Background: Structural language anomalies or impairments in autistic spectrum

disorder (ASD) aretheoretically and practically important, although underrecognised

as such. This review aims to high-light the ubiquitousness of structural language
anomalies and impairments in ASD, and to stimulateinvestigation of their immediate
causes and implications for intervention. Method: Studies of struc-tural language
in ASD are reviewed (based on a search of the literature and selected as meeting
de?nedinclusion criteria), and explanatory hypotheses are discussed. Results: Some
individuals with ASDnever acquire language. Amongst those who do, language
abilities range from clinically normal (ALN) tovarious degrees of impairment (ALI).
Developmental trajectories and individual pro?les are diverse, andminority
subgroups have been identi?ed. Speci?cally: language is commonly but not always
delayedand delayed early language is always characterised by impaired comprehension
and odd utterances,and sometimes by deviant articulation and grammar. Nevertheless,
by school age an ASD-typicallanguage pro?le emerges from group studies, with
articulation and syntax least affected, and compre-hension, semantics and certain
facets of morphology most affected. Thus, even individuals with ALNhave poor
comprehension relative to expressive language; also semantic-processing anomalies
andidiosyncratic word usage. It is argued that impaired socio-emotional-
communicative relating, atypicalsensory-perceptual processing, and uneven
memory/learning abilities may underlie shared languageanomalies across the
spectrum; and that varying combinations of low nonverbal intelligence,
semanticmemory impairment and comorbidities including speci?c language impairment
(SLI), hearingimpairment, and certain medical syndromes underlie ALI and variation
in individual pro?les.Conclusions: Structural language is universally affected in
ASD, due to a complex of shared andunshared causal factors. There is an urgent need
for more research especially into the characteristicsand causes of clinically
signi?cant language impairments. Keywords: Autistic spectrum disorder,language,
social interaction, mindreading, sensory-perceptual abilities, speci?c language
impairment,intelligence, memory.

Introduction
All individuals with autistic spectrum disorder(ASD) have, by de?nition, signi?
cantly impairedcommunication (APA, 2000; WHO, 1992), and thesocio-communicative,
pragmatic and discourseimpairments in ASD have been extensively investi-gated and
discussed. A substantial subgroup ofindividuals with ASD has additional clinically
sig-ni?cant structural language impairments (whereclinically signi?cant is de?ned
as performance atleast 1.5 SD below the mean on standardised lan-guage tests). A
substantial subgroup has little or nolanguage. Moreover, as will become apparent in
thecourse of this article, in those individuals who scorewithin the normal range on
language tests by laterchildhood, the course of structural language devel-opment is
frequently if not always atypical, withsubtle linguistic anomalies persisting even
in themost able. Despite the pervasiveness of theseimpairments and anomalies in
ASD, and their likelytheoretical and undoubted practical signi?cance,structural
language in ASD has been relatively littleresearched over recent decades The
immediate aims of this review article are tohighlight the ubiquitousness of
structural languageabnormalities in ASD and to promote discussion oftheir immediate
psychological1causes. The longer-term aim is to stimulate investigation of
clinicallysigni?cant language impairments in ASD. Socio-communicative and use of
language impairments arenot the focus of this article (but see Charman &Stone,
2007; Loukusa & Moilanen, 2009; McCann &Peppe, 2003 for relevant reviews).2Nor are
thegenetic causes and neurobiological correlates oflanguage in ASD a central focus,
although alluded toat various points (see Abrahams & Geschwind, 2008;Groen, Zwiers,
van der Gaag, & Buitelaar, 2008;Herbert & Kenet, 2007; Liu, Peterson, &
Szatmari,2008 for relevant reviews).In the ?rst main section of the review,
behaviouralstudies of structural language in verbal individuals with ASD are
reviewed in two subsections covering,respectively, studies of language normal
(ALN) par-ticipants, and studies of language impaired (ALI)participants or
unselected (mixed ability) groups.The distinction between ALN and ALI is
arti?cial inthat language abilities in ASD lie along a continuum,but is made herein
because explanations of higherand lower language abilities in ASD necessarily dif-
fer. In the studies reviewed, mean language/verbalabilities in ALN groups were
85; and in ALI groups75. These criteria do not preclude some overlapamongst
outliers. It is also accepted that standardscores are not strictly comparable
across differentlanguage tests. However, use of these criteria forinclusion in the
review enables comparisons to bemade between more and less linguistically
ablegroups with ASD.
(Psychological is used here to refer to explanations at the levelof behaviour or
mental processes, including emotional andconative as well as intellectual
processes. Cognitive is usedaccording to its dictionary de?nition to refer only
to intellectualfunctions such as thinking, knowing and reasoning.2Structural
language and communication are, in reality,indissolubly linked. An arti?cial divide
is made here to sharpenthe focus of attention onto structural language in ASD.)
Studies reviewed satisfy the following methodo-logical criteria unless otherwise
stated: (a) minimumgroup sizes 10, (b) evidence that ASD participantssatisfy
current diagnostic criteria (noting that earlycriteria were less rather than more
inclusive), (c) fewor no cases of PDD-NOS included, and (d) compari-son groups
(identi?ed in the text when included)appropriately matched for age and ability (as
iden-ti?ed in the text, language-matched indicatingmatched for vocabulary
comprehension unlessotherwise stated; well-matched indicating matchedon two or
more relevant measures). No mention ofcomparison groups signals studies making
compar-isons with standardised norms or normative data.See also before a
reference signals a study of inter-est, but not meeting the inclusion criteria.In
the second main section of the review, theoriesand evidence relating to the
psychological causes ofatypical language across the spectrum (excludingmutism) are
presented and discussed. The reviewconcludes with a brief overview in which
implica-tions for future research, including interventionstudies, are indicated.
Patterns of language abilities and impairmentsStudies of language in group s with
ALNStudies of ALN sometimes report ?ndings on Asper-ger syndrome (AS) groups (in
whom language hasbeen clinically normal from the start); sometimes onhigh-
functioning autism language normal (HFA-LN)groups (in whom currently normal
language waspreceded by early delay or deviance); and sometimeson mixed AS + HFA-LN
groups. Few differencesbetween language in AS as compared to HFA-LNhave been
reported, and studies of language in ALNgenerally are considered ?rst. Findings
from studiesspeci?cally comparing language in AS and HFA-LNgroups are noted at the
end of the section.Productive phonology (articulation) is normal inindividuals
with ALN, in terms of group averages onan articulation test (Kjelgaard & Tager-
Flusberg, 2001.
