9.3.2.1 The Crying Stage (Differentiating Cries, Reflexive Vocalization; Birth to 6 Weeks)

Cries and vegetative noises are an involuntary and biologically rooted behaviour. A newborn reflexively cries owing to hunger, pain, etc. Subsequently, crying develops to be the first form of communication (crying for attention, a need or comfort). Beginning from the fourth (fifth) week on, one can distinguish between various pleasant and unpleasant cries (indicating hunger, boredom, pain, etc.), the so-called ‘modulated cry’. The sound characteristics and voice onsets differ according to the baby’s intention of crying, and the caregivers can often interpret the intended message. The baby notices that a cry can bring food, comfort or companionship, i.e. the baby learns the basic rule of communication. Newborns also begin to recognize important sounds in their environment (e.g. the voice of their mother). By 6 months of age, most basic sounds of the native language can be recognized.

9.3.2.2 The Cooing Stage (Syn.: First Babbling Stage, Cooing and Laughter; 6–8 Weeks)

At the beginning of the second month, at the same time of the first smile, the baby starts to play with its articulatory organs. He or she produces cooing sounds not only reflexively. These ‘first vocalizations of contentedness’ are predominantly elongated vowels (‘oooo’, ‘aaaa’) and are vocal responses to the speech of others. At the end of this period, simple sequences of consonant-vowels are uttered, by producing pharyngeal, palatal or uvular sounds (Oller et al. 1999). The baby’s cooing contains the basic sounds of all languages, not just those of the baby’s mother language.

It has to be pointed out that even deaf babies coo. Their language development becomes deviant from normality at later ages.

9.3.2.3 The Babbling Stage (Syn.: Second Babbling Stage; 4–12 Months)

Like cooing, babbling provides a social reward. Babies experiment with speech sounds resulting in pitch and volume variation. Babbling infants do not articulate all the speech sounds they hear in the adult language. On the other hand, babies produce sounds that they have never heard before. Canonical babbling describes the formation of syllables consisting of consonants and vocals (e.g. ‘ba’). At the age of 6 months, the baby’s babbling can be attributed to the native language (Boysson-Bardies et al. 1984). A lacking verbal interaction at this age usually results in a later developmental disorder of speech, language and communication. The babbling consists of a wide variety of sounds and is defined as the combination of consonants and vowels in alternating sequences. Reduplicative babbling is characterized by the production of reduplicated syllables such as ‘bababa’. Variegated babbling brings about more complex syllables or two-syllable utterances or multiple syllables with constant vocals and consonants and different intonation (Harley 2001; Nathani et al. 2006; Werker and Tees 1999). The vocalizations now take a more speech-like quality. Babbling means motor exercise and communicative function at the same time. Around 8 to 9 months, the baby starts to imitate sounds of the environment. For successful imitation, normal hearing (acoustic perception and differentiation) and normal motor skills are necessary.

9.3.2.4 First Word Understanding (9 Months)

At about 8–9 months, the baby turns and looks in the direction of sounds and listens when he or she is spoken to. The baby further pays attention to prosody and intonation or mimics the expression of parents and other persons and tries to imitate adult speech sounds. The baby understands its first words at about 9 months of age, learns about the relation between object and language, recognizes words for common items such as ‘cup’ or ‘shoe’ and begins to respond to requests (e.g. ‘come here’) (Grimm 2003; Bates et al. 1994). This is preparation for the production of the first word (10–12 months). An important precursor in the preverbal development of a child is the joint attention or shared attention. This happens when one individual alerts another (usually parent and child) to an object to bring it to his or her attention using eye gaze (Moore and Dunham 1995; Zollinger 2015 (‘triangulation’)), pointing or non-verbal or verbal indications. Both the child and the caregiver direct their attention to an object of shared interest, and both are aware of the other persons perceiving that object and showing interest in it as well.

