Speech, Language and Communication

The distinction between speech, language and communica-tion may be illustrated by three child cases. Emma is a livelyand engaging 9-year-old who has difficulty making herselfunderstood because her production of speech sounds is veryunclear. However, she demonstrates normal language skills:she understands what others say to her, and can express her-self in writing using long and complex sentences. Her abilityto communicate is hampered by her speech difficulties, but sheenjoys interacting with others, and when people fail to under-stand her, she supplements her utterances with gesture and facialexpression to get her message across.

Thomas is a 6-year-old who has no difficulty in producingspeech sounds clearly, but his language skills are limited, asevidenced by his use of simple and immature sentence con-struction. Instead of saying “I’d like a drink” he says “Mewant drink.” However, although his language is far more simple than that of other 6-year-olds, he does use it to com-municate with other children and adults. In contrast, 4-year-old Jack produces a great deal of complex, fluent and clearlyarticulated language, but he does not use it to communicateeffectively. Thus, his opening gambit to a stranger might beto say: “In Deep Space Nine you can’t get to level 6 until youhave killed all the foot soldiers, but if you get to level 6, youhave to first destroy the klingons before you can enter the palaceof death.”

One way of depicting the relationship between speech, language and communication is shown in Fig. 47.1, where language is a subset of communication and speech is a subsetof language. Communication is defined by McArthur (1992,p. 238) as “the transmission of information (a message)between a source and a receiver, using a signaling system.”The primary means of communication between humans isthrough language, but communication also encompasses othermeans of signaling meaning, such as facial expression, bodilygesture and non-verbal sounds. Language differs from theseother communicative modes; it is a complex formal system inwhich a small number of elements are combined in a rule-basedmanner to generate an infinite number of possible meanings.Most human language is expressed in speech (i.e., meanings

are represented by words that are composed of a small set ofspeech sounds, or phonemes). Where learning of oral languageis compromised because a child is deaf, manual (sign) languageshave evolved, showing similar structural characteristics tospoken languages. In addition, oral language can be expressedin written form. Language involves more than speech, and com-munication involves more than language. However, it is possible for someone to speak without producing language (e.g., when a person utters meaningless gobbledegook), andit is possible for someone to produce utterances that obey theformal rules of language, yet communication is not achieved,as in the case of Jack. In evaluating children with impairments,it is important to keep these three levels in mind, and to recog-nize that a problem at one level does not necessarily entail aproblem at another.

In this chapter we make a broad division between disordersaffecting speech, and those affecting language and communica-tion. This distinction has some similarity with the distinctionmade in DSM-IV-TR (American Psychiatric Association, 2000)between phonological disorder (315.39) and language disorder(315.31), but the coverage is broader. Among speech disorders,we cover disorders affecting fluency, voice and prosody as well as problems of speech sound production that may havea neurological basis. For language and communication dis-orders, we focus heavily on specific language impairment (SLI),which is analogous to the DSM language disorder category,but we also consider other conditions required for a differential

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Speech and Language DisordersDorothy V. M. Bishop and Courtenay Frazier Norbury47

Rutter’s Child and Adolescent Psychiatry, 5th edition. Edited by M.Rutter, D. Bishop, D. Pine, S. Scott, J. Stevenson, E. Taylor and A.Thapar. © 2008 Blackwell Publishing, ISBN: 978-1-4051-4592-3.

Fig. 47.1 Relationship between speech, language andcommunication.

Communication

Language

Speech

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diagnosis, including acquired epileptic aphasia, autistic disorderand selective mutism.

General Principles of Assessment

In most instances, detailed assessment of the speech and language system will be carried out by a specialist speech-language therapist, who will have extensive knowledge of linguistics and language development, the anatomy and physio-logy that supports the language system, and access to a varietyof assessment and intervention techniques. With regard to communication, the primary decisions for the practitioner tomake at initial assessment are:1 Is the child’s communication development delayed or disordered?2 What aspects of communication are causing the most concern?3 Is referral to speech-language therapy warranted?

The first port of call in the assessment process is the casehistory. This will give the practitioner an opportunity toexplore with the child’s parents who is concerned about com-munication, and precisely what they are concerned about.Although many parents will be concerned about the child’slanguage development, others may not be aware of difficul-ties with communication. These parents may not see languageas the central problem, but will voice concerns about behavior,social skills and learning that may be related to underlyinglanguage difficulties.

As part of the case history, it is essential to obtain fromparents clear examples of what motivates the child to com-municate and how the child achieves communication. For example, does the child communicate only to get his or herbasic needs met? Does the child communicate to show othersthings that interest him or her? Does the child use words orphrases? If not, does the child gesture, vocalize and/or pointin an effort to get the message across? In addition to concreteexamples of the types of communication the child produces,it is also important to ascertain the types of communicationthe child can understand. Does the child follow an adult’s pointor eye gaze? Can he or she follow simple verbal instructionsout of context? For more able children this may not pose aproblem, but they may have difficulty following a story or getting the point of a joke.

Once the practitioner has gained an impression of the childfrom the parents, it will be necessary to determine directly thechild’s current level of functioning. Throughout the rest of thischapter, we give specific signposts to impairment in speech,language and broader communication, and suggest standard-ized assessments in each of these domains that can assist inthe diagnostic process (Table 47.1). However, it is usuallypreferable to start by observing the child’s communication ina less structured setting. This can be achieved by videoing thechild playing with his or her parents or siblings in the clinic.If the child has some verbal language, this play session canbe supplemented by asking the child to recall a favorite story,computer game or television program.

During these informal tasks, the practitioner can make a num-ber of important observations. The first concerns the child’sexpressive language output. How long and grammaticallycomplex are the child’s utterances? How rich is the child’svocabulary? Does he or she struggle to find the words for com-mon objects? Does he or she use gestures and facial expres-sion? Is the speech fluent, or is the child’s speech pepperedwith hesitations and repetitions? What is the child’s voice quality like? Is he or she shouting and hoarse, or whisperinginappropriately? Is the child intelligible, or are there numer-ous speech errors that impede understanding? Does the childtell a story as a coherent sequence of events, or does he orshe get muddled and leave important events out?

The next set of observations concerns the child’s under-standing, which may be more difficult to gauge in this setting.Nevertheless, it can be revealing to observe how the childresponds to the questions and comments of others. Are theanswers appropriate to the questions? Does the child followadult directions? Does the child understand the premise of astory or does he or she misinterpret key events? Does the childappear to understand the gestures and facial expressions ofothers? Can the child listen while engaged with something else,or must the adult focus his or her attention before speaking?

Finally, these informal interactions enable the practitionerto observe other important behaviors. How and why does thechild engage with the other people in the room? Does he orshe look up when called? Is the child’s play creative and imag-inative, or destructive and repetitive? Can the child stick withan activity, or is his or her attention span unduly short? Is thechild frustrated when he or she is not understood? Does heor she try again? Does the child recognize when he or she hasnot understood something and ask for clarification? Is the childanxious, or does he or she quickly adjust to the new situation?

In combination with the case history, this set of observationsshould provide the practitioner with a working hypothesis ofthe child’s strengths and weaknesses which will guide the assess-ment process (see chapter 19).

Speech Disorders

Speech refers to the production of oral language, which isachieved by modifications to the vocal tract while a streamof air is breathed out from the lungs. Speech difficulties in children are not difficult to detect, but accurate diagnosisrequires specialist assessment by a speech and language ther-apist. The main types of difficulty that are encountered arethose affecting the distinctive production of speech sounds,fluency of connected speech, voice, and prosody (i.e., speechmelody and intonation).

Differential Diagnosis of Speech Sound DisordersAll spoken languages encode meaning in terms of a small setof vowels and consonants: in standard British English thereare 24 consonants and 20 vowels that can be combined toyield thousands of words. When a child’s speech is difficult

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Table 47.1 Language assessments in common use in the UK.

Assessment

PhonologyGoldman–Fristoe Test of Articulation–2(Goldman & Fristoe, 2000)

Diagnostic Evaluation of Articulation and Phonology(DEAP) (Dodd et al., 2002)

Phonological Assessment Battery (PhAB)(Frederickson et al., 1997)

Children’s Test of Non-word Repetition(Gathercole & Baddeley, 1996)

SemanticsMacArthur–Bates Communicative DevelopmentInventories (Fenson et al., 1994, 2003)

British Picture Vocabulary Scales–2(Dunn et al., 1998)

Expressive/Receptive One Word Picture Vocabulary Tests (Gardner, 2000)

Test of Word Knowledge (ToWK)(Wiig & Secord, 1992)

SyntaxRenfrew Action Picture Test (RAPT)(Renfrew, 1988)

Test for Reception of Grammar–2 (TROG-2)(Bishop, 2003b)

NarrativeThe Bus Story (Renfrew, 1988)

Expression, Reception and Recall of Narrative Instrument (ERRNI) (Bishop, 2004)

PragmaticsChildren’s Communication Checklist–2 (CCC-2) (Bishop, 2003a)

Omnibus testsAssessment of Comprehension and Expression (ACE) (Adams et al., 2001)

Clinical Evaluation of Language Fundamentals–Preschool (Wiig et al., 1992) and Clinical Evaluation of Language Fundamentals (Semel et al., 2003)

Pre-school Language Scales–3 (Zimmerman et al., 1997)

Reynell Developmental Language Scales–3 (Edwards et al., 1997)

Test of Language Competence (Wiig & Secord, 1989)

Test of Language Development–3 (TOLD-3) (Newcomer & Hammill, 1997)

Age range

2–21 years

3–6 years

6–14 years

4–8 years

8–30 months

3–15 years

2–12 years

5–17 years

3–8 years

4 years–adult

3–8 years

6 years–adult

4–16 years

6–11 years

3–6 years;5 years–adult

Birth-6 years

1–7 years

9–18 years

4–12 years

Description

Naming task which samples all consonants and clusters of English ininitial, medial and final word positions. Assesses spontaneous andimitated speech