However, Shriberg, Paul, McSweeny, Klin,and Cohen (2001) reported that a third of
individualshave subphonemic articulatory distortions (e.g. animperfect/r/sound, or
slightly lisped/s/). Similarly,Cleland, Gibbon, Peppe, OHare, and
Rutherford(2010) reported that 41% of individuals with ASDand ostensibly normal
language had at least somearticulatory errors, with 12% of the total grouphaving
clinically signi?cant impairments.Regarding semantics and grammar in ALN,Asperger
described language used by his patients assuperior in breadth of vocabulary and
grammaticalcorrectness, although idiosyncratic and pedantic(Asperger, 1944/1991
translated in Frith, 1991).However, receptive and expressive vocabulary aver-aged
across groups with ALN has subsequently beenfound to be either average (Kjelgaard &
Tager-Flus-berg, 2001) or in the low normal range (Howlin, 2003).Moreover, higher
order language processing as as-sessed by the Clinical Evaluation of Language Fun-
damentals Revised (CELF-R Semel, Wiig, & Secord,1987) is more impaired than
vocabulary (Kjelgaard &Tager-Flusberg, 2001), comprehension being partic-ularly
affected (Koning & Magill-Evans, 2001; Saa-lasti et al., 2008; Seung, 2007).
Consistent with thebroad picture that emerges from these ?ndings, Min-shew,
Goldstein, and Siegel (1997) and Williams,Goldstein, and Minshew (2006) reported
intact per-formance on simple tests such as a letter-cued word?uency task or the
Vocabulary subtest from theWechsler scales (Wechsler, 1997a,b) but
impairedperformance on complex tests such as reading com-prehension or the
detection of verbal absurdities.Group based ?ndings do not, of course, entail that
allindividuals with ALN have below average languageabilities on certain tests.
However, they do show thatsuperior semantic and grammatical abilities in peoplewith
ALN are less common than is often supposed.The precise nature of the higher order
languageprocessing dif?culties in ALN is not clear. How-ever, anomalous semantic
processing is certainlyinvolved. Numerous clinicians and researchers havecon?rmed
Aspergers observation of idiosyncratic orinappropriate utterances (e.g. Mayes &
Calhoun,2001; Tantam, 1988; Volden & Lord, 1991). In theirdetailed study of natural
language samples, Voldenand Lord noted in addition that real words werefrequently
used with incorrect meaning, for examplewaves for leaves. Other evidence of
semanticanomalies in ALN is more subtle. Dunn, Gomes, andSebastian (1996) reported
an excess of low frequencyresponses in a category-cued word ?uency test,relative to
language-ability-matched groups withspeci?c language impairment (SLI) or typical
devel-opment (TD). Similarly, Walenski, Mostofsky, Gidley-Larson, and Ullman (2008)
reported superiornaming speed for low frequency but not highfrequency stimuli
compared to full scale IQ (FSIQ)-matched controls (see also Toichi & Kamio, 2003).
Instudies of verbal memory in able adults with ASD compared to verbal IQ (VQ)-
matched controls, Bow-ler, Matthews, and Gardiner (1997) showed impaireduse of
semantic clustering; and Bowler, Gaigg,and Gardiner (2008) reported that whereas
neuro-typical participants developed similar sequences inrecall of words over
repeated trials, idiosyncraticsequences were developed by participants with
ASD.Even children whose early diagnosis of PDD-NOSor other high-functioning ASD no
longer appliesshowed immature lexical knowledge on a test ofthe understanding of
verb-argument structures,whilst performing normally on tests of single
wordcomprehension and naming (Kelley, Paul, Fein, &Naigles, 2006).Some have argued
that intact use of category cuesin single word recall tasks shows that
semanticknowledge is intact in ALN (Mottron, Morasse, &Belleville, 2001;
Whitehouse, Maybery, & Durkin,2007). However, intact performance on some tests
ofsemantic knowledge does not prove that semanticprocessing is entirely normal.
Thus, Kelley et al.(2006), whose ?ndings were cited above, noted thatvocabulary
tests assess knowledge of the identi?ca-tion function of words, but do not probe
conceptualnetworks underlying word meanings. Consistentwith this observation,
Minshew, Meyer, and Gold-stein (2002) reported intact category identi?
cationcoexisting with impaired category formation. Simi-larly, Dunn and Bates
(2005) reviewed the discrep-ant evidence and concluded: Although there issigni?
cant evidence that individuals with autismcomprehend basic concepts and word
meanings,they do not appear to extract and apply commonal-ities among category
members.Behavioural observations of anomalous semanticprocessing are supported
by ?ndings of anomalousbrain activity in individuals with ALN duringsemantic
processing tasks. For example, McCleeryet al. (2010) showed abnormal brain
activation inresponse to picture-word pairs but not to picture-environmental sound
pairs in young children in apredominantly HFA-LN group (3 of 14 participantswere
diagnosed with PDD-NOS). Other studiesshowing abnormal brain activity in ALN groups
rel-ative to well-matched controls during semantic pro-cessing tasks include those
of adults by Braeutigan,Swithenby, and Bailey (2008) and by Harris et al.(2006),
and of school-age children by Dunn andBates (2005; see also Knaus, Silver,
Lindgren, Had-jikhani, & Tager-Flusberg, 2008).Compared with the solid evidence of
higher orderanomalies of semantic processing in ALN, there islittle positive
evidence, and some negative evidence,of grammatical impairments, whether of
syntax(de?ned herein as knowledge of the rules andconventions governing word order)
or morphology.Positive evidence includes Volden and Lords (1991)report that non-
developmental grammatical errors,although rare, were signi?cantly more common
inschool-age children with ALN than in controls,correlating with mean length of
utterance (MLU) andVQ. Eigsti and Bennetto (2009) reported reducedsensitivity to
grammatical errors in children withHFA-LN relative to well-matched controls.
However,reduced sensitivity occurred only when errors wereembedded in long
sentences, suggesting that mem-ory load may explain this ?nding. Negative
evidencecomes from a study by Diehl, Bennetto, Watson,Gunlogson, and McDonough
(2008) showing unim-paired utilisation of syntax to disambiguate senten-tial
meaning in an HFA-LN group, relative to controlsmatched for FSIQ- and CELF
receptive languagescores. Similarly, Kelley et al.s (2006) study of wellrecovered
cases of PDD-NOS/ASD showed intactproductive morphology and syntax, coexisting
withsubtly impaired lexical-semantics.There is correspondingly little evidence of
anoma-lous brain activity associated with grammatical pro-cessing in ALN. However,
Just, Cherkassky, Keller,and Minshew (2004) reported atypical brain activityduring
a sentence comprehension task relative toFSIQ-matched controls, which they ascribed
toatypically reduced reliance on syntactic processing.Language in AS compared to
language in HFA-LN. Four behavioural studies have comparedmature language abilities
in individuals with AS andindividuals with HFA-LN and found no signi?