9.3.2.5 The First Word (10–13, at the Latest 20 Months)

The preverbal phase ends with the production of the first words, starting with proto-words (word-like utterances) around the age of 10 months (see Sect. 11.​3). First words are mainly nouns and refer to people of particular interest (‘mama’, ‘dada’) or objects that move (‘ball’, ‘cat’). Verbs, adjectives, adverbs and prepositions are learned later, usually in that order. In the second year, babbled utterances and meaningful words appear side by side. Later on, linguistic expressions increase and babbling utterances decrease (Nathani et al. 2006).

Current theories and studies about phonological acquisition challenge Jakobson (1941, 1969) theory of children’s speech, which states that universal contrasts are learned first in all languages (‘mama’, ‘papa’, the so-called phonological universals). Among others, Fox-Boyer and Dodd (1999), Weinrich and Zehner (2003) and Fox-Boyer (2016) have summarized modern knowledge in this field. The order of acquisition starts with vocals, followed by plosives, nasals, fricatives and affricates. Topographically front consonants precede back consonants; the /p/ and /m/ sounds appear before /k/ or /h/. Single consonants are realized before multiple consonants. A child first learns to articulate fricatives at the end of a word and plosives at the word’s beginning. The production passes through a learning process and is not completely correct from the beginning.

9.3.3.1 One-Word Sentences (Holophrastic Stage, 12–18 Months)

The stage of one-word utterances (one-word sentences) begins at about 1 year of age. One-word sentences differ from babbling vocalizations by their symbolic meaning (development of the symbol function of language). One-word utterances are also called holophrases because the toddler expresses the meaning of an entire situation by just a single word (Rupp 2013). This stage of language development interacts with cognitive development, as well as with the development of deixis and gesture. (Deixis describes the fact that words or phrases may require contextual information to convey any meaning, e.g. English pronouns, i.e. their semantic meaning is fixed, but their denotational meaning varies depending on time or place or other factors.) Eventually, one-word utterances turn into longer expressions, i.e. two-word utterances.

The toddler realizes that the acoustic string (word) and the reference (object) belong together (naming insight). Holophrases do not only name objects or persons. There is enormous ambiguity in a child’s holophrases. If, for example, a toddler says ‘papa’, he or she may not mean ‘father’ exclusively but also the coat of the father or asking whether the father will come, etc. The child may declare, demand, describe or question. In conjunction with prosody, mimicry and gestures, the meaning of holophrases can be varied. Owing to the social and situational context, adults can interpret the utterances. According to the noun-bias hypothesis (Gentner 1981, 1982; Nelson et al. 1993), nouns are acquired first and make up the greatest part of the lexicon compared with other word types. In contrast, it has been observed that holophrases also comprise verbs, adjectives, relational and social-pragmatic words (Rothweiler and Kauschke 2007; Rothweiler and Meibauer 1999, Meibauer 1999). Words are frequently under-extended or overextended to inappropriate categories, e.g. all four-legged hairy creatures may be called ‘dog’. At the age of 3 years, children have acquired a balanced and targeted lexicon composition (Pomnitz and Rupp 2013).

At least for English and German languages, the majority of 16- (de Langen-Müller et al. 2011, 2012, 2016) to 18- (Menyuk et al. 1995) month-old toddlers have an active lexicon of about 50 words. The receptive lexicon precedes the active one (Rothweiler and Kauschke 2007): by 13.5 months, toddlers have a receptive lexicon of about 50 words (Menyuk et al. 1995) and by 16 months already 100 words. The phase of the first 50 words starts with the first referentially used words and ends up with the beginning of the naming explosion at the age of 18 months (Kauschke 1999, Kauschke and Hofmeister 2002, Rothweiler and Kauschke 2007).