Picture materials elicit speech with goal of differentiating betweenarticulation problems, delayed phonology and consistent versusinconsistent phonological disorder

Tests of phonological processing: alliteration, naming speed, rhyme,spoonerisms, fluency and non-word reading

A measure of phonological short-term memory; the child listens tonon-words and repeats them

Parent reports of words child understands and produces earlycommunicative gestures and early word combinations

Understanding of single words. Child matches spoken word to one offour pictures

Child either names a picture (expressive) or matches a spoken wordto one of four pictures

Expressive and receptive semantics including definitions, antonyms,synonyms, multiple meanings

Sentence elicitation task in which children describe what is happeningin 10 different pictures. Scored for information content and syntacticcomplexity

Child matches spoken sentence to one of four pictures. Assessesrange of grammatical structures

Provides age equivalent scores for story information and sentencecomplexity

Narrative assessment that provides standard scores for informationcontent, complexity of grammatical structure, comprehension ofpictured story, recall of narrative

Parental report of language and pragmatic behaviors in everydaysituations. Provides standard scores

Assesses sentence comprehension, inferencing, naming, formulatingsentences, semantics, non-literal language comprehension, narrative

Assesses basic concepts, syntax, morphology, semantics, verbalmemory. Provides receptive and expressive as well as total languagescore

Assesses listening comprehension, expressive communication andprovides a total language score

Measures receptive language (verbal and non-verbal) and expressivelanguage, including structure and vocabulary

Assesses higher level language skills such as inferencing, multiplemeanings, figurative language, sentence production in conversationalcontexts

Subtests measure both semantic knowledge and grammar

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to understand, analysis of the pattern of errors will be help-ful in distinguishing whether the difficulty is the result of astructural or motor impairment affecting the articulatoryapparatus (i.e., a dysarthria) or whether other explanationsneed to be sought (Dodd, 2005). Usually, dysarthria will beaccompanied by other evidence of physical or neurologicalimpairment, and the production of speech sounds will be dis-torted or labored.

Phonological DisorderContrary to popular belief, most childhood problems withspeech production do not have a physical basis. For many yearsthere was a belief that children’s speech difficulties could becaused by “tongue tie,” which could be cured by cutting thefrenum. However, surgery is seldom effective in improvingspeech and it is now recognized that interventions that trainchildren to perceive and produce sounds accurately are moreeffective. The key point to note is that speech productioninvolves more than articulation: in learning a language, thechild has to integrate speech perception with production, andwork out which sounds in the language are used to signal con-trasts in meaning (i.e., correspond to phonemes). To illustratethe difference between articulation and phonology, considerthe following: many native English-speakers have great dif-ficulty in correctly learning to produce the French words“rue” and “roux” distinctively. This is because the vowel con-trast in these words does not match the phonemes in English,where there is just one “oo” sound. This has nothing to dowith the structure of the articulatory apparatus, and every-thing to do with perceptual experience of a language, whichleads English-speakers to treat all instances of “oo” as onephoneme, where French-speakers divide the vowel space intotwo phonemes. Most cases of childhood speech productiondifficulties appear analogous to the problems of the secondlanguage-learner: they arise because the child has not learnedto categorize speech sounds appropriately, and so may fail todifferentiate sounds that are important for signaling contrastsin meaning. Over the years, a variety of terminology has beenused to describe such difficulties, including functional articu-lation disorder and phonological disorder/impairment.

Developmental Verbal DyspraxiaSitting somewhat uneasily between dysarthria on the onehand, and phonological disorder on the other is the categoryof developmental verbal dyspraxia, also known as develop-mental apraxia of speech. An early use of the term was byMorley (1957), who applied it to children in whom the neuro-muscular control of the articulators seemed adequate for allpurposes except the rapid integrated movements used in speech.Such children might be able to imitate accurately a simple syllable or word, but would make errors if asked to producelonger words or connected sentences. Stackhouse and Wells(1997) noted that production of longer words may be incon-sistent as well as inaccurate, so that “caterpillar” could be pro-duced as “capertillar,” “taperkiller” or “takerpillar.” The term“dyspraxia” is taken from adult neurology where it describes

a disorder of planning movement sequences that is not ac-counted for in terms of lower-level difficulties in executing individual movements. However, it is unclear whether motorprograming is at the root of the inconsistent speech difficultiesseen in children. Individuals with the clinical picture of devel-opmental verbal dyspraxia often have major problems in per-ception as well as production of speech sounds, doing poorlyon tests that require them to discriminate or classify sounds(Stackhouse & Wells, 1997). Some experts argue that devel-opmental verbal dyspraxia is simply an unusually severe kindof phonological disorder in children, reflecting an underlyingdifficulty learning the categorization of speech sounds, ratherthan having motor origins. The jury is still out on this ques-tion, not least because different experts use different diagnosticcriteria (Forrest, 2003).

One way of bypassing diagnostic difficulties has been to use the more general term “speech sound disorder” (SSD) toencompass all difficulties of speech sound production in chil-dren that do not have a physical basis, without needing tospecify whether they are motor-based or phonological in ori-gin. Although such “lumping” of disorders might seem likelyto obscure important differences between phenotypes, Lewiset al. (2004) argued in its favor. They compared family pedi-grees of children with verbal dyspraxia and children with otherforms of SSD. Verbal dyspraxia showed very high familiality,but the disorder did not “breed true,” and affected relativeswere more likely to have other forms of SSD or language impair-ment than to have verbal dyspraxia themselves. Lewis et al.(2004) concluded that the principal difference between chil-dren with verbal dyspraxia and those with other SSD was inthe degree of genetic loading for disorder.

Assessment of Speech Sound DisordersCoplan and Gleason (1988) provided guidelines to help healthprofessionals decide when to refer a child for speech assess-ment, based on a parent’s response to the question, “How muchof your child’s speech can a stranger understand?” At 2 years,referral should be considered if the child is less than 50% intel-ligible, at 3 years if less than 75% and at 4 years if less than100% intelligible. Referral to a speech-language therapist isstrongly recommended when poor speech intelligibility occursin combination with other risk factors (see p. 000).

Assessment by the speech-language therapist will involve ex-amination of the articulatory apparatus. A history of difficultywith sucking, chewing, dribbling, licking or blowing shouldalert the clinician to the possibility of physical impairment,such as submucous cleft palate, or neurological impairment.Where there is facial dysmorphology or evidence of neurologicaldysfunction, referral to specialist medical services (pediatric neurology, otolaryngology or clinical genetics) is warranted.

The speech-language therapist will construct a phonemicinventory of sounds the child is able to produce and will lookfor inconsistency of word pronunciations and the presence of “phonological processes” (i.e., consistent error patterns),such as replacing /k/ with /t/ so that “cat” becomes “tat” and“take” becomes “tate.” Many of these processes are seen in

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the course of normal phonological development; however, anSSD is diagnosed when such processes continue beyond thenormal age, or when there are numerous inconsistencies andatypical phonological processes.

“Phonological processing” is a general term used to covermore subtle difficulties in using phonological information.Phonological awareness in particular is nowadays often tar-geted in assessment as research has demonstrated links with laterliteracy difficulties (Snowling & Stackhouse, 2006). This refersto the ability to manipulate the sound segments in the languageand includes tasks such as rhyming, segmenting syllables andphonemes in words, identifying initial and final word sounds,and deleting, adding or transposing phonemes in words. Such problems can been seen in children with normal speechsound production but are often also seen in children with SSD,suggesting their difficulties do not involve the physical act of articulating speech, but rather the ability to perceive andcategorize different exemplars of the same phoneme (Bird,Bishop, & Freeman, 1995; Stackhouse & Wells, 2006).

An important point to stress is that although speech andlanguage difficulties are not the same thing, they do often co-occur. We therefore recommend that any child who presentswith a speech difficulty should have a full assessment of bothspeech and language.

Prevalence, Causes and Correlates of SpeechSound DisordersEstimates of prevalence of SSD are hampered by inconsist-encies in diagnostic criteria. Gierut (1998) cited a 1994 reportfrom the US National Institute on Deafness and Other Com-munication Disorders which estimated that phonological disorders affected approximately 10% of preschool andschool-aged children, and that in 80% of cases the disorderwas severe enough to merit clinical treatment. At 6 years ofage, the prevalence of “speech delay” was estimated at 3.8% ina US epidemiological study (Shriberg, Tomblin, & McSweeny,1999).

Campbell et al. (2003) identified a number of factors thatgreatly increased the risk of speech sound disorders in pre-school children. These included male gender, limited maternaleducation and a positive family history of speech and languagedisorder. These authors also suggested that an accumulationof risk factors exerted a greater threat to developmental outcome than individual risks. Children with only one risk factor were 1.7–2.6 times more likely than children who hadnone of these characteristics to have speech delay at 3 years;children with all three risk factors present were almost eighttimes more likely to have speech delay at 3 years.

Both family (Lewis et al., 2004) and twin studies (Bishop,2002; DeThorne et al., 2006) suggest a strong genetic etiologyfor SSD. Although verbal dyspraxia can follow an autosomaldominant pattern of inheritance in some families (Hurst,Baraitser, Auger, Graham, & Norell, 1990), in most cases thereare numerous genes that contribute to risk of poor speech and language skills, rather than a single genetic mutation. Todate, progress in the search for a molecular basis has been

limited to one report of linkage to a site on chromosome 3(Stein et al., 2004).

Intervention and Prognosis for Speech Sound DisordersA variety of techniques may be employed to improve speechintelligibility, and research to date suggests that no single treatment approach is appropriate for all children with SSD(Dodd & Bradford, 2000). Techniques might include using tactile and visual cues to enable children to produce the targetsound accurately. This will be combined with repeated practiceat producing the target sound in words with corrective feed-back. More meta-linguistic approaches involve games andexercises to develop the child’s awareness of meaningful phon-emic contrasts (Gierut, 1998).

