert studies focused their analysis on a
much smaller area in chis region that the other studies.
A question that I do not believe has been resolved is
whether reversed hemispheric asymmetry in one form
or the other serve as neurological markers for a special
kind of poor language such as SLI or whether this
is a brain feature of individuals with poor language.Co-morbidity of autism and SLI: kinds, kin and complexity
Evidence for reversed asymmetty has been reported
for children who ate dyslexic (Eckert 2004). Thus, a
conservative statement might be that children with and
without ASD who have poor language also have similar
brain morphology.
Familial patterns of SLI in ASD families
Recall that within the concept of the BAP was the notion
that milder variants of the key features of ASD could
be seen in near relatives. In fact, several of the studies
that lead to the notion of the BAP reported on elevated
language and language-related deficits in the parents
and siblings of children with ASD. These scudies were
generally done in the 1990s and therefore the idea that
SLI was running in these families was not broached,
Recall that Kjelgaard and Tager-Flusberg did propose
that these elevated rates of language problems in these
BAP familics might be reflective of SLI. The Tager-
Flusberg research group in which I was participating
(Ruser er al. 2007) compared patents of ASD, SLI of
Down syndrome on communication and language from
spontaneous language samples. The Down syndrome
sample was used as a genetic
Down syndrome does not run in families. This study
provided support for the notion that poor language
skills an in the families of ASD children just as it did
in the families of children with SLI. However, when a
distinction was made between the pragmatic skills and
the structural language skills ofthe parents, itwas shown
that scruccural deficits were more common in the parents
of children with SLI, whereas pragmati
prominent in the parents of the children with ASD.
Overall, we took these data as support for a possible
geneticoverlap between ASD and SLI. One thing to note
in this scudy is that the ASD children were not differen-
tiated into ALI and ALN subgroups. This distinction
was made in a subsequent study by Lindgren et al
(2009) that compared language, phonological process-
ing, and reading test performance in sibs and parents
of children with SLI, ALI and ALN, ‘The particular
expectation was that within the ALI relatives we would
see similar deficits to the relatives of the children with
SLI given that the arcas being measured are all language
skillsthatare troublesome for children with SLI. Instead,
wwe found that relatives of SLI children were generally
poorer than relatives of the ALI or ALN. Thus, these
data did not provide support that a particular kind of
language impairment—SLI—was running in both the
SLI and ALI families.
;nsmission contol since
oblems were
ASD and SLI co-morbidity questioned
‘What Thave done so far has been to present the evidence
that has motivated the Tager-Flusberg group to hypothe-
133
size that there is a subgroup of children with ASD
who also have SLI. As this hypothesis was published,
some raised questions as to whether these children
with ALI were indeed SLI. Recently, Whitehouse et al
(2007, 2008) have argued against this notion of an
overlap between SLI and ASD, claiming that SLI and
ASD although similar in some surface manifescations
of language deficits, differ with regard to the underly-
ing bases of these deficits. For instance, the non-word
repetition deficits in the ALI children were qualitatively
different from children with SLI. ‘They suggest that
the apparent signs of SLI among children with ASD
do not hold on closer inspection and that the overlap
in familial risk is likewise weak and not well founded.
‘These authors have concluded that there is no basis for
claiming that SLL and ASD are related at the behavioural
symptom or aetiological level. They concluded that
children with SLI present with a disorder that involves
deficits in phonological working memory and grammat-
ical development whereas children with autism have
impairments in language use and social interactions as
well as restricted interests and behaviours. Even in cases
where there appears to be symptom overlap such as
with non-word repetition, the underlying reasons for
poor repetition differs beeween the two groups. Thus,
these authors have voiced doubt that there is a sizable
subgroup of children with ASD who ae also presenting
co-morbid SLL
Recencly Williams et al (2008) reached a similar
conclusion based on a detailed analysis of the data
found in the literature. One point that was emphasized
in this review was the contrast between the profiles of
children with ALI and SLI reported in both Kjelgaard
and Tager-Flusberg (2001) and Lloyd et al. (2006). In
both cases, the ALI children had greater rates of poorer
receptive than expressive language problems and bet
speech sound abilities than the children with SLI. I do
not believe that cither of these are in fact core features
of an SLI profile. Most studies of SLI recruit children
‘who are receiving clinical services. In an epidemiological
study of children with SLI that I conducted (Tomblin
etal. 1997) most of the children with SLI were not and
often had never been identified. In this study we learned
that the rate of speech sound disorder was much lower
than had been thought but was high in children who
‘were receiving clinical services. Likewise, we found many
more children with receptive problems in the children
who had not been identified compared with those who
hhad been identified. What we had discovered is a well
known problem in medical research. ‘Those people who
seek and receive clinical help will present a different
profile of an illness than those who are also affected but
do not receive care. That is, chere are built in biases in
our clinieal process that influences the clinical profiles
of children in those services. We see very good evidence134
of this with respect to children with receptive language
problems. We have found that these children often are
not identified until their poor language comprehension
results in poor reading comprehension. It should be
‘of no surprise that the poor comprchenders described
by Nation et al, (2004) are similar to children with
SLI except that they have greater receptive problems. If
wwe return to the notion of a three-dimensional space
containing individual differences language, these biases
‘mean that children in different parts of this space have
different probabilities of getting clinically served by
speech-language clinicians or reading specialist ete. The
fact that children with SLI who enter clinical speech-
language service centres ate going to be those who
show greater problems in speech and expressive language
simply is due to the fact that these forms of communi-
cation disorder are more obvious and teachers are more
likely to send children to a speech-language clinician
if they don't talk well. The children who comprise the
ALI group get referred for their clinical services because
of other coubling behaviours and therefore even those
with good speech and poor receptive problems still
are identified. The lesson we learn from this is that
wwe cannot expect that the profiles for children who
have been identified with ASD will perfectly match the
children who have been identified with SLL
In summary, I believe that the debate over an overlap
between SLI and ASD rests on shaky ground. It assumes
that SLI defines a natural kind of language learner and
that this distinctive quality is shown in characteristic
‘markers and profiles. Instead I have argued that many
of these features can be seen in other groups of children
with poor language and that some of these features are
likely to arise from systematic biases in the referral and
case selection process. Since I do not accept that SLI
represents a distinct type of language learner, then I
‘must conclude that children who are ALI are not likely
to bea simple mixture of SLI and ASD. But this still
leaves us with the important observation that Kjelgaard
and Tager-Flasberg raised. Why is it that we see so
‘many children with ASD who also have poor structural
language? Below I will propose three reasons that this
may be so.
