Preprint of: Bishop, D. V. M. (2004). Specific language impairment: diagnostic dilemmas. In L. Verhoeven & H. Van Balkom (Eds.), Classification of Developmental Language Disorders (pp. 309-326). Mahwah, NJ.: Erlbaum.

1. Specific language impairment: diagnostic dilemmas
D. V. M. Bishop
Oxford Study of Children's Communication Impairments
Department of Experimental Psychology
University of Oxford
OX1 3UD.
Preprint of:
Bishop, D. V. M. (2004). Specific language impairment: diagnostic dilemmas. In L. Verhoeven &
H. Van Balkom (Eds.), Classification of Developmental Language Disorders (pp. 309-326).
Mahwah, NJ.: Erlbaum.
1

2. SPECIFIC LANGUAGE IMPAIRMENT: DIAGNOSTIC DILEMMAS
In very general terms, specific language impairment (SLI) is easy to define: it is diagnosed when a
child fails to make normal progress in language learning for no obvious reason. In practice,
however, this simple characterisation is deceptive. Deciding who should or should not be regarded
as having SLI can be fiendishly difficult. In this chapter, I shall discuss three issues that arise
when defining diagnostic criteria for SLI: (i) the question of whether there should be a substantial
discrepancy between IQ and language level; (ii) comorbidity with, and differentiation from, other
developmental disorders; (iii) heterogeneity of developmental language impairment. Experts differ
in their recommendations as to how these issues should be addressed. My own view is that much
of the controversy arises because people are looking for a single diagnostic solution to a range of
different problems.
Is a single definition feasible?
We need first to consider the purpose to which we will put our diagnostic definition. When we do
so, we find that the optimal way of defining SLI will vary according to the context. Many of the
early attempts to formulate diagnostic criteria for SLI were made by researchers whose goal was
either to discover the underlying cognitive basis of SLI, or to characterise the linguistic deficits of
the disorder. In this kind of study, it is important to adopt stringent criteria. One wants to select
the purest cases, so as to study the correlates of language impairment without any confound caused
by comorbid conditions, low IQ, and so on. Typically, one would look for children whose
language level was substantially below both chronological age and nonverbal ability, and who had
normal hearing. Furthermore, one would want to exclude children with additional disorders, such
as attention deficit disorder (ADD). Medical or environmental factors that might possibly
influence language development, such as a history of seizures or otitis media, or a bilingual or
impoverished home background might also be used as exclusionary criteria. However, if we import
these stringent research criteria into clinical contexts, we immediately run into problems, because
such pure cases of impairment are not the norm. In reality, there is substantial comorbidity with
other developmental disorders, and the same pattern of linguistic impairment may be seen in
children with low or high nonverbal IQ. If we insist that only 'pure' cases receive a diagnosis of
SLI, and access to the intervention that such a diagnosis brings, then many children with language
problems will be excluded. I shall argue below that an insistence on stringent discrepancy and
exclusionary criteria has no rational justification in clinical and educational contexts.