In a recent meta-analysis of the literature, Law, Garrett, andNye (2004) found that phonological interventions were gen-erally effective when compared with no treatment. The most effective treatments were those carried out by speech-languagetherapists, rather than parent-administered treatments, and thosethat lasted for longer than 8 weeks. Therapist-led treatmentsmay incorporate a variety of techniques, such as “articulationdrills” in which the child learns and practises correct produc-tion of speech sounds with visual aids such as cued articula-tion (hand gestures that illustrate the place and manner of articulation) or symbols (pictures of place and manner of articulation). Other techniques (e.g., Metaphon) emphasize ameta-linguistic approach to improving speech production(Howell, & Dean, 1994). This treatment teaches sound “con-cepts” so that children learn, for example, the differencesbetween “short” sounds (/t/ and /d/) and “long” sounds (/s/ and/f/). The therapy also utilizes “meaningful minimal contrasts,”in which the child is required to alter speech production toavoid ambiguity. For instance, if the child is “fronting” (pro-ducing /k/ sounds as /t/ sounds), the therapist might constructa game in which the child has to ask for a “key” or “tea.” Ifthe child intends to ask for the “key” but the therapistresponds with the “tea,” the child is forced to adapt his pro-nunciation to convey his or her intended meaning. Many ther-apists will use a combination of techniques depending on theneeds of the child, as there is currently no evidence that onemethod of treatment is more effective than any other method.

The longer term prognosis for children with isolated pho-nological impairments is much better than that of languageimpairment, especially if the phonological difficulties resolveby the time the child starts school. However, the child whostarts school with phonological difficulties is at increased riskof long-lasting literacy deficits (Stothard, Snowling, Bishop,Chipchase, & Kaplan, 1998).

Other Types of Speech DisorderFluency DisordersStuttering and stammering are two popular terms for dys-fluent speech. Developmental dysfluency is characterized byinvoluntary repetitions, blocks or prolongations of sounds, syllables and words in discourse. These may be accompanied

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by secondary behaviors such as physical tension in the speechmusculature, eye blinking or breaking of eye contact, move-ments of the head and limbs, and emotional reactions to thedysfluency, including anxiety and avoidance of speaking.

Persistent dysfluency is estimated to affect 1% of the popu-lation (Yairi & Ambrose, 1999), although many more childrenproduce normal dysfluencies during the preschool years. Likemany speech, language and communication disorders, it ap-pears to be strongly familial, and more boys are affected moreoften than girls (ratio of 1.65:1; Mansson, 2000). Campbell,Dollaghan, and Yaruss (2002) suggest referral to a speech-language therapist if parents report:1 Frequent part-word dysfluencies;2 Noticeable physical tension or struggle;3 Any sign that the child is frustrated or concerned about talking; or4 Concerns about any other aspect of speech and languagedevelopment.

The etiology of childhood stuttering appears to be multi-factorial, with a significant genetic component (Yairi, Ambrose,& Cox, 1996). An international study by Suresh et al. (2006)suggested a complex etiology, with the strongest linkages beingfound when separate analyses were conducted for males (link-age to chromosome 7, LOD score 2.99) and females (linkageto chromosome 21, LOD score 4.5), and when interactionsbetween sites on different chromosomes were considered.

Stuttering has been associated with early difficulties in lan-guage formulation (Bloodstein, 2006) and atypical develop-ment of the auditory temporal cortex (Foundas et al., 2004).Furthermore, comorbidity with speech sound disorders is 30%(Yairi & Ambrose, 1999). Therefore, assessment of broaderspeech and language abilities is warranted.

Approximately 75% of preschoolers will recover fromdysfluency without professional involvement (Yairi & Ambrose,1999). However, prognosis is poor for those who continue tostutter beyond the age of 7 years (Campbell et al., 2002). Thereis considerable debate regarding the most appropriate formof intervention. One approach, exemplified by the Michael PalinCentre for stammering in London (www.stammeringcentre.org), focuses on modifying the environment to reduce speak-ing pressure and working with children and families to reduceanxiety about speaking (for full description see Rustin, Cook,Botterill, Hughes, & Kelman, 2001). An alternative approach,exemplified by the Lidcombe Programme (http://www3.fhs.usyd.edu.au/asrcwww/treatment/lidcombe.htm), provides directbehavioral modification to reinforce fluent speech. There arefew, if any, methodologically sound investigations of treatmentefficacy and no studies that we are aware of that explicitlycompare the two treatment approaches. However, there is somepreliminary evidence that behavioral approaches are effectivein reducing dysfluent speech in the preschool years (Jones etal., 2005).

Voice DisordersA voice disorder, dysphonia, should be suspected when a child speaks with abnormal pitch, loudness and/or hoarseness.

These features can have profound effects on how a child isperceived by others and adversely affect socialization.

Recent prevalence estimates from a population-based studysuggest 6–11% of school-aged children present with dyspho-nia (Carding, Roulsone, Northstone, & Team, 2006). This is considerably higher than would be predicted from clinicalreferrals, but this probably reflects widespread lack of recog-nition of the problem (Boyle, 2000). Gender (male) and oldersiblings were the most significant risk factors in the Cardinget al. study. Campbell et al. (2002) reported unpublished datafrom their own sample of 427 clinical referrals to a specialistclinic; 93% of these children had abnormal voice qualityassociated with laryngeal pathology. The most common patho-logy was vocal nodules (i.e., mechanical trauma caused by onevocal fold making excessive contact with the other). Surgicaltreatment is not recommended in such cases, as nodules arelikely to return if damaging vocal behavior is not altered.Behavioral treatments can be effective and center on modify-ing the environment (i.e., reducing competing noise) andtraining the child to use the voice more appropriately.

Prosodic DisordersProsody may be defined as the suprasegmental properties of the speech signal that modulate and enhance its meaning(Paul et al., 2005). Prosody includes variations in pitch, loud-ness, duration, rhythm, tempo and pausing, and serves a widerange of grammatical, pragmatic and affective functions. Forexample, variations in stress and intonation may signal the difference between a noun (con vict) and a verb (con vict),highlight elements within the sentence for attentional focus (theblue book, as opposed to the red one), and convey a speaker’semotional state.

It is frequently reported that impaired prosody is charac-teristic of verbal individuals with autistic spectrum disorder(ASD), although it may not be universal. Paul et al. (2005)reported that 47% of the 30 adolescent and adult speakerswith ASD they investigated had prosodic abnormalities. Suchabnormalities have a negative effect on how listeners perceivesocial and communicative competence and pose significantobstacles to social integration and employment (Paul et al., 2005).

Disorders of Language andCommunication

Components of LanguageCompetent adults produce language so effortlessly that it iseasy to forget just what a complex system it is. All spokenlanguages can be studied in terms of four levels of descrip-tion: phonology (speech sounds); semantics (meaning); gram-mar (formal ways of using word order and inflection); andpragmatics (use of language to communicate). However, thereis considerable variation from one language to another at allof these levels. For instance, Chinese does not have word in-flections, whereas Turkish has numerous inflections that areappended to word stems in an agglutinative fashion. Clearly,

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the task confronting the young language learner is going tobe very different in these two languages, and in English,which uses inflections, but much more sparsely than many otherlanguages. As well as the different levels of linguistic repres-entation, language can be divided into expressive (production)and receptive (comprehension) aspects. To be a competent com-municator, the child must learn to recognize and produce the distinctive speech sounds in the language (the phonology),establish a “mental lexicon” containing representations of wordsas phoneme sequences linked to meanings, master the gram-matical structure of the ambient language, and learn how toselect a message to convey meanings economically and effect-ively to others (pragmatics). Furthermore, language processinghas to be carried out at speed.

Differential Diagnosis of Specific LanguageImpairmentWhen a child presents with language impairment, the clini-cian needs to establish whether there is any causal factor present that could explain the language difficulty, or whetherthe language impairment is part of a recognized syndrome. The majority of cases of language impairment in children have no obvious cause (Shevell, Majnemer, Rosenbaum, &Abrhamowicz, 2000), and occur in the context of otherwisenormal development. This is known as specific languageimpairment (SLI) and also as primary language impairment,developmental language disorder or developmental dysphasia.Before considering the characteristics of SLI we briefly discussother conditions that need to be considered when making adifferential diagnosis.

Low Non-verbal AbilityAn early step in the assessment of a language-impaired childis administration of a non-verbal IQ test. Cases of intellectualdisability (non-verbal IQ more than 2 SD below average) areusually straightforward enough to identify (see chapter 49).However, there are many children with slow language devel-opment who do not have a syndrome of intellectual disab-ility, but nevertheless have below-average non-verbal IQ.Traditional definitions of SLI usually require that non-verbalIQ is broadly within normal limits. More stringent definitionsalso require there should be a significant mismatch betweenlanguage ability and non-verbal IQ (equivalent to 1 SD in ICD-10). However, there is increasing disquiet about the use of IQ discrepancy criteria, because these exclude large numbersof children who are not intellectually impaired and yet haveevident language difficulties. For instance, if we require thereto be a 1 SD difference between a language and non-verbalindex, then we would exclude a child with a language level 2 SD below the mean and a non-verbal score 1.3 SD belowthe mean. This child would not meet criteria for intellectualdisability and so would be left in a diagnostic limbo and maybe denied access to intervention, even though the profile andseverity of language difficulty may be similar to that seen ina child who does meet the discrepancy criterion (Tomblin & Zhang, 1999). Furthermore, twin studies suggest the same

genetic risk factors operate for children with language diffi-culties regardless of their non-verbal IQ (Bishop, 1994). Thus,the logic of distinguishing between children who do and do notmeet strict IQ discrepancy criteria is questionable.

