SLI: diagnostic dilemmas


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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.

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SLI: diagnostic dilemmas

  1. 1. Specific language impairment: diagnostic dilemmas D. V. M. Bishop Oxford Study of Childrens 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. 2. SPECIFIC LANGUAGE IMPAIRMENT: DIAGNOSTIC DILEMMASIn very general terms, specific language impairment (SLI) is easy to define: it is diagnosed when achild 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 regardedas having SLI can be fiendishly difficult. In this chapter, I shall discuss three issues that arisewhen defining diagnostic criteria for SLI: (i) the question of whether there should be a substantialdiscrepancy between IQ and language level; (ii) comorbidity with, and differentiation from, otherdevelopmental disorders; (iii) heterogeneity of developmental language impairment. Experts differin their recommendations as to how these issues should be addressed. My own view is that muchof the controversy arises because people are looking for a single diagnostic solution to a range ofdifferent problems.Is a single definition feasible?We need first to consider the purpose to which we will put our diagnostic definition. When we doso, we find that the optimal way of defining SLI will vary according to the context. Many of theearly attempts to formulate diagnostic criteria for SLI were made by researchers whose goal waseither to discover the underlying cognitive basis of SLI, or to characterise the linguistic deficits ofthe disorder. In this kind of study, it is important to adopt stringent criteria. One wants to selectthe purest cases, so as to study the correlates of language impairment without any confound causedby comorbid conditions, low IQ, and so on. Typically, one would look for children whoselanguage level was substantially below both chronological age and nonverbal ability, and who hadnormal hearing. Furthermore, one would want to exclude children with additional disorders, suchas attention deficit disorder (ADD). Medical or environmental factors that might possiblyinfluence language development, such as a history of seizures or otitis media, or a bilingual orimpoverished home background might also be used as exclusionary criteria. However, if we importthese stringent research criteria into clinical contexts, we immediately run into problems, becausesuch pure cases of impairment are not the norm. In reality, there is substantial comorbidity withother developmental disorders, and the same pattern of linguistic impairment may be seen inchildren with low or high nonverbal IQ. If we insist that only pure cases receive a diagnosis ofSLI, and access to the intervention that such a diagnosis brings, then many children with languageproblems will be excluded. I shall argue below that an insistence on stringent discrepancy andexclusionary criteria has no rational justification in clinical and educational contexts.One reason why stringent research definitions have gone unchallenged for so long is because theyappear to conform to our notions of good scientific practice. In science, it is usually far better to erron the side of rigour than to be too lax. Suppose we screen 100 children for a research study andfind that only 20 of them meet our diagnostic criteria, but by adopting less rigorous criteria wemight include 50 children. Most researchers would conclude that the loss of statistical power is asmall price to pay for the increased purity of the sample. To include additional children with lessclearcut impairments could just introduce noise and dilute the effects of interest. In a field wherethere is typically wide heterogeneity even in carefully-selected samples, an exclusive approach todiagnosis is often seen as essential. Although it has been known for many years that researchdefinitions 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 stringentdefinitions may have scientific as well as clinical drawbacks only began to dawn on researcherswhen research on genetics of SLI got underway. In these studies, one is interested in how far 2
  3. 3. genetic relatedness can predict who will and will not have a language disorder. Thus the criticalthing is correct classification of individuals as affected or not affected. Suppose we have apedigree study, where we assess first degree relatives of children with SLI. We have to classify afather who reports that he did not have speech-language therapy as a child, but was slow to start totalk, and subsequently had literacy difficulties. We then directly assess his language abilities andfind vocabulary is in the normal range. We do not have the luxury of excluding marginal cases: wemust decide whether to regard such a person as affected or unaffected. If we settle on the wrongdefinition of the phenotype, we run the risk of obtaining misleading results about heritability ofSLI. This is not just a fictional example: the famous three-generation K family who show a classicautosomal dominant pattern of inheritance include some language-impaired individuals whosenonverbal 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 incompensated cases. Typically tests that do best at discriminating compensated from unaffectedindividuals tend to be ones that minimize the role of learned knowledge and use nonsensematerials.