One reason why stringent research definitions have gone unchallenged for so long is because they
appear to conform to our notions of good scientific practice. In science, it is usually far better to err
on the side of rigour than to be too lax. Suppose we screen 100 children for a research study and
find that only 20 of them meet our diagnostic criteria, but by adopting less rigorous criteria we
might include 50 children. Most researchers would conclude that the loss of statistical power is a
small price to pay for the increased purity of the sample. To include additional children with less
clearcut impairments could just introduce noise and dilute the effects of interest. In a field where
there is typically wide heterogeneity even in carefully-selected samples, an exclusive approach to
diagnosis is often seen as essential. Although it has been known for many years that research
definitions exclude many children who are thought, on clinical grounds, to have SLI (Stark &
Tallal, 1981), this has been seen as a problem for clinicians to resolve. Awareness that stringent
definitions may have scientific as well as clinical drawbacks only began to dawn on researchers
when research on genetics of SLI got underway. In these studies, one is interested in how far
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3. genetic relatedness can predict who will and will not have a language disorder. Thus the critical
thing is correct classification of individuals as affected or not affected. Suppose we have a
pedigree study, where we assess first degree relatives of children with SLI. We have to classify a
father who reports that he did not have speech-language therapy as a child, but was slow to start to
talk, and subsequently had literacy difficulties. We then directly assess his language abilities and
find vocabulary is in the normal range. We do not have the luxury of excluding marginal cases: we
must decide whether to regard such a person as affected or unaffected. If we settle on the wrong
definition of the phenotype, we run the risk of obtaining misleading results about heritability of
SLI. This is not just a fictional example: the famous three-generation K family who show a classic
autosomal dominant pattern of inheritance include some language-impaired individuals whose
nonverbal ability is below average (Vargha-Khadem, Watkins, Alcock, Fletcher, & Passingham,
1995). Longitudinal studies confirm that affected individuals may compensate for their problems,
so that their underlying difficulties are only evident by taking a history or by using specific tests
(e.g., Bishop, North, & Donlan, 1996; Lewis & Freebairn, 1992; Tomblin, Freese, & Records,
1992). Thus for this kind of study we need tests that are sensitive to residual problems in
compensated cases. Typically tests that do best at discriminating compensated from unaffected
individuals tend to be ones that minimize the role of learned knowledge and use nonsense
materials.
Can these etiological studies show the way forward to a better definition for clinical purposes?
Unfortunately, the answer is no. Suppose we were to use a test such as nonword repetition to
identify cases of SLI. The very characteristic that makes such a definition so useful for etiological
studies, its sensitivity to residual problems, makes it unsuitable in clinical contexts. The last thing
that clinicians need is to be swamped with 'affected' individuals who have compensated for their
underlying difficulties to the extent that they are coping well with everyday language demands. A
crucial part of any sensible clinical definition of SLI must be that the language problem interferes
significantly with communication in everyday life.
In sum, there is no single 'correct' way of defining SLI. For many kinds of research study, it is
sensible to adopt a stringent definition in order to study the correlates of the disorder in its purest
form. For genetic studies, however, we want a definition of the phenotype that gives a coherent
pattern of results, and it is important to avoid underdiagnosing SLI. For clinical purposes, the goal
is to identify children whose language impairments affect everyday functioning, and we need to
classify together children who will benefit from similar kinds of intervention. In recognising these
different uses to which definitions will be put, some of the thorny diagnostic issues become more
tractable.
These different goals of diagnosis of SLI relate quite closely to the distinctions drawn by the World
Health Organization (1980) in their Classification of Impairment, Disability and Handicap (see
table 1). This classification distinguishes different levels of description that can be used when
identifying the consequences of disease. These are the organic (impairment), functional (disability)
and social (handicap) aspects of disease. SLI can be used to illustrate these distinctions. If we find
that a child has limitations of auditory perception (e.g., Tallal, Miller, & Fitch, 1995), phonological
short-term memory (e.g., Gathercole & Baddeley, 1990), or appears to have a major delay in
acquiring a component of grammatical knowledge (e.g., Rice & Wexler, 1996), these would be
examples of impairments. Although we do not know the biological basis of such difficulties, we
assume that they reflect an underlying neurodevelopmental abnormality. Tests that assess how well
the child can use and understand language in the home or classroom, without attempting to pinpoint
specific underlying processes, would be regarded as measures of disability. Thus, we may find
that the child cannot understand complex sentences which contain more than one clause. Such a
3

4. problem could reflect an impairment in auditory processing, phonological short-term memory, or
grammatical knowledge: however, when we consider disability, we are less concerned with
underlying processes, but rather we are focusing on whether the child's communicative functioning
is adequate. It is possible for a person to have an impairment that does not lead to disability. Thus
a bright person with limited phonological short-term memory may develop strategies to compensate
for the impairment, and show normal understanding and sentence production. Handicap refers to
the social consequences of impairment and disability, and will be influenced by the environment.