Auditory ProblemsHearing should always be assessed by an audiologist in a child who presents with language impairment. As neonatalscreening programs become more widespread, it is unusual tofind an undetected sensorineural hearing loss in a language-impaired child, but one needs to be alert to the possibility of screening errors or a progressive hearing loss. Hearing loss restricted to a specific frequency range is easy to miss,because the child appears responsive to sound, yet crucial in-formation may be lost from the speech signal, leading to a pro-file of impaired language development that may look similarto SLI (Stelmachowicz, Pittman, Hoover, Lewis, & Moeller,2004).

It is much more common to find conductive losses in young children with language impairments. However, it is noteasy to know how to interpret these. Early studies suggestedunusually high rates of language and literacy problems in children who had otitis media with effusion (OME; Holm & Kunze, 1969). OME typically causes a conductive loss ofup to 40 dB, and it seems plausible that such a loss mightassume significance in a child in the early stages of languagelearning. However, more recent epidemiological studies havequestioned whether OME is a major etiological factor in language impairment (Feldman et al., 2003). A substantial number of children under 5 years of age have undetected andasymptomatic middle ear disease, particularly in the wintermonths. Prospective studies of children with and withoutprolonged episodes of OME have found little or no impacton verbal skills, suggesting that language development isresilient in the face of the mild associated hearing losses. OMEmay assume more importance if it is chronic and persistent(Feldman et al., 2003). However, we would recommend cau-tion in assuming that OME is the main causal factor if it isdetected in a child with language impairment.

There is a large body of knowledge on assessment of theintegrity of the peripheral auditory pathways in children, butmuch less agreement concerning diagnosis of central auditoryprocessing deficits. In some countries, notably the USA andAustralia, the diagnosis of auditory processing disorder (APD– sometimes prefixed with C for central) is frequently made.However, it is far less common in the UK. The principaldifficulty with the APD concept is that it is typically diagnosedusing tests that use verbal materials (e.g., listening to speechin noise) or being presented with two streams of speech in different ears (Moore, 2006). These tests have demonstratedvalidity when used to identify central auditory lesions in adultswith acquired brain damage, who can be assumed to have normal language abilities. However, their interpretation is complicated in children, because it is difficult to distinguishpoor performance resulting from a primary language problemfrom a genuine auditory difficulty (Rosen, 2005). To illustrate

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this point, consider how you would fare if you were asked to carry out a range of listening tests presented in a languagewith which you had limited competence. It is likely that underoptimal listening conditions you would do much better thanwhen words were presented in noise or in a competing speechsituation. This is because a competent speaker of a languagedoes not simply decode speech by bottom-up analysis of thespeech signal; he or she also employs top-down processing topredict and fill in information. If one uses speech-based testsin diagnosis, then one is likely to end up finding numerouscases of language impairment that appear to be caused by APD,but where the problem may in fact arise for quite differentreasons. In our experience, many children who receive a diagnosis of APD from an audiologist would be given a diag-nosis of SLI, dyslexia, attention deficit/hyperactivity disorder(ADHD) or autistic disorder if seen by a speech and languagetherapist, psychologist or child psychiatrist (Dawes & Bishop,in preparation).

In emphasizing these assessment difficulties, we do notwish to imply that APD is not a valid category; it is plausiblethat some children have immature or dysfunctional develop-ment of the central auditory pathways and this might wellimpact on language development. However, our concern is that APD is often diagnosed using instruments of question-able validity, leading to implementation of auditory-based interventions that may not be justified. It is vital to adopt aninterdisciplinary approach, whereby audiologists work togetherwith other professionals to ensure that children receiveappropriate diagnoses and intervention. It is hoped that asresearch on APD advances, better assessment methods, usingmore objective electrophysiological as well as non-verbalbehavioral tests (Liasis et al., 2003) will give a clearer picture.

Acquired Epileptic AphasiaAcquired epileptic aphasia (AEA), also known as Landau–Kleffner syndrome, is a rare cause of childhood language impair-ment which is often misdiagnosed. The typical presentationis one of deterioration in language skills in the preschool years after a period of normal development. Because the childpreviously spoke normally, the disorder may be misdiagnosedas selective mutism (see p. 000); however, in AEA, there isgenuine loss of language skills, with comprehension problemspredominating. Deafness is usually suspected but ruled out on the basis of a hearing test. Many children with AEA haverelatively selective problems with language in the context ofpreserved non-verbal ability, but in some children there areassociated behavioral disturbances, which further complicatethe diagnosis (Deonna & Roulet Perez, 2005). The epilepticmanifestations of AEA are not obvious, because overt seizuresare uncommon, and it may be necessary to carry out a sleepelectroencephalogram (EEG) to demonstrate EEG abnormal-ities. These can be marked, and there has been debate as tohow far this disorder overlaps with slow wave status epilep-ticus in sleep (SWSS). Some children, particularly those withonset after 6 years of age, can make a good recovery, but theprognosis for those with preschool onset is often poor and

substantial receptive language deficits may persist to adulthood.Our recommendation is that any child with language regres-sion accompanied by comprehension problems should bereferred to a pediatric neurologist for an evaluation of AEA.Deonna and Roulet-Perez (2005) note that pharmacologicalinterventions can be effective, but there is wide variation inresponsiveness to treatment, and in the absence of controlledclinical trials it is difficult to give precise guidelines. Deonna(2000) recommends that when receptive language difficultiespersist for more than a few weeks or months, it is crucial to provide the child with an alternative mode of communica-tion. Sign language can be effective and does not interfere with attempts to retrain comprehension of auditory language(Roulet-Perez et al., 2001).

Delayed Language Development: Late-TalkersWhen diagnosing SLI, it is important to determine when ayoung child’s language delay represents a significant departurefrom normal variation, which can be difficult when the childis younger than 3 years old. Late-talkers are identified as having severely restricted vocabulary at age 2 years (fewer than50 words). It is unclear how many late-talkers have similarlyimpaired receptive language skills, because many studiesinclude only children with normal comprehension (Rescorla,2005). Many late-talkers meet typical exclusionary criteria for SLI such as normal non-verbal ability and no hearing loss; however, most late-talking 2-year-olds will normalize language function by the time they enter school (Rescorla,2005), whereas the long-term prognosis for school-aged chil-dren with SLI is less optimistic (Stothard et al., 1998).

Dale, Price, Bishop, and Plomin (2003) followed a large sample of twins from 2 to 4 years of age. Late-talkers wereidentified as those 2-year-olds with expressive vocabularyscores in the bottom 10th centile (15 words or fewer on amodified version of the MacArthur Communicative Develop-ment Inventory). By age 4, 60% had age-appropriate scoreson parent-report measures of vocabulary, grammar and useof abstract language.

It appears that gains in language skill are maintained overtime. Paul (2000) reported that 84% of late-talkers in her cohorthad language scores within the normal range at age 7.Rescorla (2005) followed 28 late-talkers from preschool to age13 and found that, at this age, all of the children scored withinthe normal range on standard measures of language and literacy. However, their scores were significantly lower thana comparison group of typically developing children matchedfor socioeconomic status (cf. Stothard et al., 1998). Rescorlaargued that late-talkers represent a subgroup of SLI charac-terized by less severe language weakness.

Although 60–85% of late-talking children will improve without direct intervention, a minority will not (Paul, 2000;Dale et al., 2003). It is not currently possible to distinguishreliably between those children with transient and persistentimpairments. Dale et al. (2003) found that severity of lan-guage delay at age 2 did not predict language status at age 4.In addition, neither gender nor level of maternal education

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significantly predicted group outcome. Paul (2000) reportedthat children with persistent language difficulties tended to havelower non-verbal abilities, although scores on non-verbalassessments were still within the normal range and there wasconsiderable overlap between groups with good and poor out-come. In addition, high socioeconomic status and prosocialadaptive communicative behaviors were associated with goodoutcome at age 7. A much smaller scale study by Thal, Tobias,and Morrison (1991) indicated that poor receptive languageskills and failure to use gesture were associated with persist-ing language difficulties.

Given these findings, a dilemma facing practitioners is whatto do when language delay is identified during the preschoolyears. Conventional wisdom posits that early intervention is desirable, but Paul (2000) questioned the ethics of treatingchildren who are otherwise developing normally, have normallanguage comprehension and do not present with any addi-tional risk factors for a language “disorder” that they mayovercome naturally without any professional help. Instead, sheadvocates initial parent training to optimize language inputin conjunction with careful monitoring of language development.

Even though good language outcomes are often seen in late-talkers, there is evidence to suggest they should be monitoredbecause such children may be at risk for other developmentaldifficulties. In a survey of over 1000 children, Horwitz et al.(2003) found that late-talkers tended to show poor social interaction, which was in turn associated with an increasedrisk of emotional and behavioral disorders. Furthermore, itwould seem prudent to give the child support in the early stagesof reading and writing, given a suggestion that there is a risk of weak literacy skills in children who were late-talkers(Rescorla, 2005).

Autism and Pragmatic Language ImpairmentsDelayed language development and poor communication skillsare hallmarks of autistic disorder, and the issue of differen-tial diagnosis between autistic disorder and specific develop-mental language disorder frequently crops up in the clinicalsetting. Diagnosis of autistic disorder is covered in detail inchapter 46, so in this chapter we focus on areas of diagnosticdifficulty.

Autistic disorder should be considered when the child’s language difficulties are accompanied by more pervasive diffi-culties affecting social interaction, non-verbal communicationand play, or if the child shows unusual repetitive or ritual-istic behaviors or restricted interests. The clinician needs toconsider whether language development is merely delayed, orwhether there are deviant features that would not be regardedas normal at any age, such as repetitive use of stereotyped catchphrases, unusual and exaggerated intonation, pronounreversal or a frequent failure to respond when the parentattempts to attract the child’s attention.