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 toidentify cases of SLI. The very characteristic that makes such a definition so useful for etiologicalstudies, its sensitivity to residual problems, makes it unsuitable in clinical contexts. The last thingthat clinicians need is to be swamped with affected individuals who have compensated for theirunderlying difficulties to the extent that they are coping well with everyday language demands. Acrucial part of any sensible clinical definition of SLI must be that the language problem interferessignificantly with communication in everyday life.In sum, there is no single correct way of defining SLI. For many kinds of research study, it issensible to adopt a stringent definition in order to study the correlates of the disorder in its purestform. For genetic studies, however, we want a definition of the phenotype that gives a coherentpattern of results, and it is important to avoid underdiagnosing SLI. For clinical purposes, the goalis to identify children whose language impairments affect everyday functioning, and we need toclassify together children who will benefit from similar kinds of intervention. In recognising thesedifferent uses to which definitions will be put, some of the thorny diagnostic issues become moretractable.These different goals of diagnosis of SLI relate quite closely to the distinctions drawn by the WorldHealth Organization (1980) in their Classification of Impairment, Disability and Handicap (seetable 1). This classification distinguishes different levels of description that can be used whenidentifying 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 findthat a child has limitations of auditory perception (e.g., Tallal, Miller, & Fitch, 1995), phonologicalshort-term memory (e.g., Gathercole & Baddeley, 1990), or appears to have a major delay inacquiring a component of grammatical knowledge (e.g., Rice & Wexler, 1996), these would beexamples of impairments. Although we do not know the biological basis of such difficulties, weassume that they reflect an underlying neurodevelopmental abnormality. Tests that assess how wellthe child can use and understand language in the home or classroom, without attempting to pinpointspecific underlying processes, would be regarded as measures of disability. Thus, we may findthat the child cannot understand complex sentences which contain more than one clause. Such a 3
  4. 4. problem could reflect an impairment in auditory processing, phonological short-term memory, orgrammatical knowledge: however, when we consider disability, we are less concerned withunderlying processes, but rather we are focusing on whether the childs communicative functioningis adequate. It is possible for a person to have an impairment that does not lead to disability. Thusa bright person with limited phonological short-term memory may develop strategies to compensatefor the impairment, and show normal understanding and sentence production. Handicap refers tothe 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 functionaldifficulties in comprehending speech in noise. The extent to which this causes handicap willdepend on whether the child is in a large, noisy classroom, or taught in a small group with littlebackground noise. Or, consider the theory of Rice, Wexler, and Cleave (1995) which proposesthat the fundamental problem in SLI is delayed maturation of a grammatical module that specifieshow verb tense is marked. Whether or not such an underlying impairment results in disability andhandicap would depend on the language being learned. A child with such an impairment will haveobvious language problems if learning English, but will have no overt difficulties if learning alanguage such as Chinese that use no tense inflections.At the clinical level, our primary interest will be in identifying disability, and in exploring how tominimise any handicap resulting from disability. For basic research studies, however, we areusually much more interested in underlying impairment.The three-fold distinction between impairment, disability and handicap is not watertight, and hascome under some criticism (e.g., Thuriaux, 1995). In the context of language problems, where welack biological indicators of underlying disease, the boundary between impairment and disabilitycan 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 pinpointspecific component processes that influence language functioning, and those that act as more globalindicators of the ability to use and understand language in more realistic contexts.Use of IQ discrepancy criteriaTraditionally, the diagnosis of SLI is made only if there is a substantial discrepancy betweenlanguage level and nonverbal IQ. This is a clear case of a criterion that may serve a purpose inresearch studies concerned with cognitive and linguistic correlates of SLI, but which is ofquestionable validity in other contexts. Typically, when arguing, for instance, that SLI isassociated with deficits of auditory processing, of symbolic functioning, or specific syntacticknowledge, 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 effectivecontrol procedure.However, for genetic studies, there is evidence that it is over-restrictive to insist that a child has asubstantial discrepancy between verbal and nonverbal ability. In my own work I have found thatMZ twins show good concordance for language impairment, but very poor concordance forlanguage-IQ discrepancy (Bishop, 1994). Furthermore, although twin studies give high indices ofheritability for language impairment, the discrepancy between language level and nonverbal IQdoes not show significant heritability (Bishop, North, & Donlan, 1995). And this is perhaps not sosurprising when we consider that discrepancy scores are notoriously unreliable. It is amathematical fact that a difference score between two measures will be less reliable than either ofthe measures on which it is based. Cole and his colleagues have demonstrated the practicalconsequences of this; the IQ-language discrepancy is sufficiently unreliable that many children 4