9.3.3.2 Two-Word Sentences (Telegraphic Stage, 18–24 Months)

In this period, the toddler starts to combine two words and to utter basic sentences such as ‘mummy bag’; the meaning may be, e.g. ‘Mummy, give me the bag’, ‘Mummy, where is the bag?’ or ‘This is Mummy’s bag!’ As in the previous stage, there is an enormous ambiguity in these two-word utterances. The kinds of word that are likely to be omitted are articles, prepositions, pronouns and auxiliary verbs. A toddler talking to him- or herself during this stage avoids pronouns (‘baby go’ instead of ‘I go’) and is able to understand simple instructions and questions.

At the age around 18 months, together with the combination of two words, the child’s vocabulary begins to grow fast (Nelson 1973): this naming explosion or ‘word spurt’ represents a developmental milestone. Children usually add 10 words per day (Clark 2003). By 18 (not later than 24) months, the children utter on average at least 50 words (Menyuk et al. 1995), at the age of 24 months about 200, at the age of 30 months 500 and at school entry 3000–5000 (Clark 2003; Rupp 2013). Interindividual differences must be considered.

Approximately 13–20% of children (Ellis Weismer 2007) are so-called late talkers (Grimm 2003; Desmarais et al. 2008). These are defined as having an expressive vocabulary of fewer than 50 words or as lacking combinations of words at the age of 24 months. They are at risk of developing a speech-language developmental disorder. Thirty-five to fifty percent of late talkers turn out to become ‘late bloomers’, who catch up during the following year (until 36 months of age), whereas others end up with a specific developmental disorder of speech and language (Grimm 2003; Kauschke 2006; Schöler et al. 2007; Kühn and von Suchodoletz 2009; Sachse and von Suchodoletz 2013).

Typical deviant phonological processes (physiological speech sound deviations during speech-language development that show a specific error pattern at the age of 24–30 months) comprise, e.g. assimilations, omission of unstressed syllables, a reduction of initial consonants, backwarded articulation or deaffrication (see Sect. 11.​3).

The acquisition of lexicon and grammar is mutually dependent. Many theories have been established and discarded, such as the theory of Universal Grammar by Chomsky. Nowadays a use-based approach is favoured. It is discussed whether innate (modular, nativistic) or epigenetic (recognition of regularities) factors are more important (Szagun 2013; Pinker 1991, 1994). Pinker states that a child is prepared for grammar acquisition as a spider is for web construction. The so-called semantic bootstrapping (Pinker 1984) enables children to discover syntactic rules.

A child aged 4 years can speak grammatically correct language, but grammar acquisition is not completely finished. For instance, passive sentences can only be built by 9–10 years.

9.3.3.3 Multiple-Word Sentences (25–36 Months)

With increasing age and larger vocabulary, children form longer and more complex sentences and start to use conjunctions. More complex grammar structures will be acquired: more-word sentences, negations, imperatives, questions and compound sentences. The first combinations are made with matrix sentences (‘Peter falling’, ‘Peter cries’, ‘Mummy runs’). Further on, the sentences are still telegraphic although they may be quite long. Until the end of the third year, the child learns to form flexions, plurals and past forms and to use auxiliary verbs.

9.3.3.4 More Complex Sentences (37–60 Months)

From the third birthday on, development towards an adultlike grammar continues. Auxiliary verbs are being ordered correctly in questions and negatives. Grammatical markers emerge including possessive words or phrases, determiners (i.e. a word, phrase or affix that occurs together with a noun and serves to express the reference of that noun in the context) and irregular past tense verbs. A variety of early complex sentence types emerge including compound sentences, full prepositional clauses in sentences and simple infinitives. At the end of this period, later-developing morphemes are acquired.

At the age of 4, children are able to talk adequately: articulately, grammatically and semantically. They are able to use communicative language appropriately.

9.3.3.5 Perfecting (‘The Intuitive Linguistic Period’, 4–14 Years)

Although most of the language has been acquired in the period up to age 4–5 years, there are still many linguistic skills to be obtained. In the so-called intuitive linguistic period (Matthews 1996), larger words, a differentiated mental lexicon and longer and more complex sentences are used. There is also a further syntactic development after 4 years of age; for example, the child begins to understand passive sentences.