Some higher functioning children with autistic disorder (i.e.,those children with non-verbal IQs within the normal range)resemble our illustrative child Jack in having superficiallycomplex language; they may appear verbose and achieve age-

appropriate scores on tests of expressive language or simplevocabulary measures. However, such measures may overest-imate true language ability (Mottron, 2004) and the same children usually have significant comprehension deficits in lessstructured and more naturalistic discourse settings (Adams,Green, Gilchrist, & Cox, 2002).

Textbook cases of autistic disorder and SLI are relativelyeasy to differentiate, but many children present with a patternof symptoms that does not fit unambiguously in either category,while showing some features of both. Thus, their difficultiesextend beyond the characteristic grammatical deficits seen in SLI, but they do not have the full triad of impairments in severe enough form to warrant a diagnosis of autism.Differentiation between the two disorders may be hamperedby a changing clinical picture over time (Charman et al., 2005,Mawhood, Howlin, & Rutter, 2000). Conti-Ramsden, Simkin,and Botting (2006) applied standard diagnostic instruments(Autism Diagnostic Interview – Revised; Lord, Rutter, &Couteur, 1994; Autism Diagnostic Observation Schedule –Generic; Lord et al., 2000) to 76 adolescents with a historyof SLI, none of whom had been regarded as autistic in middle childhood. The majority of individuals did not meetcriteria on either measure, but 3.9% met criteria for autisticdisorder on both assessments, a prevalence rate more than three times greater than would be expected from the generalpopulation (Baird et al., 2006). A further 26% met criteriaon one or other measure but not both. Similar results wereobtained by Bishop and Norbury (2002), who noted that manychildren with language impairment displayed difficulties withbroader aspects of communication and social interaction,although restricted interests and rigid behaviors were lesscharacteristic of this population.

In cases where a child meets criteria in one or two domainsof the autistic triad or exhibits subthreshold symptomatologyacross domains, a diagnosis of “pervasive developmental dis-order not otherwise specified” or “atypical autism” is frequentlyapplied. However, there is concern that these terms may be overused, and do not provide helpful information aboutsymptom profile, nor do they facilitate decisions about educa-tional placement. Bishop (2000) suggested that the term “prag-matic language impairment” (formerly “semantic-pragmatic disorder”) might be useful for describing children who do meetfull diagnostic criteria for autistic disorder, but whose languagedifficulties affect social interaction and the use of language in context. The use of this term was not intended to imply anew and discrete disorder; rather, “pragmatic language impair-ment” is seen as a variable correlate of both SLI and milderforms of autistic spectrum disorder (Norbury, Nash, Bishop,& Baird, 2004).

In reality, the diagnostic label chosen may reflect the practitioner’s theoretical stance and the practical implicationsa particular diagnosis brings with regard to accessing appro-priate educational and remedial provision. The importantpoint to recognize is that rather than attempting to draw adiscrete diagnostic line between SLI and autistic disorder, itis more helpful to think in terms of multidimensional space,

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with children varying in terms of the severity of impairmentsin language, social interaction and range of interests.

Selective MutismOccasionally, the clinician will encounter a child who isextremely reticent in the clinic setting. In these instances, it isimportant to establish that the child does speak with othersin more familiar situations such as school and home. However,if the child’s communication varies significantly in differentsettings, the practitioner should consider the possibility of select-ive mutism.

Selective mutism (SM) is diagnosed in the child who consistently does not speak in certain situations in which thereis an expectation for speaking (i.e., school), but can and doesspeak normally in some situations (e.g., at home; Steinhausenet al., 2006). The disorder was previously known as “elec-tive” mutism, but the terminology has been revised to avoidimplying that children are being obstinate or oppositional whenthey remain silent (Cline & Baldwin, 2004; Cohan, Chavira,& Stein, 2006a).

DSM-IV-TR (American Psychiatric Association, 2000) andICD–10 (World Health Organization, 1996) criteria stipulatethat in order to receive a diagnosis, the mutism must persistfor more than 1 month (not including the first month ofschool), and cannot be accounted for by a communication disorder or a lack of familiarity with the ambient language of the social situation. Toppelberg, Tabors, Coggins, Lum, and Burger (2005) further recommend that bilingual childrenare not diagnosed with SM unless the mutism persists for longerthan 6 months and is apparent in both languages.

Prevalence estimates vary depending on the criteria used andthe population studied, with higher rates of transient mutismassociated with starting school. Cline and Baldwin (2004) estimate 6–8 cases of selective mutism per 1000 through-out childhood, with a preponderance of girls (55–65% of cases), consistent with the results of recent community studies,which have found rates of approximately 75% (Cohan et al.,2006a).

The precise cause(s) of SM is unknown; although traumamay precipitate mutism, it is not implicated in the majorityof cases (Steinhausen & Juzi, 1996). SM is generally regardedas a variant of anxiety disorder (Steinhausen et al., 2006;Vecchio & Kearny, 2005), rather than being categorized withspeech and language disorders. Rates of comorbid anxiety andphobic disorders are high, both in affected children and theirfirst-degree relatives, and some success in treatment has beenreported using drugs that effectively reduce anxiety (for a reviewsee Cline & Baldwin, 2004). However, it would be wrong toimply that social anxiety is the only problem; other factorsare also often implicated, including bilingualism and speechand language impairment, suggesting that self-consciousnessabout inadequate communication plays a part in maintainingthe disorder (Manassis et al., 2003). The consensus of opinionis that SM is the culmination of multiple predisposing, pre-cipitating and perpetuating factors (Cohan, Price, & Stein,2006b; Johnson & Wintgens, 2001).

Assessment of the child with SM may be particularly challenging, as the assessment process itself might furtherincrease anxiety and reluctance to speak. At first meeting, itis most important to create a relaxed atmosphere in which thechild feels little pressure to communicate with an unfamiliaradult. In this session, the clinician may take a detailed casehistory from the parents, focusing on where, when and withwhom the child does speak and obtaining detailed examplesof how the child communicates in different settings. Duringconversation with the parents, the clinician may unobtrusivelyobserve the child playing and, if possible, interacting with parents or siblings.

Direct assessment of expressive language may not be possible at this point, although many children with SM willcooperate with receptive language testing if this just involvescarrying out commands or pointing to pictures, and this can give valuable information about general language level(Manassis et al., 2003). Formal assessment may be supple-mented by asking parents to record the child’s language skillsin a more comfortable arena, perhaps telling a story at home,or keep a diary of what the child says and the contexts in which language occurs. Johnson and Wintgens (2001) provide further examples of techniques for gaining the child’s con-fidence to enable assessment to proceed.

The most successful treatments are thought to combine beha-vioral and psychopharmacological interventions, but thereappears to be no systematic research on the efficacy of thisapproach (Cline & Baldwin, 2004). Cohan et al. (2006a) con-ducted a critical review of psychosocial treatments publishedover a 15-year period. The techniques used in these studiesincluded positive reinforcement for speaking to classmates, sys-tematic desensitization to anxiety-provoking situations, lan-guage training, family therapy and self-modeling techniques,in which the child with SM listens to recordings of him orherself speaking in situations in which he or she is usually mute.Although the majority of these studies report increases in speaking behavior, the findings are limited by very small par-ticipant numbers and a lack of suitable control groups.

A recent longitudinal study demonstrated considerableimprovement in symptoms of SM over time, but rates of psychiatric disorder, especially social phobia, remained high(Steinhausen et al., 2006). Prognosis is especially poor whena family history of SM is present.

Assessment of Language and CommunicationApproximately 50% of children referred for psychiatric evaluation have clinically significant language impairments thatare frequently unsuspected (Cohen, 2001). In many clinical con-texts it is not possible to offer the time and expertise neces-sary for every referral to receive an in-depth assessment oflanguage. However, it can be informative to gain an overviewof the child’s language development and current communicat-ive functioning by taking a detailed case history and askingcaregivers to complete a screening checklist.

The Children’s Communication Checklist-2 (CCC-2; Bishop,2003a) is a 70-item checklist for children aged 4 years and

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over that asks parents to rate the frequency of communicativebehaviors in everyday situations, thus providing a naturalisticassessment of functioning. One advantage of this assessmentis that it covers both structural aspects of language (phonologyand syntax) as well as pragmatic aspects of communication,which are more difficult to measure on face-to-face assessment.The CCC-2 reliably distinguishes children with communica-tion impairment from typically developing children (Norburyet al., 2004) and an earlier version of the checklist identifiedchildren at genetic risk for language impairment as effectivelyas standardized tests (Bishop, Laws, Adams, & Norbury,2006b). However, it should be noted that CCC-2 is not suit-able for children who are not yet speaking in sentences.

More detailed evaluation of language and communicativefunctioning will typically be undertaken by a speech-languagetherapist or specialist psychologist. A number of standardizedassessments tapping all domains of language are available inEnglish, but this is not necessarily so in other languages. Theapplication of English language assessments to children fromnon-English speaking backgrounds is not recommended, as testscores may not accurately reflect the child’s competence in hisor her native language.

There is evidence that “knowledge-dependent” measures, suchas vocabulary tests, exaggerate cultural and socioeconomic differences between children, whereas “processing” measuresthat vary difficulty by manipulating the amount of materialthat has to be processed (e.g., nonsense word repetition), provide a culturally unbiased estimate of language ability(Campbell, Dollaghan, Needleman, & Janosky, 1997). Table47.1 provides a list of commonly used language assessmentsin the UK, including the domain of language targeted and theage range appropriate for testing.