Suppose we have a child who has major impairments in auditory processing that lead to functional
difficulties in comprehending speech in noise. The extent to which this causes handicap will
depend on whether the child is in a large, noisy classroom, or taught in a small group with little
background noise. Or, consider the theory of Rice, Wexler, and Cleave (1995) which proposes
that the fundamental problem in SLI is delayed maturation of a grammatical module that specifies
how verb tense is marked. Whether or not such an underlying impairment results in disability and
handicap would depend on the language being learned. A child with such an impairment will have
obvious language problems if learning English, but will have no overt difficulties if learning a
language such as Chinese that use no tense inflections.
At the clinical level, our primary interest will be in identifying disability, and in exploring how to
minimise any handicap resulting from disability. For basic research studies, however, we are
usually much more interested in underlying impairment.
The three-fold distinction between impairment, disability and handicap is not watertight, and has
come under some criticism (e.g., Thuriaux, 1995). In the context of language problems, where we
lack biological indicators of underlying disease, the boundary between impairment and disability
can become blurred, because, in effect, we use functional measures to evaluate impairment.
Nevertheless, it can be helpful to draw a line between measures that are intended to pinpoint
specific component processes that influence language functioning, and those that act as more global
indicators of the ability to use and understand language in more realistic contexts.
Use of IQ discrepancy criteria
Traditionally, the diagnosis of SLI is made only if there is a substantial discrepancy between
language level and nonverbal IQ. This is a clear case of a criterion that may serve a purpose in
research studies concerned with cognitive and linguistic correlates of SLI, but which is of
questionable validity in other contexts. Typically, when arguing, for instance, that SLI is
associated with deficits of auditory processing, of symbolic functioning, or specific syntactic
knowledge, then one wants to control for general intellectual level using a nonverbal IQ test.
Selecting children whose poor language is discrepant with average nonverbal ability is an effective
control procedure.
However, for genetic studies, there is evidence that it is over-restrictive to insist that a child has a
substantial discrepancy between verbal and nonverbal ability. In my own work I have found that
MZ twins show good concordance for language impairment, but very poor concordance for
language-IQ discrepancy (Bishop, 1994). Furthermore, although twin studies give high indices of
heritability for language impairment, the discrepancy between language level and nonverbal IQ
does not show significant heritability (Bishop, North, & Donlan, 1995). And this is perhaps not so
surprising when we consider that discrepancy scores are notoriously unreliable. It is a
mathematical fact that a difference score between two measures will be less reliable than either of
the measures on which it is based. Cole and his colleagues have demonstrated the practical
consequences of this; the IQ-language discrepancy is sufficiently unreliable that many children
4

5. change category from one test occasion to another (Cole, Dale, & Mills, 1990; Cole, Dale, & Mills,
1992; Cole, Mills, & Kelley, 1994; Cole, Schwartz, Notari, Dale, & Mills, 1995).
This has led to a trend for abandoning discrepancy criteria. For instance, it is noteworthy that in a
large US epidemiological study by Tomblin and colleagues (Tomblin, 1996; Tomblin et al., 1997),
SLI was defined in terms of having poor language skills in the context of a nonverbal IQ above 85
(1 SD below the mean). The definition of language impairment corresponded to a cutoff on a
composite language battery of -1.14 SD. This definition would include some children whose
language and nonverbal IQ are not substantially different: in the most extreme case, the child might
have a language standard score of 82 and a nonverbal score of 85.
Should this worry us? It will depend on one’s underlying model of language impairment. Imagine
that SLI is caused by some factor X that depresses verbal abilities, so that the distribution of verbal
scores is shifted down by 1 SD for those who have factor X. Assuming factor X has no effect on
nonverbal abilities, we would find that among children with factor X, the proportion with large
verbal-nonverbal discrepancies will be increased, relative to the general population. However, the
distribution of nonverbal ability would be same as for the general population, so that some children
would be expected to have nonverbal abilities at the lower end of the normal range. In short, we
might argue that having poor language does not protect a child from having a low nonverbal IQ.
Despite such considerations, most people are understandably nervous about abandoning
discrepancy scores. There is real concern that this will open the floodgates to hordes of children
whose low language test scores arise from a range of heterogeneous etiologies. In research
contexts, this could lead to a dilution of effects of interest. In clinical contexts, services might be
overwhelmed by inclusion of large numbers of children whose language difficulties are part of a
broader developmental delay. So what is the answer?