In this period of linguistic refinement, written language is acquired, and subsequently more sophisticated spoken and written texts are produced. Children develop further metalinguistic awareness (in the four subareas: phonological, word, syntactic and pragmatic awareness (Tunmer and Bowey 1984)) and competence. They reflect consciously upon the nature and properties of language (van Kleek 1982) and are able to talk about, analyse and think about language independent of the concrete meaning of each word. Metalingustic skills are strongly associated with reading comprehension and have also great impact on academic performance (e.g. understanding multiple meanings of words, use of irony and metaphors).

9.6.2.1 Prevalence of Specific Developmental Disorders of Speech and Language

Specific developmental disorders of speech and language (SDDSL), also named primary developmental language disorders or specific language impairment, for which thorough diagnostics do not identify language-relevant comorbidities or conditions, represent a subset of DDSL. Their prevalence is given for the North American language area, according to the criteria of the ICD-10 or the DSM-5, to be from 5 to 8% (American Psychiatric Association 2013; Tomblin et al. 1997). For European countries, similar numbers have to be expected (Neumann et al. 2009). For SDDSL the gender distribution is reported between 1.3 and 5.9 boys to 1 girl (National Institute on Deafness and Other Communication Disorders 2008; Shriberg et al. 1999; Stromswold 1998; Tallal et al. 2001; Tomblin et al. 1997).

The most often cited study on the prevalence of specific language impairment is that of Tomblin et al. (1997), who reported a prevalence of SDDSL of 7.4% for monolingual English-speaking children of kindergarten age. For 6- and 7-year-old children, Law et al. (2000) noted median prevalence estimates of 5.5% and 3.1%, respectively. Differing from that, a higher prevalence of SDDSL has been reported for the region of Victoria in Australia with 17% (Reilly et al. 2010).

9.6.2.2 Developmental Disorders with Language-Relevant Comorbidities

In general, children with language-relevant comorbidities, such as hearing loss, genetic syndromes, intellectual disabilities, multiple handicaps, pervasive developmental disorders, autism, disorders of social functioning with onset specific to childhood and adolescence such as elective mutism or specific developmental disorders of motor functions, suffer from language disorders more frequently than typically developed children. For DDSL associated with such comorbidities, prevalence is not exactly known. According to conservative estimates, the proportion of children with diseases or conditions establishing such comorbidities in the population is given at about 3% for Germany (Kany and Schöler 2007). A considerable proportion of children have to be assumed as being threatened by a DDSL if a comorbidity—for example, a hearing loss—is not timely diagnosed and treated.

In the next subsections, exemplary studies are mentioned that deal with the coincidence of DDSL with some of the above-named comorbidities.

9.8.2.1 Genetic Factors

Genetic factors are recognized as being the main cause of SDDSL (SLI Consortium 2002). The hypothesis of a polygenic-multifactorial inheritance with involvement of a ‘major’ gene and a gender-dependent threshold is favoured (Lewis et al. 1993; Monaco 2007; Newbury et al. 2002). In family aggregation studies (Lahey and Edwards 1995; Tallal et al. 2001; Tomblin 1989) and in twin studies (Bishop et al. 1995; Lewis and Thompson 1992; Tomblin and Buckwalter 1998), a familial clustering of SDDSL has been shown. Several gene loci have been identified by linkage analyses and are applicable to large groups of children with SDDSL. In a study of the SLI consortium (SLI Consortium 2002), linkages between SDDSL and gene loci at 16q and 19q have been found. Bartlett et al. (2002) reported linkages with chromosomal regions 13q and 2p. Neither study showed coherence with the chromosomal region 7q, which has been described for the KE family.