There is currently no clear consensus on what degree ofimpairment on standardized assessment constitutes a significantdifficulty. A score of –1 SD (equivalent to 16th centile) on asingle assessment may not interfere with the child’s educationalor social development, whereas consistently low scores acrossa number of language domains or an extremely low score onone measure (–2 SD or 3rd centile) may be more problematic.Tomblin, Records, and Zhang (1996) used a battery of lan-guage tests covering different aspects of receptive and ex-pressive processing, and combined these into five composites:expressive language, comprehension, vocabulary, grammarand narrative. SLI was diagnosed if two or more of these com-posites fell more than –1.25 SD below age level (10th centile),non-verbal IQ was 87 or more, and no exclusionary con-ditions were present. In a population sample, this resulted in 0.85 sensitivity (identifying true cases of impairment) and0.99 specificity (correctly identifying unimpaired cases). Notethat the definition of SLI used by Tomblin et al. was con-siderably less stringent than that of ICD-10 (World HealthOrganization, 1996), which requires that language test scoresmust be 2 SD or more below age level. Application of this criterion would give a lower prevalence rate.

In DSM-IV-TR (American Psychiatric Association, 2000) adistinction is drawn between expressive vs. mixed receptive-

expressive subtypes of language disorder. The importance of establishing level of receptive language cannot be under-estimated: poor comprehension is an important predictor ofoutcome in a language-impaired child (Stothard et al., 1998).However, if strictly interpreted, the DSM-IV system is unwork-able. This is because it defines Expressive Language Disorderas having an expressive language score that is “substantiallybelow” both non-verbal IQ and receptive language, whereasin Mixed Receptive-Expressive Language Disorder, both ex-pressive and receptive language are “substantially below”non-verbal IQ. This creates a problem of how to categorizea child with average non-verbal IQ and a mild receptive language impairment and a more severe expressive impairment(e.g., receptive language score is 0.8 SD below average andexpressive language score is 1.2 SD below average). If we interpret “substantially below” in terms of a 1-SD discrepancy,such a child would not meet criteria for either DSM subtype.Furthermore, the distinction between the two subtypes seemsartificial; both genetic and developmental data suggest that theycorrespond to points on a continuum of severity (Bishop, North,& Donlan, 1995).

Prevalence, Causes and Correlates of SpecificLanguage ImpairmentResearch on SLI is complicated by the variety of diagnosticcriteria that have been employed. It is rather unusual to findresearch that focuses on “pure” SLI in which there is a substantial discrepancy with non-verbal IQ. More commonly,an IQ cut-off is used to establish that children are withinbroadly normal limits. In addition, as noted in chapter 45, SLI is often accompanied by other neurodevelopmental dis-orders: rates of co-occurrence of ADHD, developmental co-ordination disorder and academic difficulties are all high.Studies vary in how far they explicitly include or exclude children with these comorbid conditions, with speech prob-lems or with autistic features. It is likely that estimates of prevalence, comorbidity and etiology will depend on the phe-notype that is studied.

PrevalenceThe most frequently cited prevalence figure for SLI comes froman epidemiological study by Tomblin et al. (1997), who estim-ated that 7.4% (95% confidence interval [CI] 6.3–8.5%) of 5- to 6-year-old children in an Iowa sample met diag-nostic criteria as defined above. Intriguingly, of those who didmeet criteria for SLI, only 29% had previously been identifiedas having language difficulties. If the criteria were made more stringent, to include only those with composite languagescores more than 2 SD below average, it was still the case that only a minority of affected children (39%) had beenidentified clinically. This result suggests that the features thatlead to a child being identified as having an SLI are differentfrom those that are picked up by standardized tests (Bishopet al., 2005). In general, teachers and parents will notice a child whose speech is unclear or whose language structure is so immature as to sound ungrammatical, but poor verbal

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memory, limited understanding, weak vocabulary and lack ofcomplex grammar are easier to miss.

As with many other neurodevelopmental disorders, moremales than females are affected with SLI, although the malepreponderance was far less in the epidemiological study ofTomblin et al. (1997), who reported 1.33:1 boys to girls, thanin samples recruited from clinical sources (e.g., Robinson, 1991,reported a ratio of 3.8:1). There is no evidence that differentgenetic influences are implicated in causing language impair-ment in males and females; a comparison of same-sex and opposite-sex twin pairs found similar magnitude of genetic and environmental influences in both sexes (Viding et al., 2004).

As Tomblin et al. (1997) pointed out, there is an intrinsicdifficulty in attempting to compare prevalence in different racialgroups, because even if the core language is the same acrossraces, there are likely to be cultural differences in languageuse that will lead to biased test results. Campbell et al. (1997)suggested such bias could be eliminated by avoiding languagetests that were affected by prior knowledge or experience, butwe are not aware of any epidemiological studies that used suchmeasures to compare different rates of SLI in different racesor cultures.

Correlates of SLIAlthough SLI is “specific” in so far as the language disorderis not accompanied by low non-verbal ability, there are frequently accompanying impairments in other aspects offunctioning. Literacy problems are found in most but not allchildren with SLI; the question of what characterizes those children who learn to read and write despite SLI is intriguingbut as yet not fully understood; however, poor phonologicalprocessing appears a key factor (Bishop & Snowling, 2004;Catts, Adlof, Hogan, & Ellis Weismer, 2005), Another fre-quent accompaniment to SLI is motor impairment, which may not be evident in everyday interactions, but becomes soon formal testing (Hill, 2001; Webster, Majnemer, Platt, &Shevell, 2005).

Comorbidity with Psychiatric DisorderEarly research by Cantwell and Baker (1991) demonstrated a high rate of psychiatric disorder, including but not limitedto ADHD, in children referred for speech and language dis-orders. In one of the few epidemiological studies to addressthis issue, the Ottowa Longitudinal Study, it was found thatlanguage impairment in 5-year-olds was one of the strongestpredictors of psychiatric outcome at 12 years of age, even aftermeasures of social background were taken into account (forreview see Beitchman, Brownlie, & Wilson, 1996). In this study,ADHD and emotional disorders were the most common psychiatric diagnoses. A series of studies by Cohen et al. alsodemonstrated the converse. Of children referred for psychi-atric assessment solely for socioemotional disturbances, 33%were found to have previously undiagnosed language impair-ment. When combined with those whose language impairmentshad already been identified, some 50% of school-aged children

referred to out-patient mental health clinics had clinicallysignificant language impairments (for review see Cohen, 2001).

Such co-occurrences raise a host of questions about causa-tion. An obvious possibility is that inability to express onesneeds and ideas leads to a sense of frustration and impotence,and subsequent acting-out behavior. However, if this were theprincipal route to psychiatric disorder, we would expect thegreatest evidence of psychopathology to be seen in childrenwith expressive difficulties, whereas most studies find re-ceptive language difficulties pose substantially greater risk.Failure to comprehend language can lead to inappropriate accusations in the classroom of laziness, willfulness or inat-tention, and it will also limit the opportunities to form closerelationships that would normally exert a protective effect.Redmond and Rice (1998) contrasted this latter type of“social adaptation” account with a “social deviance” modelthat regards both behavior and language problems as indicators of an underlying trait of disturbed psychosocial development. They argued that parent and teacher ratings of socioemotional status in children with SLI showed little congruence or temporal stability, supporting the idea that beha-vioral problems were consequences of specific communicativeexperiences rather than reflecting intrinsic deficits in thechild. However, rates of behavior disorder were relatively lowin their sample, and the possibility remains that more severelyaffected children have socioemotional deficits that go beyondwhat could be reasonably regarded as adaptations to poor com-munication (see also Bishop, 2000).

Another route from language impairment to psychiatricdisorder is through the experience of school failure. BothBeitchman et al. (1996) and Tomblin, Zhang, Buckwalter, andCatts (2000) found that the risk of psychiatric disorder wassubstantially raised in those children whose language impair-ment was accompanied by reading disability, and was muchlower in those who were experiencing academic success. Inboth these studies, this association was less evident when thesame children’s behavior problems were assessed before theylearned to read; this suggests that it is experience of schoolfailure that exacerbates psychiatric risk.

One further mechanism whereby language could affect psychiatric status is through its role in inner speech and self-regulation. Language is a tool for thought as well as a meansof communication, and it affects how we structure our experi-ences, plan for the future and reflect on the past. A child withlimited language understanding is anchored more firmly in thehere and now, and may find it hard to delay gratification, thinkthrough another person’s motivations or appreciate chains ofcausality. In the case of autistic disorder, verbal ability isstrongly linked to the development of understanding of otherminds, thought to mediate social understanding and inter-action (Happé, 1995) and those children with significantly lower verbal ability in relation to non-verbal ability demon-strate the most severe deficits in social interaction (Joseph,Tager-Flusberg, & Lord, 2002).

We need more research relating specific aspects of languageskill to cognitive processes and behavioral outcomes in SLI to

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evaluate the plausibility of different causal pathways to dis-order, compared with other accounts such as one that wouldregard language impairment and psychiatric disorder as independent consequences of some third factor such as poorparenting or social disadvantage. In addition, we need researchon how best to help children whose psychiatric problems areassociated with language difficulties. The role of language in thinking has implications for intervention: some childrenhave language problems that could make it difficult to use methods such as cognitive–behavioral therapy. For instance,if the child does not understand what is meant by “if . . . then”,and has difficulty thinking about events beyond the here andnow, then it may be counterproductive to try to train socialproblem-solving approaches that involve thinking about solu-tions to hypothetical situations.

Genetic FactorsTwin studies have converged in finding that SLI is a highlyheritable disorder (for review see Bishop, 2001). In 1990, excite-ment was generated by the discovery of a three-generation family, the K.E. family, in which a speech and language dis-order appeared to be inherited in an autosomal dominant fashion. The earliest account of this family focused on theirverbal dyspraxia (Hurst et al., 1990), but subsequent reportshave drawn attention to coexisting problems with broader oral language skills (Watkins, Dronkers, & Vargha-Khadem,2002). The mutation responsible for the disorder has since been identified as affecting the function of a transcription factor, the FOXP2 gene, which influences development of brain as well as other organs (for an overview see Fisher, 2005).Although other cases of speech and language impairmentlinked to FOXP2 have been reported (Feuk et al., 2006;Macdermot et al., 2005), it is evident that this is a rare muta-tion that cannot account for the majority of cases of SLI.Although it is possible that other single major genes may beinvolved in the etiology of some cases of SLI (Bishop, 2005),it is likely that for many children the etiology will involve the combined influence of several genes and environmental factors, each of small effect.