cantdifferences. Speci?cally: individuals with HFA-LNare reported to resemble
individuals with AS inhaving low normal levels of language (Howlin, 2003);a
tendency to produce idiosyncratic or inappropriateutterances (Mayes & Calhoun,
2001); comprehen-sion more impaired than expression (Howlin, 2003;Seung, 2007); and
articulatory distortions in a thirdof cases (Shriberg et al., 2001). Moreover, the
studiesby Mayes and Calhoun, Howlin, and Seung includedassessment of nonlinguistic
ASD-related behav-iours, and found no signi?cant group differences inrelationships
between language and ASD-relatedbehaviours. Consistent with these
behaviouralobservations, a small-group study comparing lan-guage-related brain
activity in individuals with eitherHFA-LN (n=8) or AS (n=2) found no differences,
thesame anomalous brain activity being observed in allparticipants relative to TD
controls (Gaffrey et al.,2007).By contrast, Howlin (2003) reported that
languagelevels were slightly lower in HFA-LN than in ASadults matched for nonverbal
IQ (NVIQ), with dif-ferences in single word naming approaching signi?-cance. Kamio
and Toichi (2007) reported thatindividuals with HFA-LN were less sensitive
tosemantic similarity than AS participants matchedfor FSIQ. Ghaziuddin et al.
(2000) reported thatparticipants with HFA-LN produced shorter, lesscomplex and less
grammatically correct sentencesthan an AS group when differences in FSIQ
werepartialled out. These ?ndings suggest that delayedlanguage in individuals with
HFA-LN is associated with subtle but persistent effects in at least
someindividuals.
Studies of language in group s with ALI and inunselected (mixed ability)
groupsUntil the 1980s, diagnostic criteria for early child-hood autism included
language impairment (Ritvo &Freeman, 1977; Rutter, 1968). Studies of languageprior
to the mid- or late-1980s therefore focusedsolely on individuals with ALI. These
studies areimportant because changes in diagnostic criteria inthe mid-1980s
resulted in a switch of researchinterest from individuals with ALI to language-nor-
mal groups (as reviewed above), and studies of ALIare now relatively rare. However,
because methodsof early diagnosis had not been established, andadults with ASD were
undiagnosed, only school-agechildren were studied in this early period.
Findingsfrom these early studies of school-age children arereviewed ?rst, below.
Improved early diagnosisenabled later researchers to study language and
itsprecursors in younger unselected groups or groupswith ALI, and ?ndings from
these studies are con-sidered in a second subsection. Findings from asmall number
of relatively recent studies of school-age children with ALI, and from rare studies
of adultswith ALI, are considered in a third subsection.Early studies: language in
school-age childrenwith ALI. These studies appeared to show delayedand limited,
rather than deviant, development ofphonology and syntax. Thus, articulation
wasreported to be superior to that of language-matchedchildren with developmental
delay (DD; Boucher,1976) or in a small-group study (group sizes 9 and12)
broadly similar to that of nonverbal mental age(NVMA)-matched children with DD
(Bartolucci,Pierce, Streiner, & Eppel, 1976). Bartolucci et al.also reported signi?
cant correlation between articu-lation and syntax in ALI participants; and Pierce
andBartolucci (1977) reported that the grammaticalsystem used by children with ALI
was rule-governedand similar to that of NVMA-matched DD and TDgroups, again
suggestive of delayed syntactic devel-opment. Similarly, Tager-Flusberg (1981)
showedthat children with ALI resembled well matchedyoung TD controls in preferring
a word order strategyto a probable event strategy in sentence compre-hension,
suggestive of mental age (MA)-appropriatesyntactic abilities. Prior and Hall (1979)
reportedthat children with autism had impaired compre-hension of transitive and
intransitive phrases rela-tive to language-matched DD and young TDchildren.
However, children with ALI resembledcontrols in their pattern of response, again
suggest-ing delay rather than deviance.Early ?ndings on morphology in school-age
chil-dren with ALI relative to established norms includedimpaired comprehension and
use of personal pro-nouns, errors of verb tense marking, impaired use ofarticles
and conjunctions, and diminished use ofclosed class words generally, especially in
the earlystages of language acquisition (Bartolucci, Pierce, &Streiner, 1980;
Howlin, 1984; see also Tager-Flus-berg et al., 1990; Waterhouse & Fein, 1982).
These?ndings were variously interpreted as indicative ofdeviant development,
impaired deixis, or DD.Semantic development, by contrast, was consis-tently
recognised as deviant. Kanner (1946) notedthe frequent use of stereotyped and
idiosyncraticlanguage, including neologisms. Bartak, Rutter, andCox (1975) reported
that an excess of stereotypic,echolalic and bizarre language constituted the
majordifference between an ALI group and a NVIQ-mat-ched but slightly older SLI
group. Other researcherscommented on the persistence of echolalia in lessable
individuals with ALI, noting the idiosyncraticbut functional usages of echoic
utterances in con-texts resembling those in which they were originallyheard (Fay &
Schuler, 1980; Prizant & Duchan,1981). Fay and Schuler wrote:If there is one
pervasive theme in the study of thelanguage of childhood autism it is the
permanence of theinitial learning situation. How can speech be broughtinto line
with adult models if the only associations are?rst associations that are
tenaciously stored and recy-cled as if they were cast in concrete? [Italics as in
theoriginal].Fay and Schuler went on to suggest that the pau-city and rigidity of
the associations to words orphrases learned by a child with autism entails
thatlanguage for these individuals denotes but does notconnote i.e. words and
phrases are used like propernames, having a single referent rather than a
rich,generalisable network of associations and meaning.Anomalous processing of
linguistic meaning wasalso indicated by studies showing impaired use oflexical or
sentential meaning to facilitate verbalrecall. Thus Fyffe and Prior (1978),
Hermelin andOConnor (1967), and others showed that childrenwith ALI differ from
language-matched children withDD in that recall of sentences or of
semanticallyrelated words is not superior to recall of unrelatedword lists. These ?
ndings led some researchers topropose that children with autism have a funda-mental
impairment in the acquisition of conceptualknowledge (Fay & Schuler, 1980; Hermelin
&OConnor, 1970; Menyuk, 1978). However, tests ofknowledge of basic and
superordinate categoriesfailed to con?rm this hypothesis (Tager-Flusberg,1985;
Ungerer & Sigman, 1987). Moreover, Tager-Flusberg (1991) showed that children with
ALI canuse semantic cues to aid verbal recall (see also Bou-cher & Warrington,
1976), even though they do notspontaneously use a clustering strategy whenrecalling
semantically related word lists. These mixed?ndings pre?gured similar observations
in individu-als with ALN, as noted in the previous section.