9.8.2.2 Behavioural-Genetic Studies

Behavioural-genetic studies, in particular twin and adoption studies, may quantify how much variance (diversity) in a population related to language competence may be referred to genetic variability and how much to environmental influences. A thorough review and meta-analysis of behavioural-genetic studies including linkage studies (Stromswold 2001) and further studies (Bishop et al. 2006; Hayiou-Thomas 2008) have shown that genetic factors are responsible for a considerable part of the variance in developmental language disabilities but only for a small part of the variance of language competence of subjects with normal language development. Hence, genetic factors are the main reason of the language competence of children with DDSL.

9.8.2.3 Environmental Factors

Environmental factors, in particular social determinants of the language environment, have much less influence on the occurrence of SDDSL, and the influence of the family-specific environment is—except for the extent of the vocabulary—obviously negligible. With caution it may be stated that poor language stimulation by the family, in particular by the mother, is not a primary cause of an SDDSL (Leonard 1987). Sachse and von Suchodoletz (2009) observed in late talkers that, in addition to deficits in speech perception, poor school education of the parents in particular reduced the probability of their children’s catching up the delay by the age of 3 years and predicted an SDDSL. It is unequivocal that institutionalized children, with whom only poor social interaction takes place; twins, who are often on their own; and children from families with many children, in particular those from socially disadvantaged groups, all exhibit developmental language deviations more often than others (Grimm 2003). The parental socio-economic status (income-to-needs ratio, family income) was not an influential factor for the appearance of an SDDSL in several large studies (among others National Institutes of Health). However, maternal sensitivity and depression, and whether the mother was married, have been shown as possibly influential, whereas maternal education has been evaluated controversially (Botting et al. 2001; La Paro et al. 2004; Stanton-Chapman et al. 2002).

9.8.2.4 Neurolinguistic Perspective

From a neurolinguistic perspective, deficient cerebral processing and representation of language may be causal for SDDSL. If mechanisms of language processing do not function effectively, the input cannot be used effectively. Hence, language acquisition runs slower and is more troublesome. Abnormalities causal for an SDDSL may also occur at the cognitive level (weakness of domain-non-specific information processing), the perceptual level (disturbed basal and higher functions of sensory processing, in particular of auditory processing) and the biological level (abnormal development and lateralization of cerebral structures and genetic factors). None of these hypotheses is sufficiently proven empirically so far or fit all children with SDDSL (de Langen-Müller et al. 2012).

Currently, predominantly genetically determined developmental factors are assumed to be causal for SDDSL, possibly with some psychosocial and environmental factors working epigenetically. Therefore, and because the aetiology of SDDSL is only identified for subgroups of children, a causal therapy of SDDSL is not available so far. Hence, the intervention focuses on specific language symptoms, independent of the assumed causality.

9.8.3.1 Developmental Disorders of Speech and Language Associated with Mental Retardation (ICD-10: F70–F79)

The prevalence of intellectual disabilities for European countries ranges from 3 to 7% of the population (for Germany 0.4% with IQ values up to ≤50 and 2.5–2.9% with IQ values >50–70) (Langen 2006; Maulik and Harbour 2010). Causes are genetic factors resulting in brain diseases and—to a lesser degree—acquired cerebral injuries such as alcohol embryopathy. In most cases (up to 75%), the causes for intellectual disabilities remain unidentified. The largest cause of mental retardation (about 15%) is Down syndrome (Bower and Petterson 2001). For most subjects with an intellectual disability, oral communication is disturbed or—less often—impossible.

9.8.3.2 Developmental Disorders of Speech and Language Associated with Hearing Loss or Central Auditory Processing Disorders (ICD-10: H90–H91; F80.20)

Hearing disorders are the most prominent comorbidities of DDSLC. In case of mild hearing loss, language deficits are often counterbalanced by compensatory strategies and speaking does not appear abnormal to other people. For children with severe hearing loss, DDSLCs are common. Their extent and pattern depend on the time of diagnosis and treatment of the hearing loss, the language talent of a child and the familial background (Moeller 2000). With timely and modern hearing intervention and rehabilitation, many children develop normal language abilities (Kiese-Himmel 2003).