Well, on the basis of what I have argued so far, you will not be surprised to hear me say that 'it
depends'. If one's interest is in studying the genetics of SLI, then the way forward is to look for a
reliable measure of the underlying impairment. Bishop et al (1996) argued that a test of nonword
repetition provided an excellent behavioural marker for genetic studies because, as well as showing
high heritability, the test revealed underlying deficits in people whose overt language difficulties
had resolved. Furthermore, this measure shows weak or nonsignificant correlations with nonverbal
IQ (Bishop et al, 1996), maternal education (Coleman et al., 1999), or ethnic background
(Campbell, Dollaghan, Needleman, & Janosky, 1997). Furthermore, in those with mental
handicap, low IQ is not necessarily a barrier to developing good phonological short-term memory:
individuals with Williams syndrome do well on nonword repetition despite poor performance on
other cognitive tests (Karmiloff-Smith et al., 1997). Quite simply, if one uses a measure like this,
IQ becomes irrelevant, because there is no indication that IQ level exerts any important effect on
task performance.
Use of qualitative markers for SLI
Another approach to identifying language impairment is to move away from IQ-discrepancy
measures and to look instead at qualitative aspects of language functioning. Many people suspect
that there is something distinctive about the nature of the language problems in children that are
typically recognised as cases of SLI, as opposed to those with 'common or garden' low language
levels. If this is right, then we have a way forward, by looking for indicators that identify children
who have a qualitatively distinct deficit. This may mean rethinking how we use standardized
language tests in diagnosis. The advantages of standardized tests are well-known. They allow us
to quantify the severity of impairment in relation to a peer group, using instruments that have been
5

6. shown to have acceptable reliability. However, most standardized tests are not well-suited for
identifying qualitative abnormalities. Typically, they are designed so as to yield a normal
distribution of scores, rather than to divide a population into an impaired and unimpaired subgroup.
Suppose, though, that what distinguishes SLI from normality is an inability to carry out certain
grammatical operations that are normally mastered by around the age of 5 years. Such a model
predicts that most children above the age of 5 years will perform at ceiling on measures of the
grammatical skill, and that failure on such a test will be a marker for SLI. In other words, we
would not expect to find a normal distribution, but rather a bimodal one. Rice (2000) has argued
that her 'extended optional infinitive' test acts in just this way. Research on this measure is still at
an early stage, but it has considerable promise, and provides a nice illustration of the different types
of measure that are required if one's underlying model of disorder is qualitative rather than
quantitative.
Should we substitute measures such as nonword repetition or extended optional infinitive tests for
conventional language assessments in clinical contexts? Well, once again, it depends. The very
point that makes nonword repetition a useful test for genetics studies - its sensitivity to residual
deficits - makes it of questionable utility as a clinical diagnostic test. Quite simply, many children
who do poorly on nonword repetition tests don't have major problems on formal language tests, and
may be coping well in everyday life. In relation to table 1, we may say that they have an
impairment but not a disability. The picture would seem rather different for extended optional
infinitives, because if a child has problems using and understanding these constructions, this is
likely to have an impact on everyday communication, and thus entails disability, and probable
handicap. And indeed, Rice has shown that this measure has good sensitivity and specificity in
discriminating children who, on clinical grounds, are deemed language impaired, from those who
are typically developing.
In the final analysis, though, the important fact to bear in mind is that a clinical diagnosis should
identify children who will benefit from specific forms of intervention and educational placement,
and whose difficulties with communication interfere with everyday life and academic achievement.
There is already good evidence that conventional psychometric tests do not always succeed in
identifying those children who attract clinical and parental concern (Dunn, Flax, Sliwinski, &
Aram, 1996). Furthermore, IQ-discrepancy indices are on the one hand unreliable, and on the other
hand exclude a substantial proportion of children who are thought, on clinical grounds, to have
specific language impairments. What is needed are improved measures of underlying impairment
that mesh better with clinical impressions of disability. I expect that as we develop such measures,
we will find that the debate about IQ-discrepancies becomes irrelevant.