ater studies: language in preschool children withALI and in unselected preschool
groups through toearly school-age. The view that language acquisi-tion is
predominantly delayed rather than deviantin ALI remained dominant until the end of
thelast century (Lord & Paul, 1997). However, onceadvances in early diagnosis made
it possible toinclude very young children in research studies, adifferent picture
emerged. Thus, Rapin and Dunn(2003) reported that 63% of children with ALIof
preschool-age (up to c. 6;0 years), fall into theclinical category of mixed
receptive/expressivelanguage disorder that includes impaired phonologyand grammar
(and which is the most commonform of SLI); whereas only 37% have
impairmentsrestricted to the higher order processing problemsthat relate most
clearly to semantic meaning. How-ever, preschool children with ALI invariably
haveimpaired language comprehension, never expressivelanguage impairment alone; and
in this they differfrom groups with SLI.Rapin and Dunns observation of delayed
anddeviant phonology in preschool children with ALIwas con?rmed in case studies of
four siblings byWolk and Giesen (2000); and the observation ofimpaired grammar in
preschool children with ASDwas con?rmed by Eigsti, Bennetto, and Dadlani(2007). In
the latter study, spontaneous languageused by 16 preschool children with ASD and
past orpresent language impairment or delay was comparedwith that of age-,
language- and NVIQ-matchedchildren with DD, and very young TD children.
Threemeasures of structural language analysis were used:the Inventory of Productive
Syntax (IPSyn; Scarbor-ough, 1990); MLU as measured in morphemes; andNumber of
Different Word Roots (NDWR) to assesslexical-semantic knowledge. The children with
ASDwere signi?cantly impaired on the IPSyn; moreover,the pattern of their scores
differed from that in con-trols, and was thus deviant rather than simply de-layed.
Children with ASD also had shorter meanMLU than the DD group, and somewhat shorter
MLUthan the TD group. By contrast, they produced asimilar number of different word
roots as the TDgroup, and signi?cantly more than the DD group,although they also
produced signi?cantly more jar-gon than controls.Two large-scale studies of
unselected groups ofpreschool children with ASD reported delayed lan-guage onset
and a slowed rate of development inmost but not all children, according to
parentalobservations (Charman, Drew, Baird, & Baird, 2003;Luyster, Lopez, & Lord,
2007). For example, in theCharman et al. study a level of phrasal under-standing
that TD children have at approximately1 year 4 months was not achieved (as a group)
untilage 4:0, and when NVMA equivalent was at least3 years 6 months. In both
studies the children withASD understood more words and phrases than
theyspontaneously used, following the normal pattern.
However, the discrepancy between comprehensionand production was much smaller in
the ASD groupthan in a TD comparison group in both studies(con?rmed by Hudry et
al., 2010), and Charmanet al. suggest that words and phrases may be usedby children
with ASD without full meaning.Taken together, these four studies of language
inpreschool children with ASD show that up to the ageof approximately 6;0 years,
most but not all children with ASD have markedly delayed languagedevelopment
that includes signi?cant abnormalitiesof phonology and grammar, contrary to ?ndings
fromearlier studies of older children. To explain this dis-crepancy, Rapin and Dunn
(2003) speculated thateither the pro?le of language impairments changeswith age in
children with ASD, or that children ingroups previously studied had higher
nonverbalintelligence than the children in their study. Thelatter explanation was
discon?rmed by Eigsti et al.s?ndings on a relatively able ASD group, whereas
theformer explanation received support from a follow-up study by Rapin, Dunn,
Allen, Stevens, and Fein(2009). In this study, children with ALI who had
beenassessed as preschoolers were reassessed agedbetween 7;0 and 9;0 years. On
reassessment, 11% ofthe group had clinically normal language, and 73%had intact
articulation with mild or moderateimpairments of higher order semantic and
syntacticcomprehension, conforming in general terms to thepro?le identi?ed in early
studies of school-age chil-dren. Of the remaining children assessed by Rapinet al.
(2009), the majority were globally impaired,intellectually and linguistically.
However, a smallsubset had unimpaired comprehension but signi?-cant articulatory
impairments, a pro?le corre-sponding to that identi?ed in the study of
individualswith ALN by Cleland et al. (2010).Rapin et al.s (2009) longitudinal
study does muchto reconcile recent ?ndings on preschool children withASD with early
?ndings on school-age children withALI. Moreover, these authors ?ndings are
consistentwith those from two other longitudinal studies. Geurtsand Embrechts
(2008) reported that at preschool-agelanguage pro?les in a majority of children
with ALIresemble those of SLI, including expressive phono-logical and syntactic
impairments; but by school-agelanguage pro?les in the two conditions have
diverged,with higher order processing and pragmatic impair-ments now predominating
in ALI. Similarly, a study byBennett et al. (2008) showed that structural
languageimpairments were more common in children with ASDwhen assessed at preschool
age than when assessedat c. 7;0 years. Moreover, the persistence of
structuralimpairments at age 7;0 was a good predictor of adiagnosis of ALI in
adolescence.Later studies: language in school-age children andadults with ALI or in
unselected school-age oradult groups. In the major study by Kjelgaardand Tager-
Flusberg (2001) cited above (also reported n Tager-Flusberg & Joseph, 2003),
language wasassessed in an unselected group of 89 children withASD aged between 4;0
and 14;0 years (mean7.3 years, therefore predominantly of school-age).Clinical
tests of articulation, single word compre-hension, single word naming, nonword
repetitionand higher order receptive and expressive languageusing the CELF
(Preschool or CELF-III versions) wereadministered to all children able to
cooperate, andparticipant scores were compared with age appro-priate norms.
Unsurprisingly, in view of the widerange of age and ability represented, results
acrossthe whole group were heterogenous. However, whendivided into ALN, language-
borderline and ALI sub-groups on the basis of vocabulary comprehensionscores, ?
ndings from this study were largely con-sistent with the classic pro?le of
linguistic strengthsand weaknesses that had emerged from the earlystudies of
school-age children with ASD. Speci?cally:articulation was unimpaired in the ALN
and bor-derline subgroups, but mildly impaired (and proba-bly MA-appropriate) in
the ALI subgroup. Expressiveand receptive single word vocabulary were moreimpaired
than articulation in all three subgroups,but most signi?cantly impaired in the ALI
subgroup.Similarly, scores on the CELF in 44 children whocompleted this test showed
that higher order recep-tive and expressive language was more impairedthan single
word vocabulary in all three subgroups,with the handful of children with ALI able
to com-plete the CELF having the most marked dif?culties.Notably, subtest scores on
the CELF in all threesubgroups were below age-related norms, withreceptive language
signi?cantly more impaired thanexpressive language, and productive syntax
leastaffected. Finally, standard scores for children testedon the Preschool version
of the CELF were lower thanstandard scores for children aged from 6:0 upwardstested
on CELF-III, consistent with ?ndings fromRapin et al.s (2009) and other
longitudinal studies.In addition to the above ?ndings, one noveland challenging ?