Research on the genetics of SLI is moving ahead on threefronts. First, there are molecular studies that have madeprogress in identifying linkages to sites on chromosomes 3,16 and 19 (Newbury & Monaco, in preparation). Second, there are behavioral genetic studies that attempt to refine thephenotype of heritable SLI. In general, these suggest that wewill make better progress in molecular genetic studies if we abandon the conventional clinical criteria for SLI and move instead to define the phenotype in terms of measures ofunderlying cognitive and linguistic processes (Bishop, 2006).One important clinical message to emerge from genetic stud-ies is that genes can increase a child’s risk of SLI, but they donot act in a deterministic fashion. Whether or not a geneticrisk is manifest as a language disorder may depend on envir-onmental factors (Bishop, 2001). Finally, there is a recogni-tion that we need to move away from focusing on individualneurodevelopmental disorders, to consider whether there are

genetic risks for SLI that also affect related conditions suchas developmental dyslexia or autistic disorder. In the case of dyslexia, it is clear that there are some genetic variants that increase the risk for both SLI and reading problems but,nevertheless, there is little overlap in the sites of significantlinkage found in whole-genome scans for these two conditions(Fisher, 2006). There has been considerable interest in the ideathat a common genetic locus might be found that increasesthe risk for both SLI and autism (Folstein & Mankoski,2000), but this has yet to be validated, and behavioral studiessuggest that phenotypic similarities between the two disordersmay be only superficial (Bishop et al., 2004; Whitehouse, Barry,& Bishop, 2007).

Environmental FactorsThere is little evidence that environmental factors alone are sufficient to cause the selective deficits in grammar andphonology that characterize SLI. However, environmentalfactors may be implicated in early language delay and can havea role in mediating the developmental course of language dis-orders and the impact of language impairment on the child’swell-being.

Family socioeconomic status (SES) has long been associatedwith child language development; with children from lowerSES environments experiencing protracted rates of languagedevelopment in relation to peers from more affluent homes.It is suggested that the relationship between SES and languageimpairment is mediated by maternal education, via the quan-tity and quality of mothers’ communicative interactions withtheir children (Hoff & Tian, 2005). However, other studieshave found that SES (as measured by income or maternal education) is not a reliable predictor of long-term languageimpairment (Dale et al., 2003; Paul, 2000). Furthermore,even when SES is implicated in language or literacy impair-ment, one must consider that environments are at least parti-ally genetically influenced (Oliver, Dale, & Plomin, 2005). Inother words, a mother may have a limited educational experi-ence and poor career prospects because of her own languagelimitations. Nevertheless, early language delay in the presenceof low SES should alert the clinician of the need to monitorlinguistic progress carefully.

In a multicultural society, one must establish whether a childis presenting with a language disorder or a language difference.Two questions must be addressed:1 Is the child impaired only in his or her ability to learn theambient language, or are language impairments evident in thechild’s home language as well?2 If the child does have language impairment, does exposureto more than one language exacerbate the child’s language learn-ing difficulties?

Studies of SLI in bilingual language learners are in theirinfancy, and there is a dearth of longitudinal data with whichto answer these important questions. For some languages, suchas Spanish in the USA, there now exists a range of culturallyappropriate, well-standardized assessments with which to assessbilingual children, but the situation is far less satisfactory for

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many other language communities. It is not safe to assumethat a straightforward translation of an English test into thechild’s home language will provide an accurate picture of thechild’s language ability. In these instances, it will be importantto obtain a picture of the child’s communicative competencefrom the primary caregiver. It may be particularly beneficialto ascertain whether the caregiver is concerned about the child’scommunication and how this child’s development compareswith other children in the family or community.

The limited research available suggests that experience withtwo or more languages does not cause or compound SLI(Paradis, Crago, Genesee, & Rice, 2003). Thus, most speech-language clinicians recommend that families continue to pro-vide rich input in the child’s home language and that, wherepossible, intervention should target both languages. However,there is a no systematic research comparing monolingual vs.bilingual therapy in such cases, and it could be argued thatthe child with SLI may be particularly handicapped by the chal-lenge of mastering two or more languages simultaneously, Onerecent study by Cheuk, Wong, and Leung (2005) endorsed thisview, but focused on preschool children; thus, it is likely thatmany would achieve normal language outcomes. Longitudinalstudies of bilingual children with SLI are clearly needed.

NeurobiologyMost children with SLI show no gross abnormalities of thebrain on structural imaging. More fine-grained analyses haverevealed evidence for four kinds of developmental brainanomaly associated with SLI:1 Abnormalities in the organization of different kinds of braincell (ectopias and microgyri; Galaburda, Sherman, Rosen,Aboitiz, & Geschwind, 1985);2 Additional gyri in frontal or temporal regions (Clark &Plante, 1998; Plante & Jackson, 1997);3 Unusual proportions of different brain regions (Herbert et al., 2003; Jernigan, Hesselink, Sowell, & Tallal, 1991;Leonard et al., 2002);4 Anomalous cerebral lateralization (De Fossé et al., 2004;Gauger, Lombardino, & Leonard, 1997; Herbert et al., 2003).However, the field is plagued by inconsistent findings: forinstance, whereas SLI was associated with small cerebral volume in studies by Jernigan et al. (1991) and Leonard et al.(2002), it was associated with large cerebral volume in the study by Herbert et al. (2003). Leonard (1997) noted that such associations as are found are weak and probabilistic, andabnormalities that are more frequent in SLI than in typicallydeveloping children may also be seen in other disorders. Inher own research, she has had some success in showing clearerrelationships between disorder and brain anomaly by distin-guishing between cases with language comprehension impair-ments and those with more restricted phonological deficits(Leonard et al., 2002, 2006).

Overall, the picture from structural brain imaging has beenconfusing and contradictory. The one thing we can concludeis that such anomalies as are found in SLI appear to arise earlyin neurodevelopment, rather than being brought about by early

acquired lesions. This fits with the view of SLI as a disorderin which genetic influences lead to a brain that is wired up ina non-optimal fashion. From a clinical perspective, it is unlikelythat brain imaging will provide information of diagnostic orprognostic utility in a child with SLI (Shevell et al., 2000).

Few functional imaging studies have been conducted withSLI, and those that have been performed are difficult to inter-pret. Thus, if one shows underactivation of regions implicatedin language processing, it is unclear if this is cause or con-sequence of the language disorder. Functional imaging can nevertheless be useful in providing evidence for unusual local-ization of specific functions (e.g., studies of the affected members of the K.E. family have shown that when they per-form a verb generation task they have diffuse bilateral brainactivation), in contrast to unaffected individuals who show more focal activation of traditional language regions in theleft hemisphere (Vargha-Khadem, Gadian, Copp, & Mishkin,2005).

Electrophysiological methods have been used to study brain–behavior relationships in children with SLI, but results are characterized by the same level of inconsistency as is seen inthe structural imaging studies (see chapter 15; Bishop &McArthur, 2005; Bishop, under review). Furthermore, researchin this field is handicapped by a lack of normative data ontypically developing children.

Cognitive FactorsTheoretical accounts of SLI have traditionally attempted toexplain the disproportionate difficulties with grammar that characterize the disorder. Many of these theories are groundedin a linguistic tradition and propose that SLI results from adelay or disruption of the development of a specialized brainsystem that serves grammatical computations (Rice, 2004; vander Lely, 2005). Tasks tapping grammatical marking of tenseand agreement, as well as comprehension of complex gram-matical relations, discriminate children with SLI and typicallydeveloping peers (Conti-Ramsden, 2003) and poor performanceon grammatical tasks has been put forward as a behavioralmarker of heritable forms of SLI (Rice, 2004).

However, a number of researchers have criticized thenotion of an innate modular language faculty and suggest thatspecialized language function is the developmental outcomeof a number of domain-general endowments acting in concert(Bates, 2004). Children with SLI are impaired not only on grammatical tasks, but also on measures of phonological short-term memory. These tasks require children to repeat stringsof unfamiliar speech sounds (e.g., “blonterstaping”), an abilitythat is seen to facilitate the learning of new words (Baddeley,Gathercole, & Papagno, 1998). Attention has also been focusedon the abilities of children with SLI to process rapid brief auditory signals (Tallal, 2000); an ability that is argued tounderpin the recognition and learning of grammatical contrastsin English (Joanisse & Seidenberg, 2003).

A recent study confirmed that deficits in nonsense word repetition, like deficits in grammatical inflection, are highly heritable and sensitive markers of SLI (Bishop, Adams, &

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Norbury, 2006a). Intriguingly, there appeared to be little etio-logical overlap between the two deficits, indicating that dif-ferent risk genes may be involved in these different aspects of language difficulty. However, auditory processing deficitsshowed no genetic influence (Bishop et al., 1999) and cannotfully account for the linguistic deficits seen in SLI (Norbury,Bishop, & Briscoe, 2001; van der Lely, Rosen & Adlard, 2004).Thus, auditory impairment may be seen as an environment-ally based risk factor that comes into play in those childrenat genetic risk of the disorder.

The conclusions that we draw from theoretical studies of SLI are that there is unlikely to be a single cognitive or bio-logical factor that can cause the variety of language profilescaptured by a diagnosis of SLI. Instead, multiple risk factorsin the child’s genetic and biological make-up are likely to inter-act with factors in the child’s environment to determine theseverity and course of language impairment (Bishop, 2006).