  5. 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 alarge 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 acomposite language battery of -1.14 SD. This definition would include some children whoselanguage and nonverbal IQ are not substantially different: in the most extreme case, the child mighthave 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. Imaginethat SLI is caused by some factor X that depresses verbal abilities, so that the distribution of verbalscores is shifted down by 1 SD for those who have factor X. Assuming factor X has no effect onnonverbal abilities, we would find that among children with factor X, the proportion with largeverbal-nonverbal discrepancies will be increased, relative to the general population. However, thedistribution of nonverbal ability would be same as for the general population, so that some childrenwould be expected to have nonverbal abilities at the lower end of the normal range. In short, wemight 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 abandoningdiscrepancy scores. There is real concern that this will open the floodgates to hordes of childrenwhose low language test scores arise from a range of heterogeneous etiologies. In researchcontexts, this could lead to a dilution of effects of interest. In clinical contexts, services might beoverwhelmed by inclusion of large numbers of children whose language difficulties are part of abroader 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 itdepends. If ones interest is in studying the genetics of SLI, then the way forward is to look for areliable measure of the underlying impairment. Bishop et al (1996) argued that a test of nonwordrepetition provided an excellent behavioural marker for genetic studies because, as well as showinghigh heritability, the test revealed underlying deficits in people whose overt language difficultieshad resolved. Furthermore, this measure shows weak or nonsignificant correlations with nonverbalIQ (Bishop et al, 1996), maternal education (Coleman et al., 1999), or ethnic background(Campbell, Dollaghan, Needleman, & Janosky, 1997). Furthermore, in those with mentalhandicap, 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 onother 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 ontask performance.Use of qualitative markers for SLIAnother approach to identifying language impairment is to move away from IQ-discrepancymeasures and to look instead at qualitative aspects of language functioning. Many people suspectthat there is something distinctive about the nature of the language problems in children that aretypically recognised as cases of SLI, as opposed to those with common or garden low languagelevels. If this is right, then we have a way forward, by looking for indicators that identify childrenwho have a qualitatively distinct deficit. This may mean rethinking how we use standardizedlanguage tests in diagnosis. The advantages of standardized tests are well-known. They allow usto quantify the severity of impairment in relation to a peer group, using instruments that have been 5
  6. 6. shown to have acceptable reliability. However, most standardized tests are not well-suited foridentifying qualitative abnormalities. Typically, they are designed so as to yield a normaldistribution 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 certaingrammatical operations that are normally mastered by around the age of 5 years. Such a modelpredicts that most children above the age of 5 years will perform at ceiling on measures of thegrammatical skill, and that failure on such a test will be a marker for SLI. In other words, wewould not expect to find a normal distribution, but rather a bimodal one. Rice (2000) has arguedthat her extended optional infinitive test acts in just this way. Research on this measure is still atan early stage, but it has considerable promise, and provides a nice illustration of the different typesof measure that are required if ones underlying model of disorder is qualitative rather thanquantitative.Should we substitute measures such as nonword repetition or extended optional infinitive tests forconventional language assessments in clinical contexts? Well, once again, it depends. The verypoint that makes nonword repetition a useful test for genetics studies - its sensitivity to residualdeficits - makes it of questionable utility as a clinical diagnostic test. Quite simply, many childrenwho do poorly on nonword repetition tests dont have major problems on formal language tests, andmay be coping well in everyday life. In relation to table 1, we may say that they have animpairment but not a disability. The picture would seem rather different for extended optionalinfinitives, because if a child has problems using and understanding these constructions, this islikely to have an impact on everyday communication, and thus entails disability, and probablehandicap. And indeed, Rice has shown that this measure has good sensitivity and specificity indiscriminating children who, on clinical grounds, are deemed language impaired, from those whoare typically developing.In the final analysis, though, the important fact to bear in mind is that