nding emerged from Kjelgaard andTager-Flusbergs study: namely that nonword repe-
tition was signi?cantly impaired in the ALI subgroup(though not in the ALN or
borderline subgroups).Findings from other studies of school-age childrenor adults
are also largely consistent with ?ndings fromthe early studies, although there have
been no recentstudies of articulation in groups with ALI. Regardingsyntactic
abilities: Condouris, Meyer, and Tager-Flusberg (2003) used the IPSyn to analyse
gram-matical structures occurring in the spontaneouslanguage of the 44 children
able to complete the CELFin Kjelgaard and Tager-Flusbergs (2001) study.Nonsigni?
cant impairment relative to establishednorms was reported on combined subtest
scores.3 (Performance was signi?cantly poor on the QuestionNegationsubtest,
probably for pragmatic and social reasons, as theauthors point out.)
Shulman and Guberman (2007) reported intact use ofsyntax in a group of rising 6;0
year old children withALI, relative to very young TD children; and superioruse of
syntax relative to age- and language (CELF)-matched) children with SLI. Two other
studies haveshown that children with ALI perform better than age-and NVIQ-matched
children with SLI on, respectively,tests of the comprehension of grammar
(Botting &Conti-Ramsden, 2003) and the processing of syntac-tic complexity (Riches,
Loucas, Baird, Charman, andSimonoff (2010).Morphology, on the other hand, is more
likely to besigni?cantly impaired. Thus, detailed linguisticanalysis of natural
language samples in seven youngadults with ALI showed that morphological errorswere
common in all the participants, generally con-sisting of truncations, omissions, or
substitutionsespecially of closed class words such as conjunc-tions, articles, or
pronouns (Dobbinson, 2000).Similarly, in the study by Condouris et al. (2003)cited
above, mean MLU as measured by morphemeswas 2 SDs. below age-related norms, despite
the factthat vocabulary comprehension was normal or bor-derline-normal in most
participants. In anotherstudy using a subset of Kjelgaard and Tager-Flus-bergs
(2001) participants, 62 children divided as inthe original study into ALN,
borderline and ALIsubgroups, were tested for their production of verbtense endings
(Roberts, Rice, & Tager-Flusberg,2004). The ALI subgroup performed
particularlypoorly. However, errors also occurred in the othertwo subgroups, use of
irregular past tense formssuch as ran, spoke being particularly
impaired.Botting and Conti-Ramsden (2003) also reporteddeviant verb tense marking
in school-age childrenwith ALI but did not note the kinds of errors made.All the
above evidence indicates that the acquisitionand use of certain morphemes is
impaired in ALI.Evidence relating speci?cally to morphosyntax (therules governing
morpheme combinations) is sparse.However, in their study of idiosyncratic language
inALN and ALI subgroups, Volden and Lord (1991)noted that the majority of
neologisms used by bothgroups resulted from combining morphemes in log-ical but
incorrect ways (e.g. redundiate to meanmake redundant), suggesting that
morphosyntax isrelatively unimpaired.Regarding lexical-semantics: in the study
byCondouris et al. (2003) mean scores on the NDWRwere, like mean MLUs, 2 SDs below
age-relatednorms. This ?nding differs from that reported byEigsti et al. (2007) in
their study of preschool chil-dren, in which NDWR was unimpaired relative toyoung
TD children, and superior to that of childrenwith DD. It is also inconsistent with
the relativelygood performance on vocabulary tests, as commonlyobserved. However,
Condouris et al.s ?nding may beexplained by the repetitious and formulaic nature
ofspontaneous language in older individuals with ALI(Perkins, Dobbinson, Boucher,
Bol, & Bloom, 2006).
Thus, Perkins et al. noted that linguistic analysis ofnatural language samples from
seven young adultswith ALI showed repeated use of preferred lexicalitems, phrases
and also grammatical frames, limit-ing the range and variety of words and word
formsused.A literature search identi?es no studies of thebrain correlates of
language in ALI groups, speci?-cally. This is no doubt partly because of ethicaland
practical dif?culties associated with braininvestigations with this group,
especially in thecase of functional studies; but is nevertheless regrettable.
Summary of empirical ?ndings on struc turallanguage at diff erent ages and across
the spectrumLanguage is often but not always delayed in ASD.Preschool children with
delayed language includingthose classed as HFA-LN by later childhood
havesigni?cantly impaired comprehension and process-ing of meaning, and
approximately two-thirds of thegroup have additional, clinically signi?cant impair-
ments of expressive phonology and grammar. Oversubsequent years, the early
occurring articulatoryand syntactic impairments tend to resolve, stabilis-ing at
MA- appropriate levels in most individuals.Certain morphological errors and
anomalies aremore persistent; and comprehension, semantics,and the processing of
meaning generally are mostreliably and severely affected in persistent cases
ofALI.When language is not delayed, or when early lan-guage delays and impairments
have largely resolvedby later childhood, an uneven language pro?le cannevertheless
be detected. This shows the same pat-tern of relative peaks and troughs as commonly
oc-curs in persistent ALI, as summarised above.Speci?cally: comprehension is more
affected thanexpression, although words and phrases may beused idiosyncratically.
Articulation is normal in allbut a small subgroup, although minor mispronun-
ciations are not uncommon. Syntax, and possiblyalso morphosyntax, is unimpaired.
However, certainmorphemic anomalies persist; and despite normalperformance on
vocabulary tests, semantic pro-cessing is anomalous, possibly in association withan
impoverished conceptual or lexical meaning base.It is important to point out, ?
nally, that the aboveASD-typical language pro?le, whether at a high levelof
overall function as in individuals with ALN or atlower levels of overall function
as in persistent ALI,emerges from group studies and masks considerableheterogeneity
amongst individual pro?les.
xplaining atypical language development inASD: Theories and evidenceTheories of
atypical language development in ASDmust explain at least the following: (a) why
language is so markedly delayed in most but not all individuals (In an
important subgroup, language development is normalinitially but then regresses or
plateaus, either temporally orpermanently (Rapin, 2006; see also Mawhood, Howlin,
&Rutter, 2000 for an account of language regression in laterchildhood). The causes
of regression at various life stages inASD are not well understood, and although of
undoubtedimportance are not considered herein), (b) why an ASD-typical language
pro?leemerges from group studies of older children andadults with ASD, (c) why
language outcomes inASD are so heterogeneous, in terms of bothindividual pro?les
and the degree to which languageis impaired, and (d) why language in some
preschoolchildren with delayed language is strikingly moreimpaired and deviant than
in most older childrenand adults. Before discussing possible answers tothese
questions, it is important to note that causalchains underlying atypical language
developmentand outcomes in ASD are complex and interactive,even when considering
psychological causes only.Single cause explanations rarely if ever apply; nordo
single effects of individual causal factors oftenoccur, as will be evident from
what follows.