Comorbidity with, and differentiation from, other developmental disorders
Comorbidity between developmental disorders is so widespread that the child with a truly specific
disorder is the exception rather than the rule. There is ample evidence that children with SLI have
high rates of ADD (Beitchman, Brownlie, & Wilson, 1996), developmental co-ordination disorder
(Powell & Bishop, 1992), literacy problems (Bishop & Adams, 1990), and impairments of social
interaction (Brinton & Fujiki, 1993). Any attempt at specifying diagnostic criteria must grapple
with this issue.
Once again, we have a situation where the research focus on 'pure' cases has had a negative impact
on clinical practice, by leading to restrictive diagnostic criteria that exclude a substantial proportion
of children. Clinicians, in seeking to arrive at a single diagnostic label, are discouraged from
considering the whole spectrum of impairments that one typically sees. My experience is that there
are many children where the particular diagnostic label that a child receives is more a function of
6

7. the specialist who makes the diagnosis, than of the characteristics of the child. The same child
might receive a label of SLI from a speech-language pathologist, dyslexia from a school
psychologist, ADHD from a pediatrician, PDDNOS from a child psychiatrist, right-hemisphere
learning disability from a neuropsychologist, and developmental co-ordination disorder from a
physical therapist.
I don't think the answer is to lump all disorders together, as tended to be the case in the past with
concepts such as 'minimal brain dysfunction'. However, it would seem important to stress the
importance of multidisciplinary assessment of a child presenting with communication difficulties,
many of whom will have associated difficulties in nonlinguistic domains. Elsewhere (Bishop,
1989, 2000) I have argued that a dimensional approach to the classification of developmental
disorders may be more appropriate than the categorical approach that has been inherited from those
working in the tradition of the medical model. On this view, the distinction between specific
language impairment and autistic disorder is not a sharp divide. Certainly, there are many children
whose differential diagnosis is quite unambiguous: these would correspond to textbook cases of
SLI or autistic disorder. However, there are others who have social and pragmatic impairments that
go beyond what one would expect to see in SLI, yet whose difficulties are not as severe or
pervasive as is typically seen in autistic disorder. I have used the term 'pragmatic language
impairment' to refer to these cases. The model could be made even more complex by
incorporating the domains of attention and motor skill. A multidimensional model appears to do a
better job in capturing clinical reality than a diagnostic system with sharp divisions between
discrete disorders. However, we cannot afford simply to abandon the diagnostic labels, even if we
recognise that they are artificial abstractions. Quite simply, a label provides a shorthand
description of a child's problems that provides access to appropriate services. Certainly, in the UK,
it can make a tremendous difference to the intervention and educational provision that is offered
whether a child receives a diagnosis of SLI or autistic disorder.
If we turn back from clinical to research questions, the comorbidity that we see poses the question
as to whether we should alter our diagnostic boundaries. Comorbidity can arise for many different
reasons (Caron & Rutter, 1991). It could be that a common genetic defect leads to diverse
behavioural outcomes, perhaps by affecting adjacent brain areas. Or it might be that environmental
risk factors for one disorder raise the likelihood of the other being present. One disorder, such as
language impairment, could lead to another, e.g. social impairment (see e.g., Rice, Sell, & Hadley,
1991). The plausibility of these different lines of explanation varies from one case to another. For
instance, it is easy to see how language difficulties might lead to reading problems, but harder to
postulate a causal route from language difficulties to motor clumsiness. As yet, we have little
understanding of the origins of comorbidity with language disorders, but genetic studies may lead
to a way forward because they can help us discover whether co-occurring disorders have common
etiological origins (cf. e.g., Stevenson, Pennington, Gilger, DeFries, & Gillis, 1993). Even though
comorbidity is widespread, one can find cases of relatively pure disorder, and these may be the
optimal cases to use for certain types of research study where one wants to study the correlates of
language difficulties in the absence of confounding factors. The critical point to remember,
however, is that such children are not representative of SLI in the general population, and the
nature and origins of their problems could be quite different.