Disturbed middle ear ventilation because of age-related anatomical characteristics of the Eustachian tube, a smaller tympanum and frequent infections of the upper airways, otitis media, and blocking of the pharyngeal ostium of the Eustachian tube by secretion or enlarged adenoids are typical conditions at toddler and preschool ages. From the first to the third year of life, about 10–30% of children have been reported to suffer from middle ear effusion with resulting conductive hearing loss; at preschool ages the value is still 10–20% and at school age 5–10% (Fiellau-Nikolajsen 1983; Northern and Downs 2002). A reduced Eustachian tube pressure may also cause a mild conductive hearing loss ranging from 10 to 30 dB; in case of a middle ear effusion, the hearing loss mostly ranges from 20 to 50 dB (Schönweiler 1992).

Specific diseases such as Kartagener syndrome, an autosomal recessive genetic ciliary disorder comprising the triad of sinusitis, situs inversus and bronchiectasis or a primary ciliary dyskinesia (PCD; same symptoms as Kartagener syndrome but without situs inversus) also lead to chronic middle ear effusion. The genetic defect causes, among other conditions, a disturbed action of cilia lining the lower and upper respiratory tract, sinuses, Eustachian tube and middle ear. Congenital or, in the neonatal period, acquired permanent hearing disorders are predominantly associated with sensorineural hearing loss. Their prevalence in Europe ranges from 1 to 3 per 1000 newborns. About 10–30% of permanent hearing loss in children has a late onset or runs progressively. Causes for permanent infant hearing loss are genetic factors, pre-, peri- or postnatal infections such as congenital CMV infection, syndromes, craniofacial malformations and ototoxic impairments, e.g. caused by aminoglycosides.

Because of both the typical recurrent or fluctuating middle ear-caused hearing loss and the occurrence of fluctuating and progressive sensorineural or mixed hearing loss, singular audiograms often do not reflect the conditions for language development well, and repeated measurements may be useful for estimating the hearing profile over a longer period and for the reduction of obtainable audio-verbal learning pattern for a child. Hence, for a middle ear effusion persisting longer than 3 months, draining ear tubes and eventually an adenectomy are recommended (Deutsche Gesellschaft für Phoniatrie und Pädaudiologie 2005).

In a study of 1300 German-speaking preschoolers with DDSL, hearing loss was diagnosed in 48% (Schönweiler 1992). In the age group up to 4 years—the most important period of language development—more than half of the children were hard of hearing. In 95% hearing loss was a mild conductive hearing loss fluctuating about 20 dB. Results of meta-analyses examining the relationship between otitis media with effusion and language development found either low effects (Casby 2001) or no to very small negative associations (Roberts et al. 2004). However, these reviews have been criticized because of systematic errors and do not seem to be generalizable for children with increased risk for a DDSL or language-relevant comorbidities.

Unilateral hearing loss as caused by hereditary factors, malformations, trauma, otosclerosis, disturbed tympanic ventilation, cholesteatoma or infections may also be associated with distorted language development and may affect scholastic skills later on (Lieu 2013).

Central auditory processing difficulties are frequently associated with DDSL (Tallal 1980). An interface between the auditory and language systems is the phonological storage component of the auditory working memory, the phonological loop (Baddeley 1992). It stores and rehearses speech-based information and is necessary for the acquisition of both native and second-language vocabulary. This loop enables a child to keep longer, not yet analyzed language portions in the phonological working memory and is an important predisposition for the production and retrieval of phonemes and the development of vocabulary, syntax, morphology as well as reading and spelling skills. Hence, the acquisition of a lexicon and grammar is closely related to this memory system. Children with DDSL perform significantly worse in the phonological working memory than peers with normal language development (Grimm 2003; Hasselhorn and Werner 2000).