Explaining delayed language in some but not all individuals Delayed language is
most readily explained by thesocio-emotional-communicative impairments thatare
characteristic of very young children who willlater be diagnosed with ASD. These
impairments ofdyadic (one-to-one) relating include lack of empathy(Charman et al.,
1997; Sigman, Kasari, Kwon, &Yirmiya, 1992); lack of preferential responsiveness
tosocial stimuli such as faces and voices (Baranek,1999; Dawson, Meltzoff,
Osterling, Rinaldi, &Brown, 1998; Dawson et al., 2004; Klin, 1991; Kuhl,Coffey-
Corina, Padden, & Dawson, 2005); lack ofspontaneous imitation of others actions
(Carpenter,Tomasello, & Striano, 2005; Charman et al., 1997);and impairment of
timing mechanisms subservingrhythmicity and synchronisation within infant-
carerinteractions (Gernsbacher, Sazuer, Geye, Schweig-ert, & Goldsmith, 2008;
Wimpory, Nicholas, & Nash,2002; see also Iverson & Wozniak, 2007).5 (It is not
established that all these abnormalities occur in-nately in all infants with
incipient ASD. However, as argued byLeekam (2005) any one such impairment would
tend to lead tothe others) These early occurring socio-emotional impairments may be
exacerbated by abnormal speech perception (shownbehaviourally by Alcantara,
Weisblatt, Moore, &Bolton, 2004; Lepistoet al., 2008, 2009; and neu-robiologically
by Cardy, Flagg, Roberts, & Roberts,2008; Jansson-Verkasalo et al., 2003; and
Redcay &Courchesne, 2008).Anomalous one-to-one socio-emotional-communi-cative
behaviours create what might be termedself-originating social deprivation. Speci?
cally: the infant does not attend to or respond to people, andthis distorts carers
interactions with the child,including the amount and kind of language that isused
(Warren et al., 2010). Impoverished and atypi-cal social interactions thus prevail
from very earlychildhood when the foundations of communicativeinterchange and
language are normally established.As pointed out by Kuhl (2004), social
deprivation,however caused, has devastating effects on languageacquisition. In the
case of ASD, diminished andanomalous child-carer/carer-child interactions havebeen
shown to be associated with poor languageoutcomes in both the short term (Bopp,
Mirenda, &Zumbo, 2009; Ruble, McDuf?e, & King, 2008; Siller& Sigman, 2008) and in
the longer term (Siller &Sigman, 2002). Moreover, if, as argued originally byHobson
(1993) and now widely agreed (Boucher, inpress), early occurring impairments of
dyadic inter-action underlie later-manifesting mindreadingimpairments in ASD, the
indirect effects of very earlyinteraction impairments on structural
languageacquisition are considerable (see below).Why, then, do not all toddlers
with ASD havedelayed language, although all are, by de?nition,socially, emotionally
and communicatively impaired?Nonverbal intelligence (NVIQ) is associated
withlanguage outcomes in ASD (Stevens et al., 2000;Thurm, Lord, Li-Ching Lee, &
Newschaffer, 2007)and high NVIQ may enable some individuals toacquire language via
an atypical route. Suggestedcompensatory routes include utilisation of superiorrote
learning and associative ability (Bloom, 2000);precocious reading ability, or
extended use of intactcomputational modules subserving the acquisitionof phonology
and syntax (Frith & Happe, 1994).Normal NVIQ does not, however, guarantee protec-
tion from clinically signi?cant language impairment,as is evident from studies of
high-functioning indi-viduals with ALI (e.g. Bennett et al., 2008; Eigstiet al.,
2007; Stevens et al., 2000).Explaining the ASD-t ypical language pro?le thatemerges
from group studiesAll individuals with full forms of ASD share certainpsychological
characteristics with potential effectson language development, and these
charcteristicsprobably underlie the ASD-typical language pro?lethat emerges from
group studies, as argued next.Impaired mindreading in its numerous manifesta-tions
is widely recognised as implicated in the com-municative impairments diagnostic of
ASD (Sperber& Wilson, 2002). Impaired mindreading can alsohelp to explain why
language comprehension hasconsistently been shown to be more affected
thanexpression, in that individuals with ASD fail to takeaccount of other peoples
knowledge, thoughtsand feelings in interpreting speech (Surian, Baron-Cohen, & Van
der Lely, 1996). Certain facets ofimpaired mindreading also help to explain some
aspects of the ASD-typical structural language pro-?le, as argued by Bloom (2000),
Frith and Happe(1994), Hobson (1993), Tager-Flusberg (2000), andothers. For
example, joint attention impairments areassociated with language delay and predict
laterlanguage competence generally (e.g. Ruble et al.,2008; Siller & Sigman, 2008).