Heterogeneity of SLI
There is little agreement on the question of how to subclassify SLI. As a field develops, the basis
of classification tends to move from superficial observable characteristics to underlying processes.
In the case of SLI, we would hope ultimately to be able to identify subtypes based on etiology and
underlying cognitive mechanisms, but as yet the field is not sufficiently advanced for this to be
7

8. possible. In general, therefore, classifications tend to be based on the linguistic characterisation of
the language impairment. Bishop (1998) argued that attempts to derive categories by using cluster
analysis with test data have been largely unsuccessful, probably because the available tests do not
cover aspects of communication which are important, such as pragmatics. More agreement has
been achieved by those adopting a clinical approach, such as Rapin and Allen (1983), and those
who combine test data with more impressionistic qualitative data, as exemplified by Conti-
Ramsden, Crutchley, and Botting (1997).
I shall close by briefly describing some subtypes of developmental speech and language
impairment about which there is at least some broad agreement among clinicians.
'Typical' SLI
A large percentage of research on SLI focuses on children who have disproportionate problems
with grammatical development. In English, this is manifested in frequent omission of grammatical
endings, such as past tense -ed, or third person singular -s. Such errors are, of course, seen also in
normally developing young children, but in SLI they persist well beyond the normal age, and the
grammatical difficulties do seem out of proportion with other linguistic problems. Leonard (1997)
provides a masterly overview of the literature on such disorders, taking into account the
manifestations in languages other than English. He also reviews the wide range of theories of
underlying impairment that have been proposed to account for this pattern of language
development. First, there are theories that postulate a low-level auditory perceptual impairment as
the primary cause of the language difficulties (Tallal & Piercy, 1973). According to this view,
which is reviewed in detail by Bishop (1997), children have difficulty in perceiving oral language
at the rate at which it is normally produced, and this leads to slow and distorted acquisition of
phonology and syntax. This contrasts sharply with theories that argue for impairment of innate
brain modules specialised for processing grammar (e.g., Gopnik & Crago, 1991). Yet another
group of researchers propose limitations in processing capacity and/or working memory as the
fundamental problem in such children (Joanisse & Seidenberg, 1998; Gathercole & Baddeley,
1990; Leonard, 1997).
It can be difficult to disentangle these theories, because they make many of the same predictions
(Bishop, 1997). On the grounds of parsimony, researchers in this area tend to look for a single
underlying cause that might explain all cases of grammatical impairment in children, but it is, of
course, possible, that different explanations apply in different cases. It is unfortunate that many
studies report only group data when testing a specific hypothesis, without indicating how typical
findings are for group members. Often, however, there can be quite substantial variation from child
to child. For instance, Bishop et al. (1999) found that children with SLI did do more poorly than a
control group on a test of auditory perception based on Tallal's theory. However, they did not show
the expected rate-specific deficit, and the effect size was relatively modest. This meant that there
were many children with SLI who were not impaired in auditory processing, and many controls
who were. A subsequent study by Bishop, Carlyon, Deeks, & Bishop (1999) on a subset of these
children considered whether the variable results simply reflected poor reliability of the auditory
test. Eleven children with SLI were compared with eleven matched controls on a range of auditory
psychophysical tasks, with repeat administration over a period of several months. On a test of
auditory backward masking, there was reasonable test-retest reliability, despite the fact that practice
led to improvements in scores for all children with repeat testing. However, there was substantial
individual variation in both control and SLI groups, and, in this relatively small sample, there was
no significant difference between them. The conclusion from this study was that auditory deficit
was neither necessary nor sufficient to cause SLI, but we suggested that it might be a risk factor
that assumed importance when it occurred in a child who had a genetic predisposition to SLI.
8

9. Although grammatical difficulties are one of the most noticeable and common manifestations of
SLI (e.g., Conti-Ramsden et al., 1997), one should beware of assuming that all children with
grammatical problems are the same. Phonological difficulties appear to be a common, but not
universal, correlate (Rapin & Allen, 1983). The existence of children who have severe problems in
understanding grammar in the context of superior nonverbal ability, good pragmatics and
phonology, and normal auditory processing is of considerable theoretical interest in demonstrating
the potential independence of grammar from other aspects of cognition (Van der Lely, 1997).