Shared aetiology
Recall that when I was talking about the three principal
dimensions of communication, I noted that these
dimensions could quite reasonably share some common
mechanisms. In this regard the independence is not
complete, This may hold for the relationship between
poor structural language and ASD. We found evidence
of just this type of aetiological overlap in the structural
brain imaging and recently another example has come
from molecular genetics.
Bruce Tomblin
CNTNAP2
The CNTINAP2 gene isin the 7435 region and has been
associated with both autism and SLI. Bakkalogla et al
(2008), Alarcon et al. (2008) and Arking er al. (2008)
simultaneously published papers showing that common
and rare genetic polymorphisms within CNTNAP2 were
associated with autism. In both the Bakkalogtu et al
and the Arking et al. studies the phenotype was based
‘on autism diagnosis. In the Alarcon et al. study the
phenotype most strongly associated with CNTINNAP2
was a quantitative trait concerned with the age at
which the parents reported the child with ASD acquired
the first word and therefore these findings implicated
CNTINAP2 as a gene that might be associated wich
language problems with or without autism. Indeed,
Vernes ef al (2008) reported that che same mutation
in CNTIAP2 that was associated with autism was
also associated with phonological short term memory
in a sample of children with SLI. These findings have
provided the first strong evidence supporting a shared
aetiology between autism and SLE; however, we could
just as easily speculate that this gene influences individ-
ual differences in language in general
Direct interactions
‘While partial aetiological overlaps in language and ASD
seem quite likely: I cannot believe that the ALI children
will be identical to children with poor language but
who are not ASD. In this regard, I return to the
notion of local warping of relationships by the direct
influence of the developmental status of one dimension
‘onto another. By definition, children with ASD have a
range of cognitive and social difficulties as well as many
behavioural difficulties that come from their rigidity,
highly focused interests and preference for repetition.
Not only are these behaviours likely to interact within
the child, they also will have
manner in which others around them interact with
them. Ik is hard to believe that language, even the
structural aspects, is so modularized that chese features
do not have an impact on their language development
believe that this is the point raised by Williams et al,
and Whitehouse er al. (2007, 2008). ‘The fact thar the
background risk factors for poor language interact with
the features of autism will make ic very difficult to tease
these apart in the language behaviours of these ASD
children.
ramatic effects on the
Aspects of diagnosis
Finally, there is a fairly obvious explanation for the
‘excess in structural language problems in ASD. Early
poor language and communication are a part of theCo-morbidity of autism and SLI: kinds, kin and complexity
conditions that must be met fora diagnosis of autism. IF
a child developed language normally from early on, itis
likely che child would be considered as having Asperger
syndrome, One of the principal early signs of ASD is
late onset of speech and language. Thus, simply on the
basis of how we sore children into diagnostic classes,
children with poor language will have a greater probably
of receiving the diagnosis.
Conclusions
I began this paper by pointing out that our clinical
classification systems reflect beliefs about the processes
that give ise to these clinical conditions. If we
distinguish between ASD and SLI, do we assume that
cach of these is a unified distinct clinical entity with its
‘own distinct causal system? Furthermore, if we observe
an excess of SLI in the population of children with ASD,
should we assume that this points to an overlap in the
aetiologies of these two? This appears to be the nature
of the debate that has been carried on during the past
decade, What Ihave attempted to do has been to redefine
cour view of SLI (and perhaps ASD) such that they
are not distinct kinds of disorders. Instead che children
with SLI and ASD are indeed children first. They, like
all children, develop from very complex developmen-
tal systems. Some of these systems when perturbed in
particular ways may tip the developmental trajectories
‘ofa child toward ASD or SLI (poor structural language
learners), thus there are likely to be some unique factors
associated with each, but also there ate likely to be shared
‘or common aetiological factors as well. Additionally, to
make things more complex, we can expect to find local
causal relationships that warp the overall independence
of subsystems or dimensions. Furthermore, we cannot
ignore that our clinical services and diagnostic schemes
are actually carving up a multidimensional space that
houses individual differences. These systems reflect
value systems and professional polities, but ultimately
shape the similarities and differences of the clinical
groups.
In conclusion, ASD and what has been known
as SLL very likely overlap, However, I doubt that
they overlap in the form of overlapping nacural kinds.
Instead, the overlap is reflective of deep complexity
that probably produces a complex mixture of similar-
ities and differences just as children with both SLI and
ASD overlap in many ways with typically developing
children.
Note
1. Siructutal language in thie cae includes both grammar and
vocabulary
135
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