More particularly,early word learning is normally based in part on theapprehension
of social cues such as the speakersdirection of gaze. Young children with ASD are
lesslikely than other children to utilise such cues (Bar-on-Cohen, Baldwin, &
Crowson, 1997; Parish-Mor-ris, Hennon, Hirsch-Pasek, Golinkoff, & Tager-Flusberg,
2007; but see Luyster & Lord, 2009),biasing towards the acquisition of unshared
i.e.idiosyncratic word meanings. Impaired mindread-ing can also explain the
problems that younger orless able individuals have in understanding andusing
person-centred (deictic) terms, such as you/me, here/there, now/then
(Hobson, Garcia-Perez, & Lee, 2010). Diminished use of mental statewords such as
think or know (Tager-Flusberg,2000), and impaired comprehension of words refer-
ring to emotions (Hobson & Lee, 1989), may also beexplained in this way.Sensory-
perceptual anomalies are probably uni-versal in ASD (Mottron & Burack, 2006), and
wouldhave certain predictable effects on structural lan-guage acquisition and
processing across the spec-trum. Anomalous speech perception has alreadybeen
mentioned as a likely contributory cause oflanguage delay, and may also underlie
the abnor-malities of pre-speech vocalisation detected in mostchildren with ASD
(Oller et al., 2010). Abnormalspeech perception might plausibly also underliethe
articulatory impairments that persist in someindividuals, although this has not
been shownempirically, and other explanations (e.g. motor inco-ordination) are
possible.Abnormalities of sensory-perceptual processingvariously conceptualised in
terms of weak centralcoherence (Happe & Frith, 2006), enhanced percep-tual
processing (Mottron, Dawson, Soulie`res, Hubert,& Burack, 2006), or enhanced
discriminability inassociation with reduced generalisation (Plaisted,2001) may have
other effects on language acquisitionin ASD. In particular, weak central
coherence/enhanced perceptual processing would predisposetowards encoding the
acoustic characteristics ofheard speech in place of meaning, as demonstratedin ALN
groups (e.g. Jarvinen-Pasley, Wallace, Ramus,Happe, & Heaton, 2008; Kamio,
Robins, Kelley,Swainson, & Fein, 2007; Toichi & Kamio, 2002) aswell as in groups
with ALI (e.g. Hermelin & OConnor,1970). This, combined with good immediate
memoryand rote learning (see below), may help to explainecholalia, and also the
formulaicity so heavily reliedon in expressive language (Perkins et al.,
2006).Plaisteds (2001) enhanced discriminability hypoth-esis, on the other hand,
is argued to be associated with reduced categorisation ability, thereby contrib-
uting (in combination with various other factors) tothe narrowed meaning that
substantive terms mayhave for people with ASD.Repetitive tendencies diagnostic of
ASD mostobviously affect the content of language used bypeople with ASD, whether at
the level of echolaliaand formulaicity, or at the level of preferred topicsand
resistance to topic change. However, a longitu-dinal study by Paul, Chawarska,
Cicchetti, Volkmar,and Rice (2008) identi?ed repetitive behaviours intoddlers (most
of whom had PDD-NOS) as a signi?-cant predictor of poor structural language at
follow-up, for reasons that are not clear.Uneven memory and learning abilities are
alsouniversal across the spectrum (Boucher & Mayes,2011). Mental age appropriate or
superior immediatememory and rote learning ability have already beenmentioned as
predisposing towards echoic and for-mulaic expression. Implicit learning of
variouskinds, including sequence learning and rule extrac-tion, is also probably
MA-appropriate, consistentwith relatively intact phonology and syntax withinthe
ASD-typical language pro?le (Frith & Happe,1994). By contrast, explicit memory for
uniqueevents episodic memory is impaired across thespectrum (Ben Shalom,
2003; Boucher & Mayes,2011; Bowler, Gaigg, & Lind, 2011). Non-autisticindividuals
with episodic memory impairment havediminished ability to acquire novel word de?
nitions(Holdstock, Mayes, Isaac, Gong, & Roberts, 2002).Impaired memory for unique
events in ASD maytherefore in combination with impaired mindread-ing and enhanced
discriminability contribute to anarrowed and idiosyncratic semantic meaning base.
Explaining heterogeneityHeterogeneity amongst individual pro?les can beexplained by
the many unshared factors that maycontribute to linguistic anomalies and
impairmentsin ASD. Some such factors occur more frequentlythan by chance, including
comorbid sensoryimpairments, epilepsy, Down syndrome, Fragile-Xsyndrome, Williams
syndrome and tuberose sclero-sis (Kielinen, Rantala, Timonen, Linna, &
Moilanen,2004). Typical language pro?les in these conditionsdiffer from each other
and from the ASD-typicalpro?le identi?ed in this article, although
somedescriptive overlaps occur (of theoretical interest,but beyond the scope of
this review to discuss).Other comorbidities occur by chance. For example,children
with ASD are as vulnerable as other chil-dren to environmental deprivation, or to
diseases orphysical traumas that may affect language out-comes, such as cleft
palate or head injury. Finally,some children with ASD bene?t from early
diagnosisand appropriate intervention but others do not, alsoaffecting language
outcomes (Woods & Wetherby,2003).
The group of nonrandomly co-occuring conditionswith effects on language probably
includes SLI, andthe relationship between SLI and ALI warrants moreextended
discussion. Comorbid SLI was originallyargued to be the main constituent of
languageimpairment in ASD (Churchill, 1972; Rutter, Bartak,& Newman, 1971). This
hypothesis was rigorouslytested in longitudinal studies reported by Bartaket al.
(1975, 1977), Cantwell, Baker, and Rutter(1978), and Mawhood et al. (2000), but was
notsupported. Interestingly, however, at the outset ofthese studies approximately
15% of potential par-ticipants were excluded on grounds of having mixedautism and
SLI.Recent behavioural, neurobiological and geneticevidence has revived interest
in links between SLIand ALI (see Williams, Botting, & Boucher, 2008 fora review of
the evidence). At the behavioural level,Kjelgaard and Tager-Flusbergs (2001)
report of im-paired nonword repetition, and Roberts et al.s(2004) con?rmation of
errors in verb tense markingdemonstrated that certain marker behavioursassociated
with SLI are also present in individualswith ALI. In addition, it is striking that
a small sub-group of older individuals with ALI continue tomanifest marked
phonological impairments in theabsence of intellectual disability or
comprehensionimpairment (Cleland et al., 2010; Rapin et al., 2009),resembling a
subgroup of individuals with SLI.Moreover, a small subgroup of children with
SLIhave pragmatic impairments similar to those uni-versal in ASD, sometimes but not
always accompa-nied by semantic impairments, but with intactphonology and grammar
(Bishop & Norbury, 2002;Botting & Conti-Ramsden, 1999; Rapin & Allen,1983). Thus, a
minority of cases of SLI resembleprototypical forms of ALI, and a minority of cases
ofALI resemble prototypical forms of SLI. This partialoverlap in language pro?les
seems unlikely to haveoccurred by chance, and suggests some degree ofoverlap in the
genetic factors contributing to eachcondition (Bishop, 2010). On the other hand,
thecanonical language pro?le in ALI clearly differs fromthat in SLI, in which
expression is more affected thancomprehension, and grammatical and
sometimesphonological impairments are prominent (Leonard,2000; Loucas et al.,
2008). Indeed, the relative rarityof phonological and syntactic impairments in
olderindividuals with ALI, and the superiority of syntacticprocessing in ALI
compared with SLI as shown insome studies, argue strongly against comorbid SLIas a
major contributor to persistent ALI.These arguments do not, however,
precludecomorbid SLI as a contributory cause in a minority ofcases perhaps
between 10% and 20% on availableevidence (Bartak et al., 1975; Cleland et al.,
2010;Rapin et al., 2009). On the assumption that thispercentage is stable across
the spectrum, the effectsof comorbid SLI should be most apparent in high-
functioning individuals with relatively pure ASD, as in the studies by Cleland et
al. and by Rapin et al. Inlower functioning groups, the effects of comorbid
SLIwould be largely masked by factors associated withlearning disabilities (as
considered below), althoughcontributing to heterogeneity amongst individualpro?