However, such children appear to be the exception rather than the rule (Bishop, Bright, James,
Bishop, & Van der Lely, 2000). More commonly, one sees children whose grammatical difficulties
co-occur with major problems in semantics and some limitations of nonverbal ability.
Severe receptive language disorder
Although one can usually find comprehension problems in children with grammatical difficulties,
these are typically less obvious and severe than their expressive difficulties (e.g., Bishop, 1979).
Much rarer are those children who have such severe problems in understanding language that they
are initially thought to be deaf. This is sometimes referred to as a childhood manifestation of
verbal auditory agnosia (Rapin, Mattis, & Rowan, 1977). Much of the research on these children
consists of single case studies, because they are so very rare. Some of these studies have
demonstrated impairment of nonverbal auditory processing in such children (e.g., Rosen, Van der
Lely, & Dry, 1997; Stefanatos, Green, & Ratcliff, 1989). This is one subtype of language
impairment that is associated with a distinctive etiology, that of acquired epileptic aphasia, or
Landau-Kleffner syndrome (see Deonna, 2000, for a review). Typically, the child starts out
developing language normally, but regresses in the preschool years, losing language
comprehension and expression over a period that may range from a few days to several months.
Although an epileptic etiology underlies this disorder, this can be difficult to demonstrate, because
often the seizures are nocturnal, and may only be evident when a sleep EEG is carried out.
Deonna (2000) raises the interesting speculation that a similar etiological process may be
implicated in some cases of milder SLI, though he notes that studies looking for elevated rates of
EEG abnormalities in children with SLI have not yielded consistent findings.
'Developmental verbal dyspraxia'
Developmental verbal dyspraxia is possibly one of the most controversial of all the subtypes of
SLI. Some authorities deny its very existence. Others accept that a clinical picture resembling
dyspraxia may be seen, but query whether the label is an appropriate one. Even those who use the
term, do so in rather different ways. In adult neurology, dyspraxia refers to difficulty in
programming movements that cannot be explained in terms of muscle weakness or sensory loss.
Typically, the patient is able to imitate individual movements or speech sounds, but has great
difficulty producing longer sequences. In developmental cases, one also sees children whose
intelligibility declines markedly when they attempt complex utterances, compared to when they are
producing individual sounds or syllables. Some authorities argue that a diagnosis of dyspraxia is
most appropriate when the child also has evidence of imitating nonspeech oral movements. Others
maintain that the programming impairment can be specific to speech production, and that the most
critical diagnostic feature is inconsistency of speech sound production from one occasion to
another. Although the term 'dyspraxia' suggests a pure output disorder, systematic studies of
phonological processing in children with a diagnosis of dyspraxia indicates that many - perhaps all-
of these children have difficulty in doing tasks that involve mentally manipulating speech sounds,
such as classic phonological awareness tasks (Stackhouse, 1992). Their difficulties may, therefore,
have more to do with problems in forming segmental phonological representations, than with
programming motor output. In contrast to children with speech disorders arising from physical or
9

10. neurological impairment of the articulators, those with verbal dyspraxia typically have major
literacy problems, and receptive language levels may be poor on tests of vocabulary and grammar
(Stackhouse, 1982; see also Bishop, 1985). Such findings suggest that the label of 'dyspraxia' may
be inappropriate in suggesting a circumscribed motor programming problem.
Pragmatic language impairment
The traditional view of SLI is of a child with normal sociability whose communication is limited
only by difficulties in mastering the structural aspects of language, i.e. phonology and syntax.