Intervention and Prognosis for Specific Language ImpairmentIntervention is usually determined by speech and language therapists, who use a wide range of techniques to stimulatelanguage learning. In preschool, intervention may involveworking with parents and caregivers to provide optimal lan-guage input for the child. Such approaches often involvevideotaping parent–child interactions and using these videosconstructively to foster better communication techniques (e.g.,The Hanen program; Girolametto & Weitzman, 2006; seewww.hanen.org for details). The advice given focuses on following the child’s lead in play, talking about what the child is doing rather than asking questions, recasting what thechild says in a grammatically correct form, and increasing com-munication opportunities by giving children choices rather thananticipating their needs.

In a meta-analysis of intervention, Law et al. (2004) foundthat treatment for preschool children with expressive languagedelays was successful when compared with no treatment, andtreatments lasting longer than 8 weeks produced the most favor-able outcomes. Parent-led interventions were as successful as direct intervention by a speech-language therapist in devel-oping young children’s language; such interventions are cost-effective and encourage generalization of language gains intoeveryday environments. With such methods, speech-languagetherapists are instrumental in identifying communicative targets for parents to work on, and supporting parents through-out the intervention program. Nevertheless, as noted by Nelson,Nygren, Walker, and Panoscha (2006), there is a dearth ofgood-quality research on long-term efficacy of interventionsfor preschool children, a problem that is compounded by thefact that existing studies are small and heterogeneous.

There is even less research on intervention for children with receptive language difficulties or school-aged children. In general, randomized controlled studies are rare and studies that explicitly compare different treatment approaches for the same language problem simply do not exist. The field isplagued with studies in which the participant numbers are small,

the interventions poorly described and methodological prob-lems abound. The studies outlined below are pilot studies in nature, but offer promise for larger scale investigations oftreatment efficacy.

Ebbels (2007) reported preliminary data for a school-basedintervention that focuses on grammar. This intervention usesvisual cues such as shapes and colors to teach children withlanguage impairment different parts of speech, and how these parts of speech may combine in different grammaticalconstructions. By situating the intervention in a school setting,classroom materials can be used in therapy to promote gener-alization. Other approaches advocate developing the child’slinguistic repertoire in more even more naturalistic settings.Fey, Long, and Finestack (2003) presented 10 principles for facilitating grammar development. Although the authorsrecognize the need to teach specific grammatical forms, theyargue that these forms should rarely be taught in isolation.Instead, the targeted forms should be embedded in natural contexts such as play or story-telling. The role of the ther-apist in this approach is to manipulate the environment so that the targeted form is salient and frequently occurring, pro-viding ample opportunity for modeling and shaping the child’sproduction.

Adams (2005) reported a series of case studies detailing treatment for children with pragmatic language impairments.Standardized assessments often lack the sensitivity to detectsubtle improvements in social communication and interaction,but using detailed conversational analysis, Adams was able todemonstrate improvement in discourse functioning in school-aged children. These studies lacked a suitable control groupnecessary to evaluate specific treatment effects, but holdpromise for larger scale studies with school-aged populationswith pragmatic deficits.

A radically different approach to treatment was developedby Tallal et al. (1996), who devised a computer-based inter-vention, FastForWord, which involves prolonged and intens-ive training on specific components of language and auditoryprocessing. The advantage of computerized presentation is that children may be persuaded to participate in thousands oftraining trials in a way that would not be possible in stand-ard therapist-based interventions. Unfortunately, after initiallypromising results using the FastForWord program (Merzenichet al., 1996), randomized controlled studies have failed todemonstrate a significant advantage of this approach over other methods in improving children’s language or literacy skills (Cohen et al., 2005; Pokorni, Worthington, & Jamison,2004; Rouse & Krueger, 2004). Children in these studies hadreceptive as well as expressive language impairments, whichappear particularly resistant to treatment (Law et al., 2004).

The limited intervention studies available suggest that thereis no cure for SLI. Despite years of intensive specialist training,many children will continue to have language deficits. However,one should bear in mind the broader aims of therapeutic inter-vention for SLI. One cannot “cure” a sensorineural hearingloss or a physical impairment; in these instances interven-tion will seek to maximize potential and lessen the impact of

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the child’s impairment on his or her social well-being and educational experiences.

In the absence of a “quick-fix,” many children with SLI willpresent with long-term special educational needs. There is alack of consensus on the most suitable type of provision forchildren with SLI. Some children will benefit from a specialschool or language unit placement where there is access to re-gular speech and language therapy and where the curriculummay be supported by using signed English or a visual symbolsystem. Others will benefit from a mainstream placement.Unfortunately, specialist support for children within mainstreamsettings is limited and almost non-existent by secondaryschool (Lindsay, Dockrell, Mackie, & Letchford, 2005).

A number of longitudinal studies have shed light on the developmental course of SLI. There is general agreement thatthe child with severely impaired understanding of language has a poor prognosis, even if the diagnosis is made early.Comprehension problems do not resolve spontaneously and,as they grow older, children with such problems experienceincreasing difficulties with social cognition and interaction(Clegg, Hollis, Mawhood, & Rutter, 2005; Howlin, Mawhood,& Rutter, 2000), non-verbal reasoning (Botting, 2005; Stothardet al., 1998) and an increased risk of psychiatric disturbance(Howlin et al., 2000; Snowling, Bishop, Chipchase, & Kaplan,2006).

For children with normal non-verbal abilities and expressivelanguage impairments, the outlook is much more positive, particularly if expressive deficits have resolved by schoolentry (Stothard et al., 1998). However, there is evidence thatliteracy skills may remain an area of weakness for these chil-dren (Botting, Simkin, & Conti-Ramsden, 2006; Rescorla,2005); although these “resolved” cases may score within thenormal range on standardized assessment, their scores are frequently lower than an IQ-matched peer group.

Conclusions

This chapter has considered various factors designed to facil-itate clinical decision-making in this complex and difficult area.It is important to realize that cases of “pure” SLI are rare inclinical practice. Rather, children present with a range of co-occurring deficits and challenges that may cloud diagnostic decisions. The most important message for clinicians toremember is that speech, language and communication skillsare critical to the cognitive and social development of chil-dren, whatever their primary diagnosis. Thus, attention to theseaspects of development is fundamental for children present-ing to psychiatric clinics.

Further ReadingBeitchman, J. H., Cohen, N. J., Konstantareas, M. M., & Tannock,

R. (Eds.). (1996). Language, learning, and behavior disorders.Cambridge: Cambridge University Press.

Bishop, D. V. M. (1997). Uncommon understanding: Develop-ment and disorders of language comprehension in children. Hove:Psychology Press.

McCauley, R. J., & Fey, M. E. (Eds.). (2006). Treatment of languagedisorders in children. Baltimore: Paul H. Brookes. [Includes exampleson DVD.]

Paul, R. (2006). Language disorders from infancy through adolescence:Assessment and intervention (3rd edn.). St. Louis: Mosby-Year Book.

ReferencesAdams, C. (2005). Pragmatic language impairment: case studies of

social and pragmatic language therapy. Child Language Teachingand Therapy, 21, 227–250.

Adams, C., Cooke, R., Crutchley, A., Hesketh, A., & Reeves, D. (2001).Assessment of comprehension and expression (6–11). Windsor:NFER-Nelson.

Adams, C., Green, J., Gilchrist, A., & Cox, A. (2002). Conversa-tional behaviour of children with Asperger syndrome and conductdisorder. Journal of Child Psychology and Psychiatry, 43, 679–690.

American Psychiatric Association. (1994). Diagnostic and statisticalmanual of mental disorders (4th edn.). Washington, D.C.: AmericanPsychiatric Association.

American Psychiatric Association. (2000). Diagnostic and statisticalmanual of mental disorders (4th edn.) Text revision. Washington,D.C.: American Psychiatric Association.

Baddeley, A., Gathercole, S., & Papagno, C. (1998). The phonolog-ical loop as a language learning device. Psychological Review, 105,158–173.

Baird, G., Simonoff, E., Pickles, A., Chandler, S., Loucas, T.,Meldrum, D., et al. (2006). Prevalence of disorders of the autismspectrum in a population cohort of children in South Thames: TheSpecial Needs and Autism Project (SNAP). Lancet, 368, 210–215.

Bates, E. A. (2004). Commentary: Explaining and interpreting deficitsin language development across clinical groups: Where do we gofrom here? Brain and Language, 88, 248–253.

Beitchman, J. H., Brownlie, E. B., & Wilson, B. (1996). Linguisticimpairment and psychiatric disorder: Pathways to outcome. In J. Beitchman, N. J. Cohen, M. M. Konstantareas, & R. Tannock(Eds.) Language, learning and behavior disorders: Developmental,biological and clinical cerspectives (pp. 493–514). New York:Cambridge University Press.

Bird, J., Bishop, D. V. M., & Freeman, N. (1995). Phonological awareness and literacy development in children with expressivephonological impairments. Journal of Speech and Hearing Research,38, 446–462.

Bishop, D. V. M. (1994). Is specific language impairment a valid diagnostic category? Genetic and psycholinguistic evidence. Philo-sophical Transactions of the Royal Society, Series B, 346, 105–111.

Bishop, D. V. M. (2000). Pragmatic language impairment: A cor-relate of SLI, a distinct subgroup, or part of the autistic continuum?In D. V. M. Bishop, & L. B. Leonard (Eds.) Speech and languageimpairments in children: Causes, characteristics, intervention andoutcome (pp. 99–114). Hove: Psychology Press.

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Bishop, D. V. M., Price, T. S., Dale, P. S., & Plomin, R. (2003).Outcomes of early language delay. II. Etiology of transient and per-sistent language delay. Journal of Speech, Language and HearingResearch, 46, 561–575.

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