les.If, as argued herein, comorbid SLI is probablypresent in a minority of
individuals with ALI, thenwhatever processing anomalies underlie SLI mayalso
contribute to language impairments in anymixed ASD-SLI subgroup. It is beyond the
scope ofthis review article to discuss theories of the causes ofSLI, but a critical
review can be found in Leonardand Deevy (2006).Heterogeneity in the sense of
differences in thedegree to which language is impaired may sometimesbe explained by
additional factors such as thosementioned above. For example, an individual withASD
and hearing impairment or Down syndrome willhave a more severe structural language
impairmentthan someone with ASD alone.However, signi?cant structural language
impair-ment frequently occurs in individuals with ASD butnone of the kinds of
additional problems outlinedabove. Moreover, an ASD-typical language pro?
leemerges across group studies of the least affected tothe most affected school-age
children and adultswith ASD, with mainly quantitative differences in thedegree to
which any facet of language is affected.This should not occur if ALI results solely
fromcomorbidities each of which is associated with aqualitatively different
language pro?le. Instead, theemergence of a typical language pro?le across
thespectrum suggests that some other causal factor(s)that are continuously
distributed as opposed topresent or not present, are the most common cau-se(s) of
differences in the degree to which language isaffected.It might be the case, for
example, that one or moreof the shared psychological characteristics underly-ing
the typical pro?le occur in mild to severe formsacross the spectrum. Alternatively,
or in addition, itmight be the case that at least in lower functioningindividuals
with ALI generalised learning disabili-ties contribute to the lower scores on
language tests.In particular, low nonverbal (?uid) intelligence isclearly
associated with generalised learning disabil-ities, including delayed and limited
language in ASD(Stevens et al., 2000).Another possibility, recently proposed by
Boucher,Mayes, and Bigham (2008a) is that individuals withALI have more pervasive
declarative memoryimpairments than individuals with ALN. Speci?cally,it is
hypothesised that individuals with ALI com-monly have semantic memory impairment
additionalto the episodic memory impairment that occursacross the spectrum.
Impaired semantic memorycould explain why verbal (crystallized) intelligenceis
lower than nonverbal intelligence in mostindividuals with ALI (Lord & Paul, 1997;
Siegel, Minshew, & Goldstein, 1996). Moreover, Ullman(2001) has argued that
declarative memory (com-prising episodic and semantic memory together) isnecessary
for the acquisition of lexical itemsincluding open class words such as nouns,
adjec-tives and verb stems, but also closed class wordswith grammatical functions,
such as articles, prep-ositions and conjunctions; also irregular grammati-cal forms
such as irregular past tense forms orplurals. If Ullmans theory is correct, then
Boucherand colleagues hypothesis could explain themorphemic impairments in ALI, as
well as helpingto explain the semantic impairments. There is someevidence of
semantic memory impairment inlower ability individuals with ASD (Boucher & Ma-yes,
2011). In addition, impairments in semanticmemory and word meaning were correlated
in indi-viduals with ALI in a study by Boucher, Bigham,Mayes, and Muskett (2008b).
However, furtherinvestigation is needed to con?rm or discon?rm
thishypothesis.Explaining why language is more pervasivelyimpaired and deviant in
preschool child ren than atlater agesIt is tempting to explain the widespread
languageimpairments in preschool children with ASD simplyas the consequences of
language delay. Delayedonset will, of course, contribute, if only because achild
who says their ?rst words at age 3;0 may wellhave immature language at age 4;0.
Eigsti and Ben-netto (2009) went further, speculating that deviantdevelopment might
result from the fact that for thechild with markedly delayed language onset,
theprocess of language acquisition might resembleeffortful second language
learning. This suggestionassumes a critical period for language acquisition(Johnson
& Newport, 1989), and is potentially inter-esting. However, it is untested. It is
also inconsistentwith the fact that correct pronunciation is rarelyachieved by
second language learners, whereasarticulation is a relative strength in most
individualswith ALI from school-age onwards. Moreover, thishypothesis cannot
explain differences in languagepro?les within preschool groups with ALI.An
alternative suggestion is that a proportion ofpreschool children with ALI have
comorbid buttransient SLI. SLI-like language impairments arecommon amongst late
talkers who are otherwisetypically developing (Bishop & Edmundson, 1987). If,as is
suggested above, persistent SLI contributes tolanguage impairments in a subset of
school-agechildren and adults with ALI, and assuming thattransient and persistent
forms of SLI are geneticallyrelated, then transient SLI-like impairments wouldbe
expected to occur in some late talking preschoolchildren with ASD. This explanation
is attractive inthat it can explain why some but not all preschoolchildren with ALI
have phonological and grammatical impairments. It also ?ts nicely with ?ndings
reportedby Bennett et al. (2008), Geurts and Embrechts(2008), and Rapin and Dunn
(2003), cited earlier.
ConclusionIn this review, current knowledge concerning struc-tural language
abilities across the spectrum hasbeen summarised, and the complexity of explana-
tions of the data has been indicated, with the aim ofstimulating further research.
The lack of recentresearch into ALI is striking and regrettable, giventhe need for
greater understanding to inform effec-tive intervention. Studies of the
characteristics andimmediate causes of language impairments in ALI not least in
adults are urgently needed. With a fewhonourable exceptions, longitudinal studies
of lan-guage across the spectrum are also strikingly lack-ing, and longitudinal
studies of unselected groupsfrom infancy through to adulthood are also badlyneeded.
Trials of interventions designed to capitaliseon known islets of ability, as well
as to counteract well established blocks to language acquisition,would also be
welcome. Although the foremost aim oftherapy must be communication by
whatevermeans, language is, for humans, the preeminentmeans, and individuals with
ALI deserve evidence-based remedial language interventions.AcknowledgementsThis
article was commissioned as a Research Reviewarticle for the journal, for which the
author has receiveda nominal honorarium. The author has declared thatshe has no
competing or potential con?icts of interest todisclose in relation to this work.
The author is gratefulto Sophie Anns for her helpful comments on an earlierdraft of
this article; and to two anonymous Reviewersfor their constructive comments and
suggestions.Correspondence toJill Boucher, Autism Research Group, Department
ofPsychology, City University, Northampton Square,London EC1V 0HB UK; Email:
jill.boucher.1@city.ac.uk

Key points Structural language impairments were originally a diagnostic criterion

for ASD, widely considered to re?ectDD rather than deviance. Recently it has
become clear that: (a) language in preschool children with ASD is frequently
deviant as well asdelayed; (b) by school age, an ASD-typical language pro?le
emerges characterised by deviant semantics andmorphology with relatively intact
articulation and syntax; and (c) nevertheless, considerable heterogeneityoccurs
across individual pro?les and in the degree to which language is affected. The
immediate causes of language anomalies and impairments in ASD are only partially
understood, and arecertain to be complex. Research into the characteristics and
causes of ALI is urgently needed to inform evidence-based interventions.

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Accepted for publication: 27 October 2011
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