However, there is a substantial literature indicating an elevated level of difficulties in the social use
of language in this population. Bishop (2000) reviewed this work and concluded that, though some
social communication problems in SLI could be secondary consequences of difficulties in
formulating intelligible utterances or comprehending what others were saying, others were less
easy to explain this way. This is particularly true in the case where the child with early language
delay goes on to make rapid progress in mastering phonology and grammar, and starts to speak in
long and complex sentences, but uses utterances inappropriately. Such children may offer
tangential answers to questions, lack coherence in conversation or narrative speech, and appear
over-literal in their comprehension. In the past, I adopted the terminology based on the nosology of
Rapin and Allen (1983), referring to these children as cases of 'semantic-pragmatic disorder', but
there is little evidence that semantic and pragmatic difficulties tend to co-occur, and I now prefer
the term 'pragmatic language impairment'. One might expect a child with language difficulties to
compensate by developing a rich repertoire of nonverbal communication, but in these cases of
pragmatic language impairment, that is not what is typically seen (Bishop, Chan, Adams, Hartley,
& Weir, 2000). A critical question is whether such children should be regarded as part of the
autistic continuum, rather than classified with SLI. They certainly share a number of features with
high-functioning autistic children, and would in most cases meet the, admittedly rather vague,
diagnostic criteria for Pervasive Developmental Disorder Not Otherwise Specified (PDDNOS) (see
(American Psychological Association, 1994). In our current state of knowledge, I regard it as
premature to conclude that all children with PLI should be placed on the autistic spectrum. Some
of these children do have clear autistic features, but others do not (Bishop, 1998). The diagnostic
overlap with the category of Attention Deficit Hyperactivity Disorder is also of interest.
Incoherent, tangential speech is often remarked upon as a correlate of that disorder, with poor
social interaction and limited narrative and conversational skills (Tannock, Fine, Heintz, &
Schachar, 1995; Tannock, Purvis, & Schachar, 1993). For clinicians, the message seems to be that
one should be alert to the possibility that a child's communicative difficulties might extend beyond
language structure, to encompass social use of language, and nonverbal communication. Most
formal language assessments are not sensitive to these problems, and so one should not assume that
they are absent, just because they don't show up on a test. Where the child does have pragmatic
problems, a multidisciplinary assessment is warranted to consider whether a diagnosis of ADD or
autistic spectrum disorder (PDDNOS) would be appropriate. It can be particularly difficult to find
appropriate educational placements for such children. Schools for children with autism tend to
focus more on the needs of those of low IQ, who may need much more focus on structured
activities and behaviour control. Schools for those with language difficulties may, however, be less
well prepared for dealing with the nonverbal and social impairments, which become increasingly
important as children grow older.
Concluding comment
Specific language impairment poses enormous challenges for both clinicians and researchers. The
existence of children with communication problems is not in doubt. There is little consensus about
diagnostic criteria, diagnostic boundaries, or subclassification. The principal message of this
chapter is that we have to consider the purpose of diagnosis, and match our methods to our goals,
10

11. rather than looking for a single 'gold standard' to apply in all situations. The pure, clearcut
categories that are described in textbooks bear little relation to clinical reality.
I have deliberately emphasised the challenges that lie ahead for those of us working with SLI,
because I believe that only by confronting them, and analysing the reasons for diagnostic
difficulties, can we resolve them. However, it would be wrong to give the impression that the
problems are insuperable. Just over the past decade, we have seen enormous advances in our
understanding of SLI on many fronts. We now know considerably more than we did 10 years ago
about the causes of SLI (e.g. Bishop, in press), the nature of linguistic difficulties (Leonard, 1997),
epidemiology (Tomblin et al, 1997), and comorbidity (e.g. Beitchman et al, 1996). We know just
how common SLI is, and we also know just how serious it is, in terms of putting the child at risk
for later problems, both academic and psychiatric (e.g., Beitchman et al, 1996; Snowling, Bishop,
& Stothard, 2000). Fortunately, we are at the same time starting to see many more scientific
studies of intervention that allow us to identify the characteristics of successful interventions (see
the five subsequent chapters in Part 3 of this volume).
11

12. Table 1
Definitions of Impairment, Disability and Handicap (World Health Organization, 1980)
 Impairment
Abnormality at the level of organ or system functioning: includes psychologic, physiologic or
anatomic abnormalities
 Disability
Restriction or loss at the functional level. Inability to carry out activities that most humans can
do
 Handicap
Social disadvantage arising from impairment: this depends on the social environment as well as
the level of impairment and disability
12

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16