a clinical diagnosis shouldidentify 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 inidentifying 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 otherhand exclude a substantial proportion of children who are thought, on clinical grounds, to havespecific language impairments. What is needed are improved measures of underlying impairmentthat 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 disordersComorbidity between developmental disorders is so widespread that the child with a truly specificdisorder is the exception rather than the rule. There is ample evidence that children with SLI havehigh rates of ADD (Beitchman, Brownlie, & Wilson, 1996), developmental co-ordination disorder(Powell & Bishop, 1992), literacy problems (Bishop & Adams, 1990), and impairments of socialinteraction (Brinton & Fujiki, 1993). Any attempt at specifying diagnostic criteria must grapplewith this issue.Once again, we have a situation where the research focus on pure cases has had a negative impacton clinical practice, by leading to restrictive diagnostic criteria that exclude a substantial proportionof children. Clinicians, in seeking to arrive at a single diagnostic label, are discouraged fromconsidering the whole spectrum of impairments that one typically sees. My experience is that thereare many children where the particular diagnostic label that a child receives is more a function of 6
  7. 7. the specialist who makes the diagnosis, than of the characteristics of the child. The same childmight receive a label of SLI from a speech-language pathologist, dyslexia from a schoolpsychologist, ADHD from a pediatrician, PDDNOS from a child psychiatrist, right-hemispherelearning disability from a neuropsychologist, and developmental co-ordination disorder from aphysical therapist.I dont think the answer is to lump all disorders together, as tended to be the case in the past withconcepts such as minimal brain dysfunction. However, it would seem important to stress theimportance 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 developmentaldisorders may be more appropriate than the categorical approach that has been inherited from thoseworking in the tradition of the medical model. On this view, the distinction between specificlanguage impairment and autistic disorder is not a sharp divide. Certainly, there are many childrenwhose differential diagnosis is quite unambiguous: these would correspond to textbook cases ofSLI or autistic disorder. However, there are others who have social and pragmatic impairments thatgo beyond what one would expect to see in SLI, yet whose difficulties are not as severe orpervasive as is typically seen in autistic disorder. I have used the term pragmatic languageimpairment to refer to these cases. The model could be made even more complex byincorporating the domains of attention and motor skill. A multidimensional model appears to do abetter job in capturing clinical reality than a diagnostic system with sharp divisions betweendiscrete disorders. However, we cannot afford simply to abandon the diagnostic labels, even if werecognise that they are artificial abstractions. Quite simply, a label provides a shorthanddescription of a childs 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 offeredwhether 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 questionas to whether we should alter our diagnostic boundaries. Comorbidity can arise for many differentreasons (Caron & Rutter, 1991). It could be that a common genetic defect leads to diversebehavioural outcomes, perhaps by affecting adjacent brain areas. Or it might be that environmentalrisk factors for one disorder raise the likelihood of the other being present. One disorder, such aslanguage 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. Forinstance, it is easy to see how language difficulties might lead to reading problems, but harder topostulate a causal route from language difficulties to motor clumsiness. As yet, we have littleunderstanding of the origins of comorbidity with language disorders, but genetic studies may leadto a way forward because they can help us discover whether co-occurring disorders have commonetiological origins (cf. e.g., Stevenson, Pennington, Gilger, DeFries, & Gillis, 1993). Even thoughcomorbidity is widespread, one can find cases of relatively pure disorder, and these may be theoptimal cases to use for certain types of research study where one wants to study the correlates oflanguage 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 thenature and origins of their problems could be quite different.Heterogeneity of SLIThere is little agreement on the question of how to subclassify SLI. As a field develops, the basisof 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 andunderlying cognitive mechanisms, but as yet the field is not sufficiently advanced for this to be 7