9.8.3.3 Developmental Disorders of Speech and Language Associated with Other Sensory Disorders and Multiple Disabilities

Blindness with or without residual vision (visus ≤2%), with a prevalence of 4–5 per 1000 newborns, is a frequent sensory disorder and may influence language development at the beginning. Its causes are hereditary malformations of the eye and the optic nerve, inflammation and impairment of the immature retina (retinopathia praematorum) or of the visual cortex in preterm babies. Most of the affected children have normal language development. Sometimes, however, the disturbed acquisition of the precursor abilities, such as the absence of referential eye contact, hinders early language development. Nevertheless, the subsequent language acquisition of blind children of normal intelligence resembles that of typically developed children with some minor qualitative deviations. This is interpreted as a result of adaptive compensatory strategies of children and parents (Perez-Pereira and Conti-Ramsden 1999).

For children with multiple disabilities, whether they are of genetic or non-genetic in origin, such as Down or Landau-Kleffner syndromes, the severity of the language impairment depends on the specific combination of physical and intellectual disabilities. The specific aetiology of some exemplary language-relevant syndromes is described in Sect. 9.8.3.6. A large synopsis of language-related syndromes is given in Sect. 9.10.

9.8.3.4 Developmental Disorders of Speech and Language Associated with Pervasive Developmental Disorders (ICD-10: F84)

Pervasive developmental disorders comprise, among others, childhood autism; atypical autism; Rett syndrome; other childhood disintegrative disorders such as dementia infantilis, disintegrative and symbiotic psychoses and Heller syndrome; overactivity disorders associated with mental retardation and stereotyped movements; and Asperger syndrome. They are characterized by qualitative deviations in social interactions and communication patterns and by a restricted, stereotypical, repetitive repertoire of interests and activities. In a study of Schönweiler (1994), 20% of children with language impairment had global developmental retardation.

Rett syndrome (see also Sect. 9.8.3.6) is a seizure syndrome that nearly exclusively affects girls but in combination with the Klinefelter syndrome can affect boys. After the first to second year of life, both cognitive and language abilities are lost (e.g. object permanence) leading to a severe impairment of language and communication.

The causes of autism are not clear up to now. The most probable cause is a pre-, peri- or post-natal brain injury. Anomalies of chromosomes 3, 7 and 15 and the X chromosome are discussed. Five per 10,000 children are affected. The gender proportion is about 4:1 boys/girls (Grimm 2003). About half of the autistic children do not acquire oral language; language development of the other half is strongly delayed and qualitatively aberrant. This does not hold true for children with Asperger syndrome, a mild form of autism that affects ~3.6 per 1000 children aged from 7 to 16 years. Here, language development is nearly undisturbed, although speech may appear formal and pedantic with a peculiar prosody (Ehlers and Gillberg 1993).

For hyperactive disturbances with reduced intelligence and movement stereotypies (ICD-10: F84.4), an ill-defined disorder of uncertain nosological validity, a severe mental retardation (IQ <35) is combined with problems of hyperactivity, attention deficits and stereotypical behaviour. Language impairment is obligatory and contributes to a specific or global developmental retardation.

9.8.3.5 Speech and Language Abnormalities Associated with Disorders of Social Functioning with Onset Specific to Childhood and Adolescence Such as Selective Mutism (ICD-10: F94.0)

Selective mutism is not a speech or language disorder but a communication disorder due to a psychically caused speech arrest. Speech and language abilities are normal in most cases. The communication may run normally or almost normally under specific circumstances (i.e. in a certain group of subjects or with a specific individual). A prevalence of selective mutism from 0.5 to 0.7 per 1000 children at early school age is reported (Schwartz and Shipon-Blum 2005).

9.8.3.6 Developmental Disorders of Speech and Language Associated with Syndromes

Many syndromes (clusters of symptoms, genetically caused in most cases) are associated with DDSLC. Subsequently, some language-relevant syndromes are listed exemplarily with a focus on their aetiology and pathogenesis. For a comprehensive systematic list of language-affecting syndromes with focus on their symptoms, see Sect. 9.10.

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