  8. 8. possible. In general, therefore, classifications tend to be based on the linguistic characterisation ofthe language impairment. Bishop (1998) argued that attempts to derive categories by using clusteranalysis with test data have been largely unsuccessful, probably because the available tests do notcover aspects of communication which are important, such as pragmatics. More agreement hasbeen achieved by those adopting a clinical approach, such as Rapin and Allen (1983), and thosewho 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 languageimpairment about which there is at least some broad agreement among clinicians. Typical SLIA large percentage of research on SLI focuses on children who have disproportionate problemswith grammatical development. In English, this is manifested in frequent omission of grammaticalendings, such as past tense -ed, or third person singular -s. Such errors are, of course, seen also innormally developing young children, but in SLI they persist well beyond the normal age, and thegrammatical 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 themanifestations in languages other than English. He also reviews the wide range of theories ofunderlying impairment that have been proposed to account for this pattern of languagedevelopment. First, there are theories that postulate a low-level auditory perceptual impairment asthe 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 languageat the rate at which it is normally produced, and this leads to slow and distorted acquisition ofphonology and syntax. This contrasts sharply with theories that argue for impairment of innatebrain modules specialised for processing grammar (e.g., Gopnik & Crago, 1991). Yet anothergroup of researchers propose limitations in processing capacity and/or working memory as thefundamental 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 singleunderlying cause that might explain all cases of grammatical impairment in children, but it is, ofcourse, possible, that different explanations apply in different cases. It is unfortunate that manystudies report only group data when testing a specific hypothesis, without indicating how typicalfindings are for group members. Often, however, there can be quite substantial variation from childto child. For instance, Bishop et al. (1999) found that children with SLI did do more poorly than acontrol group on a test of auditory perception based on Tallals theory. However, they did not showthe expected rate-specific deficit, and the effect size was relatively modest. This meant that therewere many children with SLI who were not impaired in auditory processing, and many controlswho were. A subsequent study by Bishop, Carlyon, Deeks, & Bishop (1999) on a subset of thesechildren considered whether the variable results simply reflected poor reliability of the auditorytest. Eleven children with SLI were compared with eleven matched controls on a range of auditorypsychophysical tasks, with repeat administration over a period of several months. On a test ofauditory backward masking, there was reasonable test-retest reliability, despite the fact that practiceled to improvements in scores for all children with repeat testing. However, there was substantialindividual variation in both control and SLI groups, and, in this relatively small sample, there wasno significant difference between them. The conclusion from this study was that auditory deficitwas neither necessary nor sufficient to cause SLI, but we suggested that it might be a risk factorthat assumed importance when it occurred in a child who had a genetic predisposition to SLI. 8
  9. 9. Although grammatical difficulties are one of the most noticeable and common manifestations ofSLI (e.g., Conti-Ramsden et al., 1997), one should beware of assuming that all children withgrammatical problems are the same. Phonological difficulties appear to be a common, but notuniversal, correlate (Rapin & Allen, 1983). The existence of children who have severe problems inunderstanding grammar in the context of superior nonverbal ability, good pragmatics andphonology, and normal auditory processing is of considerable theoretical interest in demonstratingthe 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 difficultiesco-occur with major problems in semantics and some limitations of nonverbal ability. Severe receptive language disorderAlthough 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 theyare initially thought to be deaf. This is sometimes referred to as a childhood manifestation ofverbal auditory agnosia (Rapin, Mattis, & Rowan, 1977). Much of the research on these childrenconsists of single case studies, because they are so very rare. Some of these studies havedemonstrated impairment of nonverbal auditory processing in such children (e.g., Rosen, Van derLely, & Dry, 1997; Stefanatos, Green, & Ratcliff, 1989). This is one subtype of languageimpairment that is associated with a distinctive etiology, that of acquired epileptic aphasia, orLandau-Kleffner syndrome (see Deonna, 2000, for a review). Typically, the child starts outdeveloping language normally, but regresses in the preschool years, losing languagecomprehension 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, becauseoften 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 beimplicated in some cases of milder SLI, though he notes that studies looking for elevated rates ofEEG abnormalities in children with SLI have not yielded consistent findings. Developmental verbal dyspraxiaDevelopmental verbal dyspraxia is possibly one of the most controversial of all the subtypes ofSLI. Some authorities deny its very existence. Others accept that a clinical picture resemblingdyspraxia may be seen, but query whether the label is an appropriate one. Even those who use theterm, do so in rather different ways. In adult neurology, dyspraxia refers to difficulty inprogramming 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 greatdifficulty producing longer sequences. In developmental cases, one also sees children whoseintelligibility declines markedly when they attempt complex utterances, compared to when they areproducing individual sounds or syllables. Some authorities argue that a diagnosis of dyspraxia ismost appropriate when the child also has evidence of imitating nonspeech oral movements. Othersmaintain that the programming impairment can be specific to speech production, and that the mostcritical diagnostic feature is inconsistency of speech sound production from one occasion toanother. Although the term dyspraxia suggests a pure output disorder, systematic studies ofphonological 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 withprogramming motor output. In contrast to children with speech disorders arising from physical or 9
  10. 10. neurological impairment of the articulators, those with verbal dyspraxia typically have majorliteracy 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 maybe inappropriate in suggesting a circumscribed motor programming problem. Pragmatic language impairmentThe traditional view of SLI is of a child with normal sociability whose communication is limitedonly 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 useof language in this population. Bishop (2000) reviewed this work and concluded that, though somesocial communication problems in SLI could be secondary consequences of difficulties informulating intelligible utterances or comprehending what others were saying, others were lesseasy to explain this way. This is particularly true in the case where the child with early languagedelay goes on to make rapid progress in mastering phonology and grammar, and starts to speak inlong and complex sentences, but uses utterances inappropriately. Such children may offertangential answers to questions, lack coherence in conversation or narrative speech, and appearover-literal in their comprehension. In the past, I adopted the terminology based on the nosology ofRapin and Allen (1983), referring to these children as cases of semantic-pragmatic disorder, butthere is little evidence that semantic and pragmatic difficulties tend to co-occur, and I now preferthe term pragmatic language impairment. One might expect a child with language difficulties tocompensate by developing a rich repertoire of nonverbal communication, but in these cases ofpragmatic 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 theautistic continuum, rather than classified with SLI. They certainly share a number of features withhigh-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 aspremature to conclude that all children with PLI should be placed on the autistic spectrum. Someof these children do have clear autistic features, but others do not (Bishop, 1998). The diagnosticoverlap 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 poorsocial interaction and limited narrative and conversational skills (Tannock, Fine, Heintz, &Schachar, 1995; Tannock, Purvis, & Schachar, 1993). For clinicians, the message seems to be thatone should be alert to the possibility that a childs communicative difficulties might extend beyondlanguage structure, to encompass social use of language, and nonverbal communication. Mostformal language assessments are not sensitive to these problems, and so one should not assume thatthey are absent, just because they dont show up on a test. Where the child does have pragmaticproblems, a multidisciplinary assessment is warranted to consider whether a diagnosis of ADD orautistic spectrum disorder (PDDNOS) would be appropriate. It can be particularly difficult to findappropriate educational placements for such children. Schools for children with autism tend tofocus more on the needs of those of low IQ, who may need much more focus on structuredactivities and behaviour control. Schools for those with language difficulties may, however, be lesswell prepared for dealing with the nonverbal and social impairments, which become increasinglyimportant as children grow older.Concluding comment Specific language impairment poses enormous challenges for both clinicians and researchers. Theexistence of children with communication problems is not in doubt. There is little consensus aboutdiagnostic criteria, diagnostic boundaries, or subclassification. The principal message of thischapter is that we have to consider the purpose of diagnosis, and match our methods to our goals, 10
  11. 11. rather than looking for a single gold standard to apply in all situations. The pure, clearcutcategories 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 diagnosticdifficulties, can we resolve them. However, it would be wrong to give the impression that theproblems are insuperable. Just over the past decade, we have seen enormous advances in ourunderstanding of SLI on many fronts. We now know considerably more than we did 10 years agoabout 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 justhow common SLI is, and we also know just how serious it is, in terms of putting the child at riskfor 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 scientificstudies of intervention that allow us to identify the characteristics of successful interventions (seethe five subsequent chapters in Part 3 of this volume). 11
  12. 12. Table 1Definitions of Impairment, Disability and Handicap (World Health Organization, 1980) Impairment Abnormality at the level of organ or system functioning: includes psychologic, physiologic oranatomic abnormalities Disability Restriction or loss at the functional level. Inability to carry out activities that most humans cando Handicap Social disadvantage arising from impairment: this depends on the social environment as well asthe level of impairment and disability 12
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